Pediatric Dentistry (Textbooks in Contemporary Dentistry) 3030780023, 9783030780029

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Textbooks in Contemporary Dentistry

Nikolaos Kotsanos Haim Sarnat Kitae Park   Editors

Pediatric Dentistry

Textbooks in Contemporary Dentistry

This textbook series presents the most recent advances in all fields of dentistry, with the aim of bridging the gap between basic science and clinical practice. It will equip readers with an excellent knowledge of how to provide optimal care reflecting current understanding and utilizing the latest materials and techniques. Each volume is written by internationally respected experts in the field who ensure that information is conveyed in a concise, consistent, and readily intelligible manner with the aid of a wealth of informative illustrations. Textbooks in Contemporary Dentistry will be especially valuable for advanced students, practitioners in the early stages of their career, and university instructors. More information about this series at http://www.­springer.­com/series/14362

Nikolaos Kotsanos • Haim Sarnat • Kitae Park Editors

Pediatric Dentistry

Editors

Nikolaos Kotsanos Department of Paediatric Dentistry Aristotle University of Thessaloniki Thessaloniki Greece Kitae Park Institute of Oral Health Science Samsung Medical Center, School of Medicine Sungkyunkwan University Seoul Korea (Republic of)

Haim Sarnat Department of Pediatric Dentistry, School of Dental Medicine Tel Aviv University Tel Aviv Israel

Originally published by Fylatos Publishing, Thessaloniki, 2015 ISSN 2524-4612     ISSN 2524-4620 (electronic) Textbooks in Contemporary Dentistry ISBN 978-3-030-78002-9    ISBN 978-3-030-78003-6 (eBook) https://doi.org/10.1007/978-3-030-78003-6 © Springer Nature Switzerland AG 2015, 2022

1th edition: © Fylatos Publishing, Thessaloniki 2015

This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

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Contents 1

Pediatric Dentistry: Past, Present, and Future . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Nikolaos Kotsanos, Haim Sarnat, and Kitae Park

2

 hild Cognitive Development: Building Positive Attitudes C toward Dentists and Oral Health . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Trilby Coolidge, Jacqueline P. Spector, and Jaap Verkamp

3

Pediatric Body Growth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Panagiota Triantafyllou and Stephanie Roberts

4

Child Dental Fear, Communication and Cooperation . . . . . . . . . . . . . . . . . . . . . . . . 37 Trilby Coolidge and Nikolaos Kotsanos

5

Behavior Guidance and Communicative Management . . . . . . . . . . . . . . . . . . . . . 61 Travis Nelson and Nikolaos Kotsanos

6

Examination, Diagnosis, and Treatment Plan Implementation . . . . . . . . . . . . . 79 Stergios Arizos, Johan K. M. Aps, and Konstantinos N. Arapostathis

7

Local Anesthesia in Pediatric Dentistry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111 Konstantinos N. Arapostathis and Jean-Louis Sixou

8

 harmacologic Behavior Management (Sedation – General P Anesthesia) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131 Dimitrios Velonis, Dimitrios Emmanouil, and Keira P. Mason

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Growth of the Craniofacial Complex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155 Fernando Pugliese, Anastasios A. Zafeiriadis, and Mark G. Hans

10

Tooth Eruption, Shedding, Extraction and Related Surgical Issues . . . . . . . . 177 Aristidis Arhakis, Ola B. Al-Batayneh, and Hubertus van Waes

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Orthodontic Knowledge and Practice for the Pediatric Dentist . . . . . . . . . . . . 207 Kitae Park, Anastasios A. Zafeiriadis, and Nikolaos Kotsanos

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Dental Caries Prevention in Children and Adolescents . . . . . . . . . . . . . . . . . . . . . 247 Nikolaos Kotsanos, Rosalyn Sulyanto, and Man Wai Ng

13

Restoration of Carious Hard Dental Tissues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281 Nikolaos Kotsanos and Ferranti Wong

14

Pulp Therapy in Pediatric Dentistry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315 Aristidis Arhakis, Elisabetta Cotti, and Nikolaos Kotsanos

15

Periodontal Diseases in Children and Adolescents . . . . . . . . . . . . . . . . . . . . . . . . . . 347 Aikaterini-Elisavet Doufexi and Frank Nichols

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Dentoalveolar Trauma of Children and Adolescents . . . . . . . . . . . . . . . . . . . . . . . . 363 Cecilia Bourguignon, Aristidis Arhakis, Asgeir Sigurdsson, and Nikolaos Kotsanos

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Contents

Developmental Defects of the Teeth and Their Hard Tissues . . . . . . . . . . . . . . . 415 Nikolaos Kotsanos, Petros Papagerakis, Haim Sarnat, and Agnès Bloch-­Zupan

18

Tooth Wear in Children and Adolescents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 465 Nikolaos Kotsanos and Dowen Birkhed

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Temporomandibular Disorders in Children and Adolescents . . . . . . . . . . . . . . . 475 Linda Van den Berghe and Louis Simoen

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Oral Lesions in Children and Adolescents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 485 Stephen Porter and Alexandros Kolokotronis

21

The Young Dental Patient with Systemic Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . 515 Aristidis Arhakis and Nikolaos Kotsanos

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 isabilities, Neuropsychiatric Disorders, and Syndromes in Childhood D and Adolescence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 527 Nikolaos Kotsanos, Luc A. M. Marks, Konstantinos N. Arapostathis, and Kazumi Kubota

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Child-Centred Dentistry: Engaging and Protecting Children . . . . . . . . . . . . . . . 553 Zoe Marshman and Helen Rodd

Supplementary Information Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 565

VII

Contributors Ola  B.  Al-Batayneh  Preventive Dentistry Department, Jordan University of Science and Technology, Irbid, Jordan [email protected] Johan K. M. Aps  School of Oral Hygiene, Artevelde University of Applied Sciences, Ghent, Belgium Department of Pneumology, Free University Brussels, Brussels, Belgium Opinident BV, Marke, Belgium Konstantinos  N.  Arapostathis  Department of Paediatric Dentistry, School of Dentistry, Aristotle University of Thessaloniki, Thessaloniki, Greece [email protected] Aristidis  Arhakis  Department of Paediatric Dentistry, School of Dentistry, Aristotle University of Thessaloniki, Thessaloniki, Greece [email protected] Stergios Arizos  Department of Paediatric Dentistry, School of Dentistry, Aristotle University of Thessaloniki, Thessaloniki, Greece [email protected] Linda  Van Den Berghe  Ghent University, Faculty of Medicine and Health Sciences, Oral Health Sciences, Department of Special Care in Dentistry, University Hospital, Ghent, Belgium [email protected] Dowen  Birkhed  Former: Department of Cariology, Göteborg University, Gothenburg, Sweden Agnès  Bloch-Zupan  Faculté de Chirurgie Dentaire, University of Strasbourg, Strasbourg, France [email protected] Cecilia  Bourguignon  Private Practice in Endodontics and Dental Traumatology in Paris, Paris, France Trilby Coolidge  Oral Health Sciences, University of Washington, Seattle, WA, USA [email protected] Elisabetta  Cotti  Department of Conservative Dentistry and Endodontics, University of Cagliari, Cagliari, Italy Aikaterini-Elisavet Doufexi  Department of Preventive Dentistry, Periodontology and Implant Biology, School of Dentistry, Aristotle University of Thessaloniki, Thessaloniki, Greece [email protected]

VIII

Contributors

Dimitrios Emmanouil  Department of Paediatric Dentistry, School of Dentistry, National and Kapodistrian University, Athens, Greece [email protected] Mark  G.  Hans  Department of Orthodontics, Case Western Reserve University, School of Dental Medicine, Cleveland, OH, USA [email protected] Alexandros Kolokotronis  School of Dentistry, Aristotle University, Thessaloniki, Greece [email protected] Nikolaos Kotsanos  Department of Paediatric Dentistry, School of Dentistry, Aristotle University of Thessaloniki, Thessaloniki, Greece [email protected] Kazumi Kubota  Department of Special Needs Dentistry, Division of Hygiene and Oral Health, School of Dentistry Showa University, Tokyo, Japan [email protected] Luc A. M. Marks  Center for Dentistry and Oral Hygiene – UMCG, University of Groningen, Groningen, The Netherlands [email protected] Zoe  Marshman  Unit of Oral Health, Dentistry and Society, School of Clinical Dentistry, University of Sheffield, Sheffield, UK [email protected] Keira P. Mason  Department of Anaesthesia, Harvard Medical School, Boston, MA, USA [email protected] Travis  Nelson  Department of Pediatric Dentistry, University of Washington, Seattle, WA, USA [email protected] Man Wai Ng  Boston Children’s Hospital, Boston, MA, USA [email protected] Frank  Nichols  Division of Periodontology, Department of Oral Health and Diagnostic Sciences, University of Connecticut School of Dental Medicine, Farmington, CT, USA [email protected] Petros Papagerakis  College of Dentistry, University of Saskatchewan, Saskatoon, Canada [email protected] Kitae  Park  Institute of Oral Health Science, Samsung Medical Center, School of Medicine, Sungkyunkwan University, Seoul, Korea (Republic of) [email protected] Stephen Porter  UCL Eastman dental Institute, University College, London, UK [email protected] Fernando Pugliese  Department of Orthodontics, Case Western Reserve University, School of Dental Medicine, Cleveland, OH, USA [email protected]

IX Contributors

Stephanie  Roberts  Attending in Endocrinology, Boston Children’s Hospital, Boston, MA, USA [email protected] Helen  Rodd  Unit of Oral Health, Dentistry and Society, School of Clinical Dentistry, University of Sheffield, Sheffield, UK [email protected] Haim  Sarnat  Department of Pediatric Dentistry, School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel [email protected] Asgeir Sigurdsson  New York University College of Dentistry, New York, NY, USA [email protected] Louis  Simoen  Ghent University, Faculty of Medicine and Health Sciences, Oral Health Sciences, Department of Special Care in Dentistry, University Hospital, Ghent, Belgium [email protected] Jean-Louis  Sixou  Department: Paediatric Dentistry, Faculty of Dentistry, University of Rennes 1, Rennes, France [email protected] Jacqueline  P.  Spector  Oral Health Sciences and Psychology, University of Washington, Seattle, WA, USA [email protected]; [email protected] Rosalyn Sulyanto  Harvard School of Dental Medicine, Boston Children’s Hospital, Boston, MA, USA [email protected] Panagiota  Triantafyllou  Scientific collaborator in Pediatric Endocrinology, Department of Pediatrics, Aristotle University of Thessaloniki, Thessaloniki, Greece [email protected] Dimitrios  Velonis  Pediatric Dentist, Oral Medicine Specialist, Pediatric Laser Dentistry, Larisa, Greece Jaap Verkamp  Clinic for Paediatric Dentistry, Kindertand, Amsterdam, Netherlands [email protected] Hubertus  Van Waes  Clinic of Orthodontics and Peadiatric Dentistry Center for Dental Medicine, University of Zurich, Zurich, Switzerland [email protected] Ferranti  Wong  Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK [email protected] Anastasios  A.  Zafeiriadis  Department of Orthodontics, School of Dentistry, Aristotle University of Thessaloniki, Thessaloniki, Greece [email protected]

1

Pediatric Dentistry: Past, Present, and Future Nikolaos Kotsanos, Haim Sarnat, and Kitae Park Contents 1.1

Brief Historical Overview – 2

1.2

Child Oral Health. Inequalities and the Dental Services – 4

1.2.1

Trends in Pediatric Dentistry in the Future – 6

1.3

Addressing Children’s Rights – 6

1.4

Breadth of Knowledge in Pediatric Dentistry – 7 References – 9

© Springer Nature Switzerland AG 2022 N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry, https://doi.org/10.1007/978-3-030-78003-6_1

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N. Kotsanos et al.

Brief Historical Overview

Meeting the oral among other health needs, in a humane manner, and successfully preventing oral disease of children and adolescents, including those with disabilities, is a right for the youth. It is also a measure of a high standard of living and is seen nowadays in many societies across the globe while it remains a goal for many others. Its fulfillment has taken long efforts of dental educating and planning pediatric dental services, and the pioneering attempts to set the foundation for today’s level of care should be acknowledged. The first organized child dental treatment efforts seem to have started at the end of the eighteenth century in New York and Paris by private practitioners’ initiatives. Examination of 5- to 12-year-old children was recorded in 1850 in Belgium, and, on the other side of the Atlantic, the Baltimore College of Dentistry in 1840 and the Harvard School of Dental Medicine in 1867 were founded. Thus, over time, dental education moved from a largely proprietary to science-based education housed within the university and/or academic health center structure [1]. In the early 1900s Europe, following the publication of the first epidemiological studies in children recording massive caries rates, the first school-­ based dental care was established in Strasbourg by the Danish dentist E. Jessen, and this model for child oral care was then followed in several countries, particularly in Scandinavia, focused at that time on the permanent teeth only [2]. At the same time, dental clinics were established in order to provide free care to impoverished children by philanthropists, Forsyth in Boston and Eastman in Rochester at US East coast. In the second quarter of the twentieth century, the first books devoted to “pedodontics” were published, and new such departments established in US dental schools (. Fig. 1.1), which, beyond theoretical courses, included clinical training. Thus, by the end of World War II, pediatric dentistry was already a separate discipline. Before then, local anesthesia was neither standardized nor as efficient as nowadays. Behavior management and guidance was during the third quarter of the twentieth century progressively based on knowledge and principles of child psychology, when the concomitant evolution of the latter allowed for it. The progress of dental science and research and the emphasis on psychological and behavioral aspects have had a great impact in changing the image of dentistry for children and adults alike. The development of post graduate programs had centered in a more total patient care approach in pediatric dentistry [3]. The dental treatment was mainly restor-

..      Fig. 1.1  A dental surgery of the second quarter of the twentieth century. Museum items

..      Fig. 1.2  Orthodontic treatment with bands bearing brackets at the third quarter of the twentieth century

 

ative, in maintaining carious primary teeth or the space from their premature loss. As for available restorative materials, the approach could not be primarily aesthetic at a time that only few children had access or happily accepted orthodontic treatment (. Fig. 1.2). Preventive dentistry and its teaching acquired its decisive role in that third quarter of the twentieth century [4], mainly connected to oral hygiene measures for dental decay. Artificial fluoridation of drinking water was established in some countries, starting with the USA, and the global spread of the use of fluoridated toothpaste significantly reduced caries in children. This was at first in industrialized countries, where fluoride toothpaste consumption has come to be today around 300 ml per person (three normal size tubes). The effec 

3 Pediatric Dentistry: Past, Present, and Future

tiveness of brushing in dental and gingival health has since been connected with a healthy mouth and a bright smile in modern culture (. Fig. 1.3). The acid etching of enamel, which was first described in 1955, was a further breakthrough. It proved to be the decisive technology for the continuous improvement of composite resins. Mainly these were the aesthetic restorative materials contributing to a more conservative approach in restoring carious teeth including sealing vulnerable fissures for caries reduction. Thus, the end of  

the twentieth century saw a shift from mainly restorative to preventive, cosmetic, and orthodontic procedures in children and adolescents [5, 6], which continues to date. Overview Milestones of pediatric dentistry in the twentieth century (from beginning to end): 1. Epidemiological recording of dental caries documents extent. 2. Pediatric dentistry textbooks get published. 3. Effective formulated local anesthesia is introduced. 4. Postgraduate pediatric dentistry programs are developed. 5. Communicative behavior management is widely taught. 6. Topical fluorides prevail and major caries decrease is evidenced in children. 7. Etching the enamel boosts fissure sealing and composite as restorative. 8. The rights of the child concept are adopted.

The American Academy of Pediatric Dentistry was founded as early as 1947 and affected the academic and professional developments in other parts of the world. Two decades later, the International Association of Paediatric Dentistry was established in 1969 [7], and after another two decades, the European and the Australasian Academies were founded in 1990 for the better coordination of the already existing national pediatric dental societies in those continents. Their major contributions are the political influence and advocacy for child oral health as well as the issuing of guidelines for improved and evidence-based dental care for children (. Fig. 1.4). Throughout the second half of the twentieth century, pediatric dentistry was increasingly recognized as a specialty of dentistry in many countries and this trend continues to date.  

..      Fig. 1.3  The bright smile reflects health and communication in modern societies

..      Fig. 1.4  Logos of world leading pediatric dentistry bodies

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 hild Oral Health. Inequalities C and the Dental Services

caries experience among 35- to 45-year-old and 65- to 74-year-old groups was still on the rise [13]. At about the same period with China, i.e., 1992–2016, a decline started showing in 2–5- and 11–15-year-olds in India [14] (. Fig. 1.6). Other reports however find caries levels to be relatively low in many emerging Asian countries, even though, for the most part, carious and periodontal needs remain there largely unmet [16]. Notwithstanding the diversity of dental caries reports in the various parts of Africa, caries does not seem to be among the prime factors influencing oral health-related quality of life [17]. Regarding restorative needs, a decrease of multi-­ surface cavities, endodontic treatment needs, and placement of preformed metal crowns in primary teeth has been noted in university pediatric dentistry clinics of countries showing significant caries decline. Though these are still widely performed there today, the most frequent recipients are those socioeconomically worse and minorities like immigrants [18–20]. Before, caries indices were high because dental caries, by affecting the majority of children in the early and mid-twentieth century, was considered a disease of modernization; there was a higher prevalence in developed countries and in individuals with higher socioeconomic status. In the late twentieth and the twenty-first century, this pattern of caries prevalence and severity changed in developing

Dental caries is the most common chronic disease in childhood [8]. For about 2/3 of the twentieth century, it posed a physical as well as a social problem for children and adults in the industrialized countries. Implementing preventive programs achieved some caries reduction in the child population after that time. For example, the mean dmfs (sum of decayed, missing, and filled primary tooth surfaces) of 4-year-olds in southern Sweden was reduced from 8 to 2 between 1967 and 1980 [9]. At the same trend, 70% of the Danish 5-year-olds in 1998 were caries-free, while the mean DMFS (same index for permanent teeth) of 12-year-olds was reduced to 1.5 [10]. Similar reductions had been observed in the USA in the 1970s. The average DMFS of children aged 5–17 years decreased from 7.1 to 4.8 with a dramatic decrease in the number of extracted first permanent molars [11]. It was remarkable that this trend was irrespective of systemic ways of fluoride use (. Fig. 1.5). In other parts of the world this improvement came somewhat delayed. In Italy, for example, a report for preschool children showed caries decline in the last decade of the past century [12]. In China this seemed to occur in the first decade of the current century, while

 

 

..      Fig. 1.5  Tooth decay (DMFT) trends of 12-year-olds in fluoridated and non-fluoridated countries. (Accessed at 7 https://fluoridealert.­org/ studies/caries01)

Tooth Decay Trends in Fluoridated and Non-Fluoridated Countries WHO data on DMFT in 12 year olds*

Ice

 

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Years 1970 through 2010 * World Health Organization (WHO). Collaborating Centre for Education, Training, and Research in Oral Health, Malmö University, Sweden, http://www.mah.se/CAPP/ (accessed June 10, 2012). ** No water or salt fluoridation.

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5 Pediatric Dentistry: Past, Present, and Future

..      Fig. 1.6  The changing pattern of caries incidence in 12-year-olds in developed and developing countries during the last two decades of the twentieth century and beyond [15]

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All countries

Developing countries

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and developed countries; low income, low education levels, and lower classes of occupations have been consistently related to high caries risk [21–25]. To effectively combat this established discriminative caries pattern, contemporary research and clinical efforts are directed toward reliably targeting high-risk children, i.e., with active disease before being symptomatic. Interventions that begin early and combine multiple strategies hold greatest potential [26]. Within this frame, refugee populations except for being subject to worse physical, mental, and social health outcomes experience difficulties accessing health services in their new country [27]. Further, in most lowand middle-income countries, oral health-care demands are beyond the capacities of their health-care systems, while in the private sector there may be an uneven distribution of dental services in the expense of rural areas [28]. Despite being largely preventable, oral diseases are still a major public health problem in child populations in many parts of the world [29]. Special needs children have, or are at risk, for chronic physical, developmental, behavioral, or emotional conditions, which can impact on their oral health and usually require increased and/or special services for dental and periodontal disease. Studies of special care needs children show much higher prevalence of caries compared to children in the general population. In two studies reporting on disabled children in Kuwait and children with autism in South Africa, the teeth most affected were the first permanent molars and their periodontal and restorative needs were mostly unmet [30, 31]. Although there is little longitudinal data on the history of oral diseases/conditions other than caries, there has been some progress in the prevalence and treatment

..      Fig. 1.7  Contemporary orthodontic treatment with tooth-­ colored material. (Courtesy of Dr. Manoukakis)

of periodontal disease and anomalies of occlusion. The idealization of smile aesthetics nowadays, which ­promotes images of healthy teeth and gums, helps the adoption of good oral hygiene habits (. Fig.  1.3). Consequently, it is very likely that the gingival health has improved [32]. Regarding orthodontics, it seems now attractive, considering the large increase of acceptance and frequency of children under orthodontic treatment (. Fig.  1.7). While it has a positive impact on the oral health-related quality of life of adolescents [33], treatment requirements – compliance to treatment, long duration, costs – pose a burden to many population groups. Dental auxiliary personnel were introduced several decades ago in industrialized countries for various reasons including the reduction of costs, which are higher  

 

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for dental education than any other health profession. One such example was in Australia’s health-care system in the mid-1960s, in trying to address the then difficult-­ to-­meet treatment needs for child dental disease. Today, oral health therapists and hygienists comprise one quarter of the dental workforce providing fissure sealants, restorations and primary tooth extractions, oral health instruction, fluoride applications, scale and cleans, and some periodontal services [34]. Thus, much of the less complex dental treatment needs are not provided by dentists themselves, and this, along with the caries decline, means that their involvement with restorative procedures has decreased significantly. Lastly, upcoming social changes bring about other issues. As many families nowadays have limited free time, either because both parents are occupied at work or because they escort children in several organized extracurricular activities (. Fig. 1.8), they become more selective in search of high-quality services for their children. Even though restorative procedures show reduction, the emphasis on quality and the increase in preventive, cosmetic, and orthodontic services compensate for it. Τhe recent pandemic of airborne Covid-19 with even asymptomatic carriers spreading the disease has challenged dentistry among other health professions. Concerns regarding dentists’ and patients’ safety during the outbreaks limited dental care to emergencies compromising preventive appointments. Among other impacts [35], the aerosols produced in several dental procedures imposed a higher level of protection than before, necessitating the use of FFP2/FFP3 masks and other protective gear. The production of successful vaccines has somewhat eased fears for dental visits, but the risk of similar viral future threats calls for constant alertness.  

1.2.1

Future trends for the practice of pediatric dentistry based on research advances may include the following: 1. Predominance of prevention of dental caries by early identifying high caries risk, informing and engaging parents, promoting oral health care at home, use of fluoride and other prevention technologies, application of fissure sealants, and establishment of efficient recall system. 2. Increased intervention in orthodontic anomalies and smile aesthetics, which already are of high interest among parents and children. 3. Improved accessibility and dental care for people with disabilities, alongside with extending the dental neglect concept to them. 4. Increased use of new technology dental equipment (e.g., evolution of laser devices [36], sophisticated electronic anesthesia techniques that increase efficiency and acceptance by children, etc.). 5. Therapeutic approaches based on the principles of preventive dentistry including minimally invasive operative approaches lead to painless and often pleasant dental procedures for children. This improved dentist’s image will further reduce phobic young adults. 6. Exclusive use of tooth-colored materials with everimproving bonding and with emphasis on safety (lack of toxicity), while these principles increasingly apply to preformed crowns. 7. Molecular biology and engineering bring potential applications in the dental practice with regeneration of dental tissue by the stem cell technology. 8. Better understanding the microbiome of the human body and its environment will allow development of preventive health measures for oral and general health.

1.3

..      Fig. 1.8  Appointment delays with families of limited free time

 rends in Pediatric Dentistry T in the Future

Addressing Children’s Rights

A growing body of evidence leads to the view that children’s development, following the social transformation of childhood in modern societies, is influenced both by family and by the social and cultural norms of society. Thus, children’s health, development, achievements, and social attainments have come to require the interest, guidance, and protection of both families and society [37]. In the United Nations Convention on the Rights of the Child [38], the term “child” refers to anyone under the age of 18. It was signed on November 20, 1989 and is commemorated on this date as world’s children’s day,

7 Pediatric Dentistry: Past, Present, and Future

and it is the most widely ratified human rights treaty (about 200 countries currently). Its purpose is to defend children’s rights and protect them from exploitation ­ phenomena, violence, and abuse. Oral health is not specifically mentioned but is nevertheless implied under general health and wellbeing. The reference to health rights in articles 23–25 briefly includes:

cause for suspecting neglect. The American Academy of Pediatric Dentistry defines dental neglect as “the willful failure of parent or guardian to seek and follow through with treatment necessary to ensure a level of oral heath essential for adequate function and freedom from pain and infection” [42].

55 No child is deprived of the right of access to highest attainable standard of health. 55 The child receives periodic review of the treatment. 55 Disabled children have effective access to and receive health-care and rehabilitation services. On the other hand, article 22 states these health rights also apply to children with refugee state, further to those for protection and humanitarian assistance. Undergraduate pediatric dentistry programs in most schools contain some clinical training on patients with disabilities. One of postgraduate orientations in pediatric dentistry is the training at competency level of oral care of these individuals at least up until early adulthood. Recognizing the need to prevent severe early childhood caries, which remains a very frequent cause of oral inflammation and pain in many population groups, impacts on child’s quality of life [39]. The first dental visit has been set to be when the first tooth erupts and not later than the child’s first birthday [40]. This is for informing and educating parents on proper child tooth care because the above severe disease undermines the rights of the children, affecting not only their physical but also their psychological health. The definition of health by the WHO includes the general state of the individual, which includes avoiding dental fear and anxiety. Informed consent of the parent and perhaps the patient is another issue. It is the legal instrument that protects the right of the patient – defended by the parent or legal guardian in case of a minor – to a repressive approach and treatment without her/his approval. While this is in a positive direction for children’s’ rights, with particularly skeptical and difficult-to-convince parents, dentists may be more prone to sedation techniques for treating more challenging young dental patients, cooperation-­wise. This poses the risk of moving to more defensive pediatric dentistry approaches. It is important for all health-care providers (including dental providers) to be knowledgeable and alert about signs and symptoms of child abuse and neglect and to know how to respond [41]. Physical abuse, sexual abuse, bite marks, bullying, and human trafficking all constitute abuse issues. All findings when there is reasonable suspicion of abuse should be reported for further investigation. The dentist should also look for adequate clothing and general and oral hygiene. Poor diet and lack of medical and dental care should be

Overview In general, a contemporary practicing dentist should: 55 Embrace risk assessment tools being prevention-­ minded 55 Utilize changing technology for improved patient care 55 Appreciate evidence-based advances in biomedical and behavioral sciences 55 Be willing to interact professionally with other health-care providers 55 Be committed to ethics both in treatment choices and electronic patient record use

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Guiding and caring each child to stay orally healthy is a serious responsibility and has an educating influence for her/his psychological maturation. If done effectively, it earns the trust of the parents, is rewarded with great satisfaction, and promotes good oral health in the long run. To adequately train the new dentists for this task (. Fig. 1.9), the discipline of pediatric dentistry needs to draw and transfer knowledge from other non-dental disciplines, primarily from the fields of medicine and child psychology, so that they acquire:  

..      Fig. 1.9  University dental school setting for pediatric dentistry clinical training (prior to the covid-19 era)

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1. Good dental knowledge, in prevention of oral diseases, restoring dental cavities, wear and various defects, pulp treatment, dental materials, oral surgery, preventive orthodontics, and certain principles of prosthetic dentistry 2. Basic knowledge of pediatrics, anesthesiology, general medicine and oral pathology, growth and development, as well as nutrition 3. Knowledge of mental, emotional development, and child psychological issues, because each child requires different management, depending on age, maturity, and other physical abilities It is apparent, however, that the dentist has an obligation to recognize the limits of his/her knowledge either in dental/medical or in the behavior management skills. In cases where the patient’s needs exceed those limits, the dentist must refer the patient to a specialist pediatric dentist. Moreover, the level of dental care provided to the child should be of quality that can be ­certified. Dental care and treatment options should not be empirical or even based only on expert opinion. Today it is evidence-based as far as possible, which means knowledge that comes from randomized control trials, systematic reviews, and meta-analyses. Research today is deemed to fill the gaps in the documentation of knowledge in pediatric dentistry, as in other fields of medicine. Pediatric dentistry has widely expanded its content, due to the recognition of the importance of child oral health and its effect on normal physical and psychological development. Its effective practice requires the pediatric dentist to collaborate with various other pediatric specialties. The extensive level of education in pediatric dentistry is not possible to be integrated in undergraduate dental programs and it is taught in postgraduate specialization programs. These, according to the principles of international bodies of pediatric dentistry [43–45], aim to specialize the trainee in all aspects in order to be able to: 55 Care of all the oral needs of infants, children, and adolescents, including the medically compromised and the young people with disabilities 55 Search for continuous improvement of his/her knowledge by continuing clinical education and acquire adequate teaching ability for disseminating this knowledge 55 Participate in interdisciplinary groups for the caring of children with special needs, e.g., the craniofacial anomalies 55 Use the authority and expertise to advocate for patient safety, improved outcomes, and intelligent regulatory oversight

55 Support training programs, advising accreditation boards, and sponsoring programs to enhance success throughout their career 55 Be competitive in pursuing and advancing collaborative research Engagement with pediatric dentistry ascribes the practicing dentist with an additional important social role as an educator, trainer, and protector of the vulnerable groups, often in collaboration with the pediatrician and many other clinicians and scientists. Along with progress in recognizing children’s rights, this is still important because access to care remains a serious public health problem, even in population sections of industrialized countries. This role includes: 55 Dynamic interventions for impoverished, neglected, or abused children 55 Undertaking interventions on preventing of dental caries, which remains a plague for certain groups of unprivileged child populations, by individual or collaborative voluntary activities (. Fig. 1.10) 55 Counseling parents and children on obesity, an epidemic of our time, discussing healthy eating habits and regular exercise  

..      Fig. 1.10  Voluntary outreach service to underprivileged children as a joint action of local pediatric dental society members working on a company-sponsored caravan transformed to a dental surgery

9 Pediatric Dentistry: Past, Present, and Future

References 1. DePaola DP. The evolution of dental education as a profession, 1936–2011, and the role of the journal of dental education. J Dent Educ. 2012;76(1):14–27. 2. Poulsen S, Koch G. Pediatric oral health care: the perspectives, Ch 1. Ιn: Pediatric dentistry; a clinical approach. 2nd edn, Koch G and Poulsen S (eds), Wiley-Blackwell, Chichester 2009. 3. Casamassimo PS.  The practical importance of pediatric dentistry, Ch. 1. In: Casamassimo PS, Fields Jr HW, McTigue DJ, Nowak AJ, editors. Pediatric dentistry; infancy through adolescence. 5th ed. St Louis: Elsevier; 2013. 4. Gerbert B. Planned change and the future of the dental education system. J Dent Educ. 1986;50(10):585–93. 5. Association of Pedodontic Diplomats. Survey of orthodontic services provided by pedodontists. Pediatr Dent. 1983;5:204–6. 6. Christensen GJ.  The future of dental practice. J Dent Educ. 1986;50:114–8. 7. Gelbier S. History of the International Association of Paediatric Dentistry. Part 3: Samuel D. Harris and some early pressures for international developments. Int J Paediatr Dent. 1995;5:123–5. 8. Oral health in America: a report of the Surgeon General. J Calif Dent Assoc. 2000;28(9):685–95. 9. Stecksen-Blicks C, Borssen E. Dental caries, sugar-eating habits and tooth-brushing in 4-year-old children 1967-1997 in the city of Umea, Sweden. Caries Res. 1999;33:409–14. 10. Holm AK, Poulsen S.  Oral health in children and adolescents. Ch 2. In: Koch G, Poulsen S, editors. Pediatric dentistry; a clinical approach. Copenhagen: Munksgaard; 2001. 11. National caries program. National Institute of Dental Research: The national dental caries prevalence survey: The prevalence of dental caries in the United States. US department of Health and Human Services, NIH Publication No 82–2245, Dec. 1981. 12. Ferro R, Besostri A, Olivieri A. Survey of caries experience in 3- to 5-year-old children in Northeast Italy in 2011 and its trend 1984-2011. Oral Health Prev Dent. 2017;15(5):475–81. https:// doi.org/10.3290/j.ohpd.a38976. 13. Liu J, Zhang SS, Zheng SG, Xu T, Si Y. Oral health status and oral health care model in China. Chin J Dent Res. 2016;19(4):207–15. https://doi.org/10.3290/j.cjdr.a37145. 14. Mehta A.  Trends in dental caries in Indian children for the past 25 years. Indian J Dent Res. 2018;29(3):323–8. https://doi. org/10.4103/ijdr.IJDR_615_17. 15. Petersen PE (2003) The World Oral Health Report 2003. www. sciencedirect.com/topics/medicine-and-dentistry/dmft-index. Accessed on 21/14/2020. 16. Saekel R. Comparison of oral health status in Asia: results for eight emerging and five high income countries or regions and implications. Chin J Dent Res. 2016;19(4):191–206. https://doi. org/10.3290/j.cjdr.a37144. 17. Malele-Kolisa Y, Yengopal V, Igumbor J, Nqcobo CB, Ralephenya TRD.  Systematic review of factors influencing oral health-related quality of life in children in Africa. Afr J Prim Health Care Fam Med. 2019;11(1):e1–e12. https://doi. org/10.4102/phcfm.v11i1.1943. 18. Waldman HB. Are minority children getting their fair share of dental services? ASDC J Dent Child. 1990;57(5):380–4. 19. Blen M, Narendran S, Jones K.  Dental caries in children under age three attending a university clinic. Pediatr Dent. 1999;21(4):261–4. 20. Ferrazzano GF, Cantile T, Sangianantoni G, Ingenito A, Rengo S, Alcidi B, et  al. Oral health status and Unmet Restorative Treatment Needs (UTN) in disadvantaged migrant and not migrant children in Italy. Eur J Paediatr Dent. 2019;20(1):10–4. https://doi.org/10.23804/ejpd.2019.20.01.02.

21. Armfield JM.  Socioeconomic inequalities in child oral health: a comparison of discrete and composite area-­based measures. J Public Health Dent. 2007;67(2):119–25. 22. Traebert J, Guimarães Ldo A, Durante EZ, Serratine AC. Low maternal schooling and severity of dental caries in Brazilian preschool children. Oral Health Prev Dent. 2009;7(1):39–45. 23. Christensen LB, Twetman S, Sundby A.  Oral health in children and adolescents with different socio-cultural and socioeconomic backgrounds. Acta Odontol Scand. 2010;68(1):34–42. https://doi.org/10.3109/00016350903301712. 24. Ferro R, Cecchin C, Besostri A, Olivieri A, Stellini E, Mazzoleni S. Social differences in tooth decay occurrence in a sample of children aged 3 to 5  in north-east Italy. Community Dent Health. 2010;27(3):163–6. 25. Marcenes W, Kassebaum NJ, Bernabé E, Flaxman A, Naghavi M, Lopez A, et  al. Global burden of oral conditions in 1990– 2010: a systematic analysis. J Dent Res. 2013;92:592–7. 26. Edelstein BL, Hirsch G, Frosh M, Kumar J.  Reducing early childhood caries in a Medicaid population: a systems model analysis. J Am Dent Assoc. 2015;146(4):224–32. https://doi. org/10.1016/j.adaj.2014.12.024. 27. Riggs E, Rajan S, Casey S, Kilpatrick N.  Refugee child oral health. Oral Dis. 2017;23:292–9. https://doi.org/10.1111/ odi.12530. 28. Saliba NA, Moimaz SA, Garbin CA, Diniz DG.  Dentistry in Brazil: its history and current trends. J Dent Educ. 2009;73(2): 225–31. 29. Watt RG, Mathur MR, Aida J, Bönecker M, Venturelli R, Gansky SA. Oral health disparities in children: a canary in the coalmine? Pediatr Clin N Am. 2018;65(5):965–79. https://doi. org/10.1016/j.pcl.2018.05.006. 30. Shyama M, Al-Mutawa SA, Morris RE, Sugathan T, Honkala E.  Dental caries experience of disabled children and young adults in Kuwait. Community Dent Health. 2001;18(3):181–6. 31. Naidoo M, Singh S.  The Oral health status of children with autism Spectrum disorder in KwaZulu-Nata, South Africa. BMC Oral Health. 2018;18(1):165. https://doi.org/10.1186/ s12903-­018-­0632-­1. 32. Dye BA, Tan S, Smith V, Lewis BG, Barker LK, ThorntonEvans G, et al. Trends in oral health status: United States, 19881994 and 1999-2004. Vital Health Stat. 2007;11(248):1–92. 33. Ferrando-Magraner E, García-Sanz V, Bellot-­Arcís C, Montiel-Company JM, Almerich-Silla JM, Paredes-­ Gallardo V.  Oral health-related quality of life of adolescents after orthodontic treatment. A systematic review. J Clin Exp Dent. 2019;11(2):e194–202. https://doi.org/10.4317/jced.55527. 34. Teusner DN, Satur J, Gardner SP, Amarasena N, Brennan DS.  Variations in Australian dental therapy practice by practitioner and workplace characteristics. Int Dent J. 2018;68(4):235– 44. https://doi.org/10.1111/idj.12382. 35. Campagnaro R, Collet GO, Andrade MP, Salles JPDSL, Calvo Fracasso ML, et al. COVID-19 pandemic and pediatric dentistry: fear, eating habits and parent’s oral health perceptions. Child Youth Serv Rev. 2020;118:105469. https://doi.org/10.1016/j. childyouth.2020.105469. 36. American Academy of Pediatric Dentistry. Policy on the use of lasers for pediatric dental patients. Pediatr Dent. 2017;39(6): 93–5. 37. Children’s Health, The Nation’s Wealth. Assessing and improving child health. National Research Council; Institute of Medicine. Washington, DC: National Academies Press (US); 2004. https://doi.org/10.17226/10886. 38. Convention on the rights of the child. At: https://www.unicef. org/sites/default/files/2019-04/UN-Convention-Rights-Childtext.pdf

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39. Chen KJ, Gao SS, Duangthip D, Lo ECM, Chu CH. Prevalence of early childhood caries among 5-year-old children: a systematic review. J Investig Clin Dent. 2019;10(1):e12376. https://doi. org/10.1111/jicd.12376. 40. American Academy of Pediatric Dentistry. Periodicity of examination, preventive dental services, anticipatory guidance/counseling, and oral treatment for infants, children, and adolescents. Reference manual 2018/19, 40 (No. 6); 194–204. 41. American Academy of Pediatric Dentistry. Oral and dental aspects of child abuse and neglect. Reference manual 2018/19, 40 (No. 6); 243–9.

42. American Academy of Pediatric Dentistry. Definition of dental neglect. Reference manual 2018/19, 40 (No. 6);13. 43. European Academy of Paediatric Dentistry. Curriculum guidelines for education and training in paediatric dentistry. At: www.eapd. eu/uploads/files/Curriculum%20guidelines%20for%20Education%20and%20Training%20in%20Paediatric%20Dentistry.pdf. 44. Australasian Academy of Paediatric Dentistry. Mission and vision. At: www.aapd.org.au/viewStory/Mission-and-Vision. 45. American Academy of Pediatric Dentistry. Residency programs. At: https://www.aapd.org/resources/member/residentresources/ residency-programs/.

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Child Cognitive Development: Building Positive Attitudes toward Dentists and Oral Health Trilby Coolidge, Jacqueline P. Spector, and Jaap Verkamp Contents 2.1

 he Dentist’s Long-Term Goal for Pediatric Patients T and an Introduction to Piaget’s Stages of Cognitive Development – 12

2.1.1 2.1.2 2.1.3 2.1.4

S ensorimotor Stage – 12 Preoperational Stage – 15 Concrete Operational Stage – 17 Formal Operational Thought – 18

2.2

 sing Memory Principles to Help Prevent the U Development of Fear – 20

2.3

Tailoring Oral Messages to the Individual Patient – 21 References – 22

© Springer Nature Switzerland AG 2022 N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry, https://doi.org/10.1007/978-3-030-78003-6_2

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 he Dentist’s Long-Term Goal T for Pediatric Patients and an Introduction to Piaget’s Stages of Cognitive Development

Helping children develop positive attitudes about dentists and oral health is an effective strategy to ensure that these patients continue to have positive attitudes about dentists and oral health throughout their lives. This long-term goal involves developing a relationship with the child and his/her parents that fosters trust, as well as providing those dental services that result in promoting oral health in keeping children healthy throughout their childhood. In our opinion, many of the difficulties dentists encounter while trying to provide dental care to young children are a result of focusing on the short-term goal of completing a particular dental procedure, rather than keeping this long-term goal in mind. A strong background in child cognitive development will provide clinicians with tools helpful for accomplishing both short- and long-term goals when working with children. The Swiss psychologist Jean Piaget studied the development of children’s thought processes for nearly 50 years (. Fig. 2.1). It became apparent to Piaget that children are not simply “little” versions of adults whose knowledge gradually increases. Rather, while their brains go through processes of biological maturation which are genetically influenced, children’s experiences interact  

..      Table 2.1  Stages of cognitive development of the child according to Piaget [2] Birth to 2 years

2–6 years

6–11 years

11+ years

Sensorimotor

Preoperational

Concrete operational

Formal operational (hypothetical/ abstract thinking)

with that physical maturation and result in the development of cognitive abilities, i.e., interaction between genetic and environmental features [1], and result in qualitatively different ways of thinking or behaving as they develop. These new ways can be identified as occurring at distinct times, or stages, during a child’s development. This concept alone will serve the pediatric dentist well. Piaget’s stage model of cognitive development provides clinicians with the structure with which to understand the thought processes of pediatric patients. Piaget stated that children go through four different stages of cognitive development (. Table 2.1) [2]. An understanding of Piaget’s model provides the clinician about what behaviors to expect from children of different ages and, important for that long-term goal, how to help create positive schemata – mental representations  – about dentists, dental visits, and good home oral health behaviors.  

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Sensorimotor Stage

Case Study

..      Fig. 2.1  Jean Piaget (1896–1980), Swiss philosopher and psychologist

You enter the operatory to find a new patient, 15-month-old Sally, and her mother. It’s Sally’s first visit to a dentist. Your assistant had seated Sally in a pediatric dental chair, and her mother is sitting on a regular chair beside her, holding restless Sally’s hand. Sally is holding a chain that has several large plastic toy keys strung on it and is putting one or two keys into her mouth and then pulling them out again. After greeting her mother, you sit in your dental chair and scoot over to Sally. As you get closer, you smile and say “Hi, Sally.” She freezes, looks at you, closes her eyes and turns her head away, and starts to cry. The plastic keys fall out of her mouth. You turn on the overhead exam light and focus it on Sally’s mouth, move in between her and her mother, and use a dental mirror to do a quick exam. Sally kicks harder and cries more loudly, moving her head back and forth.

13 Child Cognitive Development: Building Positive Attitudes toward Dentists and Oral Health

..      Fig. 2.2  Piaget’s early sensorimotor stage

The sensorimotor stage begins at birth and lasts until approximately the child’s second birthday. Children are born with reflexes (e.g., sucking), can see and hear, and explore and learn about their worlds through their senses and their ability to move (. Fig.  2.2). This means that they understand their world through what they can sense and physically interact with. One frequent way of learning about objects during this stage is to put them in one’s mouth. Other ways to learn about objects and the world around include looking and handling things with one’s fingers. Some fascinating research has demonstrated that newborns can mimic adults who are sticking out their tongues or making other facial gestures, indicating that mimicry is another method of sensorimotor exploration [3]. Especially during the first year of life, the sensorimotor child does not have a fully developed, individuated sense of self. That is, she does not consider herself to be a completely separate person from her caregivers. This is why physical contact with caregivers is soothing, while physical separation from them can be stressful. In addition, children of this age are only concerned with what they can sense in the present moment. The clinician needs to remember how a child thinks at this stage: “out of sight, out of mind.” Piaget believed that children begin to construct ­schemata or concepts – ideas about how the world works – during this stage. Schemata are mental representations about the world and include different kinds of objects, individuals, actions, descriptors or properties, and abstractions [4]. For example, parents point out a dog and say: “Look, honey, see the doggie!” Eventually, the child points to a different dog and says: “Doggie!” It seems that the child has learned that certain objects are “doggies.” In Piaget’s terms, the child has used assimilation to apply the “doggie” schema to a new object. However, it is not uncommon for children to point to a different animal (say, a cat) and say “Doggie!” From the adult’s point of view, the child is incorrect to assign a cat to the concept of “doggie.” The parent may say, “No, honey, that is a kitty,” and provide some information about why the object is a cat and not a dog. This starts the process of developing a new  

schema (“kitty”). It also further refines the child’s schema for “doggie.” According to Piaget, the child has accommodated the “doggie” schema to include the new information. The general processes of assimilation and accommodation are facilitated by the child’s growing understanding of what constitutes a prototypical example of the schema. For example, the child learns that the prototypic zebra has white and black stripes, while the prototypic horse does not. In various cultures, prototypic men and women may wear different clothes and/or have different hairstyles. Similarly, although they are both objects which one can shelter inside of, prototypic houses differ from prototypic tree forts. This raises the issue of what a prototypic dentist is like. For some adults, the prototypic dentist is someone wearing a white coat who helps people have good oral health. For other adults, the dentist is someone frightening who causes pain inside one’s mouth. Dentists and parents can each work to influence the child to develop a positive prototypic schema for dentists. The pediatric dentist and the parents can help the child learn the schemata for “dentist,” “visiting the dentist” and “oral hygiene” even before his or her first dental visit by posting current pictures of the dentist, the waiting room, and the pediatric operatory on the practice’s website, so that parents can show their children who the dentist is and what the dental office looks like. The website can also suggest appropriate pictures about children’s dental appointments and oral home care for parent and child to look at together. These pictures can provide information about what a dentist does and how to maintain good oral health through behaviors at home. These principles also apply for older children. The photographs posted on the practice’s website can help children notice that the dentist and other personnel are smiling. “Smiling” is likely to be part of children’s schemata of “good people” or “nice people.” Another photograph might show the dentist using a large toy toothbrush to “brush” the teeth of a plush alligator, which can cue the parent to say: “Look, the dentist is cleaning Mr. Alligator’s teeth! That helps him keep his teeth nice and strong!” Since “nice” and “strong” are positive qualities, this conveys that dentists are helpful people, as well as that brushing is related to the health of one’s teeth. Dentists can provide parents with descriptions of what the dental philosophy of the practice is, what will happen at a dental appointment to pass on to the child, and additional information designed to help ensure that the parent provides information about how a dentist is helpful to children. While infants use their vision to begin to build schemata of concrete objects that they can see, such as dogs,

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cats, trees, and flowers, they need input from caretakers and other people to help build schemata for concepts which may not be visible [4]. For example, a young child who is taken to the dentist for the first time without the kinds of preparation referred to above will probably be able to see if the dentist is a member of the schema for “man” or a member of the schema for “woman.” But it will be much harder for the child to understand that this person is a “dentist” unless the parent tells the child, or the child watches a cartoon story explaining what a dentist is, what he or she does, and why he or she is important for a child. Other invisible schemata include “strong teeth” and “oral health.” Young children also learn the scripts which govern who is involved with a particular activity and how the events are supposed to transpire [4]. For example, the script for “day care” may include the child traveling to a particular location with a parent, where he/she is greeted by an adult who may help with removing a coat as the parent leaves. The child is then free to enter a play area where other children are. At a certain point, a meal or snack may be served. At another point, the children are expected to lie down and take a nap, or at least lie quietly. Later, the parent will come back, the child will be helped to put on his/her coat, and then parent and child will return home. Here, too, dentists can help by providing parents with suggestions for how to describe the script for “going to the dentist.” When children first visit the dental office, they try to understand this new experience in light of what they already know. When the new experiences do not fit with their current schemata and scripts, the child is more likely to respond with uncertainty, feelings of being overwhelmed, or fear. If the clinician can provide detailed pictures or other visual examples on his/ her website of what will happen during an initial dental visit, the parent and child can use this information to help the child develop new schemata and a script for “going to the dentist.” As a result, he or she will become more relaxed and will behave more positively on the first and future visits.

in an operatory, a child being examined in a mother-­ supported position, and so on. The “script” ends with photos of the dentist thanking the child for his/her help, the child receiving a reward from a “treasure box,” and the child and parent leaving the operatory and returning to the waiting area, putting the coat back on, and leaving the office. Once the child is at the dental appointment, the dentist can help the child elaborate the script by talking to him or her during the appointment about what the dentist is doing and why. This provides the child with more information to add to his developing script about what happens during a dental visit.

An additional bonus of developing a rich schema and script about who dentists are, what they do, and why they are important is that this can help protect a child from developing dental fear and/or incorrect ideas about dentists and dental visits. In 7 Chap. 4, it is pointed out that children can become afraid of the dentist by simply hearing another person say something such as: “Dentists! I hate them! They hurt you!” However, if the child has developed complex, positive schemata and scripts for dentists and dental visits, he or she is much less likely to be influenced by these negative statements from others. Revisiting the vignette of 15-month-old Sally, kicking and crying are normal behaviors for a child of her age  – and perhaps up to a year older than her  – so it would be a mistake to conclude that she is an unruly child (. Fig.  2.3). The initial kicking provides her developing brain with information about the object which she is sitting on. Closing her eyes, looking away from the dentist’s face, and crying are signs of being overwhelmed. The increased kicking is another sign of  

 

Eye Catcher

To help the child develop a script about what happens at a dental appointment, the practice website could include photographs of the door to the practice, what one sees once that door is opened (e.g., the receptionist and waiting area, with toys, child art work on the walls, perhaps a giant toothbrush), a child who is getting parental help taking off a coat and hanging it up, the dental operatory, the dentist talking with a child

..      Fig. 2.3  Some disobedience, or even aggression, is possible at the transition from the sensorimotor to the preoperational stage

15 Child Cognitive Development: Building Positive Attitudes toward Dentists and Oral Health

distress. There are a number of reasons why she might be feeling this way. First, it is her first dental visit, so she is working hard to figure out who this new person is and what this new experience is all about. Second, she has been put into a pediatric dental chair where she is separated from her mother. Third, unless she has seen his/her photograph ahead of time, she is now being approached by a stranger. These combined are probably more than she can tolerate. Examining Sally in a parent-supported (as well as restrained) position (7 Fig. 5.15a, b) is much less stressful, because in that position she can maintain physical contact with her mother/father, which should be soothing to her. This position also allows her parent to lean in, so that Sally can be reassured by seeing his/ her familiar face, thus satisfying the central need that young children have for physical parental touch and reassurance during the sensorimotor and early preoperational stages. Another cause for Sally’s distress is that the source of control has shifted from herself to the stranger/dentist. Before the crying began, Sally was putting the toy keys in her mouth and taking them back out again, a typical behavior for children in this stage, who learn a great deal about the world by putting things inside their mouths. Notice that Sally was controlling when the keys went inside and outside, and her tongue, inner cheeks, and lips were exploring the keys as she moved them. Contrast this with the dentist’s attempt to start an oral exam by putting a mirror inside her mouth: suddenly, someone else – a stranger – is controlling what gets put inside her mouth, how it moves around, and when it is removed. Observations of children under 2 years of age receiving dental care indicated that, when the caretakers were attentive to their children, the children were less distressed. The difficulty arises from the broad definition of being “attentive.” While the physical contact of a mothersupported exam may be important, it is not necessarily sufficient. The lack of control and/or understanding of being separate from the caregiver is distressing. Even if the parent is physically present in the operatory, if he/she is distracted – perhaps by being in conversation with the dental assistant or checking his/her phone for texts – the child is more likely to become distressed.  

2.1.2

Preoperational Stage

Case Study

When 4-year-old Alex enters the operatory, he hops up into the chair, slips, and bangs his chin on the metal tray table. He sheds a few tears and is quickly calmed by his mother. However, Alex remains apprehensive the entire visit even though he cooperates

with the clinician and the examination is successfully completed. When Alex arrives home, his father asks “How was your dental visit?” Despite learning that he has healthy teeth and having had an otherwise unremarkable clinical visit, Alex breaks into tears and tells his father all about how he got hurt. Now, here is the problem with memory: as time passes, Alex may remember the fear he experienced at the dentist office, but that memory has become detached from the source of the fear. In other words, he is likely to associate his fear with the dentist and the entire experience, rather than with the brief surprise and pain he experienced when he hopped up into the chair.

In addition to Piaget’s stage theory, psychologists soon found that children’s social environment also had a profound influence on their cognitive development. Lev Vygotsky, a contemporary of Piaget, believed that culture and, specifically, the social environment of a child provide a tremendous contribution to cognitive development. Of interest to the pediatric dentist is Vygotsky’s belief that children have skills that allow them to learn from others. Vygotsky identified what he called the zone of proximal development (ZPD) as the difference between skills the child has already acquired on his own and what he would be capable of doing with some assistance (or what is sometimes called “scaffolding”) from older siblings or adults [5]. Dentists, too, can help children learn new information by utilizing the concept of the ZPD and move the child’s cognitive development forward. For example, if a child opens his mouth only slightly, the dentist can say: “Nice job, Tommy! Right now I can see your front teeth. If you open your mouth really wide, then I can see the rest of your teeth, too.” Tommy is likely to open his mouth more widely, having learned how this allows the dentist to see more of his teeth. As children progress to the preoperational stage toward 2 years of age, they increasingly use symbols to represent their world. During this time, language skills are developing rapidly, and children are acquiring an increasing number of mental images and schemata. What this tells the clinician is that children can now engage in games of make believe or pretend play. While a child in this stage has not yet developed an understanding of basic mental operations, two very important skills have emerged: representing simple concepts (i.e., children can tell whether two things are the same or different) and he/she is beginning to understand the concepts of time. Children can now think about the concept of yesterday (the past) and soon (the future). These skills allow them to begin to anticipate the consequences of their behaviors. Further, compared with infants, children in the preoperational stage are learning to control their impulses,

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and thus they have more coping resources. Adults can take advantage of the concept of the zone of proximal development to help children develop coping resources. Case Study

Sammy walked slowly into the operatory and then stood hiding behind his mother. Sammy had been to the dentist once before, just after his first birthday, but he had no memory of that event. Now he was 4 years old. His mother gently tried to coax him into the chair, but he was very hesitant. She lifted him up into the chair, and he immediately drew his knees to his chest and put his head down. I introduce myself and tell Sammy that I want to take a look at his teeth to count them. Sammy doesn’t look at me or respond. I go on to say that, to do this, I need him to lie flat in the chair and to open his mouth for me. I suggest to him that perhaps he could pretend he was a statue, and lie still. While Sammy is listening to me, he remains folded up in his little ball position. Mom then says to Sammy: “Sammy, Melanie comes to Dr. Dentist so he can keep her teeth healthy. She told me that when she ‘lies still like a statue’ and opens her mouth really wide, it makes the Doctor’s job easier.” I knew that Melanie was Sammy’s older sister, because she is my patient, too, but, since I had already asked Sammy to “lie still like a statue,” I had my doubts that his mother’s statement would work. I was surprised and happy to watch Sammy uncurl himself, put his hands at his side, and open his mouth! At the end of my exam, I complimented Sammy for his excellent ability to lie still like a statue. Sammy said that lying still like a statue worked for Melanie, so he trusted that it would work for him, too. His mother went on to say: “Sammy really adores Melanie.” He was unable to relate to pretend play as I had hoped, but, because of the example that his older sister had set, he developed a successful coping mechanism with a gentle nudge from his mother, based on the concept of the zone of proximal development.

At the same time, children in the preoperational stage have difficulty viewing the world from someone else’s perspective. This egocentrism means that children believe that other people perceive things in the same way as they do. From the child’s point of view, whatever he or she is seeing, hearing, or experiencing, the p ­ arent/sibling/dentist must also be experiencing. In other words, the child cannot “put himself/herself in another’s shoes.” For example, in the previous scenario Sammy acted as if the dentist couldn’t see him or know that he was in the operatory, because he couldn’t see the dentist when he was hiding behind his mother.

Just as the parents help the child understand who a dentist is and the upcoming dental visit by talking about what will happen, the dentist should talk to children during the dental appointment itself, explaining what he or she is doing and why he/she is doing it (“I am counting your teeth to see how many you have”). While it may be amusing to the child to experience other novel aspects of the dental office, such as feeling his/ her body recline and return to a sitting position as the back of a pediatric dental chair is lowered and raised, or fun to experience the water being squirted into his or her mouth and then suctioned out by the “straw,” probably the most important behavior for the dentist is to talk to the child about what he/she is doing – and why – before, during, and after any procedures or activities. The descriptions and explanations serve two purposes. First, they provide rationales for the child to help him/ her understand what is going on. Thus, they explain to the child what is happening, which is reassuring and can help prevent the child’s imagination from incorrectly assuming that something bad or dangerous is occurring in this new situation. Second, the information that is conveyed helps the child develop the schemata related to dentists and oral health. In addition, clinicians need to remember that preoperational children do not yet have the cognitive capacities of older children. For example, think about the directions you may give to a child patient during an appointment. Do you ask the child to open wide? Then close. Then open wide, then close. Now, perhaps you want to check the bite after a new filling, so you ask the child to open his mouth and grind his teeth backward and forward then side to side. Very young children will not be able to inhibit the well-rehearsed sequence of opening and closing their mouths and switch to the new grind backward and forward, side to side task. If tell-show-do (described in 7 Chap. 5) is used with preoperational children, the dentist should only refer to one step or action at a time. This is because children at this stage cannot remember a series of things very well. For example, if the dentist said “I need you to open your mouth very wide, and turn your head toward me, and be very still,” the child may remember the initial action that the dentist described (open mouth wide), or the last action described (be very still), but not all three. (In Sect. 2.2.1 of this chapter, we point out that, in general, memory tends to be strongest for the initial experience, due to the primacy effect, and the last experience, due to the recency effect. The same is true for hearing a list or series of words or descriptions. The issue with preoperational children is that they are not able to remember all of the contents of the list or series that are in between the first and last items as older children can.) One of the best illustrations of how children in the preoperational stage think differently from adolescents and adults can be seen in the children’s failure  

17 Child Cognitive Development: Building Positive Attitudes toward Dentists and Oral Health

to understand the principle of conservation. The classic example is to show a young child two glasses of the same size and shape, each filled to the same height with water. The child can compare the two glasses and tell you whether the amount of water in the glasses is the same or different (in this case, she will tell you that it is the same). Then, you can take a taller, thinner glass and have the child watch you as you pour the water from one of the first two glasses into this differently shaped – taller and thinner – glass. Then, when you ask the child whether the two glasses of water have the same amount of water in them, or a different amount, she will confidently tell you that they are different, and, in particular, that the tall glass has more water in it. When you ask her why, she will explain that the taller glass has more water because the water level is higher! This failure to understand that matter remains the same despite the change in height (i.e., the failure to understand conservation) extends to other changes in appearance (e.g., two lines of ten pennies each are “the same” as long as the two lines have the same length. However, once the pennies are spread out in one of the lines, then that line has “more” pennies in it.). Why does the child fail to understand conservation? Piaget said that children may only be able to focus on one aspect of a situation at a time. Thus, in the example of water, the child can only focus on the height of the two glasses  – without also being able to focus on the width of the glasses, or the fact that the volume of water must be the same even though it has been poured into a taller glass, because the child saw the adult pouring the water from the old container into the new one. On the other hand, an older child is not fooled by the increased height and will be able to tell you that the amount of water is still the same. If you ask how he knows this, he can say something such as: “You just poured the water into a new glass. If you pour it back again, you will see that it is the same amount as before.” The older child is referring to the process of reversibility. This means that dentists should not expect a child in the preoperational stage to be able to think about mentally reversing actions. For example, the following statement cannot be understood by preoperational children: “If you had done a better job brushing, the tooth bugs would not have become stuck to your teeth.” On the other hand, the dentist can take advantage of the fact that the preoperational child is likely to attribute lifelike qualities to inanimate objects and natural events, a process called “animism.” Thus, children of this age respond well to statements such as: “Let’s let your tooth rest on Mister Pillow” or “The super straw will suck up all of the extra water.”

2.1.3

Concrete Operational Stage

Case Study

Six-year-old Carlos hops up in the operatory chair with great energy and confidence. After a quick examination and a confirmation from the x-rays, I show Carlos the weakness on the enamel on his lower molar. When he asks, “How did that happen?” I explain about the decay while also including behavioral steps he can take to prevent the further breakdown of his tooth. Carlos is now old enough to understand the concept of reversibility such that he understands that, by skipping teeth brushing before he went to bed this past year, his enamel has weakened and the harmful bacteria in his mouth have multiplied and are attacking his tooth. Carlos can now perform basic mental operations, thus quickly calculating the effect his poor oral care may have on the rest of his teeth. As Carlos is now able to look at situations from a perspective outside of his own (i.e., is much less egocentric than the preoperational child), he is able to understand what I and his parents see. (For example, unlike 4-year-old Sammy, Carlos knows that the dentist could see him, or know that he was in the room, even if he tried to hide behind his mother.) I tell Carlos to imagine his teeth are like the bricks on the side of my office building. Sometimes ivy and moss start growing on the bricks and you might even think they make it look nice. But, when we pull the plants off of the brick, some of that hard brick goes with the plants. The brick on the building still looks good, but it is now weaker. When this happens over a period of years, eventually the bricks are no longer hard and strong and in some cases crumble and need to be removed. I explain to Carlos that this is like his teeth and sugar. His teeth are like the bricks, all polished and strong, and the pleasing to look at ivy is like the raisins and lollipops he is so fond of. It doesn’t happen overnight, but eventually, if the sugar is allowed to stick to the teeth without being removed every night, the enamel on his teeth, like the brick, will weaken and crumble. My story is met with a blank stare from Carlos, who says that his teeth don’t have ivy and moss growing on them! Children at Carlos’ stage of cognitive development have trouble with hypothetical and abstract reasoning. Any directions that start with “imagine” or “let’s pretend…” are doomed as children at this stage understand concrete concepts and have not yet developed the skill to think in the abstract.

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He admits that he is smoking now, “like all the other guys” in his circle of friends, but goes on to say that he’ll never get lung cancer because he’ll quit way before that happens.

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..      Fig. 2.4  Elementary schoolchildren are at the concrete operational stage

By the time a young child is in elementary school, she has entered the concrete operational stage (. Fig. 2.4). She can understand some of the concepts that were difficult earlier, such as reversibility and conservation. The ability to control impulses increases in this stage, allowing the child to use an increasing number of strategies to deal with difficult or unpleasant situations. The primary limitation of this stage is that children cannot think abstractly or with hypotheticals.  

2.1.4

Formal Operational Thought

Case Study

Your hygienist put her head inside the operatory where you are working on a patient, and asked: “May I see you in your office when you have a moment, Doctor?” A few minutes later, you excuse yourself and meet with the hygienist. “It’s Kenny, Doctor. I’ve spoken with him about his oral hygiene during the last two visits, but he’s still not brushing his teeth very often. And today I can smell cigarette smoke, which is new.” Kenny is a 14-year-old who has been in your practice since he was in elementary school. He’s a bright teen who is interested in marine biology, and hopes to study this in college. You invite him to join you in a private room. When you ask about his brushing, he says “Yes, I know about brushing off the food bits, but I don’t like to brush. I haven’t had a cavity in years, so I figure that I’m not going to get anymore.”

Piaget believed that children will enter the final stage of cognitive development – formal operational thought – at around 11 or 12  years. While children in the concrete operational stage can solve problems, they must physically manipulate objects in some way in order to do so. By contrast, youth are increasingly able to solve problems by mental processes. Adolescents in this stage can think about things and arrive at solutions without having to actually manipulate objects. For example, if presented with the following information: “Tom is taller than Bob, and Bob is taller than Joe, and Joe is taller than Chris” and then asked: “Who is taller, Chris or Tom?”, the adolescent in the formal operational thought stage can answer: “Tom is,” because he or she understands how to solve word problems using his/her knowledge of logic. By contrast, a child in the concrete operational stage will need to look at a drawing showing the three people and their relative heights to figure this out. The use of logic signifies an increasing ability to use abstract thought processes, such as using and understanding metaphors and analogies; ponder things that don’t exist (“I wonder what the moon would be like if there was water on it?”); think about abstract concepts, such as “health,” “justice,” and “love”; think about the outcomes of an action which hasn’t been taken yet; and understand causation (. Fig. 2.5). Thus, an adolescent can understand the scientific reasoning about why he/ she should use a toothbrush regularly, why consuming acidic drinks or having a dry mouth can pose risks to dental health, and the like. On the other hand, due to what Piaget referred to as “adolescent egocentrism,” even adolescents who can articulate the biological processes related to caries development may act as if the science doesn’t apply to them. Thus, some adolescents do not practice oral self-care and/or do not attend a dentist regularly; these individuals are more likely to have untreated dental needs [6–8]. The increased inhibitory abilities that were noted for younger children continue in adolescence. For example, in one cross-sectional study, adolescents younger than 16 years old stated that they preferred to take a smaller reward immediately, rather than wait for a larger reward in the future. On the other hand, the adolescents who were 16 or older wanted to wait for the larger reward, indicating a greater ability to inhibit the desire to have the reward immediately. The older adolescents also  

19 Child Cognitive Development: Building Positive Attitudes toward Dentists and Oral Health

that the dentist knew about her hobbies and interests, which included Irish dancing, and together they had decided that she could distract herself by “practicing” her Irish dancing steps during the treatment (as long as she was able to curtail the arm movements, which typically involved lifting her arms above her head). The deliberate foot movements were a scaled-down version of the kicks and other steps that were involved in the dances.

Having a sense of control helps individuals cope with stressful situations [18]. Since the amount of desired control will vary from person to person and from circumstance to circumstance, it is important to consider both the amount of desired control that an individual has when faced with a stressful situation and the amount of perceived control that the individual feels he/she actually has in that situation. The Revised Iowa Dental Control Index (R-IDCI) is ..      Fig. 2.5  At formal operational stage, children and adolescents a nine-item scale which measures these two constructs are capable of abstract thinking in the dental situation. Adult patients who experienced less control in the dental setting than they preferred to described themselves as being more likely to think about have rated themselves as having experienced higher levels of anxiety and pain during dental treatment, as well the future, compared with the younger ones [9]. Thinking about the future is associated with a num- as having higher levels of dental fear in general [19]. The ber of health-promoting behaviors, such as engaging in nine-­item R-IDCI has also been used with youth aged exercise and making healthy food choices [10]. Future 11–15 years in the United States, Australia, and Japan, orientation is also related to obtaining regular health where it was compared with a measure of preferred conscreenings. For example, adults who are more future-­ trol strategies for children in the dental setting (Child oriented are more likely to have had a recent dental Dental Control Assessment, CDCA) [20] and measures checkup [11]. By contrast, homeless youth who are less of dental fear [21]. The results indicate that the CDCA future-oriented are more likely to go to a dentist when and the R-IDCI perform well with adolescents and they have a problem, rather than for routine checkups, could provide the dentist with rich information about and are more likely to neglect their oral home care [12]. patients’ preferences for various strategies that the denCompared with children, adolescents are more likely tist can use during a dental appointment, as well as the to use cognitive, approach-oriented control strategies, patients’ potential for experiencing pain and anxiety such as information seeking, positive self-talk, and cog- during dental treatment if they prefer to have greater control than they actually feel that they have during nitive distraction [13–17]. dental treatment. Case Study

One of us (TC) observed a teen as she underwent a restoration. The observer noticed that the teen was moving her feet in a deliberate way on the chair (while taking care not to jostle herself), and asked the teen about this once the treatment was completed. Sitting upright, the patient explained that she had been anxious about whether she would be able to handle the discomfort of the injections and the length of time that the treatment would take. She went on to say

Eye Catcher

Sample Revised Iowa Dental Control Index items: Desired Control: 55 To what degree would you like control over what will happen to you in the dental chair? Predicted Control: 55 Do you feel you have control of what will happen to you in the dental chair?

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Eye Catcher

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55 55 55 55

2.2

Sample Child Dental Control Assessment Items: I want the dentist to tell me what will happen. I want the dentist to answer my questions. I want the dentist to tell me how long things will last.

 sing Memory Principles to Help U Prevent the Development of Fear

Returning to 4-year-old Alex, who banged his chin at his dental appointment, let us focus on what dentists can do to prevent children from developing dental fear. This is particularly important given that we want children to return for routine dental care on a regular basis, and it is possible that children may also need to undergo some appointments that involve restorations or other invasive treatments. Unfortunately, the negative memory from one appointment may impact a child’s behavior on subsequent visits [22]. Given the pervasive negative valence surrounding dental appointments in our culture (how often has one heard “It was like pulling teeth” or “Ugh, I’d rather have a root canal”), children may have heightened anxiety and arrive at their first dental visit prepared to experience something awful. Some research focuses on restructuring memory of visits or procedures so as to prevent negative memories growing with the passage of time [23–25]. General memory principles help guide the restructuring procedure followed in cognitive intervention [23]. These include: Use the primacy effect concept identified by memory researchers. We have already recommended that dental offices offer stimuli (e.g., photos of the dentist and the dental office on the practice website) and previsit activities (e.g., books for parents and children to look through) to help prepare children for their initial visit. Dentists also need to ensure that the initial visit – and the initial aspects of that visit  – is as positive as possible. These initial experiences are likely to be strongly remembered, as they are the primary experiences that the child has. When children form their first impression of their visit, they will use that information as a lens through which they experience and interpret all subsequent information, and have additional time to explore, think about, and analyze this initial information. This results in a strong encoding and thus a stronger recall. Since 4-year-old Alex had a painful experience at the onset of his dental appointment, it is not surprising that his memory of the visit – as he described it to

his father – focused on this initial experience. This demonstrates the power of the primacy effect. However, if the dentist (and/or parent) had found ways to use some of the behaviors described below, Alex would have been better able to put the initial experience in context. Important behaviors for the dentist who wants to prevent the development of dental fear: 55 Have the child repeat the information that you want him/her to remember. You can ask the child “What did you learn today?”, as well as “What are you going to tell your dad [i.e., the parent who was not in the operatory with the child during the visit] about your trip to the dentist today?” 55 Have the child talk about what she learned and how well she did today, because this helps to ensure that she remembers these positive aspects. 55 If the child refers to “negative” behavior, reframe this in a truthful way to put it in perspective, and include a reference to some aspect of positive behavior that you noticed. For example, if the child says “I cried, it hurt,” you can reply: “Yes, it’s true that you did cry when you got the shot, and I am sorry that it hurt you. But you only cried for a minute or two, and then you were able to lie very still and that helped me finish the work quickly. Overall, you really did well today!” 55 After walking the child back out to the waiting room, be sure that she overhears you tell her parent what a good job she did today. 55 Focus on simple, salient facts while suggesting important ideas peripherally. Suppose the main important idea that you want the child to understand is: “Make sure you cover your teeth with toothpaste every time you brush.” To make that message salient, talk about how “the fluoride in the toothpaste kills the bacteria that eat your tooth enamel. When you cover your teeth with toothpaste, you are protecting them.” 55 Children (and adults) find it easier to remember information if it is associated with them. For example, the dentist should talk to the child during the appointment about how well he is helping. The dentist can say: “Thank you for lying nice and still.” “Thank you for letting me know that you need a little break now.” “You know how to open your mouth really wide!” In addition to ensuring that the beginning of the dental encounter is positive (primacy effect concept), according to the recency effect concept the last experiences at the dental office are also central to the child’s memory of the visit. In other words, the dentist needs to ensure that these last experiences are positive. The end of the appointment provides an excellent opportunity

21 Child Cognitive Development: Building Positive Attitudes toward Dentists and Oral Health

to reinforce concepts first introduced, and any positive behaviors exhibited. Remind children how they helped the dentist take care of their teeth. The dentist can say: “You really helped me today! You sat nice and still, you opened your mouth really wide, which made my job so much easier. You also followed my directions really well. You know, you helped me so much today, and that made my job so much easier.” Always praise the child for something positive, even if the appointment was difficult. For example, even the child who cries during the entire examination can be told what a great job he did opening his mouth very wide when the dentist asked so that the dentist could see his teeth much more easily. To illustrate the power of the last experiences of a dental visit, imagine the memory that this young patient – observed at the end of an appointment which included a restoration – will have of his dental visit: The father heard his son crying in the operatory and came to the doorway. When he saw his child in the dental chair, extremely upset, he said: “Ahhh, now I know what to do to punish you in the future. Next time you misbehave I’m going to bring you back here!”

2.3

 ailoring Oral Messages T to the Individual Patient

Dentists (and other dental personnel) often find themselves wanting to give information or advice to their patients and/or the parents of their patients. Sometimes they feel frustrated when their advice doesn’t seem to be heeded. We would like to offer some suggestions about how to tailor the information in specific ways, which have been found to be more effective in terms of resulting in actual behavior change. Of note, individuals are motivated both by the promise of receiving rewards and the risk or threat of receiving punishment, although some individuals are more motivated by one of these two possibilities [26]. An individual’s relative preference for one of these two possibilities can be assessed by the BIS/BAS Scale [26], where BIS is short for the “behavioral inhibition system” (i.e., that which operates to reduce the risk of receiving punishment) and BAS is short for the “behavioral activation system” (i.e., that which operates to increase the likelihood of receiving rewards). A 10-year longitudinal study found that adolescents’ endorsement of the BIS items increased with age [27], indicating that inhibition tendencies increase with experience and maturation.

Eye Catcher

Sample BIS item: “I feel worried when I think I have done poorly at something important.” Sample BAS item: “When I want something I usually go all out to get it.”

Given the seeming paradox between understanding the reasoning behind, say, suggestions to brush but at the same time not brushing, dentists are likely to find the results of one study team intriguing. In several studies, Sherman, Updegraff, and Mann [28] experimented with the wording of the messages they created to learn whether they were successful in motivating college students to change an oral behavior. First, they created two messages about flossing. One was gain-oriented (“Great Breath, Healthy Gums Only a Floss Away”) and referred to the benefits of flossing, while the other was loss-­oriented (“Floss Now and Avoid Bad Breath and Gum Disease”) and referred to the downsides of not flossing. Importantly, the same information was included in both messages. For example, the gain-oriented message included the statement that “flossing your teeth daily removes particles of food in the mouth, avoiding bacteria, which promotes great breath,” while the loss-­oriented message included the same information, but worded differently: “If you don’t floss your teeth daily, particles of food remain in the mouth, collecting bacteria, which causes bad breath.” The team recruited college students and measured their relative preferences for approaching (to receive a reward) or avoiding (to avoid punishment) with the BIS/BAS scale. The researchers postulated that the students who were higher on BIS would respond more to a message focused on losses, while the students who were higher on BAS would respond more to a message focused on gains. The students were then randomly assigned to receive either the gain or the loss message. After they read the message, they received individual packets of dental floss. After a week, the students were asked how many packets they still had. The results were that students who had received the message which was congruent with their motivational style flossed significantly more than the students who had received the message which was incongruent with their motivational style [28]. The take-away message is that the dentist who specifically tailors his/her description of the outcome of a desired behavior (e.g., more frequent dental visits, such

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as checkups; increase or decrease in oral self-care behavior at home, etc.) to match the patient’s motivational style (or the parent’s motivational style, in the case of a child patient) is likely to be more effective, compared with a dentist who tends to provide the same description to all of his/her patients and parents. Dentists can create gain- and loss-oriented descriptions of behaviors which they would like to influence, such as reducing smoking, increasing tooth brushing, and the like. Typically, these messages contain the same information, but worded differently to either focus on the costs or gains associated with the behavior. Eye Catcher

Sample part of a loss message for quitting smoking for adolescents: 55 What are the costs of continuing to smoke? –– Your appearance: By continuing to smoke, you will have premature wrinkling and aging of your face and lips. Your teeth will also be more yellow, since cigarette smoke stains your teeth…. Sample part of a gain message: 55 What are the benefits of quitting smoking? –– Your appearance: By quitting smoking, you will avoid premature wrinkling and aging of your face and lips. Your teeth will also be whiter, since cigarette smoke stains your teeth… (Of course, other information – such as about risks/ gains to lungs, teeth, and sexual performance, the amount of money that will be spent on cigarettes/ saved by stopping smoking, etc.  – can be added to these samples.)

Returning to the vignette about 14-year-old Kenny, it appears that this adolescent is currently motivated by an approach motivation (although the dentist could check this by asking him to complete the BIS/BAS Scales), so it would be best to frame messages that stress the benefits of quitting smoking (i.e., quitting smoking means that you could save X dollars per month; your clothes and hair will smell fresh, since they won’t be exposed to tobacco smoke; etc.) Similarly, it would be best to frame messages about regular tooth brushing that stress the benefits of this behavior (e.g., brushing regularly means that your breath will be fresher, you’ll be more likely to keep your teeth for a lifetime, etc.).

References 1. Bjorklund DF. Cognitive development: an overview. In: Zelazo PD, editor. The Oxford handbook of Developmental Psychology, Vol 1: body and mind. New York: Oxford University Press; 2013. p. 447–76. 2. Piaget J.  The construction of reality in the child. New  York: Basic Books; 1954. 3. Meltzoff AN, Moore MK. Imitation of facial and manual gestures by human neonates. Science. 1977;198:75–8. 4. Gelman SA. Concepts in development. In: Zelazo PD, editor. The Oxford handbook of Developmental Psychology, Vol 1: body and mind. New York: Oxford University Press; 2013. p. 542–63. 5. Vygotsky LS.  Mind in society: the development of higher psychological processes. Cambridge, MA: Harvard University Press; 1978. 6. Coolidge T, Heima M, Johnson EK, Weinstein P.  The dental neglect scale in adolescence. BMC Oral Health. 2009;9:2. 7. Skaret E, Raadal M, Berg E, Kvale G. Dental anxiety and dental avoidance among 12 to 18 year olds in Norway. Eur J Oral Sci. 1999;107:422–8. 8. Sarri G, Evans P, Stansffeld S, Marcenes W.  A school-based epidemiological study of dental neglect among adolescents in a deprived area of the UK. Brit Dent J. 2012;213:E17. https://doi. org/10.1038/sj.bdj.2012.1042. 9. Steinberg L, Graham S, O’Brien L, Woolard J, Cauffman E, Banich M.  Age differences in future orientation and delay discounting. Child Dev. 2009;80:28–44. 10. Joireman J, Shaffer MJ, Balliet D, Strathman A. Promotion orientation explains why future-oriented people exercise and eat healthy: evidence from the two-factor consideration of future Consequences-14 scale. Pers Soc Psychol B. 2012;38:1272–87. 11. Bradford WD.  The association between individual time preferences and health maintenance habits. Med Decis Mak. 2010;30:99–112. 12. Coolidge T, Pickrell J, Raykhman M, Trippel C, Riedy CA.  Smoking, dental attendance, and the CFC-14  in homeless youth. Presented at the second international conference on time perspective, July 29 – August 1, 2014; Warsaw, Poland. 13. Band EB, Weisz JR. How to feel better when it feels bad: Children’s perspectives on coping with everyday stress. Dev Psychol. 1988;24:247–53. 14. LaMontagne LL, Hepworth JT, Johnson BD, Cohen F.  Children’s preoperative coping and its effects on postoperative anxiety and return to normal activity. Nurs Res. 1996;45:141–7. 15. Hodgins MJ, Lander J.  Children’s coping with venipuncture. J Pain Symptom Manag. 1997;13:274–85. 16. Fields L, Prinz RJ.  Coping and adjustment during childhood and adolescence. Clin Psychol Rev. 1997;17:937–76. 17. Olson AL, Johanssen SG, Powers LE, Pope JB, Klein RB. Cognitive coping strategies of children with chronic illness. Dev Behav Pediatr. 1993;14:217–23. 18. Compas BE, Jaser SS, Dunn MJ, Rodriguez EM.  Coping with chronic illness in childhood and adolescence. Annu Rev Clin Psycho. 2012;8:455–80. 19. Brunsman BA, Logan HL, Patil RR, Baron RS.  The development and validation of the revised Iowa dental control index (IDCI). Pers Indiv Differ. 2003;34:1113–28. 20. Weinstein P, Milgrom P, Hoskuldsson O, Golletz D, Jeffcoat E, Koday M. Situation-specific child control: a visit to the dentist. Behav Res Ther. 1996;34:11–21.

23 Child Cognitive Development: Building Positive Attitudes toward Dentists and Oral Health

21. Coolidge T, Heima M, Heaton LJ, Nakai Y, Höskuldsson Ó, Smith TA, Weinstein P, Milgrom P.  The child dental control assessment (CDCA) in youth: reliability, validity and cross-cultural differences. Eur J Paediatr Dent. 2005;6:35–43. 22. Quas JA, Bauer A, Boyce WT.  Physiological reactivity, social support, and memory in early childhood. Child Dev. 2004;75: 797–814. 23. Pickrell JE, Heima M, Weinstein P, Coolidge T, Coldwell SE, Skaret E, Castillo J, Milgrom P.  Using memory restructuring strategy to enhance dental behaviour. I J Paediatr Dent. 2007;17:439–48. 24. Chen E, Zeltzer LK, Craske MG, Katz ER. Alteration of memory in the reduction of children’s distress during repeated aversive medical procedures. J Consult Clin Psych. 1999;67:481–90.

25. Bruck M, Ceci SJ, Francouer E, Barr R. I hardly cried when I got my shot! Influencing children’s reports about a visit to their pediatrician. Child Dev. 1995;66:193–208. 26. Carver CS, White TL.  Behavioral inhibition, behavioral activation, and affective responses to impending reward and punishment: the BIS/BAS scales. J Pers Soc Psychol. 1994;67: 319–33. 27. Almy B, Kuskowski M, Malone SM, Myers E, Luciana M.  A longitudinal analysis of adolescent decision-­making with the Iowa gambling task. Dev Psychol. 2018;54:689–702. 28. Sherman DK, Updegraff JA, Mann T. (2008). Improving oral health behavior: a social psychological approach. J Am Dent Assoc. 2008;139:1382–7.

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Pediatric Body Growth Panagiota Triantafyllou and Stephanie Roberts Contents 3.1

Normal Growth – 26

3.1.1 3.1.2

 rowth Phases – 26 G Growth Evaluation – 26

3.2

Growth Disorders – 30

3.2.1 3.2.2 3.2.3

I ntrauterine Growth Retardation and Small for Gestational Age Newborns – 30 Short Stature – 30 Tall Stature – 32

3.3

Puberty – 34

3.3.1

Disorders of Puberty – 34

References – 35

© Springer Nature Switzerland AG 2022 N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry, https://doi.org/10.1007/978-3-030-78003-6_3

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Growth and development in addition to onset and progression of puberty are important topics in the field of pediatrics and that of pediatric dentistry. Growth is the term which is referred to children’s linear growth, whereas development is referred to cognitive and emotional maturation and milestones’ achievement written in 7 Chap. 2.  

and sex steroids is essential for fetal growth. Thyroid hormones are very important for growth after birth but do not seem to be essential during fetal period given that the growth of newborns with athyreosis is unaffected. Male fetus starts to produce testosterone at tenth fetal week. Elevated testosterone levels perinatally drive to a higher weight and less adipose tissue of male newborns [1–5]. 3.1.1.2

3.1

Normal Growth

Human growth is a complex and dynamic process which starts at the time of ovum’s fertilization and continues until the end of puberty with the fusion of the long bones’ epiphyses. At any stage, normal growth is evidence of good health. The process of growth is controlled by many interacting factors such as endogenic (genotype), exogenic (nutrition and environment), and internal regulatory systems (hormones and growth factors) [1–3]. The role of the above factors depends on the stage of growth. The rate of growth on the other hand is neither the same nor symmetric for all the organs. There are four phases of growth: the prenatal, the infantile, the childhood, and pubertal [1–5].

Overview

Infantile Growth

Following birth, infants continue to grow rapidly. By the end of first year of life, the infant has increased his length 50% (approximately 25  cm) and has tripled his weight. Growth during this period is influenced mainly by nutritional factors and less by genetics, thyroid, and growth hormone [1–4]. 3.1.1.3

Growth in Childhood

In the second year of life, height velocity is 10–13 cm/ year, and in the third year it is 7.5–10  cm/year. Thereafter, childhood growth is relatively constant and from age 3 years to puberty, height velocity is 5–6 cm/ year. Weight gain is approximately 2–3 kg/year in both genders. During this period growth is predominantly regulated by growth hormone, IGFs, and thyroid hormone. Nutrition is less important in this stage but a positive energy status is important to avoid falloff in linear growth [1–5].

Pubertal Growth

Prenatal

Conception to birth (newborn 0–28 days)

3.1.1.4

Infantile

1–23 months

Childhood

2–12 years

Puberty

12–16 years

Children generally enter puberty on average at age 10  years in girls and age 12  years in boys. Following quiescence of the hypothalamic-pituitary-gonadal axis after the mini-puberty of the fetal and neonatal period, pubertal onset results from gradual increase in GnRH pulsatility and secretion followed by increased pulsatile release of LH, FSH, and sex steroids. Moreover, sex steroids (mainly estradiol in girls and testosterone in boys) stimulate growth directly and indirectly by augmenting growth hormone production. The first clinical sign of pubertal onset of girls is breast budding and in boys it is testicular enlargement. Additionally, pubertal growth spurt in girls begins at the onset of puberty, whereas in boys it happens approximately 2  years later. The combination of a longer period of prepubertal growth and greater amplitude of pubertal growth results in greater adult height in male [1–5].

3.1.1

Growth Phases

3.1.1.1

Prenatal Growth

The intrauterine development of the zygote into the 50-cm newborn is the first and most impressive period of growth. It is divided into three trimesters. The completion of organogenesis in the first trimester is followed by the rapid acceleration during the second trimester with maximum velocity of 2.5  cm/week, whereas during the third trimester it is mainly the weight which is accelerated. Intrauterine growth depends on maternal nutritional status, the size of uterus, the placenta, and the influence of insulin growth factors (IGFs). Genetics and growth hormone play a minor role during this period, although skeletal dysplasias like achondroplasia or severe growth factors’ deficiency do influence intrauterine growth. In terms of hormones and in addition to the insulin-like growth factors (IGFs), fetal insulin production in response to maternal glycemia, placental lactogen,

3.1.2

Growth Evaluation

3.1.2.1

Weight and Height Measurement

Precise anthropometric measurements are the basis of an accurate growth assessment. Infants are weighed without any clothes and children with minimal clothing and

27 Pediatric Body Growth

without shoes. For children from birth to 2 years of age, supine length should be measured, and it requires two persons to obtain a reliable measurement. The one holds child’s head and the other straightens the legs. Over the age of 2 a stadiometer should be used to measure height in standing position without shoes. Measurements should be plotted on standardized growth charts [3, 5]. Standardized growth charts can be obtained from either national surveys or the World Health Organization website (. Figs. 3.1 and 3.2). For patients who have trisomy 21, Turner syndrome, Klinefelter syndrome, and achondroplasia, specific growth charts are available that should be used [3]. In every growth chart there are five curves usually referred to third, 15th, 50th, 85th, and 97th percentile. For instance, when the height of a child is plotted on the 15th percentile, it means that 15% of children matched for age and gender are shorter and 85% taller than that child. To evaluate weight gain, it is preferable to use BMI (body mass index) growth charts according to which children are categorized as underweight, normal, overweight, or obese. In children less than 2 years, weight-for-length is used instead of BMI. Moreover, head circumference, arm span, upper segment/lower segment ratio, and sitting height are body proportion measurements that can be considered for growth evaluation if there is a clinical concern for short or tall stature, falloff in growth velocity, or an underlying syndrome.  

3.1.2.2

Growth Velocity

Normal growth is assessed by growth velocity. It is calculated by the difference of two measurements in a time interval of 6–12 months. Shorter intervals such as 3 months may lead to inaccurate evaluation of growth. There are specific charts for growth velocity (. Fig. 3.3). Growth velocity follows seasonable variability given that it is accelerating in spring and summer than fall and winter [3, 6]. Assessment of growth velocity depends on the stage of pubertal development and pubertal tempo during puberty and depends on the timing of pubertal growth spurt. Family history is an important part of the history to assess the anticipated onset of puberty and growth spurt.  

3.1.2.3

Midparental Height or Target Height

The evaluation of a growth pattern should be based on the genetic potential since adult height is in part genetically determined. For instance, we do not worry for a child growing at the tenth percentile if parents are healthy and their height is also at the tenth percentile and the child has a normal growth velocity for age. By contrast, if the parents are very tall, even if this child’s height is in normal range, it is short for the genetic potential and needs further investigation. Therefore, the

child’s adult height potential can be estimated by calculating midparental (MPH) or target, height. Having measured parents’ heights, the target height is occurring by calculating mean parental height and adding or subtracting 6.5 cm for male or female child, respectively. Two standard deviations for the calculated target height is approximately ±10 cm [1]. 3.1.2.4

Bone Age

Linear growth depends on skeletal maturation which in normal children follows an orderly development. Skeletal maturation depends on the appearance of epiphyseal centers, the length of long bones, and the fusion of the epiphyses that marks the cease of growth. Estrogen fuses the growth plate in both girls and boys. Bone age is a method of assessing skeletal maturation by comparing left hand and wrist radiograph with given age-­appropriate standard radiographs of healthy children (. Fig. 3.4). There are two main methods for the evaluation of bone age: a) the most widely used Greulich and Pyle hand standards and b) the Tanner and Whitehouse method mainly used in Great Britain [1, 6–10]. Retarded bone age may be seen in hypothyroidism, growth hormone deficiency, Cushing’s syndrome, chronic malnutrition, and underlying chronic disease. Advanced bone age results from hyperthyroidism, precocious puberty, androgen excess, or obesity. Furthermore, bone age, in addition to child’s height at a specific moment, can be used for prediction of final height, commonly performed using the BayleyPinneau method [9, 10]. Height predictions must be used in caution in children with abnormal growth patterns and/or underlying pathology that may impact growth.  

3.1.2.5

Dental Age

The appearance of teeth in an orthopantomographic (OPG) radiograph aids in estimating the dental age of a child according to mineralization/maturation stage of the dental hard tissues. Such information is useful, inter alia, in anthropology and forensic medicine/dentistry. Among several methods, the one most commonly used is Demirjian’s, which is based on the recording of all teeth – except for the third molars – of the left side of the mandible from the OPG. It records eight stages, beginning from the mineralization of the tips of their cusps to full root apex formation, in relation to chronological child age (. Fig.  3.5). The method is considered relatively accurate (± 1 year) for finding dental maturity of single children, although there may be an overestimation in puberty [11]. Dental age, despite being considered more reliable than eruption age of the teeth, does not show a high correlation with bone age [12].  

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Height-for-age BOYS

a

5 to 19 years (percentiles)

97th

190

3

190

85th 180

180

50th 170

15th

170

Height (cm)

3rd 160

160

150

150

140

140

130

130

120

120

110

110

Months 100

Years

3 6 9

5

3 6 9

6

3 6 9

7

3 6 9

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3 6 9

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3 6 9

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3 6 9

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3 6 9

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3 6 9

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3 6 9

14

3 6 9

15

3 6 9

16

3 6 9

17

100

3 6 9

18

19

Age (completed months and years) 2007 WHO Reference

Height-for-age GIRLS

b

5 to 19 years (percentiles) 180

180

97th 85th

170

170

50th 160

160

15th 3rd

Height (cm)

150

140

140

130

130

120

120

110

110

100

100 3 6 9

Months

Years

150

5

3 6 9

6

3 6 9

7

3 6 9

8

3 6 9

9

3 6 9

10

3 6 9

11

3 6 9

12

3 6 9

13

3 6 9

14

3 6 9

15

3 6 9

16

3 6 9

17

3 6 9

18

19

Age (completed months and years) 2007 WHO Reference

..      Fig. 3.1  Height for age WHO curves from fifth to 19th year of age of children. Frequently used percentiles are marked at the right side. a. Boys. b. Girls

3

29 Pediatric Body Growth

Weight-for-age BOYS

a

5 to 10 years (percentiles) 45

45

97th

40

40

85th

Weight (kg)

35

35

50th 30

30

15th 25

25

3rd

20

20

15

15 3

Months

Y e a rs

6

9

5

3

6

9

6

3

6

9

7

3

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3

6

9

9

10

Age (completed months and years) 2007 WHO Reference

Weight-for-age GIRLS

b

5 to 10 years (percentiles)

97th

45

40

45

40

85th

Weight (kg)

35

35

50th 30

30

15th 25

25

3rd

20

20

15

15 3

Months

Y e a rs

5

6

9

3

6

6

9

3

7

6

9

3

8

6

9

3

9

6

9

10

Age (completed months and years) 2007 WHO Reference

..      Fig. 3.2  Weight for age WHO curves from fifth to tenth year of age of children. Frequently used percentiles are marked at the right side. a. Boys. b. Girls

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9

22

3

Centimetres per year

18

8

Boys Girls

16

6

14

Peak

12

5

10

4

8

3

6

2

4

1

2 0

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 Age Rate of height increase

0

..      Fig. 3.3  Height velocity curve for boys and girls (50th percentile)

a

Growth Disorders

3.2.1

7 Inches per year

20

3.2

I ntrauterine Growth Retardation and Small for Gestational Age Newborns

The terms intrauterine growth retardation and small for gestational age newborns many times are used identically. However, the first is the pathologic counterpart to the second. The term intrauterine growth retardation (IUGR) is referred to a newborn whose growth did not achieve genetic potential, whereas the term small for gestational age (SGA) is referred to a newborn with weight and/or length below the third or tenth percentile for gestational age. Therefore, the SGA newborns have low birth weight and/or length due to genetic or constitutional factors or intrauterine growth retardation results from maternal, placental, or fetal factors [3, 6, 13].

b

Overview 55 Intrauterine growth retardation – newborn growth did not achieve genetic potential 55 Small for gestational age – newborn’s weight and/or length 

>

Pain

/? (evoked)

+ (spontaneous)

Intense hemorrhage on exposure

+

Radiographic findings

/+

14.1.2.1  Antimicrobial Medication

in Emergency Cases

Acute orofacial infections are mostly  of dental origin and usually respond well to dental treatment. A fundamental principle of treating infections of dental origin is to control the endodontically established microbial factor; this is achieved with extraction or root canal treatment of the tooth involved. If however these are left untreated, they may lead to a dangerous spread of the infection, e.g., to obstruction of airways [9]. In such cases, the dentist may need to cooperate with the pediatrician and possibly hospitalize the child. Antimicrobial (antibiotic) medication should generally be administered when the overall condition of the child is serious or in cases of intense progressive cellulitis where there is a risk of the infection spreading to more vital organs. A conservative use of antibiotics is indicated for minimizing the risk of developing resistance to current antibiotic regimes [6, 14]. In many countries phenoxymethylpenicillin (penicillin V) is still recommended, while if anaerobic infection is suspected, metronidazole may be used at a dose of 7.5 mg/kg of body weight every 8 hours for 5–6 days [14]. Semisynthetic penicillins are usually preferred, such as amoxicillin and its more recent forms with the addition of clavulanic acid. Another antimicrobial is clindamycin. Despite reservations in the past about side effects, such as pseudomembranous colitis, clindamycin is used due to its good absorption and antimicrobial spectrum, which includes numerous anaerobic microbes. Dosage is 15–40 mg/kg of body weight, divided into 3–4 equal doses. However, it may not be found in suspension and being suitable for children weighing 35–40 kg or older, in adult dosages. In cases of hypersensitivity to penicillin, in addition to clindamycin, more recent forms of macrolides, such as clarithromycin, are preferred, due to their better pharmacodynamics and dosage schemes compared

+/

+

..      Table 14.2  Antimicrobial medication in suspension form and usual dosage schemes for pediatric inflammations of dental origin; in cases of serious infections the dosage can be doubled Amoxicillin

40–50 mg/kg bw/24 hours, in 3 doses, for 7–10 days

Amoxicillin with clavulanic acid

40(32 + 8) mg/kg bw/24 hours, in 3 doses, for 7–10 days

Clindamycin

20–30 mg/kg bw/24 hours, in 3 doses, for 7–10 days

Clarithromycin

15 mg/kg bw/24 hours, in 3 doses, for 7–10 days

to erythromycin [6, 14, 19]. Usual dosages are presented in . Table 14.2.  

14.2  Treatment of Pulp Pathology

in Primary Teeth

14.2.1  Indirect Pulp Capping of Primary

Teeth

The aim of indirect pulp capping (IPC) is to maintain pulp integrity. It has been proposed for teeth with very deep carious lesions, in trying to avoid iatrogenic pulp exposure [20]. Prerequisite for IPC is the absence of clinical or radiographic signs of nonreversible pulpitis, and the only acceptable symptom may be short evoked pain that soon subsides without analgesics. In performing IPC, most bacteria-rich soft carious dentin is removed while the relatively hard, possibly discolored, dentin close to the pulp remains. This still contains some bacteria, the number and activity of which is drastically reduced when the cavity is restored with appropriate biocompatible material; its hermetic sealing deprives

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Description of an Emergency Case Dental History A 4-year old boy with no medical history was referred for consultation after a 9-day hospitalization with IV antimicrobial and analgesic/anti-­inflammatory medication for a persistent submandibular edema (the patient’s parents had sought emergency treatment at a local hospital’s pediatric department because of weekend holiday). Prior intense pain was in remission, and his temperature was 38 °C. Dental Examination The child was burned out and his cooperation low. Extraorally Chronic submandibular edema was still present (. Fig. 14.11), while local submandibular lymph nodes were found swollen and tender to palpation. Intraorally Clinically, the tongue presented a fungal infection. Two clinically sound, class II back-to-back composite resin restorations in the mandibular right first and second primary molars were present. Inadequate oral hygiene regionally, absence of intraoral edema but positive percussion signs from the first primary molar, was evident.  

The periapical radiograph indicated the mandibular right first primary molar as the responsible tooth (. Fig. 14.11). Diagnosis An extensive inflammation spread with no signs of purulence, originating from the carious pulp of the mandibular right first primary molar, was diagnosed as the cause. The tongue fungal infection had obviously been caused by the continued administration of antimicrobials. Treatment Based on the radiographic image of its sound roots, it was decided to immediately start root canal treatment of the respective tooth, under inferior dental block anesthesia and use of rubber dam. Debriding and irrigating the canals with sodium hypochlorite and filling root canals with calcium hydroxide led to full edema resolution; after 10 days, root canal filling with zinc and eugenol paste (ZOE) of the respective first primary molar and restoring both right first and second primary molars were made possible under the patient’s full cooperation. Oral hygiene was reinstituted, and treatment success was confirmed in follow-ups (. Fig. 14.11).  

 

a b

14

c

..      Fig. 14.11  a Persistent right submandibular edema after 9-day hospitalization of a 5-year-old. b The tongue presents fungal infection secondary to long chemotherapeutic treatment. c Radiograph reveals deep, back-to-back, restorations of mandibular right primary molars with residual carious dentin. A

d

difuse furcation bony lesion suggests the first primary molar as the responsible tooth (please disregard the dark thick artefact line above its pulp chamber). d The annual follow-up radiograph confirms the ­successful outcome of the root canal treatment

325 Pulp Therapy in Pediatric Dentistry

the bacteria of nutrients. The carious process is thus interrupted and any carious dentin that remains hardens (remineralizes) [7]. Following IPC, the pulp-dentin complex is preserved by activating the reparative pulp mechanism for secondary dentin apposition [21]. 14.2.1.1  Technique

the acceptance of sealing the soft infected dentin of primary molars under a PMC placed by the Hall technique. Attention should be paid to fully removing carious dentin located at the peripheral cavity walls and, particularly, the cervical one where most mistakes occur. The restorative material must be seated on healthy dental tissues (. Fig. 14.10). Otherwise, existing leakage risks caries progression. The use of a round bur (usually Νο. 4 or 5) at very low rotation speed provides quite a good sense of the hardness of deep dentin to be removed, in the effort to avoid pulp exposure. On the contrary, the use of a hand excavator, although very useful at initial removal of gross carious dentin, when approaching the pulp is more likely to result in its exposure. For the same reason, the use of the dental probe to sense the dentin hardness should be completely avoided, contrary to an old view for checking if all carious dentin is removed. The ART technique (discussed in 7 Chap. 13) for removing carious dentin using only hand instruments (usually without local anesthesia) is another form of IPC [22].  

The tooth is anesthetized and isolated with rubber dam. All carious dentin is removed except for that very close to the pulp, which, if removed, might lead to pulp exposure. This requires familiarization of the clinician with the pulp chamber shape and dimensions of primary teeth and with the radiographic image of deep primary molar caries. The risk of exposure is much higher approaching the primary tooth pulp horns, whether from the axial or the supra-pulpal cavity wall (. Fig. 14.12). While it is generally advised that following caries excavation only hard and discolored dentin remains, in fast-progressing active lesions no dentin with such characteristics is often found. This increases the risk of unnecessary pulp exposures. All these apply to anterior teeth as well. The properties of lining materials such as (RM)GIC allow for minimal remnants of soft dentin surrounding the pulpal horn [20]. These materials seem to possibly satisfy the need for both an indirect capping material and a filling material according to a clinical study [9], an approach that also reduces chair time. The same principal governs  

a

 

14.2.1.2  Materials

If the pulp is healthy or with signs of reversible pulpitis, it is sufficient to cover the pulpal cavity wall with conventional GIC or RMGIC [23]. Other biocompatible materials may be used like a quick-setting calcium hydroxide or ZOE. The latter was formerly used as temporary filling material in the so-called stepwise excavation [20]. For primary teeth in general, reentry to the cavity is not recommended and IPC and restoration are better completed in one session. Although there is a view that lining the deep cavity with calcium hydroxide is advantageous due to the initially high pH, what seems to be important is the tight seal from bacteria rather than the type of material used to cover the pulpal wall of the cavity [21]. 14.2.1.3  Effectiveness

b

c

..      Fig. 14.12  a Radiographically the occlusal carious dentin in the second primary molar is in contact with both pulp horns but not with central supra-pulpal wall. b The preparation of this deep cavity respects the pulp chamber shape. c Checking the finished restorations for early contacts after rubber dam removal

IPC success rates of 83–96% have been reported for primary teeth that present no signs or symptoms of nonreversible pulpitis [23]. IPC using preferably calcium hydroxide and GIC is taught as the technique of choice at 70% and 83% of American and British dental schools, respectively [24]. IPC has the same indications as pulpotomy in primary molars with deep carious lesions without pulp exposure [25] and may therefore be preferred over pulpotomy, since their success is similar [26].

14.2.2  Direct Pulp Capping of Primary Teeth

Direct pulp capping (DPC) may be implemented when the pulp tissue is exposed. The tooth must be asymptomatic and, to avoid further contamination, one should

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not risk a DPC without using a rubber dam. With extra careful carious dentin removal, there may be cases that exposure is borderline with no bleeding (. Fig. 14.13). Following DPC, the pulp is expected to preserve its vitality and “defend itself ” by reparative dentin deposition. This technique may be selected ideally for small carious pulp exposure cases in permanent teeth with an open apex. If we suspect that the inflammation extends to a large part of the pulp chamber, treatment failure and full-blown pulpitis are probable. In primary teeth, DPC may be selected based on strict criteria indicating absence of pulp inflammation, i.e., in clinical terms, absence of spontaneous or continuous pain of pulpal origin and limited self-contained hemorrhage after minimal pulp exposure [17, 25]. The documentation of such instructions is however low, based on a few old studies and expert opinions; more  recently, randomized controlled clinical trials with contemporary pulp capping materials support DPC as an option in carious primary molars, with success rates comparable to pulpotomy [18, 27]. Instead of direct capping per se in cases of carious primary teeth, some authors have adopted partial pulpotomy with calcium hydroxide or MTA (. Fig. 14.14). In performing it, about 2  mm of pulp  – the part considered to be inflamed – is removed using a high-speed diamond bur. This variation has produced success rates 75% after 3 years [28]. Since it is a preferred option in pulp exposures of traumatized permanent teeth, it is described in 7 Chap. 16.  

 

 

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14.2.2.1  Technique

DPC procedure requires ideal conditions. Gross carious dentin removal at pulpal walls and cavity preparation must have been completed before exposure occurs. Thus, the most dentin infected with bacteria will have already been removed. If uncontrollable hemorrhage is observed at minimal primary tooth pulp exposure, extensive inflammation is present and other pulp treatment options are chosen among those presented below [20]. If there is little hemorrhage leading soon  to spontaneous hemostasis, possibly aided with a short light dressing with a cotton pellet dump in saline, DPC is possible. After gently drying the pulpal wall, the minimally exposed primary tooth pulp may be covered under no pressure with calcium hydroxide (Ca[OH]2) or mineral trioxide aggregate paste (ΜΤΑ), before placing a PMC or a well-sealed restoration, which again does not require significant condensation (. Fig. 14.15).  

14.2.2.2  Materials

Biocompatible materials for DPC are the following.

Calcium Hydroxide Pure calcium hydroxide (Ca[OH]2) has been, and still is, the gold standard. Its water mixture provides good disinfection, because of high pΗ [12], and prevents microbial growth; it has a superficial caustic effect to the pulp tissue and is very soluble (it does not set). This is why it is also employed in the form of quick-setting cement with the addition of salicylate esters (commercial brands, e.g., Dycal, Life, etc.); this increases mechanical stability and easier handling (it sets very soon). As a cement has much lower pH [9] which may explain the lower success rates when compared with pure calcium hydroxide in direct pulp capping. The pulp reacts forming ideally a “bridge” of hard tissue, preserving pulp vitality. The quality of this “bridge” has been studied in permanent teeth and shown to be less solid than the one formed with the use of ΜΤΑ [29], allegedly because the latter bonds much better with dentin and remains stable in the long-term, thus preventing microbial leakage. Nevertheless, calcium hydroxide is still the most user-­friendly and affordable material [30].

Mineral Trioxide Aggregate (MTA) The basic ingredients of ΜΤΑ is a mixture of dicalcium and tricalcium silicate and tricalcium aluminate, 20% bismuth oxide added for radio-opaqueness and, in smaller amounts, and iron and magnesium oxides. It has found various dental applications as final root canal sealer, in direct pulp capping and pulpotomy, root penetration, and apical plugs [30, 31]. Less documentation is available for the similar material Portland cement [32]. When the powder form is mixed with water, it becomes colloidal and hardens within about three hours; its pH is 12.5, similar to that of pure calcium hydroxide. The main product of the reaction of these cements with water is calcium hydroxide, which explains their similar effect on the pulp. ΜΤΑ setting is accelerated in a humid environment; this is why, after placing it at the exposure site, dump cotton wool is temporized in the cavity, with the final restoration placed the following day. This is a disadvantage in clinical practice but some studies of one visit for MTA application and restoration in primary teeth have shown good results [28]. ΜΤΑ strength is at least equivalent to that of ΖΟΕ and other similar cements. Disadvantages are its relatively high cost and the necessity to be packaged in single doses because atmospheric humidity degrades it, thus other packaging forms have appeared (. Fig. 14.16).  

Other Materials Under Investigation Dentin bonding agents proposed for direct pulp capping do not promote the creation of secondary dentin, and their bonding capacity to carious dentin is limited leading to pulp inflammation [33]. TGF-β pathway

327 Pulp Therapy in Pediatric Dentistry

a

b

c

d

e

..      Fig. 14.13  a Extremely deep cavities in both mandibular primary molars, radiographically in contact with the pulp cavity, and possible furcation involvement of the first one. There was history of only provoked pain. b Occlusal aspect of oversize class II cavity preparations. c Wide borderline pulp exposure with no bleeding was evident

in both molars after extra careful carious dentin removal at pulpal walls. Caries removal was complete at axial and cervical walls. d The finished restorations with RMGIC after calcium hydroxide cover of exposure site on both molars. e Follow-up radiograph at 30 months shows pulp treatment success and healthy bone furcation

growth factor and bone morphogenetic proteins have been used in pulp capping cases in animal experiments [34], but further investigation is necessary to explain the mechanisms of their action and their potential for clinical application. Other substances have also been tested, such as an enamel matrix derivative, which has performed successfully in a clinical primary teeth study [35]; however, additional evidence is sought.

14.2.2.3  Effectiveness

The relevant guidelines state that direct pulp capping may only be selected in the absence of pulp inflammation [8, 25]. More recent findings regarding the use of calcium hydroxide or MTA [18, 27, 36, 37] report high success rates in carious primary molars, which approximate those of permanent teeth [38]. Until more randomized controlled trials (RCTs) are available on whether

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a

b

c

Pulpotomy is indicated following pulp exposure due to caries or injury in cases of asymptomatic teeth with vital pulp or with pulpitis symptoms limited to the crown pulp [8, 25]. The latter is confirmed when after the excision of the crown pulp hemostasis is achieved within a few minutes. Pulpotomy is contraindicated for primary molars with extensive pulp inflammation, something indicated by a history of spontaneous or long-lasting pain, edema or abscess, tenderness on percussion, pathologic mobility, furcation bone lesion, and internal or external pathologic root resorption [12]. Pulpotomy indications and contraindications are not, in effect, different from those for indirect pulp capping [8, 25], and this is why the former should be selected over the latter only after pulp exposure has occurred. The evaluation of long-term pulpotomy success in primary teeth is based on clinical and radiographic criteria. Clinical success criteria are the absence of pain, mobility, and inflammation including abscess or fistula. Radiographic criteria for pulpotomy success are normal periodontal space and no furcation or periapical radiolucency, as well as normal eruption path of the permanent successor tooth. 14.2.3.1  Technique

14

..      Fig. 14.14  a Radiographic image of mandibular second primary molar of a 6-year-old boy referring recent, short-duration, evoked pain (its apical distal root resorption seems unrelated). b Partial pulpotomy with MTA and placement of a PMC was preferred along with restoring the first molar. c Progressive root canal obliteration is observed under the MTA at 2-year recall

After local anesthesia administration and rubber dam placement, carious dentin is fully removed from the cavity walls using a Νο. 4 or 5 round bur at a low speed handpiece. Thus, additional bacterial contamination when the pulp is exposed is prevented. If the pulp is exposed, the supra-pulpal wall of the crown chamber is removed using a cylindrical diamond bur on a high-­speed handpiece with water spray. The bur follows the outline of the crown chamber, as defined by the pulp horns, starting from the exposure point (. Fig. 14.17). The pulp segment in the crown chamber may be amputated using a new (sharp) sterilized excavator or a new round No. 4–6 bur on a low speed handpiece. The pulp is amputated at the root canals entries, a procedure requiring familiarity with their topography. Ample rinsing of the pulp chamber with saline solution helps prevent the entry of infected dentin debris into root canals. The entire crown pulp must be carefully removed as any inflamed remnants continue to bleed impeding diagnosis and making it impossible to visually examine the root canal entries. Root pulp hemorrhage is controlled by placing a cotton wool plug impregnated with saline for 3 minutes (. Fig. 14.18). The tooth is considered suitable for pulpotomy only when hemorrhage stops after that. Placing a cotton wool plug impregnated with 5% sodium hypochlorite solution for 1 minute may help in  

direct pulp capping is a reliable long-term option for carious primary teeth as well, it should only be chosen in the light of the precautions listed above [18, 30]. 14.2.3  Primary Molar Pulpotomy

Pulpotomy is the excision and removal of the inflamed crown pulp segment. The healthy radical segment remains and is covered with some material so as to promote healing at the dissection point with the generation of hard tissue, thus allowing the radical pulp to preserve its vitality. In cases of anterior teeth, partial pulpotomy or pulpectomy is preferred over pulpotomy because there is no abrupt narrowing of the pulp chamber in its transition to the radical pulp.

 

329 Pulp Therapy in Pediatric Dentistry

..      Fig. 14.15  a Radiograph of carious primary teeth. b Pulp exposure of maxillary second primary molar after spontaneous hemostasis. c The 2-year follow-up radiograph after DPC with ΜΤΑ and IPC of maxillary and mandibular second primary molars, respectively, shows the success of both pulp treatments. d, e Clinical view of the restorations

a

b

c

d

a

b

e

c

..      Fig. 14.16  a Individual packaging of white ΜΤΑ (ProRoot, Dentsply, and Angelus) in power sachets and distilled water. b White ΜΤΑ (Medcem GmbH) with powder in capsules. c Allegedly less sensitive to moisture white ΜΤΑ (NuSmile)

the disinfection and hemostasis, although reservations to that have been expressed [20, 25]. Root stumps are particularly sensitive to new irritation, e.g., by new contact with dry cotton fibers and bleeding may reappear. If even minimal hemorrhage continues, the procedure may be repeated once more. If it is still not controlled, this indicates inflammation of the root pulp and pulpectomy should follow [39]. Following hemostasis, the pulp stumps are covered by the material of choice. The pulp chamber is then filled under no pressure (before hardening starts) by fast setting ZOE or by RMGIC. A PMC is carefully cemented or another restoration placed providing complete cavity sealing.

14.2.3.2  Materials and Effectiveness

of Pulpotomy

Various materials have been used for pulpotomy. The ideal material should be bacteriostatic, nonirritating for the pulp and surrounding tissues, promote pulp healing, and not interfere with normal root resorption [12]. A contemporary well-documented material is MTA, but other medicaments and techniques are being or have been used, as well.

Mineral Trioxide Aggregate MTA as well as Portland cement are highly biocompatible pulp capping materials not resorbed over time like calcium hydroxide and present fewer toxic properties

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a

c

b

..      Fig. 14.17  a A cylindrical diamond bur has been used to cut away supra-pulpal dentin of a mandibular second primary molar with a large distal carious cavity. The supra-pulpal-dentin is ready

a

to be detached. b Cotton wool dumped in formocresol is pressed in the pulp chamber after careful inflamed pulp remnants. c The pulpal chamber with complete hemostasis

c

b

d

e

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..      Fig. 14.18  a Series of pulpotomy actions following radiographic examination, local anesthesia, and rubber dam isolation. a Hyperplastic pulpitis of mandibular left second primary molar. b Cavity preparation with removal of supra-pulpal dentin with pear-shaped diamond at high speed under water cooling. c Amputation of crown

pulp and placement of cotton wool plug impregnated with saline solution for 3 minutes. d Hemostasis is controlled. e Filling the pulp chamber with quick-setting ZOE preparation following capping of pulp stumps with MTA

than other materials [40–42]. Their mode of action was explained earlier in DPC. A small quantity of 1–2 mm thickness is placed at root canal entries. The absence of internal root resorption, biocompatibility, and capacity to induce “dentin bridge” creation has increased MTA preference for pulpotomies. Some root canal

obliteration is a frequent finding, but this does not seem to be clinically significant (. Fig. 14.14). Success rates are over 95% for 1- to 2.5-year follow-up period, [20, 43, 44], although lower rates have been reported when placed by pediatric dentistry trainees (Dimitraki et  al. 2019) [18].  

331 Pulp Therapy in Pediatric Dentistry

Formocresol

Other Techniques and Medications

Formocresol was the most popular primary tooth pulpotomy and reference material for more than 70 years. In the new century, there has been renewed reflection to the cytotoxicity and potential mutagenic action of the formaldehyde (19%) it contains, which has caused concern in the scientific community, leading to recommendations for stopping its use [25]. Dilution of formocresol with glycerine, at a ratio of 1:5, was found to be as effective [43], and this has been employed more frequently in recent decades to mitigate the undesirable effects of formaldehyde. Formocresol is a potent antiseptic that does not promote dentinogenesis but causes fibrous degeneration and fixation, under the site of pulp amputation. Despite animal studies eliciting its negative effects, formocresol has remained clinically acceptable [45], and its use was until recently taught at dental schools in the USA and Europe. Success rates have been reported in the order of 80–90%, close to those for ΜΤΑ [39, 46, 47].

A different approach is electrosurgery to cauterize the pulp, leaving a clot at radical pulp stumps. A retrospective study reported high clinical and radiographic success rates (96% and 84%, respectively) (Lin et al. 2014). Additionally, various laser methods have been assessed on animals and in dental praxis, such as Nd:YAG, Er:YAG, carbon dioxide laser, laser diode, and argon laser [50, 51]. Data so far do not support the general adoption of laser and electric surgery techniques for primary molar pulpotomy.

Ferric Sulfate When this coagulating agent comes into contact with blood, a ferric ion and protein complex is formed in the form of a membrane mechanically covering vessels and inducing hemostasis. This complex covers the root canal amputated pulp preventing clot formation (Srinivasan et  al. 2006) [46]. This 15-second impregnation with ferric sulfate (. Fig. 14.17b) is followed by mild irrigation of the crown chamber with water and light drying with a moist cotton wool pellet. A ZOE cover of root canal entries is succeeded by the permanent restoration. A wide range of ferric sulfate success is reported (43–97%) which is lower than those of MTA [17, 48]. Ferric sulfate has no systemic toxic action. In the “post-formocresol era,” it remains a popular medication in primary tooth pulpotomy [24, 49].  

14.2.4  Pulpectomy/Root Canal Treatment

of Primary Teeth

Pulpectomy means the full removal of pulpal tissue. Following chemical and mild mechanical processing of root canals, these are filled with a biocompatible material to prevent any bacteria remaining within them. Root canal treatment is indicated when there are signs and symptoms of chronic pulpitis or necrotic pulp (pulpless tooth) without radiographically apparent internal or external pathologic root resorption. Local pus presence is not a contraindication as it can be managed by endodontic drainage. Contraindications to root canal treatment leave extraction as the alternative (. Fig.  14.19). Extraction is preferred for primary teeth with extensive crown destruction that cannot be restored even with a PMC. When, in mixed dentition, the roots of a primary molar have been resorbed, either naturally or pathologically, to the degree that there is no furcation bone up to the permanent successor tooth crown, the primary molar extraction is preferred and there is no need to maintain space [3]. When space maintenance is an issue, preserving the primary tooth in the dentition is significant especially before the first permanent molars erupt [25].  

c

a

b

..      Fig. 14.19  a External and internal resorption of mesial roots of mandibular second primary molar and major furcation bone resorption in an 8-year-old boy call for its extraction. Some bone is visible

on top of the successor’s crown, indicating the need for space maintenance. b, c Radiographic and clinical view with space maintainer in place after 3.5 years, respectively

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Anatomical Features of Primary Molar Roots

The shape and form of root canals in anterior teeth are simple. In molars, however, many variations of their basic anatomy exist, emphasizing the importance of the clinician being familiar with the morphology of root canals to ensure successful root canal treatment. Maxillary and mandibular primary molars sometimes exhibit more than the usual three root canals. In the mandible, a network of thin accessory canals is usually found between buccal and lingual aspect of the second molar distal root. In about one quarter of second molars in both jaws, there is a very wide root canal dividing before the apex (. Figs. 14.20 and 14.21) [ 52, 53]. Primary molar roots present considerable curvature embracing the successor tooth germ, so that care is needed to avoid perforating them. The furcation lesions found almost exclusively in primary molars with inflamed/necrotic pulps signifies that mechanical debridement should focus in the cervical half of the roots, thus reaching their apical part with files being purposeless most of the time.  

14.2.4.1  Technique

In the first session it is necessary to administer local anesthesia to avoid any pain during pulpectomy and/ or debridement. It also makes the rubber dam more

14

..      Fig. 14.20  Root canal variations of mandibular a and maxillary b primary molars [52] (by permission)

a

acceptable by the child. Removing the supra-pulpal dentin is done as for pulpotomy, but the axial walls may deviate more if necessary for easy access of root canal filing and rinsing [54]. Every canal entry has to be located and the canal tissue remnants removed by appropriately sized Hedstroem or K files. The buccal root canals of maxillary primary molars (particularly the distal one) and the lingual root canals of mandibular primary molars are usually thinner, and pulp extirpation or debridement usually starts with files Νο. 25–35 [54, 55]. The length of files preferred for primary molar teeth is 21  mm since this, except for being sufficiently long, facilitates working in the smaller opening of a child’s mouth (. Fig.  14.22). If satisfactory opening of the mouth is not possible, some authors recommend permanently bending a file (. Fig. 14.23). In order to avoid files penetrating the apex, the working length is set at 2–3 mm shorter than the actual one [54, 55]. Root canals are disinfected with 5% sodium hypochlorite or chlorhexidine under continuous suction for removing organic residues, while mildly filing slightly short to apex [54]. In pulpitis not extending further than the root canals, endodontic treatment may be completed in one session, while in pulpless (septic) teeth or if inflammation extends to the alveolar bone, treatment completion requires more than one session [17]. Two sessions usually suffice, with root canals cleaned as above in the first session, dried with paper points and filled with  

 

b

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b

a

c

d

palatal

mesial distal ..      Fig. 14.21  3-D models of second primary molars [52] (by permission). a Maxillary molar with auxiliary root canal in the apical half of mesiobuccal root. b Maxillary molar with early canal termination in the palatal root, possibly the result of external root

b

distal

mesial

resorption. c Mandibular molar with a single, wide root canal in the distal root. d Mandibular molar with bifurcated root canal in the middle and apical thirds of the distal root

c

a

d

e

f

..      Fig. 14.22  a Periapical radiograph in this 5-year-old boy shows moderate furcation bone resorption of mandibular right second primary molar with deep occlusal cavity involving the pulp. b After inferior alveolar nerve block anesthesia, the rubber dam was placed. c Mild filing of mesiobuccal root (with 21 mm length, No.25

Hedstroem file) is done under rinsing with NaOCl. d Final restoration of the cavity followed the filling of root canals with ZOE at the next session. e Post-op radiograph. f The 3-year follow-up radiograph confirms the successful treatment outcome. Some resorption of the inner wall of the mesial root is without clinical significance

calcium hydroxide with the help of a lentulo spiral or high pressure syringe and temporized [56]. In the second session, 10–14 days later, rinsing is repeated and, if there is no exudate or other signs of inflammation, the root canals are dried by paper points and carefully filled with an appropriate paste (see types below). The pulp chamber is then filled with a quick-setting ZOE preparation [57, 58], a post-op radiograph taken, and final restoration or PMC placed.

14.2.4.2  Root Canal Filling Materials

and Effectiveness

The differences in growth/development, anatomy, and physiology between primary and permanent teeth impose changes also in the criteria for root canal filling materials. The ideal material for primary teeth should. 55 Be absorbable at a rate comparable to the rate of root resorption

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comparison with permanent teeth does not decrease the value of such results. Iodoform paste has shown clinical and radiographic success rates of 84% [60]. In a study of 30 primary incisors and 51 primary molars with 78% successful root canal treatment rates using ΖΟΕ, some undesirable sequelae were observed in permanent successor teeth, such as premolar deviation from eruption path at a frequency of 21%, palatal eruption of maxillary incisors in crossbite at 20%, as well as prolonged retention of primary teeth at 36% [61]. 14.3  Pulp Treatment of Young Carious

Permanent Teeth

..      Fig. 14.23  Hand instruments of 21  mm length for root canal therapy. Top: Lentulo. Middle: Hedstroem Νο. 25 file. Bottom: Bended Νο. 30 file for mesial roots, in cases of inadequate mouth opening

55 Be harmless to periapical tissues and the germ of the permanent successor tooth 55 Be absorbed quickly if pushed through the apex 55 Be antiseptic 55 Be easy to handle 55 Bond to the canal walls 55 Show no contraction 55 Be easy to remove if such a need arises 55 Be radio-opaque 55 Not cause tooth discoloration

14

Gutta-percha points are excluded, unless there is aplasia of permanent successor, and, consequently, preserving the primary tooth in the arch is important, even if it is heavily carious. The materials that most closely fulfill most of the abovementioned criteria and used today are ZOE and iodoform paste. The use of ZOE is taught in 2/3 of undergraduate programs in the USA [49] and recommended by most pediatric dentistry and endodontology bodies. A moderate foreign body reaction in cases of overfilling and different absorption rates than those of the root remain its disadvantages [59]. However, its residues may remain in the alveolar bone for a long time without any significant clinical impact. The difficulty in adequate pulp removal/debridement of root canals in primary molars, particularly when working without a rubber dam, the uncertainty regarding the impact of handling files or medication on developing permanent successor, and the frequent cooperation problems encountered when working with child patients under stress discourage many dentists from preferring this technique. Nevertheless, reported success rates of root canal treatment are quite high (78– 93%) [10]. The fact that, in the case of primary teeth, less strict radiographic success criteria may be applied in

Procedures to manage the anterior teeth with pulpal involvement following trauma in children and adolescents are presented in 7 Chap. 16. Indeed, trauma is by far the main reason for pulpal damage of these teeth in youth. For the biological background of these procedures and root canal treatment of teeth with mature roots and closed apices, readers are referred to appropriate endodontology books and relevant publications. In this chapter we report specifically diagnostic procedures and treatment options and protocols for treating young permanent teeth presenting pulp pathology combined with deep carious cavities. Most of such teeth are molars, the first ones in particular. The root canal treatment of permanent immature teeth (open apices) aims at allowing root development and restoring function. If the prognosis is poor, preserving these teeth along with their supporting bone until adulthood allow for a permanent solution (prosthetic/ implant). These decisions should be made in the best interests of the young patient and may include orthodontic consultation. For example, extraction rather than endodontic treatment of a badly broken down tooth at an appropriate time followed by orthodontic space closure may be preferred as a best solution in the long run [62].  

Eye Catcher

The pulp tissue of young permanent teeth, particularly those with an open apex, responds more positively to microbial inflammation and trauma, due to the better hemodynamics of its vascular network, and to the broader communication with the densely vascularized periapical tissues [63]. On traumatic or iatrogenic exposure, pulpal tissue is healthy and can be entirely preserved, if properly treated. When the pulp is exposed in the presence of carious dentin, it always presents some degree of infection and inflammation that is already chronic (. Fig. 14.24) or in the process of partial or total necrosis.  

335 Pulp Therapy in Pediatric Dentistry

..      Fig. 14.24  a Hemorrhagic pulp exposed while preparing occlusal cavity in a young permanent molar with spontaneous pain history indicates nonreversible pulpitis. b. Septic carious dentin with pulp abscess (hematoxylin/eosin stain, By permission [64])

a

Concerning the diagnosis of probable pathology of young permanent teeth based on clinical signs and symptoms as well as radiographic findings, readers are referred to . Table  14.1 which presents a summary regarding primary teeth, the only exception being that permanent pulp response to sensitivity testing is more reliable.

b

a

 

14.3.1  Indirect Pulp Capping

IPC in the case of young permanent teeth follows the procedures described for the corresponding pulp treatment of primary teeth. If preferred, capping should embrace the clinical and radiographic criteria to confirm the absence of nonreversible pulp inflammation (. Fig.  14.25). An alternative is represented by the “stepwise excavation” procedure [25] which, when permanent teeth are involved, is often preferably completed in two sessions, with an interval between the two that may extend to several months. These teeth usually present symptoms of evoked pain. In the first session, after all carious dentin has been removed except for that in direct proximity to the pulp, quick-setting calcium hydroxide preparation is inserted and covered with a GIC filling for the period mentioned. This treatment aims at alleviating the symptoms and drastically reducing the risk of pulp exposure upon reentering the cavity [65, 66], because during the time interval tertiary

b

 

..      Fig. 14.25   a Cotton wool pellet impregnated in ethyl chloride spray for cold pulp testing. b Electrometric testing for pulp vitality is done without gloves for contactivity purposes

(reparative) dentin is deposited on the respective pulpal wall. The advantage of this technique is that the practitioner is given the opportunity to evaluate the success of the treatment and modify the therapeutic scheme accordingly.

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Another approach is to complete tooth restoration in one session by stepwise excavation, just as is done for primary teeth (. Fig.  14.26). This does not offer the possibility to confirm the reversibility of pulp inflammation securing a safer prognosis. In choosing the best option, all the relevant factors for the individual patient must be considered on a case-by-case basis, because long-term prognosis in the relevant literature does not favor either of the two options [67].  

14.3.2  Direct Pulp Capping

Evidence on the suitability of carious permanent teeth for DPC, as well as the relevant clinical procedure, do not differ from that presented for primary teeth. Traditionally, the material of choice has been calcium hydroxide, while the more recent so-called Bioactive Endodontic Cements have shown excellent results [68]. a

14

One such  is a calcium silicate cement  (Biodentine™, Septodont, France), which appears to promote equally dense reparative dentin as that produced by ΜΤΑ [69] (. Fig. 14.27). In the past, adhesive dentin agents were experimentally used in contact with the exposed pulp, but they did not meet with success. This supports the view that besides hermetically sealing the cavity from bacteria, the capping material should promote reparative dentin formation. When a small carious exposure of healthy or, more likely, reversibly inflamed pulp occurs, and after possible hemorrhage is controlled, the capping material of choice is placed over the exposure without pressure. If it is a quick-setting calcium hydroxide, it is then coated with a GIC followed by a sound restoration to fully prevent microleakage. If the choice is MTA, it should be covered with a dump cotton pellet before the tooth is temporarily filled. It takes a few hours for the MTA to set, so cotton is removed and final restoration placed at  

b

..      Fig. 14.26  a Deep occlusal  carious lesion of mandibular first  permanent molar. b Indirect pulp capping with quick-setting calcium hydroxide, GIC lining and final composite restoration in one session appears to be successful at the 6-month review ..      Fig. 14.27  a Deep carious lesion of mandibular first permanent molar in a 17-year-old girl with a history of provoked pain. b Non-­hemorrhagic pulp exposure during partial caries excavation. c The cavity is filled with Biodentine™ cement for 6 months, before composite resin replaced the outer part of the cement for a permanent restoration. d Biodentine™ capsule and water dose

a

b

c

d

14

337 Pulp Therapy in Pediatric Dentistry

a

b

..      Fig. 14.28  a Deep carious lesion of a mandibular first permanent molar without a history of spontaneous pain. Despite the effort toward indirect pulp capping, exposure occurred, and the pulp was

directly capped with Biodentine™ cement. b This radiograph was taken 4 months later, before placing a permanent restoration. The tooth was asymptomatic

a later time. If the material is Biodentine™ cement, it can be left as a temporary filling material for up to 6 months or be coated after its 12-minute setting time with the permanent restoration (. Fig.  14.28) [70]. Direct capping is considered successful if the pulp survives and the radiograph confirms the deposition of reparative dentin at the exposure site. Furthermore, in teeth with an open apex, success is confirmed when the root continues developing and apex formation is completed (apexogenesis). The effectiveness of DPC in young permanent teeth with deep carious cavities has been better documented than in primary teeth; consequently the technique is included in the  relevant guidelines [71]. If only teeth with vital pulp with no more than reversible pulpitis are selected, and a sound procedure is followed, studies show that DPC of permanent teeth shows success rate of 73% for over 3 years follow-up [72] or even 80% for 6 years follow-up [73]. In a specialist endodontic private practice, success rates at 9 years follow-up of 98% for young teeth with mature apex have been reported, which rose to 100% in the 15 teeth with immature apices [38].

14.3.3  Partial Pulpotomy and Cervical

 

Eye Catcher

Pulpotomy

In partial pulpotomy only the superficially inflamed pulp next to exposure site is removed, and the healthy pulp is covered with any biological material listed above for DPC.  It is considered the treatment of choice for permanent incisors with crown fractures that expose the pulp; for a description of the procedure see 7 Chap. 16. In a carious exposure of a permanent molar, this technique is considered to be more successful than DPC and especially indicated for teeth with undeveloped apices [76]. Partial pulpotomy is acceptable as a permanent pulp treatment (. Fig. 14.29). Wide acceptance of DPC and partial pulpotomy in young permanent teeth affected by caries has restricted the choice of cervical (deep) pulpotomy exclusively to cases when hemorrhage can only be controlled at the level of pulp stumps at the entries to root canals. Even then, it is meaningful to choose this procedure only in immature teeth so that apices may be completed, while in mature teeth full pulpectomy and root canal treatment should be preferred [77]. Once again, the capping materials of choice for deep pulpotomy are MTA or calcium hydroxide (. Fig.  14.30). A theoretical disadvantage of the technique, in case of failure, may be the difficulty to access root canals for further treatment due to possible formation of a hard tissue bridge under the capping material.  

 

 

Various bioactive molecules are being investigated, including growth factors and molecules of extracellular enamel or dentin matrix. These are considered capable of activating the endogenous stem or ancestor cells, enhancing the local regenerative potential. Animal studies have shown that the use of bioactive molecules in pulp capping produced a thicker layer of homogenous reparative dentin, while research continues in the quest whether carious dentin is capable of repair [74]. For example, collagen infiltrated with hydroxyapatite and silicon nanoparticles provided scaffolding for increased crystal formation toward carious dentin remineralization, if environmental conditions were favorable [75].

14.3.4  Root Canal Treatment of Immature

Carious Teeth

The detailed procedures of endodontic procedures of mature teeth can be found in textbooks of endodontology. In this part of a pediatric dentistry book, the emphasis is given to the treatment of irreversible pulpal inflammation or pulp necrosis, with or without apical

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periodontitis, in immature carious teeth with open apices. Recent advances in regenerative endodontics have offered more biological possibilities for immature teeth [78]. The majority of young carious permanent teeth that usually require root canal treatment are first molars with pulpitis, most usually in patients with severe forms of Molar Incisor Hypomineralization. These patients often present as emergencies with history of recent spontaneous pain, often complaining of a sleepless night. Following the taking of periapical radiograph and diagnosis, effective local anesthesia to allow cooperation of the young patient, and rubber dam placement, access to the pulp chamber and root canals is achieved.

a

b

c

14.3.4.1  Apexification

..      Fig. 14.29  a Deep carious cavity with pulp involvement in a mandibular first permanent molar of a 14-year-old girl. b Partial pulpotomy of inflamed part of the pulp, dressing with MTA and temporary restoration. c At the 6-month review, the restored by PMC tooth is asymptomatic

14

Under copious irrigation with 1.5% sodium hypochlorite, delicate instrumentation is carried out using hand files to remove the inflamed/necrotic content. Sodium hypochlorite in teeth with immature apices may be alternated with irrigation by sterile saline solution. A file working length is set 1–2  mm before the radiographic apex, since the open apex often has uneven shape. At this point either traditional apexification or “MTA plug” techniques may be selected [79]. For the traditional apexification technique, after drying with absorbent paper cones or intracanal aspirating tips, the canals are carefully filled with calcium hydroxide (powder or paste), using a lentulo spiral or a syringe and endodontic pluggers, until the material meets the apical tissues. Calcium hydroxide can help dissolve small amounts of residual necrotic pulp tissues while exerting

a

c b

d

..      Fig. 14.30  a An emergency case of immature carious first permanent molar with extensive crown pulp inflammation. b Hemostasis and placement of MTA at root pulp stamps following cervical

e

pulpotomy. c Radiographic image with temporary filling. d Continued apexogenesis is seen at the 6-month review. A preformed metal crown had been placed. e Clinical occlusal view

339 Pulp Therapy in Pediatric Dentistry

antisepsis [80]. The access cavity of the tooth is sealed with a temporary restoration which should be at least 3 mm thick. The goal of the apexification treatment is to promote healing of the periapical tissues and the formation of an apical hard tissue barrier which will act as a stop for a future endodontic obturation. The apical barrier is achieved within a period which ranges from 6 to 18 months (average 12 months), during which the canal may need calcium hydroxide refilling two or three times because of gradual resorption at its apical portion [81]. The need, however, to change calcium hydroxide during the apexification is debated. After the clinical procedure is completed, the patient will be followed at 1 week, 1 month (for symptoms), and then every six months with a clinical and radiographic evaluation. The formation of the apical barrier is confirmed radiographically. The roots are permanently filled with gutta-percha (best if thermoplasticized) and root canal sealer (. Fig. 14.31). If the “MTA apexification” procedure is selected, after the canal has been instrumented and disinfected, a preformed barrier of MTA blocks the open apex for a minimum length of three millimetres [25]. The MTA barrier can be introduced in the canal with different carriers and compacted using endodontic pluggers. If the tooth is very immature (i.e., stage 1–2), then the entire canal may be filled with MTA.  Following positioning of the apical barrier, the access cavity is sealed with a wet cotton pellet and a temporary cement. In the next appointment the tooth is reaccessed, the MTA is checked for its proper setting, the remaining root is filled with gutta-percha and sealer, and the tooth is restored with adhesive techniques. According to some authors, the treatment can be also completed in one appointment, without waiting for the MTA to set. The patient is checked for symptoms after one week and followed-up clinically and radiographically to monitor the mineralized barrier. The advantage of using a preformed apical  

a

b

..      Fig. 14.31  a Radiograph of a heavily carious and abscessed mandibular first permanent molar with large diffused periapical radiolucency at immature distal root. b Obturation of the canals with gutta-percha following the temporary calcium hydroxide fill

plug consists in completing the endodontic treatment of an immature tooth soon, by sealing the open apex and still promoting the hard tissue barrier formation in the next 6 to 18 months as in the traditional technique (. Fig. 14.32). The MTA’s very hard consistency, however, does not forgive mistakes. This procedure can be followed both in traumatized teeth and in teeth with carious pulp necrosis. If the tooth is necrotic, local anesthesia may not be necessary, except for a minimal amount to numb the gingiva for clamp placing. MTA apexification may be performed using also alternative bioactive cements [79]. Successful apical barrier formation, following the placement of an MTA apical plug in 22 pulpless immature permanent incisors, was as high as 95% [82]. For posterior carious permanent teeth with open apices, there have been only case reports [83, 84].  

14.3.4.2  Revascularization

In the context of a “regenerative” endodontic approach, revascularization of the pulp space of anterior traumatized immature necrotic teeth has been attempted in an effort to avoid later root fractures because of thin canal walls [78]. The rationale of this technique is to activate the stem cells of the apical papilla. According to the suggested protocols, the tooth should be lightly rinsed in the coronal to middle third of the root. A delicate instrumentation to this level may be also attempted. The disinfected space is then filled with a triple antimicrobial paste (ciprofloxacin, metronidazole, and minocycline), and the tooth is temporized (. Fig.  14.33). In the absence of symptoms, three weeks later, the tooth is reopened, using an anesthetic solution without vasoconstrictor, the canal is rinsed, and bleeding is induced by pushing an endodontic file passed the working length [85]. When a coagulum is formed, the coronal portion of the root is sealed with MTA or other bioactive endodontic cement,  

c

and ongoing healing of the periapical tissues. c Three-year follow-up radiograph of the tooth with preformed metal crown showing complete healing, resorption of the extruded material, and intact lamina dura [84] (By permission)

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..      Fig. 14.32  Radiograph of a carious mandibular left second premolar presenting apical lesion around its immature root apex. b K file is in the root canal without local anesthesia. c The restored tooth with MTA plug at a distance from open apex. d After one year, apical closure and the excellent periapical healing are seen

a

b

a

b

c

d

c

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..      Fig. 14.33  a Periapical radiograph showing the mandibular permanent right first molar of a 7-year-old boy, affected by deep caries and showing signs of apical periodontitis at the apex of the distal root. The tooth did not respond to sensitivity test. Tooth revascularization treatment was attempted using triple antibiotic paste. b

6-months recall: the tooth is asymptomatic and the bone lesion is healing. c 18 months recall: the tooth is still asymptomatic, periapical tissues look healthy, the root canal walls appear thickened, and the apical opening narrowed, but the root has not increased its length

and the tooth is hermetically restored. By this procedure the stem cells from the papilla should be able to migrate and use the coagulum as a scaffold, and growth factors are released from the dentinal walls. The migration of stem cells should recreate the pulp tissue. So far, the clinical cases studied have shown success in achieving

thicker dentinal walls and consequently more fracture-­ resistant roots [86, 87]. Histopathology reports have shown that the endodontically grown tissue was mostly of periodontal origin being cementum bone-like and fibrous connective tissue [78, 88]. The revascularization mechanism, the type of tissue coming in contact with

341 Pulp Therapy in Pediatric Dentistry

a

d

b

c

e

f

..      Fig. 14.34  a Partial pulpotomy with white MTA in an 8-year-old girl, of the immature maxillary right central incisor having suffered a complicated crown fracture. b The 3-month radiographic follow­up shows the reattachment of the fragment with composite resin. c Successful outcome after 5 years, with some canal obliteration. d, e

The patient however complained of localized crown discoloration at the fracture line, which becomes more evident as enamel and dentin are progressively removed. f The discoloration was related to the MTA. Most of it was removed and cavity restored with opaque and enamel-colored composite resin

pulpal walls, and the long-term clinical consequences are therefore still under investigation. Finally, several experimental animal studies and recent limited trials in humans indicate that stem cell treatment may play a significant role in the future of dentistry. The first applications will most probably concern the pulp and periodontal tissues, after the possible epigenetic stability of populations emerging from stem cell cultures has been investigated. What have also to be determined are the protocols to test regenerated dental tissues before they are clinically used to ensure desirability of shape, size, and color [89].

even in conservative pulp treatments of permanent incisors (. Fig. 14.34). Discoloration related to endodontic treatment has always been an aesthetic problem, arising in pulpless teeth before or after treatment. Before treatment, it is caused by the degeneration of necrotic pulp tissues due to patient neglect for seeking treatment. After endodontic treatment, it stems from inadequate treatment procedures allowing leakage, for example, an unsuitable access shape to pulp chamber allowing for degenerating pulp remnants to remain unnoticed. Restoring normal color by internal bleaching may be achieved following the procedure described below. After radiographic examination of the tooth and placement of the rubber dam, the filling is removed and unobstructed lingual approach to the pulp cavity is achieved. The pulp contents are removed up to a few millimeters beyond the clinical cervix; using a round bur at a low speed, discolored dentin is removed in so far that tooth strength is not compromised. A thin layer of cement, e.g., white GIC, is cervically placed so as to prevent microleakage of the bleaching agent into the root or the periodontium through the dentinal tubules. The dentin is etched internally and then cleaned of fatty ingredients with an acetone impregnated cotton wool pellet.

14.3.5  Restoring the Color of Discolored

Teeth

Since gray MTA has been considered responsible for the discoloration due to its ferric oxide content, white MTA has been developed and marketed, particularly for use with anterior teeth. Despite the use of white MTA, however, in 5 of the 22 anterior teeth receiving root canal treatment in a clinical study of children of an average age of 10 years, some crown discoloration was observed [82]. It has indeed been observed after the use of white MTA

 

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a

b

c

d

..      Fig. 14.35  a-d Gradual color restoration in four sessions of a discolored maxillary right central permanent incisor that had received root canal treatment. (Courtesy of Dr. P. Beltes)

The cavity is filled up to the dentin borders with a dense paste produced by mixing sodium perborate powder with 3% hydrogen peroxide. The enamel walls are cleaned and a temporary restoration, e.g., RMGIC, offers a hermetic seal [90]. If necessary, the process is repeated. In the last session, the cavity and tooth are thoroughly rinsed with water, due to a risk of chemical damage to the gingiva and of external cervical resorption of the root by the bleaching agents. Then cavity is wiped with cotton wetted with chloroform and restored with a white shade of composite (further enhancing the bleaching effect) after etching and bonding. If every stage is performed with care, the outcome is good and stable, particularly in light yellow and gray discoloration cases, as compared to those of dark yellow and black (. Fig. 14.35) [91].  

References

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56. Barcelos R, Santos MP, Primo LG, Luiz RR, Maia LC.  ZOE paste pulpectomies outcome in primary teeth: a systematic review. J Clin Pediatr Dent. 2011;35:241–8. 57. Chandrasekhar S, Prasad MG, Radhakrishna AN, Saujanya K, Raviteja NVK, Deepthi B, Ramakrishna J.  A comparative In vivo efficacy of three spiral techniques versus incremental technique in obturating primary teeth. J Indian Soc Pedod Prev Dent. 2018;36:71–5. https://doi.org/10.4103/JISPPD.JISPPD_365_16. 58. Walia T, Ghanbari AH, Mathew S, Ziadlou AH.  An in  vitro comparison of three delivery techniques for obturation of root canals in primary molars. Eur Arch Paediatr Dent. 2017;18:17– 23. https://doi.org/10.1007/s40368-­016-­­0258-­­4. 59. Chen X, Liu X, Zhong J.  Clinical and radiographic evaluation of pulpectomy in primary teeth: a 18-months clinical randomized controlled trial. Head Face Med. 2017;13:12. https://doi. org/10.1186/s13005-­017-­0145-­1. 60. Holan G, Fuks AB. A comparison of pulpectomies using ZOE and KRI paste in primary molars: a retrospective study. Pediatr Dent. 1993;15(6):403–7. 61. Coll JA, Sadrian R. Predicting pulpectomy s­ uccess and its relationship to exfoliation and succedaneous dentition. Pediatr Dent. 1996;18(1):57–63. 62. Conde MCM, Chisini LA, Sarkis-Onofre R, Schuch HS, Nör JE, Demarco FF. A scoping review of root canal revascularization: relevant aspects for clinical success and tissue formation. Int Endod J. 2017;50:860–74. https://doi.org/10.1111/iej.12711. 63. Hargreaves KM, Giesler T, Henry M, Wang Y.  Regenera tion potential of the young permanent tooth: what does the future hold? J Endod. 2008;34:S51–6. https://doi.org/10.1016/j. joen.2008.02.032. 64. Slootweg PJ. Dental pathology, Ch. 8. In: Disorders of the dental pulp. 2nd ed. Springer-Verlag; 2013. 65. Ricketts DN, Kidd EA, Innes N, Clarkson J.  Complete or ultraconservative removal of decayed tissue in unfilled teeth. Cochrane Database Syst Rev. 2006;3:CD003808. https://doi. org/10.1002/14651858.CD003808.pub2. 66. Hayashi M, Fujitani M, Yamaki C, Momoi Y. Ways of enhancing pulp preservation by stepwise excavation-­ a systematic review. J Dent. 2011;39:95–107. https://doi.org/10.1016/j. jdent.2010.10.012. 67. Thompson V, Craig RG, Curro FA, Green WS, Ship JA. Treatment of deep carious lesions by complete excavation or partial removal: a critical review. J Am Dent Assoc. 2008;139: 705–12. 68. Parinyaprom N, Nirunsittirat A, Chuveera P, Na Lampang S, Srisuwan T, Sastraruji T, et al. Outcomes of direct pulp capping by using either ProRoot mineral trioxide aggregate or biodentine in permanent teeth with carious pulp exposure in 6- to 18-year-old patients: a randomized controlled trial. J Endod. 2018;44:341–8. https://doi.org/10.1016/j.joen.2017.10.012. Epub 2017 Dec 21 69. Tran XV, Gorin C, Willig C, Baroukh B, Pellat B, Decup F, et  al. Effect of a calcium-silicate-based restorative cement on pulp repair. J Dent Res. 2012;91:1166–71. https://doi. org/10.1177/0022034512460833. 70. Rajasekharan S, Martens LC, Cauwels RGEC, Anthonappa RP, Verbeeck RMH. Biodentine™ material characteristics and clinical applications: a 3 year literature review and update. Eur Arch Paediatr Dent. 2018;19:1–22. https://doi.org/10.1007/s40368-­ 018-­0328-­x.

71. Santos PSD, Pedrotti D, Braga MM, Rocha RO, Lenzi TL.  Materials used for indirect pulp treatment in primary teeth: a mixed treatment comparisons meta-analysis. Braz Oral Res. 2017;31:e101. https://doi.org/10.1590/1807-­­3107/2017. vol31.0101. 72. Aguilar P, Linsuwanont P. Vital pulp therapy in vital permanent teeth with cariously exposed pulp: a systematic review. J Endod. 2011;37:581–7. https://doi.org/10.1016/j.joen.2010.12.004. 73. Dammaschke T, Leidinger J, Schafer E.  Long-­term evaluation of direct pulp capping--treatment outcomes over an average period of 6.1 years. Clin Oral Investig. 2010;14:559–67. https:// doi.org/10.1007/s00784-­009-­0326-­9. 74. Chatzistavrou X, Papagerakis S, Ma PX, Papagerakis P. Innovative approaches to regenerate enamel and dentin. Int J Dent. 2012;2012:856470. https://doi.org/10.1155/2012/856470. 75. Besinis A, van Noort R, Martin N. Remineralization potential of fully demineralized dentin infiltrated with silica and hydroxyapatite nanoparticles. Dent Mater. 2014;30:249–62. https://doi. org/10.1016/j.dental.2013.11.014. 76. Mejare I, Cvek M.  Partial pulpotomy in young permanent teeth with deep carious lesions. Endod Dent Traumatol. 1993;9: 238–42. 77. Bjørndal L, Reit C, Bruun G, Markvart M, Kjaeldgaard M, Näsman P, et  al. Treatment of deep caries lesions in adults: randomized clinical trials comparing stepwise vs. direct complete excavation, and direct pulp capping vs. partial pulpotomy. Eur J Oral Sci. 2010;118:290–7. https://doi.org/10.1111/j.1600-­0722.2010.00731.x. 78. Simon SR, Tomson PL, Berdal A.  Regenerative endodontics: regeneration or repair? J Endod. 2014;40:S70–5. https://doi. org/10.1016/j.joen.2014.01.024. 79. Harlamb SC.  Management of incompletely developed teeth requiring root canal treatment. Aust Dent J. 2016;61(Suppl 1):95–106. https://doi.org/10.1111/adj.12401. 80. Hasselgren G, Olsson B, Cvek M. Effects of calcium hydroxide and sodium hypochlorite on the dissolution of necrotic porcine muscle tissue. J Endod. 1988;14:125–7. https://doi.org/10.1016/ S0099-­2399(88)80212-­7. 81. Deepti A, Shifa S, Muthu MS, RathnaPrabhu V. Apical closure of immature molar roots: a rare case report. Int J Clin Pediatr Dent. 2008;1:54–7. 82. Moore A, Howley MF, O'Connell AC.  Treatment of open apex teeth using two types of white mineral trioxide aggregate after initial dressing with calcium hydroxide in children. Dent Traumatol. 2011;27:166–73. https://doi.org/10.1111/j.1600-­9657.2011.00984.x. 83. Woelber JP, Bruder M, Tennert C, Wrbas KT.  Assessment of endodontic treatment of c-shaped root canals. Swiss Dent J. 2014;124:11–5. 84. Musale PK, Kothare S.  Non-surgical endodontic manage ment of immature permanent mandibular first molar: a 3 year follow-up. Eur Arch Paediatr Dent. 2018;19:373–7. https://doi. org/10.1007/s40368-­018-­0350-­z. 85. Cotti E, Mereu M, Lusso D.  Regenerative treatment of an immature, traumatized tooth with apical periodontitis: report of a case. J Endod. 2008;34:611–6. https://doi.org/10.1016/j. joen.2008.02.029. 86. Cehreli ZC, Isbitiren B, Sara S, Erbas G.  Regenerative endodontic treatment (revascularization) of immature necrotic molars medicated with calcium hydroxide: a case

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series. J Endod. 2011;37:1327–30. https://doi.org/10.1016/j. joen.2011.05.033. 87. Tzanetakis GN, Giannakoulas DG, Papanakou S, Gizani S, Lygidakis N. Regenerative endodontic therapy of immature permanent molars with pulp necrosis: a cases series and a literature review. Eur Arch Paediatr Dent. 2021;22(3):515–25. https://doi. org/10.1007/s40368-020-00550-w. 88. Shimizu E, Ricucci D, Albert J, Alobaid AS, Gibbs JL, Huang GT, Lin LM.  Clinical, radiographic, and histological observation of a human immature permanent tooth with chronic apical abscess after revitalization treatment. J Endod. 2013;39:1078– 83. https://doi.org/10.1016/j.joen.2013.04.032.

89. Mitsiadis TA, Papagerakis P.  Regenerated teeth: the future of tooth replacement? Regen Med. 2011;6:135–9. https://doi. org/10.2217/rme.14.78. 90. Marin PD, Heithersay GS, Bridges TE. A quantitative comparison of traditional and non-peroxide bleaching agents. Endod Dent Traumatol. 1998;14:64–8. 91. Abbott P, Heah SY. Internal bleaching of teeth: an analysis of 255 teeth. Aust Dent J. 2009;54:326–33. https://doi.org/10.1111/ j.1834-­7819.2009.01158.x.

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Periodontal Diseases in Children and Adolescents Aikaterini-Elisavet Doufexi and Frank Nichols Contents 15.1

Diseases Restricted to Gingiva – 348

15.1.1 15.1.2 15.1.3

 ingivitis – 348 G Localized Juvenile Spongiotic Hyperplasia – 350 Gingival Hyperplasia – 351

15.2

Periodontitis – 352

15.2.1 15.2.2 15.2.3 15.2.4

 hronic Periodontitis in Children and Adolescents – 353 C Periodontitis Associated with Systemic Disease – 356 Diabetes Mellitus and Periodontal Disease – 357 Acute Ulcerative Gingivitis/Periodontitis – 357

15.3

Mucogingival Deformities – 358

15.3.1 15.3.2

 ingival Recession – 358 G Frenum Pull – 358

References – 360

© Springer Nature Switzerland AG 2022 N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry, https://doi.org/10.1007/978-3-030-78003-6_15

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Children and adolescents commonly present with periodontal diseases. The dental clinician should be aware of and be able to diagnose and timely treat such diseases for the following reasons: [1] 1. The prevalence of periodontal disease in children and adolescents is high. 2. Superficial or localized periodontal lesions in children may lead to more severe and generalized periodontal diseases in adulthood. 3. There is strong evidence for an association between general-systemic diseases and periodontal diseases. 4. Families at high risk for periodontal disease (e.g., due to predisposing genetic factors) can be identified early and placed into individualized prevention programs and more vigilant treatment. 5. The prevention and treatment of most forms of periodontal disease is straightforward and effective. Eye Catcher

The most common periodontal disease in children and adolescents is gingivitis. Common in youth are also mucogingival problems, gingival hyperplasias, and necrotizing ulcerative gingivitis/periodontitis. Periodontal attachment loss occurs infrequently in children, but when it does, it is usually aggressive. Severe periodontal attachment loss in children and adolescents should raise concern for an underlying systemic disease of genetic predisposition.

15.1  Diseases Restricted to Gingiva

15

15.1.1  Gingivitis 15.1.1.1  Definition, Epidemiology,

and Clinical Findings

Chronic gingivitis is a reversible disease of periodontal tissues with signs and symptoms of gingival inflammation without attachment loss. Under the general title “gingivitis,” we could describe three different forms: (a) Acute or chronic gingivitis of exclusively microbial etiology. (b) Gingivitis in which the inflammatory reaction is modified by hormones, specifically gonadotrophins (elevated estrogen and/or progesterone levels in puberty, during pregnancy, and when taking oral contraceptives). (c) Gingivitis secondary to drug-induced gingival hyperplasia. The primary etiologic factor associated with these forms of gingivitis is dental plaque on tooth surfaces of children. Other factors may be important predisposing factors that complicate the development of the inflammatory process, i.e., by differentiating host response.

Gingivitis presents with the same clinical findings in children and adults: gingival redness, edema of free gingivae, bleeding on probing, and often loss of stippling [2]. The gingival margin becomes rounded due to edema and bleeds upon any mechanical challenge (. Fig. 15.1). If gingivitis is left untreated, the gingival tissue can become more fibrous and the interdental papillae may appear hyperplastic, thereby increasing the depth of the gingival crevice [2]. This leads to pocket development without loss of attachment (“pseudo-pocket”). Epidemiological data indicate that in children aged 4–9  years, gingivitis occurs at rates of 40–60%. Its prevalence increases with age [3]. Approximately 82% of teenagers suffer from gingivitis in the USA, while in various other countries teenagers show a similar or higher prevalence [4, 5]. Experimental gingivitis studies after discontinuation of oral hygiene showed that longer time was required for its appearance in children than in adults [6–9]. The bleeding index (GI, gingival index) in various age groups (children, adolescents, adults), with similar plaque index scores, was also found to increase with age [7]. The different inflammatory responses in various age groups could be partially attributed to different levels of hormones, particularly in females. The inflammatory response of the gingiva to plaque accumulation is typically more severe around erupting permanent teeth and is frequently termed “eruption gingivitis.” [10] The main reason is simply related to the substantially greater bacterial load due to ineffective oral hygiene in the tooth eruption sites. Access to and cleaning of the tooth eruption area with the brush requires more time and effort. Another reason might be that degenerative changes in the attached epithelium undergoing remodeling at the eruption site may lead to a diminished immune response with an altered ability to mount a suitable inflammatory response [10].  

15.1.1.2  Microbiological and Histological

Findings

Although the signs and symptoms of gingivitis in children are less pronounced than in adults, the microbiota is generally similar and is characterized by elevated levels of subgingival Prevotella sp., Actinomyces sp., ­ Capnocytophaga sp., Leptotrichia sp., and Selenomonas sp. [11–13]. Histologically, gingivitis in children is characterized by ulceration of the epithelium of the gingival sulcus and infiltration of the underlying connective tissue by inflammatory cells [2]. Dominant cells in the region of gingival inflammation are T lymphocytes in contrast to adult gingivitis where B lymphocytes predominate. The total number of leukocytes in the sulcus is generally reduced in children compared to adult gingivitis [2, 14, 15]. Moreover, elevated estrogen and progesterone levels in adolescents may contribute to increased vascularity and a more pronounced inflammatory response of gingival tissue to bacterial plaque [2, 11, 16].

349 Periodontal Diseases in Children and Adolescents

a

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..      Fig. 15.1  a. A seven-year-old boy with chronic generalized gingivitis manifested by edema of free gingivae. b. Heavy plaque deposits due to the absence of oral hygiene are evident to the naked eye. c. Plaque disclosure with fuchsine dye and demonstrating spontaneous

bleeding upon plaque removal are educational to the child. d. Clinical appearance 6 weeks after the treatment of gingivitis (oral hygiene instructions, removal of deposits). Tooth crowns appear longer, due in part to the resolution of edema

15.1.1.3  Etiology and Treatment

The causal relationship of dental plaque with gingivitis has been demonstrated with experimental gingivitis studies in both adults and children [6, 7, 12]. However, several predisposing factors, local and systemic, regulate the onset of disease [8]. Such local factors for gingivitis in children and adolescents are those favoring plaque accumulation and retention, including: 1. Carious cavities. 2. Overhanging restorations. 3. Hypoplastic cervical tooth areas. 4. Orthodontic anomalies, particularly with severe tooth crowding (. Fig. 15.2). 5. Fixed orthodontic appliances (. Fig. 15.3).  

 

On the other hand, factors that affect host defense responses may include: 55 Mouth breathing which leads to dry mouth, causing local vasoconstriction and thus reducing microbial defense responses. Clinical signs of mouth breathing are the glossy dry surface of the gingiva and mucosa, enlarged interdental papillae and free gingival margin, and bleeding on probing [8]. These findings are usually most pronounced in the maxillary anterior region. 55 Increased levels of estrogen and progesterone in adolescence may contribute to increased vascularity of gingival tissue, and this may be associated with increased bleeding index scores and inflammation [2, 8] (. Figs. 15.3, 15.4). 55 Various systemic diseases that will be discussed as a separate entity.  

..      Fig. 15.2  A girl 14 years of age scheduled for orthodontic treatment. Ineffective oral hygiene and tooth crowding contributed to localized gingivitis (edema of free gingivae). Arrows indicate the localized gingival recession, consistent with ectopic (labial) tooth positioning

Gingivitis in children and adolescents is fully reversible with effective daily plaque removal and possibly additional oral hygiene measures. It is imperative for the clinician to demonstrate oral hygiene practice to adolescents  – and/or to parents of younger children  – and evaluate their performance frequently. If calculus is present, scaling with hand or ultrasonic instruments is necessary. Reevaluation every 6 months is necessary, especially in children with orthodontic abnormalities or children wearing fixed orthodontic appliances, and if oral hygiene is poor, this ought to be more frequent [8]. Care of local and systemic predisposing factors is also very important [2, 8]. For example, mouth breathing should be identified

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c ..      Fig. 15.3  a. Clinical appearance of hyperplastic form of gingivitis, modified by hormonal changes of puberty in a 14-year-old female under orthodontic treatment. Edematous gingivae are indicative of inflammation. b. After removal of orthodontic brackets, good oral hygiene, and periodontal treatment, periodontal health is fully restored. The result could (and should) have been achieved with equal success during the orthodontic treatment

and cared for by the dental clinician and orthodontist and possibly by the otorinolaryngologist [8].

15 Eye Catcher

An important goal for adolescents is to increase their motivation and make them a partner in their oral hygiene effectiveness self-assessment of the techniques, as parental supervision ceases or is not welcome. Success in addressing this challenge will support their self-esteem and awareness to care for their own health and aesthetics and will help them minimize bad breath and gingival bleeding.

15.1.2  Localized Juvenile Spongiotic

Hyperplasia

Localized juvenile spongiotic gingival hyperplasia (LJSGH) is a poorly understood distinctive inflammatory hyperplasia occurring in children and juveniles but may infrequently occur in adults. It was reported, for example, that, out of 27 cases with a median age of 13 years, three were patients

..      Fig. 15.4  a. Clinical image of severe gingivitis in a 15-year-old male presenting with heavy calculus and bacterial accumulation and orange stain. b. Initial treatment with ultrasonic scaling was followed by oral hygiene instructions. c. At follow-up, a degree of gingival inflammation persists. The fear of bleeding at brushing combined with pubertal hormonal effects in some adolescents calls for additional topical chemotherapeutic support, e.g., periodic use of chlorhexidine

over 60 years of age [17]. The most commonly affected site is the anterior maxillary gingiva, without any explanation offered for this so far. LJSGH presents as a solitary, red, and papillated lesion affecting one tooth, but cases with multiple affected teeth have been reported [18]. There is an abrupt transition from LJSGH to normal mucosa. Typical microscopic findings include elevated areas of variably acanthotic, spongiotic nonkeratinized epithelium (. Fig. 15.5). There are no sex hormone (estrogen or progesterone) receptors as investigated immunohistochemically. No etiologic relationship has been established.  

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b

a

..      Fig. 15.5  a. Clinical image of localized juvenile spongiotic gingival hyperplasia (LJSGH) in a 10-year-old boy extending full width in the attached gingiva of the right central and only in the free gingiva of the left central incisor (courtesy of Dr. R.  Steffens). b.

LJSGH does not respond to conventional oral hygiene measures unlike and plaque-related and/or puberty-related gingivitis. Anecdotal evidence of spontaneous remission has been mentioned. Excision or cryotherapy has been met with some success and may be tried in a symptomatic or cosmetically unsightly lesion. However, as there is no long-term follow-up documentation, in the cases of asymptomatic lesions, observation would be justified [18]. Plasma cell gingivitis (PCG), being again a rare, also benign inflammatory condition of unclear etiology possibly involving allergic reaction to food additives such as cinnamon, seems to not be so frequent in children. When encountered, standard, professional oral hygiene procedures and nonsurgical periodontal therapy, including antimicrobials, have been reported to produce marked improvement [19].

Histological picture of LJSGH. The epithelium demonstrates hyperplasia, spongiosis, and exocytosis. A dense mixed inflammatory cell infiltrate is seen in the underlying connective tissue. (Courtesy of Dr. N. Nikitakis)

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15.1.3  Gingival Hyperplasia 15.1.3.1  Drug-Related Gingival Hyperplasia

The main cause of gingival hyperplasia is systemic medications. Severely hyperplastic gingivae produce aesthetic problems but may also impair mastication, tooth eruption and position, and speech, as well as act as predisposing factors for periodontal destruction. Four drugs, phenytoin, nifedipine (and other calcium channel blockers), cyclosporine, and amphetamine, have been identified as the most common cause of gingival hyperplasia in children and adolescents [8, 20]. In more than 50% of drug-related cases, hyperplasia is caused by the chronic administration of phenytoin (. Fig.  15.6), a drug used to treat epilepsy. Gingival hyperplasia occurs 2–3  weeks after the initiation of systemic medication  

..      Fig. 15.6  a. Clinical features of hyperplastic gingivitis in a 10-year-old child under phenytoin. Gingival enlargement is evident with coexisting acute and chronic inflammation. b. Plaque deposits are the absolute prerequisite for the inflammatory process and secondary hyperplasia to occur

administration to children and has increased incidence and intensity compared to adults. Gingival hyperplasia is mainly localized in the anterior region [20]. The combined administration of nifedipine and cyclosporine in

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children under organ transplantation and therapy of autoimmune diseases increases the frequency and severity of gingival hyperplasias [20]. Another group of drugs associated with gingival hyperplasia are amphetamines administered to children with attention deficit hyperactivity disorder (ADHD). These children may represent up to 5–10% of the school population in the USA and nowadays constitute the largest percentage of children referred for treatment of gingival hyperplasia [8]. Interestingly, most studies show a positive correlation between the frequency and severity of hyperplasia and plaque index and bleeding index, despite there being no clear causal relationship between poor oral hygiene and gingival hyperplasia [20]. The most effective treatment of drug-induced gingival hyperplasia is to replace the drug causing the hyperplasia [21]. This, however, is solely in the responsibility of the attending physician, and in most cases medication substitution is not possible. Therefore, treatment of drug-induced gingival hyperplasia is mainly preventive and includes:

Initial treatment includes oral hygiene instructions, maintenance therapy with root planing, and, in some cases, surgical removal of hyperplastic gingivae (gingivectomy) [22]. It should be noted that, in 40% of these patients, recurrence of hyperplasia after gingivectomy appears 18  months after surgical treatment, which is frequently associated with gingival inflammation due to poor compliance [21, 22]. Surgical interventions should necessarily be followed by frequent and meticulous maintenance therapy.

and absence of inflammatory cells. Although the fibrous gingival hyperplasia does not directly cause alveolar bone loss, it creates gingival anatomical conditions that predispose for plaque accumulation with bone loss as a possible consequence. The most common complications are tooth migration, resulting in tooth spacing and over-­ retention of primary teeth. Indicated treatment is gingivectomy for the improvement of aesthetics, speech, and masticatory function [20] (. Fig. 15.8). Neurofibromatosis type I, also termed von Recklinghausen’s disease, is an inherited disease with varying expression, depending on the type of mutation that causes it (see 7 Chap. 21). Intraorally, gingival hyperplasia may present with tooth impaction, orthodontic anomalies, high plaque and caries indices, and periodontal attachment loss.

15.1.3.2  Congenital Fibrous Gingival

15.2  Periodontitis

Other causes of gingival hyperplasia in children and adolescents are congenital fibrous hyperplasia, neurofibromatosis type I, and leukemia [20]. Hereditary gingival fibromatosis (HGF) is an inherited autosomal dominant syndromic disease (. Fig.  15.7). The syndrome may be associated with epilepsy, mental retardation, and hypertrichosis, but in most cases gingival hyperplasia is the only clinical manifestation. It presents with equal frequency in boys and girls, and usually its onset coincides with eruption of the permanent dentition [20]. Histologically, it differs from the drug-related gingival hyperplasia mainly in that the gingival connective tissue shows a high percentage of collagen fibers

The previous classification of periodontal diseases in 1999 [23] describes three forms of periodontitis, i.e., chronic periodontitis, aggressive periodontitis, and periodontitis as a manifestation of systemic disease. The first category, chronic periodontitis, occurs exclusively in adults by this classification. The most current classification in 2018 [24] excludes the category of aggressive periodontitis and classifies periodontal disease to stages and grades. Stages are supposed to describe the disease state, whereas grades are supposed to describe the rate of disease progression and the systemic and environmental factors that can affect disease progression.

55 Emphasis on oral hygiene instruction. 55 Frequent (every 3  months) professional removal of hard and soft bacterial deposits. 55 Use of antimicrobial solutions.

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..      Fig. 15.7  Hereditary gingival fibromatosis in a 30-month-old boy with primary molars covered with fibrous gingivae. (Courtesy of Dr. R. Steffens)

Hyperplasia

 

 

 

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..      Fig. 15.8  a–d. Clinical appearance of congenital fibrous gingival hyperplasia in a 10-year-old girl. The patient presents with “pseudo-­pockets” and swollen gingivae composed of fibrous tissue, especially in the upper and lower anterior regions. Exceptions are the

Eye Catcher

Children and adolescents can experience one of the following forms of periodontitis based on the most recent classification of periodontal diseases in 2018: 1. Chronic periodontitis. 2. Periodontal disease as a manifestation of systemic disease. Aggressive periodontitis can occur in children and adolescents and can be generalized or localized. Chronic periodontitis in young individuals is caused by specific bacteria and dysfunction of the immune system.

15.2.1  Chronic Periodontitis in Children

and Adolescents

Chronic periodontitis occurs not only in adults but also in children and adolescents. Briefly, the clinical signs include rapid attachment loss and severe gingival inflammation and may show a familial aggregation [11, 23] (. Fig.  15.9). Secondary features include defects in phagocytosis and excessive activity of macrophages/  

interdental papillae between the maxillary central and lateral incisors, which have clinical signs of chronic inflammation, i.e., smooth, red, and spongy texture. e–j. The radiographic images show normal bone levels in the hyperplastic anterior region

monocytes. Polymorphonuclear leukocytes may have reduced capacity for chemotaxis and phagocytosis, reduced bactericidal capacity, and reduced capacity to produce leukotrienes [11, 25–27]. Chronic periodontitis in children and adolescents progresses more rapidly than the chronic periodontitis in adults and can be localized or generalized in distribution [11, 28]. Localized aggressive periodontitis  – as defined by the previous classification in 1999  – is characterized by attachment loss around at least two permanent first molars or incisors and up to two other teeth in the absence of systemic disease [11, 29] (. Fig.  15.10). Retrospective studies in patients with localized aggressive periodontitis show that attachment loss in the primary teeth can precede that in the teeth of the permanent ­ dentition [30]. In contrast, generalized aggressive periodontitis is determined by recording attachment loss in three or more teeth other than molars or incisors [11]. Some clinicians and periodontal researchers believe that localized aggressive periodontitis is not a precursor disease to other forms of periodontitis, while others maintain that it can evolve into generalized aggressive periodontitis [11, 31, 32] (. Figs. 15.11 and 15.12). The incidence of aggressive  

 

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..      Fig. 15.9  Three African-American sisters present with characteristics of aggressive periodontitis, such as severe periodontal lesions, loss of teeth due to periodontal disease at a young age, periodontal destruction in incisors and molars, and genetic predisposition. a1–3. The oldest girl of the family (19 years old) has already lost a central incisor and a first lower molar due to periodontal disease. The lower molar has been replaced with a fixed partial denture. During periodontal surgery advanced intraosseous periodontal lesions were detected in the mandibular molar region of the contralateral side. b1–3. The middle sister (17 years old) has already shown buccal displacement of the upper central incisors. Radiographs showed

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a

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significant periodontal destruction around the maxillary central incisors, which can account for their significant buccal displacement. Radiographic evidence indicates also the advanced periodontal lesions around the first maxillary molars. c1–4. The youngest girl of the family shows significant loss of the attachment between the upper central incisors with the characteristic loss of papilla. By contrast, there is no loss of periodontal attachment in the lower incisors. According to the dental history, both parents lost their teeth due to periodontal disease. Overall, the pediatric dentist should collaborate with a periodontist in the diagnosis, prevention, and treatment of aggressive periodontitis in children

periodontitis  – generalized or localized  – ranges between 0.1 and 3.8% depending on the report and has a higher frequency in African-Americans (2.5%) than in Caucasians. 15.2.1.1  Clinical, Microbiological,

and Immunological Findings

..      Fig. 15.10  a. Significant attachment loss on the buccal surface of the mandibular right first permanent molar of a 7-year-old girl detected with the periodontal probe, while there are minimal clinical signs of inflammation (edema and bleeding on probing). b. Radiographic examination of the area reveals some bone loss of the newly erupted first molar, compatible with a probably self resolving buccal bifurcation cyst. This does not comprise localized aggressive periodontitis. (Courtesy of Dr. N. Kotsanos)

Based on many clinical reports and impressions, the prevailing clinical view holds that localized chronic periodontitis in children and adolescents is characterized by a relatively low accumulation of supragingival plaque and calculus, but others report similar accumulation of supragingival plaque as with other forms of periodontitis [11, 29, 33–35]. Bacteria that have been associated causally with the disease are usually anaerobic gram-­negative rods [36, 37]. Many periopathogenic bacteria isolated from diseased sites are common with those of adult patients with chronic periodontitis, but show greater prevalence in patients of younger age. Some of these

355 Periodontal Diseases in Children and Adolescents

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..      Fig. 15.11  a. 9-year-old boy with localized aggressive periodontitis. A. Acute hyperplastic inflammatory lesion is seen in the gingiva of the maxillary and mandibular molars. b, c. The radiographic examination reveals significant alveolar bone loss in the central maxillary and the lateral mandibular incisors. d. Eighteen months later,

radiographic examination reveals significant bone loss on the molars as well. e. Five years after baseline examination, the periodontitis has progressed significantly with the maxillary right second premolar having a hopeless prognosis. (Courtesy of Drs. N. Kotsanos and A. Gofa)

are Porphyromonas gingivalis (P.g.), Peptostreptococcus micros, Campylobacter rectus, and Tannerella forsythia. The Aggregatibacter (formerly Actinobacillus) actinomycetemcomitans (A.a.) is also a periopathogenic bacterium and is frequently recovered as a substantial percentage of the flora at localized periodontitis sites. Among the five different serotypes of A.a. isolated, serotype b has been associated with aggressive and chronic periodontitis and serotype c with periodontal health. However, a single subgingival organism has not been implicated as the causative organism for localized periodontitis [4, 11, 12, 38–40] Both localized and generalized periodontitis in children and adolescents are characterized by dysfunction of the immune system. Patients show polymorphonuclear leukocyte dysfunction and impaired immunoglobin production (immunoglobins come from B lymphocytes). For both localized and generalized periodontitis, polymorphonuclear leukocytes typically show impaired chemotaxis (although this is not universal) and reduced GP-110 expression, which is a glycoprotein found on the neutrophil cell surface and acts as a receptor of chemotactic factors. The IgG immunoglobulins are classified into four isotype classes (IgG1–4). After infection with

A.a., the IgG2 antibody produced against A.a. is specific for the high molecular weight lipopolysaccharide (HMWLPS) generated by A.a. [11]. Production of IgG2 antibodies against A.a. appears to be protective against aggressive periodontitis [11, 41, 42] since patients with higher concentrations of IgG2 show less attachment loss compared to patients with lower titers of IgG2. The immune response in young patients with chronic periodontitis is determined by other factors as well. For example, the levels of IgG2 in serum are influenced by genetic and environmental factors. Specifically, high levels of serum IgG2 have been detected in Blacks with aggressive periodontitis, while low levels of IgG2 are typically observed in subjects with a smoking history [11] 15.2.1.2  Treatment

As mentioned before, aggressive periodontitis is probably caused by either a specialized subgingival flora or a dysfunctional immune reaction to the subgingival flora. Thus, the treatment of aggressive periodontitis aims to reduce the microbial load and to strengthen host defense mechanisms [11].

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A.-E. Doufexi and F. Nichols

..      Fig. 15.12  a. Routine radiographic examination for detection of caries revealed localized aggressive periodontitis in the primary molars in an 8-year-old girl with no systemic disease. The patient was scheduled for oral hygiene instructions and root scaling and planing. b. Three years later no attachment loss was detected for the permanent teeth, as the patient was prompt in following her recall appointments after phase I periodontal therapy

a

c

Eye Catcher

The antimicrobial therapeutic approach for chronic periodontitis in children and adolescents is similar to the classical periodontal disease management protocol, i.e., the combination of the following: (a) Conventional debridement treatment with root scaling and planing. (b) Surgical treatment. (c) Local or general administration of antibiotics (antimicrobials) [11].

15

The treatment of chronic periodontitis requires eradication of the biofilm by root scaling and planing and typically includes surgical intervention and the administration of antibiotics (. Fig.  15.13). Indeed studies indicate that levels of A.a. were significantly reduced only after periodontal surgery, while the conservative treatment with the administration of antibiotics does not significantly reduce the levels of A.a. [3, 11, 42, 43]. Since in most cases of periodontitis other periopathogenic bacteria are detected besides A.a., administration of systemic antibiotics is often recommended [11]. Young people usually have an excellent healing capacity, and, therefore, the combination of surgery and systemic administration of antibiotics can be successful in promoting substantial osseous fill in infrabony lesions or furcation involvement associated with aggressive periodontitis. In localized periodontitis, tetracyclines are the systemic antibiotics most frequently used. Specifically, the administration of doxycycline (100  mg once a day for 13 days) in combination with surgical debridement-root scaling and planing has been found to significantly reduce the levels of A.a. [44–47]. Metronidazole in combination with amoxicillin with or without clavulanic acid has also

b

d

been used with successful results, especially in the cases of resistant to tetracyclines A.a. Administration of metronidazole (250  mg) in combination with amoxicillin (375 mg 3 times daily for 7 days) may be more effective in eradicating (or substantially reducing) the A.a. and P.g. in most patients with rapid progression of periodontitis [2, 11, 48]. The same antibiotic regimen can be used in the cases of generalized periodontitis. Use of alternative antibiotics may be required in patients who do not respond to conventional antibiotic therapy. In this case, laboratory techniques, such as bacterial culture, polymerase chain reaction (PCR) detection of genetic products, ELISA, or DNA probes, can be used to detect periopathogenic bacteria or that resist conventional antibiotic treatment [11].

 

15.2.2  Periodontitis Associated

with Systemic Disease

Periodontal disease associated with systemic disease may be a manifestation of these diseases. Examples include: 1. Papillon-Lefèvre syndrome (7 Fig. 10.29) 2. Hypophosphatasia 3. Neutropenia 4. Chediak-Higashi syndrome 5. Histiocytosis X 6. Acrodynia 7. HIV infection 8. Leukocyte adhesion deficiency 9. Leukemias  

Leukemia is the most common cancer in children, and the characteristic clinical appearance of the gingiva may help in the early diagnosis of this disease. The clinical signs of leukemia are gingival inflammation and hyperplasia due to invasion of the connective tissue and the

357 Periodontal Diseases in Children and Adolescents

a b

c

d

e

..      Fig. 15.13  a. A 5-year-old boy with no systemic diseases who was diagnosed with aggressive periodontitis shows significant clinical signs of acute gingival inflammation (edema and loss of stippling appearance). b. Radiographic examination reveals significant attachment loss in deciduous molars. The patient was treated with root

scaling and planing and systemic antibiotics. c–e. Eighteen months after treatment completion, the patient presents with periodontal health. The patient complied with frequent recall appointments. Orthodontic treatment will be initiated in the future for the posterior crossbite. (Courtesy of Drs. N. Kotsanos and D. Apatzidou)

underlying bone by transformed leukocytes. Children with leukemia might have fever, bleeding disorders, and malaise. Gingivitis signs and symptoms in children with leukemia will be recurrent, if the systemic disease is not treated. Periodontal disease associated with systemic diseases in children and adolescents typically shows severe symptoms, including severe inflammation, ulceration, rapid bone loss, tooth mobility, and tooth loss. For further reading on the relationship between systemic diseases and periodontal disease, the reader is directed to Williams and Paquette [49], while other diseases, such as neutropenia, histiocytosis X, HIV infection, and leukemia, are further described in 7 Chaps. 20 and 21.

subgingival plaque of diabetic children with periodontitis [55]. Therefore, children with type I diabetes are at higher risk of developing destructive periodontal disease. A significant correlation is also reported between body fat index and the presence of periodontitis in children and adolescents [56]. The authors conclude that a healthy diet and physical activity may be factors that inhibit the onset and progression of periodontitis. The mechanism linking obesity with periodontitis may involve elevated levels of cytokines including IL-8 and TNF-α in crevicular fluid of obese patients that might contribute to periodontal destruction. However, there are some common predisposing factors for obesity and periodontitis, such as unhealthy diet and low socioeconomic status. Therefore, it appears that the two diseases are associated not only through common biological mechanisms but also through common risk factors.

 

15.2.3  Diabetes Mellitus and Periodontal

Disease

It should be noted that, according to the classification of periodontal disease in 1999, diabetes is not included in the category of periodontitis as a manifestation of systemic disease. Nevertheless, diabetes, particularly type I diabetes, is an important predisposing condition for all forms of periodontitis [50, 51]. Several researchers have studied the relationship between juvenile diabetes and aggressive periodontitis. Children with type I diabetes, especially with uncontrolled diabetes, have a higher bleeding index over healthy subjects [52, 53]. The prevalence of aggressive periodontitis in children with type I diabetes has been found to be 10% [54]. Attachment loss in diabetic children is usually localized to molars and incisors, but it can also be generalized. A.a. and Capnocytophaga sp. have been isolated from

15.2.4  Acute Ulcerative Gingivitis/

Periodontitis

The frequency of acute periodontal disease and particularly acute necrotizing periodontal diseases in children and adolescents is very low  – less than 1%  – in Europe and the USA, [8, 11] while they occur more frequently in children and adolescents of developing countries in Africa, Asia, and South America (2–5%) [11]. Necrotizing ulcerative gingivitis usually occurs in young children with systemic disease, while in adolescence it is associated with high levels of physical or mental stress. The two most common diagnostic criteria for necrotizing

15

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A.-E. Doufexi and F. Nichols

15.3  Mucogingival Deformities

a

15.3.1  Gingival Recession

b

..      Fig. 15.14  A 17-year-old girl presented with clinical signs of acute ulcerative gingivitis (pain, halitosis, necrosis of the dental papilla, pseudomembranes). a. Characteristic ulcerative lesions in dental papillae. The patient was a heavy smoker, and she reported that she was under significant stress and malnourished. b. Formation of pseudomembranes in a dental papillae area

Localized recession occurs in 10–15% of children and adolescents. Recession usually occurs on labial surfaces of the lower incisors in children, whereas during teenage years, recession is typically detected on the buccal surfaces of the canines, premolars, and molars. Causes and predisposing factors for gingival recessions in children and adolescents are [8]: 1. Poor oral hygiene, especially if the patient is undergoing orthodontic treatment. 2. Traumatic toothbrushing. 3. Malpositioned teeth. 4. Thin gingival biotype. 5. Piercing of tongue and lips. 6. Frenum pull. 7. Traumatic habits (. Fig. 15.15).  

ulcerative gingivitis are necrosis of the interdental papillae and the acute pain (. Fig.  15.14). Bacteria associated with acute ulcerative gingivitis include spirochetes, especially Borrelia vincentii and Prevotella intermedia.  

Eye Catcher

15

Predisposing factors for acute necrotizing ulcerative periodontal diseases are viral infections including infection with HIV, systemic diseases, poor nutrition, smoking, inadequate sleep, and mental and physical stress. Necrotizing ulcerative periodontitis is characterized by formation of pseudomembranes, necrosis of interdental papillae, and acute pain. It is exceedingly rare in children and is usually associated with severe immunodeficiency associated with AIDS or ARC (AIDS-related complex).

If necrotizing ulcerative gingivitis is left untreated, it may progress to periodontitis. Treatment of necrotizing ulcerative gingivitis involves removing plaque and calculus, oral hygiene instructions, administration of metronidazole or penicillin if there are other systemic symptoms, and frequent recall appointments. If the patient is a smoker, he/she should be informed about the role of nicotine to gingival tissue responses and referred for smoking cessation therapy. Scaling using ultrasound has proven to be very efficient and leads to rapid relief of symptoms. It is also recommended to use a soft toothbrush, at least in the initial phase of therapy, because of severe pain with each contact of the gingiva, and mouthwashes with 1.5% hydrogen peroxide or 0.2% chlorhexidine can cause significant burning sensation.

It is important to identify the exact causes (traumatic toothbrushing or inflammation) and predisposing factors (gingival biotype, teeth alignment) before treating gingival recession. For example, the buccal alveolar bone position on the facial aspect of a tooth may be a predisposing factor for recession. Before any surgical treatment of recession on a facially tipped tooth, the tooth position must be corrected by orthodontic treatment. After the completion of realigning, the existence and severity of recession is reassessed, and usually no further surgical treatment of the recession is needed. Piercing of the tongue and lips is one of the modern causes of gingival trauma that may cause recession [8]. The continuous pressure on the gingiva created by tongue jewelry can also cause severe attachment loss in addition. Studies show that about 1/3 of patients with tongue jewelry have at least one area of lingual recession and 80% of patients with lip jewelry have one or more areas of recession [57, 58]. Informing patients about the consequences of piercing can prevent future recession due to piercing (. Fig. 15.16). Recognition of the factors responsible for the genesis of recession can also help to prevent failure of mucogingival surgery.  

15.3.2  Frenum Pull

Another common finding in children is frenum pull between the maxillary central incisors accompanied by diastema (. Fig. 15.17). In most cases there is no reason for immediate treatment until eruption of permanent incisors and canines, when usually the diastema closes spontaneously. If the patient elects to have orthodontic treatment, surgical incision or excision of the frenum is  

359 Periodontal Diseases in Children and Adolescents

a

b

..      Fig. 15.15  a, b. A 4-year-old boy presented for dental caries treatment. Clinical examination revealed extensive gingival recession in the area of the maxillary lateral incisors. The child confessed

a

b

..      Fig. 15.16  a. Lip jewelry can cause chronic trauma intraorally to corresponding periodontal tissues. b. The adolescent girl agreed to change to flat surface buttoning to prevent this from happening

postponed until the end of orthodontic treatment and only if it impedes the movement of the two central incisors. On the other hand, there are reports that frenum excision before orthodontic treatment may provide better access for frenum removal due to the presence of the diastema. Moreover, some studies indicate that the diastema might disappear only by frenum excision with no orthodontic treatment, suggesting that early surgical intervention may be more cost-effective as well as less time-consuming [59, 60]. The excision of the frenum can be accomplished in various ways, i.e., surgical removal can be as simple as a frenotomy or may include apical displacement of the frenum and a free gingival graft. A free gingival graft in the frenectomy area might cause aesthetic concerns due to different thickness and color between the graft and the adjacent gingiva. Moreover, a frenectomy can be accompanied with a lateral sliding flap by which primary closure can be achieved over the site where the frenum was previously located [60, 61]. The ankyloglossia (tongue-tie) is a malformation characterized by high attachment of a short lingual frenum, occurring at a frequency of about 1.5–4.5%. The short lingual frenum limits the tongue movement anteriorly and superiorly in the mouth, limiting its

scratching his gingiva with his nails. Treatment will include gingival recession as well as management of underlying stress. (Courtesy of Dr. Arhakis)

mobility and causing difficulties with physiological functions. Various frenum classifications have been proposed in the literature. One of them is the following [7]: (a) Light (a very thin frenum of mucosa). (b) Moderate (the frenum and the genioglossus muscles showing fibrous consistency). (c) Complete (the tongue is attached to the floor of the mouth). Ankyloglossia may result in difficulty with speech, but this is usually not serious. However, surgical excision of a short lingual frenum in a few cases contributed to the restoration of the speech of young patients who had severe difficulties in speech. Because the evaluation of the results from each speech therapist is subjective, controversy exists in speech therapy studies as to whether the surgical correction of ankyloglossia improved speech. Whether there is real benefit after surgical excision of the lingual frenum could be assessed by randomized controlled clinical trials comparing speech difficulties before and after frenectomy [62]. Frenectomy of the lingual frenum is indicated if the child cannot touch the labial surface of the lower incisors with his/her tongue. If decided in infancy, it can be done under general anesthesia (7 Fig. 8.18). In cooperative children it may be performed under local anesthesia with cautious placement of a few sutures due to the vascularity of the floor of the mouth. It has recently been reported that frenectomy can be done by the use of diode, Nd:YAG, or CO2 laser, a method associated with less postoperative pain and discomfort and also better healing compared to traditional surgical techniques. The laser excision technique is simple and efficient, readily achieves the required frenum release with minimal bleeding, and can be accomplished without anesthesia even in infants with severe ankyloglossia.  

15

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A.-E. Doufexi and F. Nichols

a

b

c

d

..      Fig. 15.17  a, b. Frenum pulls on the upper lip in the primary and permanent dentitions, respectively. Frenum excision is better postponed until after orthodontic treatment. c. The high frenum attachment can impair plaque control and promote gingival inflammation.

d. Medium ankyloglossia in a 7-year-old girl. The patient did not undergo surgical treatment, since her speech was not impaired. (Courtesy of Dr. N. Kotsanos)

References

13. Murakami S, Mealey BL, Mariotti A, Chapple ILC.  Dental plaque-induced gingival conditions. J Periodontol. 2018;89(Suppl 1):S17–27. 14. Ramseier CA, Anerud A, Dulac M, Lulic M, Cullinan MP, Seymour GJ, Faddy MJ, Bürgin W, Schätzle M, Lang NP.  Natural history of periodontitis: disease progression and tooth loss over 40 years. J Clin Periodontol. 2017;44:1182–91. 15. Seymour GJ, Crouch MS, Powell RN. The phenotypic characterization of lymphoid cell subpopulations in gingivitis in children. J Periodontal Res. 1981;16:582–92. 16. Nakagawa S, Fujii H, Machida Y, Okuda K.  A longitudinal study from prepuberty to puberty of gingivitis. Correlation between the occurrence of Prevotella intermedia and sex hormones. J Clin Periodontol. 1994;21:658–65. 17. Wang MZ, Jordan RC.  Localized juvenile spongiotic gingival hyperplasia: a report of 27 cases. J Cutan Pathol. 2019;46(11):839–43. https://doi.org/10.1111/cup.13549. 18. Siamantas I, Kalogirou EM, Tosios KI, Fourmousis I, Sklavounou A. Spongiotic gingival hyperplasia synchronously involving multiple sites: case report and review of the literature. Head Neck Pathol. 2018;12(4):517–21. 19. Arduino PG, D'Aiuto F, Cavallito C, Carcieri P, Carbone M, Conrotto D, et  al. Professional oral hygiene as a therapeutic option for pediatric patients with plasma cell gingivitis: preliminary results of a prospective case series. J Periodontol. 2011;82(12):1670–5. https://doi.org/10.1902/jop.2011.100663. 20. Doufexi A, Mina M, Ioannidou E. Gingival overgrowth in children: epidemiology, pathogenesis, and complications. A literature review. J Periodontol. 2005;76:3–10. 21. Dongari-Bagtzoglou A. Drug-associated gingival enlargement. J Periodontol. 2004;75:1424–31. 22. Ilgenli T, Atilla G, Baylas H. Effectiveness of periodontal therapy in patients with drug-induced gingival overgrowth. Longterm results. J Periodontol. 1999;70:967–72.

1. Pari A, Ilango P, Subbareddy V, Katamreddy V, Parthasarthy H. Gingival diseases in childhood - a review. J Clin Diagn Res. 2014;8:ZE01–4. 2. Oh TJ, Eber R, WangHL. Periodontal diseases in the child and adolescent. J Clin Periodontol. 29:400–10. 3. Burt B. Position paper: epidemiology of periodontal diseases. J Periodontol. 2005;76:1406–19. 4. Albandar JM.  Epidemiology and risk factors of periodontal diseases. Dent Clin N Am. 2005;49:517–32, v-vi. 5. Albandar JM, Tinoco EM. Global ­epidemiology of periodontal diseases in children and young persons. Periodontol 2000. 2002;29:153–76. 6. Loe H, Theilade E, Jensen SB. Experimental gingivitis in man. J Periodontol. 1965;36:177–87. 7. Matsson L, Goldberg P.  Gingival inflammatory reaction in children at different ages. J Clin Periodontol. 1985;12(2):98– 103. 8. Studen-Pavlovich D, Ranalli DN.  Periodontal and soft tissue prevention strategies for the adolescent dental patient. Dent Clin N Am. 2006;50:51–67. 9. Bimstein E, Lustmann J, Soskolne WA.  A clinical and histometric study of gingivitis associated with the human deciduous dentition. J Periodontol. 1985;56:293–6. 10. Trombelli L, Farina R. A review of factors influencing the incidence and severity of plaque-induced gingivitis. Minerva Stomatol. 2013;62:207–34. Review. 11. Califano JV.  Position paper: periodontal diseases of children and adolescents. J Periodontol. 2003;74:1696–704. 12. Moore WE, Holdeman LV, Smibert RM, Cato EP, Burmeister JA, Palcanis KG, Ranney RR.  Bacteriology of experimental gingivitis in children. Infect Immun. 1984;46:1–6.

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23. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol. 1999;4:1–6. 24. Papapanou PN, Sanz M, Buduneli N, Dietrich T, Feres M, Fine DH, et al. Periodontitis: consensus report of workgroup 2 of the 2017 world workshop on the classification of periodontal and Peri-implant diseases and conditions. J Periodontol. 2018;89(Suppl 1):S173–82. 25. Cogen RB, Roseman JM, Al-Joburi W, Louv WC, Acton RT, Barger BO, et al. Host factors in juvenile periodontitis. J Dent Res. 1986;65:394–9. 26. Van Dyke TE, Hoop GA. Neutrophil function and oral disease. Crit Rev Oral Biol Med. 1990;1:117–33. 27. Van Dyke TE, Zinney W, Winkel K, Taufiq A, Offenbacher S, Arnold RR.  Neutrophil function in  localized juvenile periodontitis. Phagocytosis, superoxide production and specific granule release. J Periodontol. 1986;57:703–8. 28. Waerhaug J. Subgingival plaque and loss of attachment in periodontosis as evaluated on extracted teeth. J Periodontol. 1977;48:125–30. 29. Catunda RQ, Levin L, Kornerup I, Gibson MP. Diagnosis of aggressive periodontitis: a dilemma? Quintessence Int. 2018:49173–80. 30. Sjödin B, Matsson L, Unell L, Egelberg J. Marginal bone loss in the primary dentition of patients with juvenile periodontitis. J Clin Periodontol. 1993;20:32–6. 31. Brown LJ, Albandar JM, Brunelle JA, LöeH. Early-onset periodontitis: progression of attachment loss during 6 years. J Periodontol. 1996;67:968–75. 32. Gunsolley JC, Califano JV, Koertge TE, Burmeister JA, Cooper LC, Schenkein HA. Longitudinal assessment of early onset periodontitis. J Periodontol. 1995;66:321–8. 33. Albandar JM, Brown LJ, Brunelle JA, Löe H.  Gingival state and dental calculus in early-onset periodontitis. J Periodontol. 1996;67:953–9. 34. Araujo M. Localized juvenile periodontitis or localized aggressive periodontitis. J Mas Soc Summer. 2002;51:14–8. 35. Butler JH.  A familial pattern of juvenile periodontitis (periodontosis). J Periodontol. 1969;40:115–8. 36. Newman MG, Socransky SS. Predominant cultivable microbiota in periodontosis. J PeriodontalRes. 1977;12:120–8. 37. Slots J. Subgingival microflora and periodontal disease. J Clin Periodontol. 1979;6:351–82. 38. Asikainen S, Lai CH, Alaluusua S, Slots J.  Distribution of Actinobacillus actinomycetemcomitans serotypes in periodontal health and disease. Oral Microbiol Immunol. 1991;6: 115–8. 39. Han NM, Xiao XR, Zhang LS, Ri XQ, Zhang JZ, Tong YH, et al. Bacteriological study of juvenile periodontitis in China. J Periodontal Res. 1991;26:409–14. 40. Moore WE, Moore LV.  The bacteria of periodontal diseases. Periodontol. 2000. 1994;5:66–77. 41. Califano JV, Gunsolley JC, Nakashima K, Schenkein HA, Wilson ME, Tew JG.  Influence of anti-­Actinobacillus actinomycetemcomitans Y4 (serotype b) lipopolysaccharide on severity of generalized early-onset periodontitis. Infect Immun. 1996;64:3908–10. 42. Califano JV, Pace BE, Gunsolley JC, Schenkein HA, Lally ET, Tew JG. Antibody reactive with Actinobacillus actinomycetemcomitans leukotoxin in early-onset periodontitis patients. Oral Microbiol Immunol. 1997;12:20–6. 43. Albandar JM.  Aggressive periodontitis: case definition and diagnostic criteria. Periodontol 2000. 2014;65:13–26. Review. 44. Aitken S, Birek P, Kulkarni GV, Lee WL, McCulloch CA. Serial doxycycline and metronidazole in prevention of recurrent peri-

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363

Dentoalveolar Trauma of Children and Adolescents Cecilia Bourguignon, Aristidis Arhakis, Asgeir Sigurdsson, and Nikolaos Kotsanos Contents 16.1

Introduction to Dentoalveolar Trauma – 364

16.1.1 16.1.2 16.1.3 16.1.4

 lassification – 364 C Epidemiology – 364 Etiology of Dental Trauma – 366 Examination: Diagnosis – 367

16.2

Dental Trauma to Primary Teeth – 370

16.2.1 16.2.2 16.2.3 16.2.4

F ractures of Primary T – 370 Luxation Injuries to Primary Teeth – 372 Follow-Up and Complications of Trauma to Primary Teeth – 376 Consequences of Primary Tooth Trauma to Their Permanent Successors – 377

16.3

Dental Trauma to Permanent Teeth – 380

16.3.1 16.3.2 16.3.3 16.3.4 16.3.5

F ractures of Permanent Teeth – 380 Luxation Injuries to Permanent Teeth – 389 Post-traumatic Complications of Permanent Teeth – 396 Follow-Ups of Injured Permanent Teeth – 401 Endodontic Evaluation and Management of Injured Permanent Teeth – 401

16.4

Prognosis of Injured Teeth – 405

16.5

Orthodontic Management of the Traumatized Dentition – 406

16.6

Prevention of Dentoalveolar Trauma – 407

16.6.1

Mouth-guards – 407

References – 409

© Springer Nature Switzerland AG 2022 N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry, https://doi.org/10.1007/978-3-030-78003-6_16

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C. Bourguignon et al.

16.1  Introduction to Dentoalveolar Trauma

Injuries to the lower face occur in about one third of the general population and most of them are managed by dental practitioners. Dental and oral injuries occur frequently in children and may have medical, functional, and psychological consequences. The term dentoalveolar, or dental as a short expression, refers to injuries to the teeth themselves, to their supporting periodontal ligament and bone, to soft tissues covering the oral cavity or being in contact with the teeth, or to a combination thereof. Such injuries may cause pain, inflammation, and discomfort of different intensities. They are often combined with injuries in other parts of the face or body. Dental traumas in children usually cause extreme anxiety both to themselves and to their parents. Treatment may thus be a challenge for the dentist. If optimal prognosis is to be ensured, good knowledge, careful planning, efficiency, and a calm attitude are “must to have” skills for the dental practitioner. 16.1.1  Classification

16

The present classification is based on a system adopted by the World Health Organization (WHO) in 1992 in its Application of international classification of diseases to dentistry and stomatology. Later, JO and FM Andreasen suggested some adjustments in the classification, which include the groups below [1]. Injuries to the hard dental tissues and the pulp: 55 Incomplete enamel fracture. Fracture without enamel loss (enamel infraction) 55 Complete enamel fracture. Loss confined to the enamel 55 Crown fracture (enamel/dentin), no pulp exposure; also known as uncomplicated crown fracture 55 Crown fracture (enamel/dentin), pulp exposed; also known as complicated crown fracture 55 Crown/Root fracture with or without pulp exposure 55 Root fracture; no enamel involvement Injuries to the periodontal tissues: 55 Concussion. Periodontal trauma without tooth loosening 55 Subluxation. Loosening without tooth displacement 55 Extrusive luxation. Partial excursion of the tooth while still in its socket 55 Lateral luxation. Non-axial (horizontal) tooth displacement 55 Intrusion. The tooth is impacted into the alveolar bone 55 Avulsion. Complete excursion of the tooth out of its socket

a

b

..      Fig.16.1  a Extraoral wound 24 hours after its suturing. The soft tissue laceration was due to impact on hard floor surface, which also led to palatal displacement of the right maxillary primary incisors. b Intraoral lacerated mucosal marks from the traumatized teeth

In addition to the above groups, there are “injuries to the supporting bone” and “injuries to gingiva or oral mucosa included” [1]. Dentoalveolar trauma is often accompanied by soft tissue injuries. Unless there is bleeding that interferes with dental treatment, soft tissue injuries should be dealt with only after the tooth/pulp is securely treated. If there is an open soft-tissue injury, it needs disinfection and suturing so that proper healing may be achieved (. Fig. 16.1). Radiographic examination of the soft tissues may be necessary, as described later, regarding tooth fractures. If there is notable swelling, the edema will start subsiding the third day after trauma (. Fig.  16.2). Tooth displacement (luxation) is often accompanied by alveolar bone fracture, which is discussed in the subchapter on this topic. There may also be maxillary or mandibular trauma, most often occurring at the mandibular condyles. Oral injuries are common among teenagers, usually after a fight (. Fig.  16.3), but may also be a component of more serious non-oral injuries, for example, those occurring at motor accidents. Whether mandibular/maxillary fractures should be treated simply by splinting or if surgical correction is necessary lies beyond the scope of a pediatric dentistry textbook, and readers are referred to other sources, e.g., maxillofacial surgery literature.  

 

 

Eye Catcher

Traditional classifications usually separate endodontic from periodontal injuries. This is not in principle justified, since injuries usually affect both tissues concomitantly. Additionally, there are mutual relations between these tissues from a healing and prognosis perspective.

16.1.2  Epidemiology

Oral traumas where patients seek help at dental practices and hospitals are frequent and represent 5% of all body trauma cases. Their incidence is probably even higher,

16

365 Dentoalveolar Trauma of Children and Adolescents

a

b

Number of Accidents 25 21

22

21

20

19

17

15 10 5

5 ..      Fig. 16.2  a Upper lip edema a few hours after a 2-year-old toddler had fallen. b Intraoral view of the dentoalveolar trauma

a

2

0

1

up to 1 up to 2 up to 3 up to 4 up to 5 up to 6 up to 7 up to 8

..      Fig. 16.4  Age distribution of 106 successive patient arrivals with 200 traumatized primary teeth at University of Gottingen Dental Clinic, Germany [3]

(. Fig.  16.4). The teeth most frequently involved in trauma are central maxillary primary incisors at a rate of 68–75%, since they are more exposed than any other teeth on the dental arch. The next most frequent group is that of lateral maxillary primary incisors and maxillary canines [2, 4]. Posterior tooth trauma is rather rare, and it is typically caused by jaw fracture; it usually involves longitudinal crown-root fractures (. Fig.  16.5). More rarely, such trauma may be accompanied by mandibular condyle fracture. Although the reported range of findings is wide, varying from 1:1 to 3:1, boys generally appear to be more susceptible than girls to primary tooth trauma [3–5]. Of particular interest is the finding that 87% of children arriving at a dental practice because of trauma have already suffered prior trauma to one or two teeth [6]. Thus, a recent dental trauma radiograph may show atypical root resorption, indicating an older trauma for which no treatment had been sought (. Fig. 16.6).  

 

b

 

16.1.2.2  Permanent Teeth

..      Fig. 16.3  a Chin blow in a 17-year-old boy following a fight. The TMJ is painful and the occlusion hindered by lateral displacement of the mandible. b Coronoid process and condyle fractures (arrows) in the patient’s right ramus as seen in the panoramic radiograph

because in mild dental trauma cases patients often do not seek treatment or are not officially registered, since they do not represent issues of concern to them [2]. 16.1.2.1  Primary Teeth

At least 30% of children have suffered some type of trauma to their primary teeth [2]. Such injuries occur most frequently between the ages of 2 and 5  years and about 80–85% of them are caused by falls [3, 4]

A study from Denmark reported a 22% dentoalveolar trauma incidence for permanent teeth [2]. There is a huge variation in trauma prevalence, explained by differences in trauma investigation methodology, age group choice, geographical regions, and various socioeconomic factors. Still, among youngsters with anterior permanent teeth, boys have been reported to be about twice as likely to suffer dental trauma than girls; however, this gap is likely to be diminishing now [7, 8]. The highest incidence is encountered among individuals of up to 10  years, while during adolescence, there is a marked reduction in numbers, almost leveling off in adult life [4] (. Fig. 16.7). The distribution of permanent teeth most frequently involved in trauma is similar to that of primary teeth, and it is presented in . Table 16.1. The most frequent condition is isolated dental trauma, but there are cases of multiple dental traumas as well [4, 7].  

 

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a

c

b

..      Fig. 16.5  a Crown-root fracture with pulp exposure of a mandibular primary first molar after blow to the chin. b Radiographic image of the crown-root fracture. c, d Treatment involved pulpotomy

d

and placement of a stainless-steel crown after removal of the fractured fragment rather than tooth extraction. Regular monitoring of the tooth is necessary

16.1.3  Etiology of Dental Trauma

Dental trauma etiology is associated with accidents and impacts related to biological, socioeconomic, psychological, and behavioral factors [4]. 16.1.3.1  Primary Teeth

..      Fig. 16.6  The parents were not aware of any trauma episode; the occlusal radiograph, however, shows changes consistent with prior trauma to primary central incisors: an apical radiolucency is visible on the right one; there is pathological root resorption of both and pulp canal obliteration of the left one

a

16

 

b

Dental trauma distribution

60

The main cause for dentoalveolar trauma in primary dentition is the unstable gait of young children, which results in frequent falls at home or at school. Falls are frequent causes for the avulsion of primary teeth among children aged 9 months to 4 years. Other common causes are collision and falls while playing at school or cycling accidents [4, 10]. The abused child syndrome is another, less frequent, etiological factor that might escape the attention of dental practitioners. Incidents that seek delayed medical help are suspicious for child battering or abuse (. Fig. 16.8) [10].

90 80

50

Permanent teeth Primary teeth

NUMBER OF PATIENTS

70 40

Males

Females

60 50

30

40 20

30 20

10 0

10 0-4

5-9 10-14 15-19 20-24 25-29 30-34 35-39 >40

0

Assault

AGE GROUPS (YEARS)

..      Fig. 16.7  A sample of 323 Australian individuals who sought treatment for dental trauma [4]. a Distribution of patients according to age and gender. Prevalence differences between males and females

Bike

Fall

MVA

Other

Play

Sport

Work

CAUSE OF INJURY

do not become apparent prior to school age. b Causes of traumatized primary and permanent teeth (MVA motor vehicle accident)

16

367 Dentoalveolar Trauma of Children and Adolescents

..      Table 16.1  Distribution of frequency of permanent incisors dental trauma Lam, Abbott et al. 2008 [4]

Roberts and Longhurst 1996 [9]

Upper central incisors

63%

73%

Upper lateral incisors

18%

18%

Lower central incisors

10%

6%

Lower lateral incisors

5%

3%

interference or impact on fixed surfaces of reduced hardness mainly causes luxation injuries. The outcome is, of course, dependent on the force of the impact. The most common predisposing factor is increased overjet with protrusion of maxillary incisors. It has been reported that an increase from 0–3  mm to 3–6  mm leads to twice as many trauma rates, while if protrusion exceeds 6 mm, incidence triples [14] (. Fig. 16.9). Insufficient lip coverage seems to play a role as well. The Swedish Council on Technology Assessment in Health Care (SBU) presented a systematic overview in 2005 of the literature and concluded (evidence 3) that there is an increased risk of a traumatic dental injuries (TDI) to the upper front teeth if the patient has a pronounced overjet with protrusion in combination with inadequate lip coverage [15]. Hyperactive children, as well as those with frequent epileptic seizures or motor disabilities, are also more susceptible to dental trauma, depending on the severity of their disability and on whether they are on medication or not [16, 17].  

Eye Catcher

Biological factors that affect the type of primary tooth trauma are the structure of the supporting alveolar bone, which is of reduced hardness among young children and therefore sustains higher deformity, and root length, which is shorter when compared to permanent anterior teeth. Due to these factors, tooth displacement is more frequent (85%) than tooth fracture (15%) in primary teeth [6].

16.1.4  Examination: Diagnosis 16.1.4.1  Medical History

16.1.3.2  Permanent Teeth

Almost half of permanent tooth trauma cases in the 7–18-year-old age group occur at school. Of the rest, 10% are caused by road accidents, if bicycles are also included [2]. Sport injuries are frequent, particularly in contact sports, such as football, basketball, handball, and boxing [11]. However, many of those “sport” injuries actually do not occur during an organized event but rather in backyard play where prevention is much harder to achieve [12]. Naturally, rates may vary among societies with different lifestyles. Crown fractures are caused by direct impact of teeth against hard objects or surfaces [13]. Soft tissue ..      Fig. 16.8  a Case of an abused child for whom delayed medical help was sought. b The panoramic radiograph indicates alveolar fracture in the anterior maxilla with extrusion of three incisors (courtesy of Dr. C. Stavrianos)

a

A medical history is taken to find out about possible allergies, coagulation disorders, cognitive disorders, or other information that might affect the treatment plan. Part of this history taking should be assessment of any possible central nervous system (CNS) injuries, like brain concussion or intracranial hemorrhage. This is because every dental trauma is by definition a head injury, and it has been shown in a systematic review of over 12,750 mild head injuries that the mean prevalence of intracranial hemorrhage was over 8% [18]. The most common signs of a CNS injury are loss of consciousness or post-traumatic amnesia; however, delayed reactions like loss of/or diminished consciousness, situational confusions, headache getting worse, nausea/vomiting,

b

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b

c

..      Fig. 16.9  a Face of an 8-year-old with increased risk of dental trauma due to overjet of maxillary central incisors >10  mm. b, c A 7-year-old girl with epilepsy. There is a 15 mm maxillary permanent central incisor overjet with deep bite. Previous trauma caused an enamel-dentin fracture. A sinus tract is now evident labially to the right central incisor

and or behavioral changes/unexplained irritation can be also signs [19]. Therefore, it is essential to do at least some rudimentary CNS evaluation prior to any further treatment is rendered. If there are any signs of brain injury, the patient needs to be referred immediately to appropriate emergency services. 16.1.4.2  Dental Trauma History

16

Whether at the initial phone call or once the patient has arrived at the dental office, the dentist needs to know what happened. For collecting reliable and comparable data, it is recommended that a standardized dental trauma sheet should be filled out [20]. The most important questions that should be answered first are the following: 55 When did the injury happen? The time intervening between the injury and the beginning of treatment is decisive for selecting the therapeutic protocol and for prognosis. 55 Where did the injury happen? This information is important in order to find out how far the patient is from the dental office and also for social or/and legal purposes. If the injury happened in contaminated soil, anti-tetanus protection should be checked. 55 How did the injury happen? The nature of the impact can lead to suspicions about the type of injuries to be expected. For example, a blow to the chin often results in condyle fracture or crown/root fracture in molars or premolars. 55 Was there loss of consciousness or other signs/symptoms? If the patient fainted, vomited, had amnesia, suffered headaches, or presented hemorrhage or loss of cerebrospinal fluid from the nose or the ears, he needs to be referred to a hospital immediately.

Dizziness, which may occur quite a few hours after the accident, or photophobia and difficulty in visual focusing are also indicators of possible craniocerebral injury. 55 Have the teeth been counted? Is any missing? If there is suspicion that a tooth may have been aspired into the respiratory tract, the patient is referred for a chest radiograph. 55 Is there any difficulty in closing mouth or a malocclusion? If yes, there might be tooth displacement, alveolar process or jaw fracture, displacement, or/ and fracture of a TMJ component. 55 Did any tooth become mobile? If yes, a luxation injury is suspected. 16.1.4.3  Extraoral Examination

The patient is checked for the presence of abrasions, edemas, bruising, hematomas (particularly in the conjunctivas), and hemorrhagic foci. Facial bones should be palpated to locate any abnormalities that might lead to fracture diagnosis. If the edema or pain does not allow direct palpation, appropriate radiographs should be taken. The patient is to be asked to open and close his/ her mouth so as to identify whether there is limitation or deviation in the mandibular movement and to diagnose condyle fractures (e.g., temporomandibular disorders, see 7 Chap. 19, 7 Fig. 19.4).  

 

16.1.4.4  Intraoral Examination

The patient is carefully examined for: 55 Edema or hemorrhaging in the gums or the mucosa 55 Malocclusion 55 Missing, displaced, loosened, or fractured teeth or teeth with enamel cracks. The following are also examined: 1. Mobility: at the horizontal and vertical levels, considering the normal mobility of primary teeth ready to fall out and of permanent teeth recently erupted. 2. Percussion: sensitivity or pain means injury to the periodontal ligament, while a sound similar to that of an impacted metal object indicates the tooth has intruded into the bone, 3. Crown discoloration: it is likely to happen a few days after the accident, or it might have preexisted due to prior injury to the same tooth. 4. Reaction to sensitivity testing: the first few days, measurements may be unreliable but should be done because the information is useful for comparison purposes at later sessions or to other noninjured teeth. Every injury to the lower face needs to be assessed for possible traumas caused to dental tissues and for any coexisting periodontal tissue trauma [21].

369 Dentoalveolar Trauma of Children and Adolescents

16.1.4.5  Radiographic Examination

It is imperative that radiographs should be taken, depending on the tooth and the type of trauma, so that clear conclusions may be drawn concerning the presence or absence of a root fracture, the potential displacement of the injured tooth, the periapical and periodontal condition, the stage of root development, and, in the case of a primary tooth, its relation to its permanent successor [22]. Since maxillary central incisors are most frequently affected teeth, the IADT (International Association of Dental Traumatology) recommends that three periapical radiographs be taken with different horizontal angulations, plus an occlusal radiograph [21]. Radiographic examination is imperative in certain reviewing checks, based on the protocols recommended, because, in the long run, this is a fundamental criterion of a successful or unsuccessful outcome. For example, halting of normal pulp space width reduction in young teeth or discovery of a periradicular radiolucency or of a pathologic external root resorption on primary or permanent teeth confirms pulp tissue necrosis and infection. This is explained by the diffusion of necrotic/septic material from the root canal through the apex and dentinal tubules. In these situations, endodontic treatment needs to be started as soon as possible. Radiographic examination of primary teeth in very young children who cannot cooperate is performed with them sitting on the parent’s lap while the parent is holding a No. 2 biting conventional or phosphor plate (. Fig. 16.10). In cases of crown fractures and wounds of adjacent soft tissues, such as lips or tongue, the latter need to be examined radiographically to check for possible shard laceration. The radiographic exposure time has to be reduced accordingly [23] (. Fig. 16.11). Although cone beam examinations should be avoided in young patients in order to minimize radiation exposure, they may be helpful visualization aids for better diagnosis. They should be prescribed occasionally, only when needed to improve treatment decision-­making (see 7 Chap. 6).

..      Fig. 16.10  Positioning a young child on the parent’s lap, while the parent is holding between fingers a No. 2 biting plate, for taking a radiograph of the anterior primary teeth

a

 

b

 

 

>>The IADT (International Association of Dental Traumatology) Guidelines Since 2001, the International Association of Dental Traumatology (IADT) has through its Board of Directors developed a series of guidelines for treatment of all types of traumatic injuries affecting primary and permanent teeth. The IADT has additionally revised and updated these guidelines in 2007, 2012, and 2020 [21, 23, 24]. The 2012 IADT Trauma Guidelines can be loaded using this link: 7 www.­iadt-­dentaltrauma.­ org or the smartphone application “ToothSOS.” The IADT is in the continuous process of revising and updating its guidelines to provide the best treatment  

..      Fig. 16.11  a Previous day’s chin blow of a 7-year-old boy and associated crown fracture of maxillary permanent left central incisor. Lip laceration is suspicious for possible lip entry of the fragment. b Radiograph of lower lip confirms the presence of crown fragment

recommendations for patients and dentists. The IADT Guidelines are endorsed by the American Association of Endodontists (AAE) and by both the American and European Academies of Pediatric Dentistry (AAPD, EAPD). Based on the IADT’s Guidelines, a recent interactive website called Dental Trauma Guide, at 7 http://www.­dentaltraumaguide.­org, was created as a joint venture between IADT and Copenhagen University Hospital under the supervision of Dr. Jens Andreasen, eminent author and researcher for dental trauma [25].  

16

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C. Bourguignon et al.

to avoid lip and tongue injury. When a fracture is more extensive involving the dentin, restoration with composite resin may be performed in children capable of cooperating. Otherwise, because dentinal tubules are exposed, it is imperative that these should be covered with glass ionomer cement, a process demanding far less cooperation [23].

a

c

b

zz Follow-up

No follow-up is necessary in the case of infractions. In an enamel-dentin fracture without pulp exposure, clinical recall should be performed at 6–8  weeks after the injury [23] (See also . Table 16.2).  

16.2.1.2  Crown Fracture with Pulp Exposure ..      Fig. 16.12  a Hypoplasia of maxillary right central primary incisor and absence of the lateral incisor in a 2-year-old born at 26th week. b Radiograph shows the lateral with severe dysplasia (odontoma). c This photograph of another boy explains why a metal laryngoscope for achieving intubation may be incriminated for causing such trauma to forming incisors, had this been necessary in the prematurely born infant

16.2  Dental Trauma to Primary Teeth

Before describing trauma to erupted teeth, one needs to refer first to the fact that children who had to undergo orotracheal intubation for various reasons (premature delivery, corrective surgical treatment, etc.) are more likely to present dental abnormalities. Such abnormalities are considered to be resulting from trauma to the alveolar process caused by the metal laryngoscope during intubation at a time when the development/calcification of anterior maxillary primary teeth is taking place (. Fig.  16.12). There is evidence of analogous trauma cases in the permanent dentition, and this is a risk that pediatric anesthesiologists should be aware of [26].

Such cases represent 5% of traumas in primary dentition, and most times, there is hemorrhage or the edge of the pulp horn revealed appears as a red spot [6, 23, 27]. Following clinical examination, it is imperative that an anterior occlusal radiograph be taken so as to assess the integrity, the developmental stage, or the extent of physiologic root resorption. zz Treatment

Treatment recommended for pulp exposure includes pulpotomy, either partial or complete, and root canal treatment, provided the patient is capable of cooperating. When the two techniques were used for primary incisors with caries, success rates showed no significant difference [28]. The fractured crown is then reconstructed using composite resin (. Fig.  16.13). If there is no hemorrhage from a recent trauma (within a few hours), the pulp may be covered immediately. In cases of patients incapable of cooperating, extraction might be necessary [23, 29].  

 

16

16.2.1  Fractures of Primary T 16.2.1.1  Enamel Infraction, Enamel-Dentine

Crown Fracture Without Pulp Exposure

This usually occurs in the mesial incisal angle or the incisal edge of central maxillary incisors. Radiographic examination with a periapical radiograph should follow the clinical examination. zz Treatment

In limited fractures, which do not significantly affect esthetics, it is preferable to grind sharp enamel borders

zz Follow-up

The first clinical recall is performed after a week has passed. Clinical and radiographic recall is performed at 6–8  weeks and a year later [23] (See also . Table 16.2).  

16.2.1.3  Crown-Root Fracture

A crown-root fracture varies depending on the fracture line position, and there is usually pulp exposure. This fracture type usually appears to 2–4% of primary dentition teeth [6]. The fracture might be vertical in the case of incisors; otherwise, the coronal component is the one that presents the highest mobility and small to medium displacement [6, 23]. The radiolucent line of the fracture is sometimes discernible in periapical radiographs. zz Treatment

If pulp exposure cannot be clinically or radiographically excluded, the two components have to be

371 Dentoalveolar Trauma of Children and Adolescents

16

..      Table 16.2  IADT recommended clinical and radiographic follow-up scheme on dental trauma of primary teeth [23] Type

1st w

4w

8w

6 m

1y

Annuallya

Enamel fracture c+rb

Enamel-dentine fracture Crown fracture with pulp exposure

c+rb

c+rb

c+r

Crown-root fracture

c+rb

c+rb

c+r

c+rb

c+rb

c+rb

c+rb

c+rb

c+rb

Root fracture:  

Without crown part displacement

 

Extraction of crown part

Concussion – Subluxationb

c+rb

Lateral luxation

c+rs+rb

Intrusive luxation Extrusive luxation

c+rb s+rb

c+rs+rb

c+rs+rb

c+rb

c+rb

c+rb

c+rb

c+rb

c+rs+rb

c+rb

c+r+s

c+rb c+rb

c+rb

c+rb

Avulsion Alveolar bone fracture

c+rb

c+rb c+rb

c+rb

c+r

c+rb

c clinical examination, r radiographic examination, s splint removal, rs review if repositioned and splinted aAnnually until exfoliation bRadiographs are only indicated where clinical findings are suggestive of pathosis

a

c

b

..      Fig. 16.13  a Clinical and radiographic image of crown fractures to both maxillary primary central incisors in a 3-year-old child. The left central presents with extensive pulp exposure. b Images after pulpotomy of the left central incisor and crown buildup of

separated. If the pulp is not exposed, remove the movable part of the tooth and, if feasible, reconstruct the remaining part. If the pulp is exposed and restoration of the radicular part is being considered, after the crown has been removed root canal treatment ensues. In cases when patients are not very cooperative or when the fracture line ends intraosseous, which is a rather

both central incisors with composite resin. c Twelve months after the initial injury no pathologic findings are observed (courtesy Dr. G. Vadiakas)

frequent finding, the treatment of choice is extraction [29, 30] (. Fig. 16.14).  

zz Follow-up

Clinical recalls are performed after a week has passed and then 6–8  weeks later. Clinical and radiographic recall is performed at 1  year. Consequently,

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a

a

b

b

..      Fig. 16.14  a Complicated crown-root fracture of maxillary primary right central incisor. b The apparent vertical fracture line in the occlusal radiograph is a reason for extraction

c

clinical recall during annual check-up sessions suffices until the permanent successor erupts [23] (see also . Table 16.2).  

16.2.1.4  Root Fracture

d

Root fractures appear at a 24% rate in primary dentition, mainly involving central incisors [6]. The tooth becomes mobile and sensitive to percussion, while the crown part may have been displaced. zz Treatment

16

If the coronal fragment is not displaced and is immobile, no treatment is necessary [23]. If it is slightly mobile and if the child is cooperative, splinting with wire and composite resin may be recommended. Parents need to be informed that after the splint is removed, the tooth may become mobile and may fall out after some time, especially if a new trauma occurs. In cases when the crown part has been displaced and prevents occlusion, or when a root fracture is accompanied by alveolar bone trauma, the treatment of choice is to extract the coronal fragment and leave in situ the apical fragment. To prevent trauma to the permanent successor germ, the apical fragment is allowed to be normally resorbed [23, 29] (. Fig. 16.15).  

zz Follow-up

If the coronal fragment has been splinted, the case should be reviewed in a week. The splint should be left in place for 4 weeks. Clinical recalls are performed after 6–8 weeks and 1 year has passed after the injury. Regular annual clinical recall suffices until the permanent tooth erupts (see also . Table 16.2).  

..      Fig. 16.15  a Radiographic imaging of horizontal root fracture of a maxillary primary right central incisor. b The ensuing edema results in extrusion of the coronal fragment from the socket. c Root canal treatment of the coronal fragment up to the fracture line; incisal crown reduction was done to avoid traumatic occlusion. d At 12  months follow-up, the apical fragment has been normally resorbed, while there is also root canal obliteration of the left central incisor. Follow-up is necessary

16.2.2  Luxation Injuries to Primary Teeth 16.2.2.1  Concussion

This is encountered in about 11% of primary dentition trauma [6]. There is no clinical movement, mobility of the tooth, or significant hemorrhage from the gingival sulcus, because there is no significant periodontal ligament rupturing. However, there is pain on percussion. Radiographically, the periodontium presents no pathologic post-traumatic finding [23]. Due to mild symptoms, such cases are often missed by parents who only visit the dentist if signs/symptoms, like discoloration, appear [31].

16

373 Dentoalveolar Trauma of Children and Adolescents

zz Treatment, Follow-up

The tooth should remain under observation, with clinical recall at 1 and 6–8 weeks after the injury [23]. 16.2.2.2  Subluxation (Loosening)

This is quite a frequent phenomenon and concerns about 1/3 of dental trauma to primary dentition [6]. The tooth injured has not been displaced but has become mobile due to partial periodontal ligament rupture. This mobility might be mild to medium, horizontal, or vertical in direction. The gingival sulcus often presents limited hemorrhage. In the radiograph, periodontal tissues appear normal [23]. zz Treatment

If the patient is cooperative, when mobility exceeds 2 mm (at the incisal edge), splinting is applied for 2 weeks; if oral hygiene is good, tooth mobility will tend to return to normal. zz Follow-up

Clinical recall at 1 and 6–8  weeks after the injury [23] (see also . Table 16.2).

splinting, is an option [23]. However, repositioning a laterally displaced primary tooth carries a higher risk of pulp necrosis [32]. Furthermore, due to their age and fear following the injury, young patients are often noncooperative. To avoid another possible injury to permanent successors, it is preferable not to attempt to reposition a laterally displaced primary tooth. It is recommended that it should be left to return naturally to its position with the help of tongue pressure [31]. In cases of minor occlusal interference, selective grinding is recommended. Extraction is considered when the crown has been significantly displaced labially causing significant occlusal interference and in neglected cases of such trauma when there is often perforation in the vestibular alveolar bone plate (. Fig. 16.17) [23].  

zz Follow-up

Clinical recalls takes place at 1  week, 6–8  weeks, 6 months, and after 1 year. Regular annual clinical recall suffices until the permanent tooth erupts [23] (see also . Table 16.2).  

 

16.2.2.3  Lateral Luxation

Lateral luxation or displacement is the type of trauma when the crown is displaced horizontally, more frequently in a palatal direction, and interferes with occlusion. Lateral luxation is frequently accompanied by alveolar bone injury [23, 32]. Initial radiographic examination comprises of an anterior occlusal and an extraoral lateral radiograph. The former is used to detect any periapical space enlargement, while the latter sometimes allows the clinician to determine the proximity to the permanent tooth germ or the labial alveolar bone plate displacement (. Fig. 16.16) [23].  

zz Treatment

A study that followed 545 displaced primary incisors indicated that only 5–22% of them did not return to their original position with time [5]. Gently digit repositioning of the tooth, followed with a 4 weeks flexible

a

b

..      Fig. 16.16  a Lateral laxation of maxillary primary left central incisor seen the next day of the accident. b Palatal displacement is emphatically shown in the occlusal radiograph. c Because of traumatic occlusion, tooth repositioning under local anesthesia was

16.2.2.4  Intrusive Luxation

Intrusive luxation is insertion of the tooth deep into the alveolar bone, which suffers fracture of various severity levels. Compared to other types of trauma intrusion is one of the most common, particularly in the early primary tooth dentition, with the primary tooth displacement causing sometimes serious complications to the permanent successor tooth [23]. The tooth is immobile and, on percussion, produces a dull metallic sound, characteristic of ankylosis (i.e., direct contact to supporting bone). Complete intrusion of the tooth into the socket may be wrongly perceived by parents as tooth loss (. Fig. 16.18). Differential diagnosis is based on radiographic data. The most common apex displacement is in a labial direction. Palatal displacement toward the permanent tooth germ occurs only if the child has an object in the posterior teeth when she/he falls. The direction in which tooth displacement occurred is revealed through palpation and radiographic examination. Lateral extraoral  

c

d

successfully attempted in this cooperative 3-year-old and tooth splinted rigidly. d At the 6-month recall, the tooth was free of signs and symptoms

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radiograph shows both the apex displacement new position and the very likely fracture of the vestibular palatal bone plate, as well as its relationship with the labial surface of the permanent successor (as in . Fig. 16.16).  

a

zz Treatment

In a study with 172 intruded primary incisors, the apex had been intruded in labial direction in 80% of the cases; only 2 presented ankylotic signs and all remaining ones erupted, while 2/3 survived without complications at the 3 years recall after the injury [33]. Therefore, the tooth is left to erupt irrespective of the direction of displacement [23] and wait for spontaneous healing of the alveolar bone. Tooth descent is completed in 4–8 weeks, but its final position may be lagging behind its initial one (. Fig.  16.19). If there is suspicion that the apex has been displaced into the germ of the permanent successor, which may possibly be seen radiographically, or if the tooth does not erupt, extraction is chosen [33].  

zz Follow-up

Clinical recalls take place at 1  week, 6–8  weeks, 6 months, and after 1 year. Regular annual clinical recall suffices until the permanent tooth erupts [23] (see also . Table 16.2).

b

 

16.2.2.5  Extrusive Luxation

..      Fig. 16.17  a Neglected trauma of primary maxillary central incisors. Severe crown discoloration of both teeth and inflammatory fenestration of alveolar bone plate and mucosa related to the right one. b Occlusal radiograph shows apical radiolucencies indicative of pulp necrosis and infection

In cases of extrusive luxation, the tooth has been extruded but remains attached in the socket and is somewhat mobile, while it also interferes with occlusion. The incidence of extrusive luxation is low (3.8%) as compared to other displacement dental trauma [6]. Radiographic assessment presupposes a periapical radiograph using a No 0 plate or an equivalent digital sensor. zz Treatment

If the tooth is not interfering with the occlusion, it should be left to spontaneously reposition itself. If c

16

a

b

..      Fig. 16.18  a Multiple intrusion of three maxillary incisors and avulsion of the fourth one in a 26-month-old. b The parents perceived two incisors as lost. c Extraoral radiograph of another intrusive incident shows both central incisor apices in labial displacement

after having fractured the alveolar plate. The nasal spine is visible more superiorly. The trace drawing indicates the previous tooth and bone plate positions (stippled lines) in relation to intruded positions (continuous lines)

16

375 Dentoalveolar Trauma of Children and Adolescents

a

b

c

..      Fig. 16.19  a Intrusion of maxillary primary left central incisor (after 24 hours) in a 16-month-old boy. b Spontaneous re-eruption with 45° rotation in 8 weeks. c Radiograph of the tooth with retention (splinting with the right central incisor) at 4-year follow-up,

extrusion is more than 3 mm and the tooth excessively mobile, extraction might be the treatment of choice [23].

d

after orthodontic alignment was undertaken when age 3  years at parents’ request. Pulp obliteration indicates pulp remained vital. d Clinical view at age 6 years

b

a

zz Follow-up

Clinical recalls take place at 1 week, 6–8 weeks, and after 1  year. Regular annual clinical recall suffices until the permanent tooth erupts [23] (see also . Table 16.2).  

16.2.2.6  Avulsion

Avulsion means the tooth is completely out of its socket and its prevalence represents 5–18% of displacement trauma. About 90% of avulsed teeth are primary maxillary incisors [6]. Radiography confirms that the tooth was not intruded. It is good to search for the avulsed tooth, because there is also a risk that the tooth went accidentally into the respiratory tract. Symptoms in such cases are coughing, tachypnea, and high temperature [23].

zz Follow-up

It is necessary to perform clinical review at 6–8 weeks. Further follow-up at 6  years of age is indicated to monitor eruption of the permanent tooth [23] (see also . Table 16.2).  

16.2.2.7  Alveolar Bone Fracture

zz Treatment

If there is complete avulsion of a primary tooth, its replantation is not recommended (. Fig.  16.20), contrary to a permanent tooth, due to either the direct risk of causing mechanical injury to the underlying permanent tooth germ or to indirect risk resulting from possible inflammation. Replantation might be possible only under ideal conditions of immediate repositioning when the infant is cooperative. Besides, complications may arise such as the following: pulp necrosis and infection requiring either endodontic treatment or extraction and ankylosis of the replanted primary tooth and pathologic root resorption. There have been some reports of primary avulsed teeth that were replanted, most of which, however, were ultimately removed 2–24 months later due to subsequent complications [34]. Although there are no functional impairments, i.e., related to mastication or articulation, this premature loss of anterior primary teeth is often of esthetic concern to parents. If they so wish, a suitable fixed restoration may be constructed (7 Fig. 13.49).  

 

..      Fig. 16.20  a Dentition after avulsed maxillary primary left central incisor. b Parents brought the avulsed primary tooth only to be informed that its replantation is not recommended

This usually accompanies displacement of one or several teeth, which move together on inspection because they are attached to the fractured bone segment. A periapical radiograph provides information about the extent of the fracture and its relation to other primary and the permanent successor teeth (. Fig. 16.21).  

zz Treatment

Treatment comprises of repositioning the fractured bone segment and displaced teeth, if possible, and their splinting for 4 weeks [23]. If there is contusive trauma to the gingiva or the mucosa, this is sutured. Good oral hygiene performed by the parents improves healing. zz Follow-up

The first clinical recall is performed 1  week after the injury. Clinical and radiographic examination should then be done at 4 weeks and then 1 year. Regular annual clinical recall suffices until the permanent tooth erupts [23] (see also . Table 16.2).  

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a

b

dentinal tubules and are degraded, affecting the color of the tooth. In mild trauma cases, such discoloration may reverse, whereas, in more serious cases leading to pulp necrosis, it persists and often is the only early post-­ traumatic finding. Such endogenous discoloration may be distinguished into three categories: 55 A pink shade appears a few days following the tooth trauma, usually after mild concussion or subluxation trauma types; this is mainly due to intrapulpal hemorrhage (extravasation of erythrocytes). Such discoloration may subside in a few weeks, indicating some recovery of the pulpal tissue, or grow darker. 55 A yellowish shade may be associated diminished pulp by root canal obliteration (see below). This color change is evident several months after trauma. 55 A dark shade, usually blue-gray or brown-gray, most likely indicates pulp necrosis (. Fig.  16.22). Such discoloration is often observed and usually appears gradually within a period of 2  months after the injury [29]. The involved tooth may remain until it sheds naturally, without any other pathologic findings. Dark discoloration on its own is not an indication for root canal treatment or extraction, unless there are radiographic signs of periapical pathosis,  

..      Fig. 16.21  a Neglected trauma in the maxillary primary right central incisor to right canine region 2  weeks after the injury. Soft tissue healing is delayed due to alveolar process fracture. b The radiograph reveals part of the fracture line (arrows)

16.2.3  Follow-Up and Complications of

Trauma to Primary Teeth

a

Follow-ups are extremely important to prevent or detect complications early. They should be carried out for all types of trauma as in . Table 16.2. Besides complications to their permanent successors, traumatic injuries of primary teeth may cause any of the following complications to these own teeth:  

16

16.2.3.1  Pulpitis

Pulpitis is the initial reaction of the pulp in cases of direct tooth injury such as in fractures or in cases of luxation injuries. Pulpitis may be fully reversed or lead to pulp degeneration and necrosis without any pain or symptoms. Teeth with reversible pulpitis may be sensitive to concussion. However, pulpitis may be due to bacterial contamination, whether the fracture exposes the pulp or not, whereupon septic pulp necrosis ensues with signs of periapical inflammation. In such cases root canal treatment becomes necessary, or, if there is no patient cooperation, the tooth has to be extracted [29]. 16.2.3.2  Discoloration of the Traumatized

Tooth

Discoloration appears in almost half of primary tooth trauma cases [5]. It is common for the pulp capillaries to bleed following trauma. Blood elements enter the

b

..      Fig. 16.22  a The dark brown-gray shade of symptomless maxillary primary right central incisor indicates pulp necrosis. b The radiograph shows small apical radiolucency and a larger one at asymptomatic left central incisor, which has a slightly wider root canal than its right counterpart. Follow-ups are necessary to determine if treatment becomes necessary

377 Dentoalveolar Trauma of Children and Adolescents

discoloration, as well as radiographic findings, such as periapical lesion and pathologic root resorption.

a

16.2.3.5  Root Resorption

Post-traumatic root resorptions may vary greatly. Within a few months, the largest part of the root may be resorbed. External root resorptions occur when trauma damaged the cementum and the periodontal ligament, such as in severe luxation injuries. They may be of the inflammatory type, in case of pulp infection. The question then arises whether to do root canal treatment or extract the primary tooth, depending also on patient cooperation. Or they may be of the ankylosis type when the alveolar bone comes into direct contact with the tooth root. During the normal exfoliation process, the root may be resorbed leading to the disappearance of the ankylotic area. If the eruption of the permanent successor is delayed or ectopic, the ankylosed primary tooth has to be extracted [29]. These resorptions should not be confused with physiologic primary tooth resorption.

b

..      Fig. 16.23  a Yellowish shade and partial re-eruption of a maxillary primary right central incisor, after having suffered intrusion in the past. b The occlusal radiograph shows marked pulp canal obliteration

and/or symptoms and signs of periapical inflammation, such as pain, appearance of an abscess, or fistula. Parents are informed accordingly; besides attending the usual dental recalls, they also need to regularly raise the upper lip of their child and check for these signs [23].

16.2.4  Consequences of Primary Tooth

Trauma to Their Permanent Successors

Eye Catcher

Permanent teeth may suffer consequences from ­traumatic injuries to predecessor primary teeth only if they are at an early developmental or mineralization stage. That’s why knowledge relevant to tooth formation timing and sequence is important (please see 7 Chap. 17). Since the most frequently traumatized primary teeth are the maxillary incisors, the permanent teeth mostly suffering such consequences are their homologous successor teeth. Regarding enamel defects, these are more frequently found in the labial surface because this surface is close to the apex of primary incisors.  

16.2.3.3  Pulp Canal Obliteration

It is usually discovered clinically by the yellowish color of the crown of such teeth. The pulp chamber and root canals become significantly stenotic by mineralized dentin like tissue formed at fast rate (. Fig. 16.23). This phenomenon is quite frequent and appears in 52% of intruded teeth [33]. Pulpal necrosis has been observed in only 10% of primary teeth with pulp space obliteration within 3 years [35]. Therefore, prognosis should be considered favorable, and these teeth do not need root canal treatment if there is no periapical lesion shown in the radiograph and no clinical signs of pulp necrosis and infection.  

16.2.3.4  Pulp Necrosis

Pulp necrosis is a frequent, yet unpredictable, consequence of primary tooth trauma, with an incidence rate of 25% [5]. Diagnosis is based on signs and symptoms such as pain, swelling, fistula, tooth mobility, gray crown

Traumatic injuries to primary teeth may affect the underlying permanent successors by any of the following mechanisms: 55 Direct physical damage (. Fig. 16.24) 55 Aseptic inflammation ensuing soon after trauma 55 Septic inflammation following pulp infection of the primary tooth 55 Combination of the above  

The most common sequalae are:

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..      Fig. 16.24  a Maxillary primary left central incisor of a 6.5-year-­old boy a week after intrusion injury on a steel object. b A difficult to interpret finding at the periapical radiograph led to a decision for CBCT, which revealed an incisal fracture of the permanent successor inflicted by the primary tooth root. c At 1-year follow-up, the successor tooth has not erupted presenting a hard palatal swelling related to the incisal fragments. d The periapical radiograph reveals its root anomaly probably as an intrusive domino effect. e The fractured permanent incisor erupted 8 months later

b

a

c

d

e

16.2.4.1  White or Yellow-Brown Spots

on the Enamel

16

These hypomineralized porous enamel spots have the appearance of demarcated opacities of various size on the enamel (. Fig. 16.25). Their frequency of appearance is as much as 23% of primary tooth trauma cases and do not seem to correlate with any specific trauma type [36, 37].

a

b

 

zz Treatment

Because porous enamel of such spots usually occupies the full thickness of the enamel, grinding and composite resin restoration are preferred, similar to the restoration of hypomineralized incisors in an MIH case (see 7 Chap. 17). Using the opaque tint of composite resin may allow a more conservative removal of the enamel. The microabrasion technique is not indicated. The more recent technique of resin infiltration, using the Icon® kit, for instance, may be effective.  

16.2.4.2  Enamel Hypoplasia

This comprises 12% of trauma-related developmental defects. Such lesions occur when the permanent successor germ is still developing, i.e., before it is adequately mineralized. The type of trauma to the primary

..      Fig. 16.25  a Well-demarcated white enamel opacities; differential diagnosis is necessary between trauma to predecessor primary teeth and molar incisor hypomineralization (MIH). b Severe mid-­ crown enamel hypoplasia of a maxillary left permanent central incisor probably related to trauma/inflammation of the predecessor primary tooth

dentition that most often leads to appearance of such lesions is intrusive and extrusive laxations [37]. The hypoplastic enamel region may be small or extensive and may include areas of hypomineralization as well (. Fig.  16.25). Radiographically, hypoplasias may often be diagnosed prior to tooth eruption.  

zz Treatment

Such lesions should be treated by removal of discolored enamel and/or dentin and restoration with composite resin.

379 Dentoalveolar Trauma of Children and Adolescents

16.2.4.3  Crown Dilaceration

Such dysplastic defects are due to primary tooth impact onto the germ of the permanent successor tooth, resulting to a bend at the developing cervical part, which is softer in relation to the already mineralized crown [36, 37]. In a report of anterior permanent teeth with dysplastic defects related to primary tooth trauma, dilaceration was found in 25% of the cases [37]. Crown angulation varies depending on the developmental phase and the germ location at the time of injury, as well as on the direction of the trauma-causing force. The crown of dilacerated maxillary incisors is usually rotated anteriorly and nasally (7 Fig. 17.20). Almost half of these teeth remain impacted. About 3% of trauma cases to primary dentition lead to such abnormalities [36]. It is inferred that the accidents occur earlier than age 5 years, i.e., when more than half or all the permanent crown has developed. Most commonly correlated trauma cases are extrusive and intrusive laxations of predecessor primary teeth [37].  

rotation during the descent may lead to vestibular root appearance [38]. The decision depends on the crown integrity and the severity of dilaceration. If the tooth erupts on its own, its position in the dentition is assessed along with the possibility of correcting the crown shape using composite resin. 16.2.4.4  Other Rare Developmental Disorders

Rare dysplasias of successor permanent teeth are reported as follows [36, 37]: 55 Odontoma-type dysplasia (. Fig. 16.26) 55 Root duplication 55 Lateral root bending (. Fig. 16.27) 55 Partial or complete interruption of root development continuity 55 Permanent tooth germ necrosis  

 

Types of trauma most often correlated with these specific abnormalities are intrusive and extrusive laxations of primary teeth [37]. zz Treatment

zz Treatment

As soon as dilaceration is discovered, it is followed up using lateral extraoral radiographic examination and probably other auxiliary radiographs, like CBCT. If the tooth does not erupt, a decision about extraction and orthodontic correction of the diastema or orthodontically guiding the tooth to occlusion must be made. If the latter solution is chosen, attention is necessary in the case of intense tooth dilaceration, because crown a

b

d

e

..      Fig. 16.26  a Radiographic image of dysplastic unerupted four maxillary permanent incisors in an 8-year-old boy with a history of severe trauma at age 9 months. A “wait and see” approach was adopted. b He returned 1  year later with left-side labial edema. c, d The partially erupted left lateral already had septic pulp, probably due to pulp communication with the oral environment due to

In some cases, such as lateral root bending, dysplastic permanent teeth do erupt. If possible, orthodontic traction is applied to the dentition if certain teeth erupted, to temporarily conserve alveolar osseous mass until more permanent treatment is possible. In the remaining cases, however, extraction and correction of the space is recommended to allow future prosthetic restoration [36, 37]. c

f

dysplasia. e, f Patient aged now 12 years is under orthodontic treatment, while the right central with dysplastic crown has been temporarily built up, the left central and right lateral have been extracted as untreatable, and the left lateral was endodontically treated. Final esthetic/prosthetic rehabilitation will follow orthodontic treatment as a multidisciplinary approach case

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a

a

b

b c

d

..      Fig. 16.27  a Labial ectopic and delayed eruption of maxillary permanent left central incisor in an 8-year-old boy with a serious oral trauma history at age 2  years. b Its radiograph reveals lateral root bending, a sort of mild dilaceration. c, d The annual review, following the extraction of predecessor primary incisor, shows further descent and almost complete apex development

16.2.4.5  Consequences to Permanent Tooth

Eruption

zz Diagnosis

Cracks follow various directions and stop close to the dentin-enamel junction [40]. Diagnosis is facilitated by the light scattering observed, due to the crack, when a light beam falls almost perpendicularly to the longitudinal tooth axis (. Fig. 16.28). Radiographic examination is recommended [41]. Response to pulpal sensitivity tests is normal. In case of severe infractions, etching and sealing with bonding resin should be considered; otherwise, no treatment is required.  

Following trauma to anterior primary teeth, there are often disorders observed in the time or path of permanent successor tooth eruption (see 7 Chap. 10). Delayed permanent tooth eruption was noted in 1/3 of primary tooth trauma cases [39]. It is reported that this may last up to 1 year and adversely influence occlusion in the mixed dentition. A permanent tooth may often be at crossbite along with delayed presence of the primary tooth in the dentition (7 Fig. 11.42), while there have been cases of ectopic labial eruption observed (7 Fig. 10.17). On the contrary, it is rather rare for a permanent tooth to erupt prematurely following the loss of its primary predecessor due to trauma, because there is no bone destruction present, as is the case when the tooth is extracted due to severe carious periapical inflammation.  

 

16

..      Fig. 16.28  Incomplete enamel fractures (infractions). a Clinical view b By LED illuminating the maxillary permanent central incisors at an appropriate angle, the infractions become visible on both incisors of right side

 

zz Follow-up

Clinical and radiographic recalls are not necessary in the cases of sole infractions [21] (see also . Table 16.3). Pulpal necrosis rate is 3.5% and most probably caused by tooth concussion or loosening, which occurred at the same time as the enamel infraction but escaped attention. When an associated luxation injury is suspected, the cracked tooth should be followed more closely (see further down in this chapter in the 7 Sect. 16.3.4).  

 

16.3.1.2  Complete Enamel Fracture 16.3  Dental Trauma to Permanent Teeth 16.3.1  Fractures of Permanent Teeth 16.3.1.1  Enamel Infraction

Incomplete enamel fracture (infraction) is frequent (10– 12.5%) in permanent teeth, but often missed [2, 7]. It is caused by direct impact onto a hard object or surface and may appear along with other fracture types to the same or adjacent teeth. There is no loss of tooth mass.

In this type of crown fracture, there is a partial enamel loss due to impacting on a hard object. The range of incidence rates in permanent teeth (26–76%) depends on the extent to which treatment is sought for such small injuries [2, 42]. zz Diagnosis

After the appropriate trauma form has been completed, an investigation should ensue as to whether additional trauma of a different kind occurred, such as root fracture. Root developmental stage affects tooth prognosis [41].

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381 Dentoalveolar Trauma of Children and Adolescents

..      Table 16.3  Follow-up table for fractured permanent teeth, according to IADT Guidelines 2020 [21] 4w

6–8 w

3 m

4 m

6 m

1 y

5 y

Enamel infraction Complete enamel fracture

c+r

c+r

Enamel-dentine fracture without pulp exposure

c+r

c+r

Enamel-dentine fracture with pulp exposure

c+r

c+r

c+r

c+r

c+r

c+r

c+r

c+r

c+r

c+r

c+r

Crown-root fractures

c+r

c+r

Root fracture

c+r+s

c+r

c+r+s*

This follow-up regimen is recommended when there is no luxation injury associated to the fracture at the time of trauma. If a concomitant luxation injury occurred, the luxation follow-up regimen prevails (please look . Table 16.4) c+r: clinical and radiographic examination s: splint removal (for mid-root and apical third fractures) s*: splint removal (for cervical third fractures)  

zz Treatment

a

Treatment, depending on fragment size and patient’s esthetic requirements, may comprise grinding to improve incisal edge appearance or crown reconstruction using tooth fragment if available or composite resin (. Fig. 16.29).  

zz Follow-up b

Clinical and radiographic recalls as well as vitality tests should be performed at 6–8 weeks and 1 year after the injury [41, 21] (see also . Table  16.3). Pulpal necrosis rate is a mere 1.7% [43]. However, if an associated luxation injury occurred or is suspected, the tooth should be monitored more closely (see further later in this chapter on the topic “Follow-ups for Luxation Injuries of Permanent Teeth”)  

16.3.1.3  Enamel-Dentine Fracture Without

Pulp Exposure (Uncomplicated Crown Fracture)

This is the highest fracture incidence (40%) to permanent teeth [2]. The tooth needs to be restored the soonest possible, not only for comfort or esthetic purposes but also to prevent pulpal microbial infection due to exposure of a high number of dentinal tubules to the oral environment in addition to avoiding issues such as deviation of adjacent teeth or overeruption of antagonists. It has been calculated that 1  mm2 of dentin contains about 20,000–45,000 dentinal tubules, which provide direct communication between the pulp and the oral cavity and allow bacteria as well as chemical and thermal stimuli to be transmitted [44, 45]. A significant role

..      Fig. 16.29  Enamel fracture at the incisal edge of maxillary permanent right central incisor and its reconstitution with composite resin

in pulp infection risk has the thickness of dentin remaining after the injury. zz Diagnosis

Radiographic examination is imperative to exclude the possibility of root fracture or tooth displacement [21]. zz Treatment

Restoring young permanent incisors with a ceramic crown should be avoided. Reconstruction of the fractured incisor crown with composite buildup is the treatment of choice. Rubber dam should always be used.

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Isolating with a double lip retractor is not sufficient, since breathing vapors contaminate the etched surfaces and compromise adhesion. Local anesthesia is not always necessary, since even if a thin dentin wall remains, it may be covered with a base such as glass ionomer cement (GIC) and blowing or rinsing the tooth causes no pain any more [21]. According to some authors, beveling broken enamel reinforces retention and improves esthetic result. Following rubber dam placement, dentin coverage if needed, etching, and the application of an adhesive, the composite resin (CR) should be applied using a celluloid partial or full strip crown, depending on whether the fracture is angular or almost horizontal, respectively (. Figs. 16.30 and 16.31). A more elaborate composite resin buildup may be made by taking a silicone impression and pouring a plaster model which is sent to a lab technician who will reconstruct the tooth and fabricate a “silicone key” or a mouth-guard. The clinician will then use one of those as a palatal matrix to gradually add layers of enamel and dentin composite in different shades and forms trying to mimic a natural tooth. Finishing and polishing are essential steps to obtain a good tooth-composite interface and an esthetically pleasing restoration [21]. If the broken fragment is found intact, it is an interesting esthetic option to consider bonding it back  

a

[46–48]. The technique involved is described as follows. The crown fragment should be kept moist or be rehydrated in water for at least 15 minutes before it is bonded [49]. This improves bonding quality and strength. A length of adhesive wax may be added to the incisal edge of the broken fragment so as to facilitate manipulations. It has been suggested that the enamel on both fractured surfaces be beveled prior to reattachment, but this may prevent optimal coaptation of the two fragments. The enamel of both fragments is then etched and the adhesive applied. By placing and light curing a minimal quantity of composite resin between the two edges, the broken piece is accurately repositioned. Any gaps left are filled and the fracture line is reinforced with more composite resin. In the last three decades, this restoration type has been in use (. Fig. 16.32); some authors have reported on technique details. For example, beveling of the fracture line did not seem to increase the strength of the restoration [46]; however, it aids in masking the fracture line. Adding composite resin on the fracture line did not increase bond strength when compared to using solely the adhesive on its own [48]. No sound clinical data regarding time endurance as compared to solely composite resin reconstruction techniques have been reported. Rubber dam isolation should always be used in restorative procedures, even if there is no pulp  

b

c

16 ..      Fig. 16.30  a Clinical view of enamel-dentine oblique crown fractures on three maxillary permanent incisors of a 9-year-old child. b, c Clinical and radiographic view after the crown buildup was made using composite resin. (Courtesy Dr. G. Vadiakas)

a

b

c

..      Fig. 16.31  a Enamel-dentine crown fracture without pulp exposure on mandibular permanent right lateral incisor after covering the dentin with GIC and enamel beveling. b Appropriate size strip crown filled with composite. c Placement of strip crown on the fractured

d

tooth followed etching and bonding. All was done under rubber dam isolation, which is now removed for finishing the restoration. d Oneyear recall

383 Dentoalveolar Trauma of Children and Adolescents

a

b

..      Fig. 16.32  Reattachment of a fractured crown fragment in a 9-year-old girl. a Oblique enamel-dentine crown fracture on maxillary permanent left central incisor. b, c Reattachment of the tooth

exposure, to avoid saliva and breathing humidity contamination (. Fig. 16.33).

c

d

fragment using a non-radiopaque composite available at early 1990s. d Recall of the adult patient 14 years later with no other intervention. A slight shade change of the composite can be detected

a

 

zz Follow-up

Clinical examinations including vitality testing and periapical radiographs need to be repeated at 6–8 weeks and 1 year following the injury. Pulpal necrosis has been shown to occur in 9% of such traumas [50], but this rate also depends on how soon after trauma the pulp was protected. If trauma to periodontal tissues happened as well, pulpal necrosis likelihood rises to 28% [51– 53]. The presence of a periapical radiolucency or root development interruption of young permanent incisors means that the pulp became necrotic and infected. This makes root canal treatment imperative [21] (see also . Table 16.3).

b

 

16.3.1.4  Enamel-Dentine Fracture with Pulp

Exposure (Complicated Crown Fracture)

These crown fractures are also called “complicated fractures.” The pulp is exposed to the oral environment and bacterial contamination starts immediately. That’s why treatment should be provided the soonest possible. zz Diagnosis

Crown fracture with pulp exposure does not automatically cause pain, but sensitivity to hot and cold stimuli, as well as low intensity pain during mastication [21]. The scale of pulp exposure and the time interval between injury and treatment are parameters with a direct effect on the inflammatory reaction extending into the pulp. At the initial examination, pulp sensibility tests are unreliable and pulp vitality can be perceived visually. Radiographic examination is imperative, similar to the previous types of trauma, so as to exclude the possibility of root fracture and to confirm apex status [21]. zz Treatment

The aim of pulpal treatment is to maintain pulp vitality to allow immature teeth to complete their root

..      Fig. 16.33  a, b Rubber dam isolation improves adhesion of composite buildups. There are several ways to apply the rubber dam: placing the clamps away, as shown here, is one of them. Alternatively, dental floss can be knotted on each tooth. WedjetsR can also be used interdentally. Direct clamping of an immature incisor is not recommended due to the high risk of fracture of these fragile teeth

development. Root canal treatment should thus be avoided. Treatment depends on root formation stage and degree of pulpal inflammation. Such treatment options include the following: (1) direct pulp capping, (2) partial pulpotomy, (3) cervical pulpotomy, or (4) root canal treatment. The first three treatment types are described below, while for root canal treatment, the reader is invited to look in this chapter in section “Endodontic Management of Injured Teeth.” All these treatment options should always be carried out under rubber dam isolation. Direct pulp capping  The success rate of this procedure is

lower than Cvek’s partial pulpotomy; therefore, direct pulp capping is not frequently recommended [54, 55]. Ideal clinical prerequisite conditions for direct pulp cover are to observe a vital pulp where the pulp exposure is limited (up to about 1 mm) and for the intervention to take

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place soon after the trauma (up to several hours). Besides, the pulp should be free of inflammation owed to another cause, e.g., deep caries. Technique steps are: 55 Local anesthesia without vasoconstrictor. 55 Tooth isolation with rubber dam. 55 Cleaning of tooth surfaces and disinfection of tooth and rubber dam with iodine, chlorhexidine, or sodium hypochlorite. 55 Rinsing and disinfection of the pulpal exposure with saline solution, chlorhexidine, or sodium hypochlorite. Blood clot presence reduces the likelihood of healing, either by preventing direct contact of therapeutic agents with pulp tissue or because the space left after its decomposition is inviting bacterial presence [56]. 55 Once hemostasis is obtained, calcium hydroxide (CH) powder mixed with saline or anesthetic solution to the consistency of a paste is applied; this remains the gold standard for pulp coverage. Alternatively, ΜΤΑ® has been used in the recent past years and has been shown to favor dentin bridge formation and pulp vitality maintenance as well. However, MTA, whether gray or white, has been shown to create tooth discoloration, and its use is not recommended anymore for pulp capping [21, 57], especially in anterior teeth. Biodentine®, a new bioceramic cement, seems to be a promising material for pulp capping, but more studies are a

b

needed before its widespread use can be safely recommended. 55 When Ca(OH)2 is used as the pulp dressing material, it should be covered hermetically. Glass ionomer cements seem to provide an adequate marginal seal before the tooth is restored with composite resin [58]. Partial pulpotomy  In cases of more extensive pulp expo-

sure and delayed arrival at the surgery (up to 2 days following the injury), partial pulpotomy is preferred (Cvek technique) in order to remove the inflamed portion of the pulp first [54]. The aim is to obtain a dentin bridge formation below the cover material. The technique is recommended for either mature or immature teeth. After anesthesia and rubber dam isolation, the technique steps are the same as described above for direct pulp capping; however, an additional step is required, the partial amputation of the pulp before the placement of the capping material [21] (. Fig. 16.34). The amputation is done as follows: 55 A small reservoir of approximately 2  mm deep is created by amputation of the exposed pulp with a high-­speed sterile bur under copious water spray. A diamond causes less damage than a low-speed bur or an excavator (. Fig. 16.35a) [59, 60].  

 

c

16 d

e

..      Fig. 16.34  a The maxillary permanent left central incisor of an 8-year-old boy presents a horizontal crown fracture with pulp exposure. The right one presents an oblique crown fracture without pulp exposure. b The radiographic examination shows that the incisors have open apices. c View of the pulp exposure. Following placement

of the rubber dam, the exposed pulp is excised to about 2 mm deep, Ca(OH)2 paste is applied on the remaining pulp, and GIC covers the paste and the exposed dentin of both teeth. d The final crown buildups with composite resin. e Post-op radiographic image. (Courtesy Dr. G. Vadiakas)

385 Dentoalveolar Trauma of Children and Adolescents

3–4 days. This is sometimes indicated for teeth that have also suffered other injuries as well [54]. The technique is the same as partial pulpotomy; however, pulp amputation is done at the cervical level of the tooth.

a

Restoration  After any of the three pulp treatments described above, crown restoration is performed as already discussed, with composite resin reconstruction, possibly with the “silicon key” technique, or with reattachment of the broken crown fragment. Quite often though, tooth eruption is in process, and part of the fracture line may lie under the gingiva. In these cases, the cervical area may be restored by using resin modified glass ionomer cement (RMGIC) or, even better, the total reconstruction can be made by using exclusively RMGIC, which can be considered as temporary until the tooth has sufficiently erupted.

b

zz Follow-up

..      Fig. 16.35  Cvek’s partial pulpotomy. a A small reservoir, almost a box of approximately 2  mm, is created by amputation of the exposed pulp with a high-speed sterile bur under copious water spray. A diamond causes less pulp damage than a low-speed bur or an excavator. b After obtaining hemostasis, the pulp is covered with a thick calcium hydroxide paste (mixture of calcium hydroxide powder with saline or anesthetic solution). A hermetic seal covering the calcium hydroxide should then be placed before fragment bonding or composite buildup. Please note rubber dam isolation during treatment

55 Pulp bleeding can be arrested by placing a cotton pellet soaked in saline on the pulp stump with light pressure for a few minutes or by rinsing gently the pulp wound with sodium hypochlorite [61]. Allowing time for hemorrhage control is important. However, if hemostasis is not achieved, this likely means that the inflammation extends beyond the prepared zone and that it is necessary to amputate the pulp further, more cervically. 55 In Cvek’s pulpotomy technique, the pulp is then covered with a thick calcium hydroxide paste (mixture of calcium hydroxide powder with saline or anesthetic solution) (. Fig. 16.35b) [54, 60].

In all three treatment modalities described above to tackle exposed vital pulps, clinical and radiographic examinations, in combination with sensibility testing, are important and should be repeated on follow-up visits at 6–8 weeks, 3 months, 6 months, and 1 year following the injury [21] (see also . Table 16.3). Clinically, it should be confirmed that there is no pain or apical inflammation and that the crown color is normal. Radiographs should confirm continuing root development (. Figs.  16.36 and 16.37). If a periapical radiolucency appears, root canal treatment should be performed.  

 

a

b

 

Cervical pulpotomy  As in the case of pulp exposures due

to caries (see 7 Chap. 14), cervical pulpotomies are usually performed on immature permanent teeth when the objective is to attempt to maintain root pulp vitality. This is preferred in cases when the inflammation is quite advanced due to major pulp exposure and when a longtime interval since trauma has elapsed, maybe exceeding  

..      Fig. 16.36  Partial pulpotomy and fragment reattachment. a Radiographic image of crown fracture with pulp exposure of maxillary permanent left central incisor in a 7-year-old child. The root is at an early developmental stage. Treatment comprised of partial pulpotomy and reattachment of the broken piece. b Treatment objectives were achieved: completion of root development and absence of pathologic findings at 3-year follow-up. However, some pulp space obliteration is evident coronally. Follow-ups should be continued. (Courtesy Dr. G. Vadiakas)

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a

b

zz Treatment

Prior to attempting any treatment, a decision must be made on whether the remaining tooth structure will be mechanically strong enough to support a future restoration. If not so, it is wise to consider the possibility of submerging the root, rather than attempting to extrude it to create restorable margins. Options for treating this type of fracture are discussed below: Eye Catcher

..      Fig. 16.37  Cervical pulpotomy. a Radiographic preoperative view of horizontally crown fractured maxillary permanent central incisors in an 8-year-old boy, who presented with a week’s delay. The left one has pulp exposure with minimal vitality signs and the right one responds normally. Both teeth are immature. b A cervical pulpotomy was performed on the left incisor, and both teeth were restored with composite. This is at the 12-month recall

zz Prognosis

In complicated crown fractures, the pulp survival rates for pulp capping range from 63% to 88%. Success rates of partial pulpotomy range from 94% to 100% [62]. When, however, dental trauma with pulp exposure is accompanied by periodontal tissue trauma (luxation injury), pulp necrosis likelihood increases up to 14% [51, 62]. 16.3.1.5  Crown-Root Fracture

16

Crown-root fractures to permanent anterior teeth are not so common. They have been reported to appear in 0.5–5.5% of all dental trauma cases to permanent teeth [2]. Treatment depends on the depth of the fracture line within the bone socket and the ensuing difficulty of isolation and restoration. The more apically the fracture line ends, the worse the prognosis [63, 64]. zz Diagnosis

Diagnosis is achieved through clinical and radiographic examination to exclude the possibility of additional root fracture or displacement. CBCT can be considered for better visualization of the fractured path, its extent, and its relationship to the marginal bone [21]. The typical crown-root fracture is oblique in a labial-palatal direction (. Fig. 16.38); it starts a few mm supragingivally on the labial surface and ends 2–5 mm subgingivally in the palatal aspect. In this case, radiographic diagnosis presents some difficulties. If the crown component is retained in place by periodontal fibers, it may present a wide range of mobility levels, depending on how far subgingivally its palatal border lies. There is usually a pulp exposure. More rarely, the fracture line may be almost parallel to the longitudinal tooth axis.  

Treatment options for crown-root fractures depend on the subgingival extension of the fracture line, on whether the fracture is located in an esthetically sensitive region and on the stage of root development. Due to the endodontic, periodontal, and prosthetic issues involved, tooth overeruption using orthodontic forces or surgical extrusion is often carried out in order to expose the fracture line to the gingival level so that proper treatment and restoration may be performed under humidity and hemorrhage control. In immature teeth of children and teenagers, the advantages/disadvantages of orthodontic traction or surgical extrusion should be put into balance, especially in patients at risk for new trauma episodes. They are not necessarily good options for immature teeth.

Removal of the crown part and restoration  This is the

most conservative way to treat a fracture, and it may be preferred if part of the fracture line lies only slightly subgingivally [63, 64]. The crown part may be restored by reattaching the broken fragment, by composite resin buildup or through a prosthetic crown. However, isolation problems usually prevent ideal ­bonding at the subgingival border [21]. Gingivectomy (and osteotomy, if necessary)  This may be indicated in cases where the subgingival fracture line lies in a region of no esthetic concern, e.g., in the palatal surface [21, 63]. However, there is risk of failure due to the development of persistent periodontal inflammation palatally. Orthodontic extrusion of the tooth with or without gingivoplasty (. Fig.  16.39)  This approach is more time-­  

consuming when compared to the surgical approach, since it usually takes 5 weeks to obtain 2–3 mm extrusion, as well as at least another 8–10 weeks of splinting to retain the tooth in its new position [65, 66]. The depth of the fracture line is important because the crown/root ratio following extrusion should be at least 1:1 after crown reconstruction. Since there is concomitant displacement of the bone and periodontal tissues along with the tooth move-

387 Dentoalveolar Trauma of Children and Adolescents

a

b

c

..      Fig. 16.38  Crown-Root fracture. Surgical extrusion of the tooth. a Radiographic view of the crown-root fracture of a maxillary permanent right central incisor in an 11-year-old boy. A previous dentist had started the endodontic treatment and had placed a radiopaque paste inside the canal. b Clinical view of the tooth after removal of the temporary filling. The fracture line extends subgingivally well below the crestal bone level. c Clinical view after surgical

d

repositioning of the tooth in a more coronal position in order to create restorable margins. Root canal treatment was finalized, and the crown was buildup with composite. d Radiographic view at 9-year follow-up. The tooth is still functioning and asymptomatic and no pathologic signs are present. Due to coronal repositioning, its tooth apex is located more coronally compared to the left central incisor

c a

d

b

..      Fig. 16.39  Crown-root fracture of 11-year-old boy is candidate for orthodontic traction. a Clinical image of maxillary permanent right central incisor after emergency treatment. b A mobile mesio-­ palatal fragment is apparent (arrow). c The periapical radiograph

fails to document the course of this fracture line. d One angle of the cone beam tomographic scans reveals the fracture line to end mesially at crestal bone level (arrow)

ment, lateral fiberotomy has to be performed every 7–10  days during the orthodontic traction period. Alternatively, bone and gum remodeling may be performed in a single procedure at the end of orthodontic traction.

been proposed [70] (please see the “Replacement Resorption (Ankylosis)” section later in this chapter). Retaining the root contributes toward maintaining alveolar crest volume so that it may be removed as late as possible after puberty, only if necessary and when the timing of implant placement is deemed appropriate [71]. A midterm prosthetic appliance will have to be made for the patient. Allowing the root to remain submerged and placement of a Maryland bonded bridge is also a very good option for these patients.

Surgical extrusion of the tooth  This is an intentional partial avulsion so that the root is repositioned to a more coronal position to allow fracture margins to lie at the level of the gingiva (. Fig. 16.38). Following splinting in the new position, the tooth should receive root canal treatment. Prognosis is good, but there is 5% possibility for the root to resorb within 3 years [67] or, according to other authors, 12% in 4 years [68, 69].  

Extraction  Finally, there is the option of extracting the

tooth if none of the solutions above is suitable. Prosthetic treatment at a later stage may, however, be quite complex, because alveolar bone resorption increases with time [21]. This is why the solution of allowing the tooth root to remain, through the excision and removal of only the coronal fragment followed by suturing of the gingiva, has

zz Follow-up

Clinical and radiographic examinations, in conjunction with vitality testing, are important and should be repeated at 1  week, 6–8  weeks, 3  months, 6  months, and then yearly for at least 5  years [21] (see also . Table 16.3).  

16.3.1.6  Root Fracture

Root fracture is a combination of pulp, dentin, cementum, and periodontal membrane trauma; it appears relatively rarely at a rate of 0.5–7.5%. Teeth

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most often involved are maxillary central incisors, at a rate of 75%. In young patients, whose permanent incisors are immature and at various eruption stages, root fracture is a rather rare event [72]. Socket elasticity probably makes such teeth more susceptible to displacement and avulsion rather than root fracture. Root fractures may be horizontal (transverse), oblique, or vertical (longitudinal). The latter often appears in mature teeth with an intraradicular post and prognosis is bad. Horizontal and oblique fractures are more frequent and are distinguished into simple and multiple ones. Simple ones have a better prognosis. They are distinguished into apical third, middle third, and cervical third fractures of the root. Prognosis is worse in cervical to middle third fractures due to less periodontal support during their potential healing process.

It is also likely that the radiograph does not reveal a root fracture immediately after the injury, but at a later point in time. This is most probably due to either ­hemorrhage or granulomatous tissue formation at the fracture line, which gradually displaces the coronal fragment incisally [73]. Additionally, depending on the direction of the radiograph beam, some root fractures may be undetectable. That’s why, according to IADT, radiographic assessment comprises taking three periapical radiographs from different angles, plus an occlusal radiograph [21]. Cone beam computerized tomography (CBCT) examination is also extremely helpful to diagnose the true extent of root fractures. The real trajectory of fracture lines is usually undetectable in a single periapical radiograph (. Fig. 16.40).

zz Diagnosis

The basic principle for treating root fractures in permanent teeth is to reposition the luxated and mobile coronal fragment and immobilize it with a splint (. Fig. 16.41). Repositioning is performed under local anesthesia and confirmed through radiographic examination. Splinting is performed, for instance, with a passive twist flex wire and composite resin on the labial surface of affected and adjacent teeth. The splint should be semiflexible and passive, without applying forces on the teeth. Splinting should remain for about 4  weeks but may stay up to 4 months if the fracture is located at the cervical third of the root [21].

Horizontal and oblique root fractures may be difficult to diagnose clinically. Indeed, sometimes they may be erroneously diagnosed as tooth loosening (subluxation) or lateral displacement (lateral luxation) since clinical characteristics are the same. Furthermore, they may be missed, due to the presence of a more visible dental trauma, such as a crown fracture. Involved teeth might be sensitive to percussion and palpation, and the coronal fragment may be slightly displaced lingually, labially, and/or incisally (. Fig. 16.40) [65].  

a

b

 

zz Treatment

 

c

16

..      Fig. 16.40  a Periapical radiographic view of maxillary permanent right central incisor presenting a horizontal middle third root fracture. b The cone beam coronal view shows the same. c However, the cone beam sagittal view reveals that the fracture line is oblique and more complex: from the labial, it starts horizontally but then

takes a vertical direction downward to the alveolar bone crest palatally. There is a chance that the fracture may heal. Before the advent of cone beam examination, many oblique root fractures were misdiagnosed as “horizontal” and healed

389 Dentoalveolar Trauma of Children and Adolescents

Eye Catcher

Four types of reactions have been described following a root fracture [73, 74]: 1. Hard tissue healing. The fracture heals through the formation of a dentinoid or cementoid callus uniting the fragments. It is the “ideal” kind of healing. 2. Healing with interposition of connective tissue. 3. Healing with interposition of connective tissue and bone between the fragments. 4. Interposition of granulation tissue between the fragments. This failure to heal is related to pulpal necrosis and infection of the coronal fragment. Clinically, the tooth is sensitive to horizontal or vertical percussion, while an abscess is likely to appear at the fracture level. Radiographically, the fracture line widens, there is lamina dura loss, and there are alveolar bone radiolucencies at the fracture level.

The protocol for clinical and radiographic recalls of fractured permanent teeth is summarized further in . Table 16.3.  

zz Prognosis

Immature teeth are more likely to heal and maintain pulp vitality as compared to mature teeth [75, 76]. Pulp necrosis appears in 20–44% of root fractures [77, 78]. Necrosis usually concerns the coronal fragment only (. Fig.  16.41), while the apical component remains vital in almost all cases [75, 79]. As with every fracture type, a negative response to sensibility testing does not necessarily indicate pulp necrosis. The degree of dislocation of the coronal fragment is one of the most important factors influencing prognosis, and reapproximating the two halves is key to pulpal healing [77].  

16.3.2  Luxation Injuries to Permanent Teeth

zz Follow-up

16.3.2.1  Concussion

Regardless of fracture type, clinical and radiographic examinations should be performed at 4 and 6–8 weeks as well as at 4, 6, and 12  months and yearly for 5  years, in accordance to the IADT Guidelines [21].

When a permanent tooth suffers concussion, there is minimal trauma to periodontal tissues and pulp. The impact is usually along the tooth axis and there is no displacement or mobility of the tooth.

a

d

c

b

e

..      Fig. 16.41  a Root fracture in the middle third with extrusive and lateral luxation of maxillary permanent left central incisor in a 12-year-old boy (closed apex). b, c The tooth was repositioned, and a semiflexible wire passive splint was bonded with composite. Incisal edge was ground by 1  mm to avoid occlusal interference. d

f

Five weeks later root canal treatment of the coronal fragment was initiated due to pain symptoms. e At the 3-year follow-up, the tooth remains asymptomatic with normal mobility but with crown 1 mm shorter. f Healing has occurred by bone tissue between the fragments. Note the canal obliteration of the apical fragment

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zz Diagnosis

The tooth is asymptomatic, although in some cases mild pain may appear during mastication and it may be sensitive to percussion. There is no laceration of periodontal fibers or hemorrhage from the gingival sulcus. Pulp vitality testing usually leads to positive results, since pulp vascularity is hardly affected. The clinical and radiographic image of the tooth is normal.

when there is no tooth mobility or interference with occlusion, and in any case, it should not be kept for more than 2  weeks for the risk of promoting external root resorption [21]. zz Follow-ups, prognosis

Clinical and radiographic recall is at 4 and 6–8  weeks, 6 months, and 1 year following the injury [21] (see also . Table 16.4). Prognosis depends on the extent of periodontal tissue trauma and on stage of root development. Pulp necrosis in 0–2% immature teeth and 3.5–15% mature teeth after 7–11 years has been reported [81].  

zz Treatment

Treatment comprises monitoring of pulp vitality. Proper oral hygiene and a soft diet for 2 weeks are recommended [21]. zz Follow-ups

It is most frequent in the 8–12-year age group [82, 83].

Clinical and radiographic recall is performed at 4 and 6–8 weeks and 1 year following the injury [21]. Prognosis is very good. After 11-year follow-up, 4% necrosis of mature teeth and 0% of immature teeth have been reported [80]. 16.3.2.2  Subluxation (Loosening) zz Diagnosis

During clinical examination, there might be hemorrhage from the gingival sulcus. There is some tenderness to percussion. On palpation there is small, usually horizontal tooth mobility due to partial laceration of periodontal fibers. Due to periodontal edema, there may be premature contact with antagonists, which may lead to traumatic occlusion [21] (see also . Table 16.4). No response to initial pulp sensibility testing may indicate pulp injury. Radiographic image is usually normal [10].  

zz Treatment

16

16.3.2.3  Lateral Luxation

Treatment other than monitoring is usually not needed but, depending on symptoms and the extent of mobility, passive and flexible splinting may offer relief to the patient in some cases. The splint may soon be removed

zz Diagnosis

The tooth is displaced in a new position, and there is bleeding from the gingival sulcus. It may either be quite mobile or be immobile. If the coronal part has been displaced in a palatal direction, it often interferes with occlusion. The tooth apex is frequently displaced labially, locked out of its socket, with the buccal plate of its alveolar bone frequently fractured and displaced labially with it. This can be well visualized in cone beam examination, but palpation of the buccal plate is also very informative. This occurs more frequently to maxillary incisors with fully developed apices; the tooth sound is metallic on percussion, similar to ankylosed teeth. The responses to pulp sensibility testing may be negative initially, but in cases of open apex without apical displacement, they may become positive after about 3  weeks [21]. Radiographic examination comprises of 4 radiographs (periapical, occlusal, and two eccentric exposures in opposite direction to each other) to check for potential root fracture, possible periapical alveolar space creation, and stage of root development [22].

..      Table 16.4  Follow-up table for luxation injuries of permanent teeth, according to IADT Guidelines 2020 [21] 2w Concussion

4w

12w

6 m

c+r

Subluxation

c+r+s

Lateral luxation

c+r

c+r+s

Intrusive luxation

c+r

Extrusive luxation

c+r+s

aFor

8w

1y

Annuallya

c+r c+r

c+r

c+r

c+r

c+r

c+r

c+r

c+r

c+r+s

c+r

c+r

c+r

c+r

c+r

c+r

c+r

c+r

c+r

c+r

c+r

at least 5 years c+r: clinical and radiographic examination s: splint removal

391 Dentoalveolar Trauma of Children and Adolescents

a

b

c

..      Fig. 16.42  a, b Lateral luxation of right lateral with subluxation of right central incisor in a 10-year-old girl. c Emergency management consisted of repositioning the lateral, removing the very mobile

primary canine, and carefully etching available teeth on either side for splinting with flexible orthodontic wire and composite resin

zz Treatment

performed at 6 months, 1 year, and every year for 5 years [21] (see also . Table 16.4). There are quite a few different reports of laterally luxated teeth surviving. One study reports that immature teeth present low rates of pulp necrosis (9%), while mature teeth present high rates (77%) [80].

Laterally luxated maxillary incisors may be repositioned ideally during the first 12 hours after the injury, under local anesthesia, − buccal and/or palatal  – or after infraorbital nerve block [84]. To disengage a locked apex, it is pressed from the buccal, using a finger with simultaneous mild pull of the tooth crown incisally, which also achieves concurrent reduction of any alveolar bone fracture that may be present (. Fig.  16.42). Tooth splinting should be semiflexible and performed with a passive wire retained on the labial tooth surfaces using small amounts of composite resin for dental/gingival hygiene. The purpose of splinting is to maintain the tooth in position, while allowing physiologic mobility. This has been shown to improve periodontal healing and be helpful in the prevention of ankylosis. The splint is usually kept for 4  weeks [21], since lateral luxation is usually associated with alveolar bone fracture. No investigation using a periodontal probe is allowed during this time. If it is certain that no associated bone fractured occurred, the splint time may be reduced to 2 weeks. The integrity of the alveolar bone plate is checked radiographically and, in case of marginal bone breakdown, splinting is extended for another 3–4 weeks [21]. If the trauma is not recent, it is preferable to reposition the tooth through orthodontic forces after initial periodontal healing [85]. The patient should be rescheduled to come at 2 weeks post-trauma to check good initial healing, perform endodontic evaluation, and possible removal of the splint. If the injured tooth is mature and the apex was severely displaced, the chances of pulp survival are low and endodontic treatment should likely be performed soon in order to prevent pulp infection and inflammatory root resorption. Pulp space healing, most often by spontaneous revascularization, may be expected in 70% of immature teeth with this type of injury [86].  

 

16.3.2.4  Intrusive Luxation

Intrusive luxation occurs due to axial force applied to the tooth’s incisal edge. This is considered to be the most serious trauma type, since it is associated with extensive lesions of the pulp, periodontal cells, and cementum and often with alveolar bone plate fracture [87]. It is a traumatic lesion of particularly bad prognosis, particularly if the patient did not comply with proper treatment (. Fig. 16.43).  

zz Diagnosis

Intrusion is often a component of serious trauma involving several teeth and bone fracture. Clinically, the crown of the injured tooth appears shorter than that of adjacent teeth. Diagnosis is easier during puberty. On the contrary, among 7–8-year-old children, the intruded tooth looks like an erupting one, and differential diagnosis can benefit from mild percussion, which produces a metallic sound [82]. Since this is displacement trauma, radiographic examination should include four radiographs, as in the case of lateral luxation. The absence of periodontal tissue at the apical region or along the entire radical length is a typical finding [21]. zz Treatment

There are no satisfactorily documented recommendations as yet concerning the treatment of a permanent tooth that has suffered intrusion. Treatment depends on the degree of root development and degree of intrusion.

zz Follow-up, prognosis

zz Immature teeth

Initial clinical and radiographic recall is performed at 2, 4, and 6–8 weeks after the injury. Later recalls should be

Teeth with open apices have the potential to re-erupt spontaneously to their original position. This may

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a

b

c

d

..      Fig. 16.43  Consequences of a neglected intrusion case. a Serious trauma to an 8-year-old girl at the playground swing, with intrusion of all 4 maxillary permanent incisors and severe lateral luxation of many primary teeth. b Same patient 8 weeks later. Partial re-­eruption of the incisors (more limited for the right central one, which is also rotated). c Patient reappearance 20  months after the initial injury.

a

b

d

e

The right central incisor did not re-erupt and produces an ankylotic sound on percussion, while the left lateral incisor presents a fistula. d Root development continued in the right lateral and left central incisors, but not in the other two incisors. Prognosis for right central incisor is bad, especially that its presence is impeding anterior alveolar bone growth. Family compliance is needed to improve prognosis

c

16

..      Fig. 16.44  a Intrusion and non-complicated crown fracture of a maxillary permanent left central incisor in an 8-year-old. b Palatal view. c Radiographic view (open apex). d Six months monitoring after pulp protection with glass ionomer cement. Spontaneous

re-­eruption occurred, but only partially. e Outcome 12 months later, after repositioning the left central incisor by orthodontic means and stabilization splinting over a 3-month period

happen within 3  months [88, 89]. Given that about 2/3 of such teeth become necrotic during this waiting period, the teeth need to be monitored so that necrosis may be diagnosed in good time [86, 90]. If within a few weeks there is no sign of re-eruption, the tooth is repositioned using orthodontic means [21] (. Fig.  16.44).

If the intrusion is severe, more than 7  mm, the IADT Guidelines recommend to reposition the tooth either surgically or orthodontically. It has also been proposed that a mild attempt to disengage the tooth using a tooth extraction forceps should be made immediately after the injury [21].

 

393 Dentoalveolar Trauma of Children and Adolescents

zz Mature teeth

If the tooth is intruded less than 3 mm, it is worth trying to wait for spontaneous re-eruption. If after 2–4 weeks there is no sign that re eruption is on its way, surgical or orthodontic repositioning is indicated. If the mature tooth is intruded more than 7 mm, surgical repositioning is recommended by the IADT Guidelines [21]. The figures below show orthodontic (. Fig. 16.45) and surgical (. Fig.  16.46) repositioning of intruded mature teeth, the former being considered a more acceptable solution from a biological point of view. Surgical repositioning is performed using bone forceps and digital compression to the socket. After repositioning, splinting is required for 4–8 weeks [21]. Because the rates of necrosis are high among such teeth [82], it is necessary for root canal treatment to start earlier than 3  weeks after the injury, at about 10 days, with temporary intracanal Ca(OH)2 filling initially for a few months and gutta-percha final filling later on. Soft food is recommended for 10–14  days as well as good oral hygiene including local application of chlorhexidine (0.1%) twice a day for a week [21].  

 

zz Follow-up, prognosis

Clinical and radiographic examination, regardless of the degree of root development, similarly to lateral luxation, should be performed at 2, 4, and 6–8 weeks, 6

a

b

and 12 months, and every year for 5 years [21] (see also . Table 16.4). Healing is complex due to the high likelihood of pulp necrosis and external tooth resorptions, both replacement and inflammatory. After follow-up of many years, it was confirmed that the pulp became necrotic in 2/3 of intruded permanent teeth with open apex and in 98–100% of those with a closed apex [89].  

16.3.2.5  Extrusive Luxation

Extrusive luxation is caused by a lateral force impact that leads to serious injury of the periodontal ligament. The tooth may still be kept in position by some periodontal fibers. zz Diagnosis

Clinically the tooth appears to have “gone down,” with a longer clinical crown, and there is bleeding from the soft tissues around the tooth. The tooth is very mobile. There is usually no response to pulp sensitivity testing. Radiographic examination reveals increased width of the periodontal space [21]. zz Treatment

Repositioning might have been performed immediately at the site of the accident. If performed in the dental office, following local anesthesia, the tooth is pushed back into the socket with mild digital pressure. In case

c

d

..      Fig. 16.45  Orthodontic repositioning of intruded teeth. a Severe intrusion of both maxillary central incisors, concomitant with extensive crown fracture in a 14-year-old adolescent from a bike accident. b Starting orthodontic repositioning with traction of central incisors.

c Completion of root canal treatment. d Crown buildups with composite resin and alignment of incisors using fixed orthodontic appliances. Clinical and radiographic follow-ups will continue. (Courtesy of Dr. G Vadiakas)

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a

b

d

16

c

e

f

..      Fig. 16.46  Surgical repositioning of intruded teeth. a, b Severe intrusion of maxillary permanent right central incisor, moderate intrusion of left central incisor, fracture to their crowns, and concomitant fracture of the alveolar bone plate in a 10-year-old girl. Teeth are quite mature. c Immediate surgical repositioning of central incisors with forceps. Caution should be taken not to damage the

root cementum with the forceps. d Splinting with orthodontic wire and composite resin and suturing of interdental gingival papillae. e Esthetic restorations with composite resin following root canal treatment of the two central incisors. Soft tissues healed well. f 4-year follow-up radiographic image without signs of root resorption or other pathologic findings. (Courtesy of Dr. G Vadiakas)

of recent trauma, the blood clot will spread out from the apical region of the socket. In extrusions neglected for several days, the blood clot has become organized. Some authors recommend orthodontic intrusion of those teeth if they are mature. If, however, the tooth is severely interfering with occlusion, it may be extracted and repositioned in its normal position following clot curettage (. Fig.  16.47). Flexible splinting, with a passive wire and composite resin, ensues for 2  weeks to allow time for periodontal ligament healing. The patient is given the same instructions as those given for intrusion injury. Continuous monitoring of the tooth is necessary so that any root resorption may be noticed. In cases of immature teeth, pulp space revascularization is confirmed if root development continues. In mature and immature teeth, continuous negative reaction to pulp sensibility testing, presence of apical radiolucency, swelling, or fistula indicates pulpal necrosis, whereupon root canal treatment is indicated.

on the stage of root development. In immature teeth, pulpal necrosis rates are 9%, while in mature teeth, rates reported are 55–98% [80, 91]. The protocol for clinical and radiographic recalls in cases of luxated permanent teeth is summarized in this chapter, in the 7 Sect. 16.3.4, in . Table 16.4.

 

zz Follow-up, prognosis

Following clinical and radiographic examination 2 weeks after the injury, the splint is removed. Recall follows the protocol applied for luxation injuries [21] (see also . Table 16.4). Tooth preservation rates are high following extrusion injuries, while pulpal survival depends  

 

 

16.3.2.6  Avulsion

This type of trauma appears more frequently among young individuals, when the apex has not yet fully developed and the alveolar bone is more resilient. The aim of emergency treatment is to replant the avulsed tooth as soon as possible, ideally within minutes, at the site of the accident. Parents, sport coaches, and the population in general should be instructed to do so [24]. If debris are present on the root surface, they should be gently removed by rinsing the tooth in water, milk, or saline prior to replantation. No wiping or scraping should be done, since they damage the cementum and periodontal ligament cells covering the root surface. The combination of the three parameters presented below determines the treatment of choice as well as the prognosis. 55 Root development stage: Spontaneous pulp space revascularization is considered unlikely in the case of a replanted mature tooth (closed apex). In a tooth with open apex, the likelihood of pulp space

395 Dentoalveolar Trauma of Children and Adolescents

a

b

c

d

e

f

..      Fig. 16.47  Extrusive luxation with delayed repositioning. a A 17-year-old girl presents 6  days after extrusive luxation of maxillary permanent right central incisor, with crown fracture of this and the left lateral incisor. There is significant occlusion interference. b Radiograph shows that the teeth are mature (closed apex). The apical socket space probably contains an organized clot. c, d The extruded incisor is extracted and, after the blood clot is curetted away, is

immediately replanted and splinted for 2 weeks. e Signs of pulp canal obliteration on both teeth at the 8 months recall. f Reconstruction of the crowns with composite resin at this stage, although this should have been carried out earlier in order to cover the exposed dentin. Follow-up continues in case of root canal treatment need and signs of root resorption

revascularization and, consequently, of the root continuing development is higher, particularly if the root surface is treated with tetracyclines, such as doxycycline or minocycline, prior to replantation [92, 93]. 55 Time the tooth remained out of the socket: The longer the tooth remains outside its socket, the higher the likelihood of periodontal cell necrosis due to desiccation. Consequently, the sooner replantation takes place, the more favorable the results [94–98]. If the extra-alveolar dry time is less than about 15  minutes, periodontal tissues may well heal. If the tooth remains outside its socket for more than an hour, even in humid environment, healing is impaired and any therapeutic intervention aims at limiting the phenomenon of replacement resorption [95]. 55 Tooth preservation medium: A preservation medium may decelerate the destruction of periodontal cells caused by dehydration. –– An extra-alveolar dry environment (air) soon causes necrosis of periodontal fibers resulting in root resorption [95].

–– Hank’s Balanced Salt Solution (HBSS) is an isotonic solution with a neutral pH, which contains ingredients necessary for cellular metabolism and is suitable for cell culture [99]. –– Viaspan solution is used in medicine for preserving organs to be transplanted; therefore, it is ideal for preserving teeth [100]. However, neither of these two solutions are readily available. –– Dentosafe® and Save-A-Tooth® are kits that contain a medium for the preservation of avulsed teeth. They are a cell culture medium that contains mineral salts, amino acids, vitamins, and glucose [101]. –– Milk is a good medium for PDL preservation and is readily available. It has the appropriate osmotic properties, neutral pH, and nutrients and no toxic ingredients. Low-fat milk seems to be most suitable as compared to full fat and low temperature possibly improves cell survival [101, 102]. –– Other media. Saliva is less suitable than milk, because it is more hypotonic, but it is always readily available. Saline solution is preferable to water, which is the most hypotonic and causes quicker cell lysis [103].

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Emergency Treatment of an Avulsed Tooth Mature Teeth (Closed Apex)

(. Fig. 16.48). An apexification procedure is then needed (please look further down in this chapter).  

The tooth has already been replanted  The proper posi-

tion of the replanted tooth is verified clinically and radiographically. The area is thoroughly rinsed and any gingival lacerations are sutured. The tooth is cleaned and splinted with a passive and flexible splint for 2 weeks. Even though antimicrobial medication is sometimes prescribed (e.g., tetracyclines, for patients older than 8  years) to prevent socket infection and inflammatory root resorption, there is no strong evidence as of today to support systemic antibiotic use [24]. If the tooth has contacted soil, the child should be referred to the pediatrician, unless anti-tetanus coverage is documented. Soft food is recommended for 10–14  days, brushing with a soft toothbrush and local application of chlorhexidine 0.1% 2 times a day for a week [24]. After 7–10 days, root canal treatment should start; Ca(OH)2 should be applied in the canal for at least 3–4  weeks before the final gutta-percha filling. However, in cases of teeth with signs of inflammatory resorption, Ca(OH)2 should be applied for at least 3  months [104]. This approach reached success rates of 97% after an 8-month period [105].

for closed apices, with the administration of antimicrobial preparations and root canal treatment performed as soon as pulp necrosis is confirmed (. Fig. 16.49) [104].  

Time outside the socket exceeds 60 minutes dry  Prognosis is

poor, but replantation should still be done, not only for mid-term esthetic, functional, and psychological purposes but also for preserving the outline of the alveolar bone, the ultimate aim being to facilitate bonded bridge or implant placement later and improve soft tissue esthetics. The final outcome is ankylosis and root resorption with possible tooth loss, although there have been reports of cases, albeit exceptional, with a favorable outcome. zz Follow-up

Clinical and radiographic examinations are performed 4 weeks later, at 3 months, 6 months, and 1 year, with continuous annual follow-ups [24] (see also . Table 16.5).  

The tooth remained outside its socket up to 60 minutes in a favorable medium (like milk, Hank’s, Viaspan, Dentosafe® solution)  The tooth is grasped by the crown while the

16.3.3  Post-traumatic Complications of

root and socket are rinsed with saline solution. The tooth is repositioned into its socket with mild digital pressure; its position is checked clinically and radiographically, and then the tooth is splinted with a passive and flexible splint. The same procedures as in the previous case are followed [24].

A range of complications may appear following traumatic injuries to permanent teeth. The most common are pulp canal obliteration, pulp necrosis, and different types of root resorption.

Time outside the socket exceeds 60 minutes dry  The likeli-

16

The tooth remained outside the socket up to 60 minutes in a favorable medium  The process followed is the same as

hood of successful periodontal healing is minimal and, therefore, efforts are made to delay the onset of ankylosis and root replacement resorption as long as possible [106]. The root is rinsed, and any soil residues or nonviable soft tissue attached to the root surface is removed gently using gauze; the socket is rinsed with saline solution [24]. It has been suggested that the tooth is bathed in a 2% stannous fluoride solution so as to delay resorption [107]. The tooth is repositioned and the same procedures as in previous cases are followed. Root canal treatment may take place extraorally before the replantation or 7–10  days later [24]. Immature Teeth (Open Apex) The tooth has already been replanted  The procedure fol-

lowed is the same as for teeth with closed apex. Because there is a possibility that the pulp space may become revascularized, root canal treatment is not performed until later, only if pulp necrosis gets confirmed

Permanent Teeth

16.3.3.1  Pulp Canal Obliteration

Root canal obliteration, as in the case of primary teeth, leads gradually to pulp chamber and root canal stenosis. It can be interpreted as a tentative healing and as a defense mechanism. There are several ways by which pulp space obliteration can occur. It is not fully understood how cells are activated to drastically accelerate intracanal calcified tissue production. The clinical result of this phenomenon is reduction or complete loss of tooth sensitivity and a shade change of the crown. Eye Catcher

Obliterated teeth tend to become discolored, usually toward yellow but sometimes toward brown-gray. If endodontic treatment was necessary, intracoronal bleaching may be performed on those teeth after root canal filling and placement of a hermetic seal on top of it (see 7 Chap. 14 and 7 Fig. 14.35). Otherwise, external bleaching may be attempted (see 7 Chap. 17).  

 

 

397 Dentoalveolar Trauma of Children and Adolescents

a

b

c

d

e

..      Fig. 16.48  a Avulsion of 5 maxillary teeth in 6.5-year-old girl: both permanent central incisors and 3 primary, left canine, and both lateral incisors. Central incisors remained dry for 10  minutes and then placed in milk for another 1  hour 40  minutes. Following replantation, sutures to the attached gingiva (secured with a spot of composite) held teeth in place for 1 week in the absence of adjacent teeth to splint with. b Radiograph immediately after replantation. c Radiographs at 14  months show that revascularization and

a

e

b

obliteration of the pulp space is occurring in the avulsed right central incisor. d The teeth are asymptomatic with no sign of ankylosis. e The 30-month radiograph shows complete obliteration of the right central incisor’s pulp space. Meanwhile paucity of root development and apical radiolucency of the left central incisor had dictated initiation of endodontic treatment. An apexification procedure using Ca(OH)2 was selected

c

f

g

..      Fig. 16.49  a Avulsion of the maxillary permanent right central incisor (dry for 10  minutes, in milk for another 40  minutes) and partial extrusion of right lateral incisor with alveolar fracture and lacerations to labial gingiva in an 8-year-old boy. b Avulsed incisor rinsed with saline. c, d Replantation of avulsed central incisor and repositioning of extruded lateral incisor, sutured gingiva and splinting using passive orthodontic wire and composite resin. Exposed dentin was protected with GIC and hygiene instructions given. e,

d

h

f Following the restoration of the crown fracture, after 12  weeks, an apical radiolucency is observed on the right central incisor. g After Ca(OH)2 filling followed by Portland cement apical plug (not radiopaque), the remaining canal was filled with gutta-­percha. The 6-month radiograph shows apical healing while the extruded lateral incisor shows root canal obliteration. h At 2 years, infraocclusion is the result of ankylosis of the avulsed tooth

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..      Table 16.5  Follow-up table for avulsion injuries of permanent teeth, according to IADT Guidelines 2020 [21]

Avulsion

2w

4w

3 m

6 m

1y

Annuallya

c+r +s

c+r

c+r

c+r

c+r

c+r

aFor

at least 5 years c+r: clinical and radiographic examination s: splint removal

Despite radiographically appearing full root canal obliteration, a minimal canal space might exist, depending on how the obliteration evolved. Pulp space obliterations are most often observed in cases of immature teeth (with open apices), which suffered extrusion traumas or lateral luxation and intrusion, thus raising suspicions that the disorder may be related to pulp space revascularization mechanisms [108]. Only in 8–13% of such cases was pulp necrosis observed, and periapical inflammation appeared 5–20 years after the injury, which brings the 20-year pulp survival estimation to 84% [105, 109, 110]. Endodontic treatment is usually feasible even in such necrotic cases, albeit with some difficulty, because the root canal remains accessible and prognosis is good [111]. However, the calcified tissue may form from a coronal to apical direction without leaving a canal space as we usually know it. Or the pulp space might get colonized by an osteoid or cementoid type of calcified tissue (. Fig.  16.48) originating from the periradicular tissues, in which cases there is no presence of a “canal” structure. That’s why, before intervening endodontically on those teeth, a careful preoperative investigation must be made by comparing previous periapical radiographs to understand how the obliteration developed. Additionally, a preoperative cone beam tomographic examination (CBCT) is recommended (. Fig. 16.50). The use of the operative microscope is helpful to find and treat infected obliterated canals. Referral to a trained endodontist is advised.  

16

 

16.3.3.2  Pulp Necrosis

Pulp necrosis is the most common post-traumatic complication. It often occurs in cases of displacement (luxation) injuries, where pulp neurovascular supply has usually been severed [51]. It occurs less often in teeth with open apices, because small displacements of those teeth do not necessarily lead to apical blood vessel rupture; even if rupture does occur, a young pulp has a higher potential for healing. Pulp necrosis usually appears in the first 3 months after the injury; however, in some cases, it might take up to 2 years for it to be confirmed. Diagnosis is based on symptom assessment; clinical examination, including palpation, percussion, sensibility testing, and evaluation of tooth color

changes; and radiographic findings such as presence of radiolucencies and signs or root and/or bone resorption. Laser Doppler flowmetry and oximetry are promising technologies that have been shown to allow reading of pulp status or pulp space revascularization status in a matter of few weeks [112–114]. Change of tooth color  Even relatively mild trauma such

as concussion and subluxation may lead to blood supply rupture or disruption at the apical foramen. Intrapulpal hemorrhage can cause the crown to become slightly pink. If the blood supply recovers, which means that the pulp preserves its vitality, normal tooth color is self-restored. If the tooth crown gradually turns gray – several weeks or even months after the injury – then suspicion of necrosis is raised, since this discoloration likely indicates necrotic pulp tissue decomposition [115]. Pulp sensibility testing  Most permanent teeth that have

suffered loosening (subluxation) or displacement (luxation) do not initially respond to cold or electrometric vitality testing; yet, several regain their sensitivity later, within 2–3 months. However, there have been cases, when it was up to 2  years before teeth regained their normal reaction. Besides, young patients and immature teeth seem to respond in an unreliable fashion to pulp sensitivity testing [116]. Therefore, a negative response to cold or to electric sensibility test per se is not sufficient, and root canal treatment should be postponed until at least one more clinical or radiographic indication of pulp necrosis arises. Last but not least, sometimes the nerve fibers seem to be the last ones to die, possibly giving false-positive responses to testing [117]. For all these reasons, pulp sensitivity interpretation can be seen as a “challenging art.” Radiographic signs of pulp necrosis  Radiographic tech-

nique should be reproducible, so that, as time passes, images may be compared to each other. Radiographs to help diagnose pulp necrosis should only be taken at a point in time when pathologic findings are expected to be present. This may be 3 weeks after the injury, although it often takes quite a few months before an apical radiolucency becomes visible in the radiograph [24]. In teeth with open apices, necrosis of Hertwig’s epithelial root sheath

399 Dentoalveolar Trauma of Children and Adolescents

a

b

..      Fig. 16.50  Pulp canal obliteration. Maxillary permanent right central incisor of a 28-year-old female had suffered a severe luxation injury while she was a child. a Periapical radiograph showing

means that apex development is inhibited. Signs of root resorption and root development interruption of immature teeth are also indicators of possible pulp necrosis.

16

c

absence of a visible canal. b, c Cone beam examination (CBCT) shows no trace of a visible canal. The tooth is asymptomatic with no signs of pathology. No treatment other than follow-ups is necessary

a

b

16.3.3.3  Root Resorption

A tooth displacement (luxation) trauma often results in some form of root resorption [118]. Partial surface resorption  In such cases, small cavities

appear on the root surface, covered by periodontal membrane; these can be confirmed with 3D radiographic techniques (cone beam computer tomography, CBCT) [119]. This form of resorption is transient and self-limiting and appears frequently after mild luxation injuries. No treatment is required if the pulp is vital. Replacement resorption (ankylosis)  This is a serious complication, mainly associated with intrusion or delayed replantation of an avulsed tooth. It is related to severe and extensive destruction of the cementum and periodontal ligament, resulting in fusion (ankylosis) of the alveolar bone with dentin. Clastic cells then resorb the root, which is gradually replaced by bone. A characteristic metal sound is produced on percussion, and the tooth is deprived of physiological mobility. Radiographically, areas of periodontal ligament space have disappeared. Within a few years, full resorption may be seen with complete root replacement by bone (. Fig.  16.51). In young patients, the affected tooth tends to become infraoccluded as both growth of the alveolar process and eruption of adjacent teeth continue. Decoronation has been suggested as a temporary measure to maintain alveolar ridge dimensions [120, 121] (. Fig.  16.52). If replacement root resorption evolves slowly, buccal, lingual, and vertical bone dimensions will be better preserved for longer, and this facilitates implant placement later. Implants should be placed as late as possible since alveolar bone growth has been shown in patients aged 35–45 years old, indicat-

..      Fig. 16.51  Replacement resorption. Maxillary permanent right central incisor was avulsed and replanted when patient was 9 years old. a 6-month post-injury. There is an ankylotic sound to the percussion test and radiographically there are signs of replacement resorption (arrow). b At 18 months replacement resorption is clearly visible: the periodontal ligament space has almost completely disappeared all around the right central incisor root; the bone is in direct contact with the root dentin; the root is getting gradually replaced by bone. In this case, the pulp seems to have remained vital

ing it is continuous throughout life [122–125]. Ankylosis clearly complicates full mouth orthodontic planning as well as future prosthetic or implant treatments.

 

 

Inflammatory root resorption  As in replacement root

resorption, this type of resorption is related to severe and extensive damage to the cementum and periodontal ligament, the root protective layers. But it’s also related to associated pulp necrosis and infection. Bacterial by-­ products and endotoxins from the infected pulp travel through the dentinal tubules toward the root surface. In areas deprived of cemental and precemental layers, they act as stimuli for the body’s defense mechanisms. An intense odontoclastic activity results on the root surface,

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a

b

d

e

c

f

g

h

..      Fig. 16.52  Replacement resorption and decoronation. Maxillary permanent right central incisor was avulsed, replanted, and splinted. The extra-alveolar time was 3 hours dry. a Radiographic view immediately after replantation and splinting. b–d Ankylosis evolution at 4  weeks, 15  months, and 30  months. e The avulsed incisor became severely infrapositioned due to ankylosis. f Clinical view of the

decoronation surgery. g Radiographic view immediately after decoronation. h Radiographic view 13 months post-­decoronation. Note the bone formation coronally to the resorbing root. The presence of the decoronated root helps to delay bone volume loss and maintain alveolar ridge dimensions

which is responsible for the resorption. In children aged 6–10 years, this type of resorption tends to be extremely aggressive, causing sometimes tooth loss in a matter of a few weeks. This happens, because at this age, dentinal tubules are wide and the distance from the pulp canal to the root surface is small [126, 127]. Radiographically, inflammatory root resorptions may appear initially as if the periodontal ligament space is wider and irregular on both the alveolar bone and on the root side. Subsequently, distinctive radiolucent lesions will form on the root surface and in the adjacent bone. The first signs of inflammatory root resorption (most commonly located in the cervical 1/3rd of the root) can be apparent radiographically as early as 2  weeks after the injury, especially in young teeth [128]. If diagnosed early, inflammatory root resorption can be successfully treated. The key to successful treatment is to completely disinfect the root canal space. Calcium hydroxide intracanal medication has been shown to be beneficial to treat inflammatory root resorption, and its use is recommended [21, 24, 105] (. Fig. 16.53). Once the canal space is disinfected, radiolucencies around the root should disappear, and the periodontal ligament width may return to normalcy and follow the new contours of the root surface. Final filling of the canal with gutta-percha and sealer ensues.

Cervical root resorption  These resorptions are usually late complications of dental trauma, so they will not be fully discussed in the scope of this chapter. In short words, cervical resorptions tend to appear below the epithelial attachment of the tooth and are inflammatory in nature. It has been assumed that the presence of sulcular bacteria is responsible for the maintenance of the lesion once it has formed [129]. They occur equally in vital and in non-vital teeth. Radiographic evaluation will reveal a radiolucent area in the cervical area of the tooth adjacent to the crestal bone (. Fig.  16.54). The lesion seems to have the tendency to develop confined in dentin, in an apical/ incisal direction along the pre-cementum and the predentin, but without perforating those protective layers and without penetrating into the pulp canal space or into the PDL space [130–133]. Their management can be complex, particularly if diagnosed late, where either the involved tooth ends up with a periodontal pocket or needs to be extracted.

 

 

Internal resorption  This is a rare post-traumatic complication likely caused by chronic pulp inflammation. It appears without any clinical symptoms and is usually diagnosed radiographically years after the injury. If the tooth involved is treated early, before the resorption extends and causes root perforation, root canal treat-

401 Dentoalveolar Trauma of Children and Adolescents

a

b

c

..      Fig. 16.53  Inflammatory root resorption. Accident of an 11-year-­ old female caused avulsion of maxillary permanent left central incisor, which was replanted several hours after the injury. a Diagnostic radiograph 1 year after the injury. There is a radiolucent zone in the bone all around the root. Radiolucent “holes” on the root and on the adjacent bone are also visible. Diagnosis of inflammatory resorption is made. b Endodontic treatment with calcium hydroxide is started and the canal space “disappears.” c After 5  months, the

d

e

radiolucent zones around the root have subsided; there is calcified tissue apposition on the root resorption lacunas; normal periodontal ligament width is reestablished. These signs are positive as they indicate that healing is in progress and that the resorption process has likely stopped. d The root canal is filled and the access cavity is restored. e 2  year follow-up. The tooth is fine but still has to be frequently monitored, especially that orthodontic treatment was deemed necessary

ment may be successful to stop the resorption (. Fig. 16.55).  

16.3.4  Follow-Ups of Injured Permanent

Teeth

All traumatized teeth should be carefully reevaluated periodically after an injury, irrespective of its apparent severity. . Tables 16.3, 16.4, and 16.5 show the IADT’s recommendations for a recall schedule after each type of injury [21, 24].  

16.3.5  Endodontic Evaluation

and Management of Injured Permanent Teeth

16.3.5.1  Pulp Status Evaluation and Diagnosis

Following Trauma

It is important to remember that a tooth can sustain multiple injuries at the same time. This does impact the outcome. For example, a luxation injury can occur in combination with an uncomplicated crown fracture [52, 53, 134, 135]. After emergency treatment, a close follow­up is essential to ensure that that the pulp has survived. If guidelines are followed, more favorable outcomes can be expected when compared to cases treated without

..      Fig. 16.54  Cervical resorption. Radiograph of tooth # 11, 6  years after trauma of a 15-year-old male. Root development stopped; an apical radiolucency indicative of pulp space infection is present. Resorption of the cervical type is visible disto-cervically. In this case, endodontic treatment should be carried out first, prior to managing the resorption per se

compliance to the guidelines [136]. At every evaluation, a radiograph needs to be taken as well as all clinical signs and symptoms associated with pulp necrosis explored. The pulp might remain unresponsive to sensibility testing for several months; however, if no other signs are evident, it is advisable to do no treatment but rather schedule recalls, especially if the patient’s tooth is

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a

b

..      Fig. 16.55  Internal resorption. a The coronal part of the canal is obliterated. The arrow points at mid-root where the internal resorption is located. b After endodontic treatment and root filling. Endodontic treatment was necessary to stop the internal resorption process

immature. Additional signs to look for are color changes of the crown, the width of the periodontal ligament, periapical lesions, and other signs of infection, like fistula, tissue swelling, and/or pain [80, 110, 137, 138]. If in doubt about the pulp status diagnosis, a timely referral to a specialist is strongly recommended, because root resorption associated with necrotic and infected pulp space can cause quite a rapid and irreversible loss of root structure in a matter of weeks. 16.3.5.2  Keeping the Pulp Alive and Favoring

Spontaneous Pulp Space Revascularization

16

As mentioned previously in this chapter, one of the main goals of post-traumatic management is the maintenance of pulp space vitality. For instance: if proper emergency treatment is provided to crown-fractured teeth, whether with or without pulp exposure, the pulp has high chances of remaining vital; because of the larger vascular supply and larger apical opening in immature teeth, pulpal survival or spontaneous pulp space revascularization is a possibility subsequent to severe luxation injuries [118, 139]. It is a desirable mode of healing. However, while waiting for this revascularization, the tooth has to be monitored against the risk of pulp necrosis, infection, and root resorption, which can severely compromise the tooth. 16.3.5.3  Endodontic Treatment of Necrotic

Teeth

Signs and symptoms of pulp necrosis and infection are as follows: pain, swelling or discomfort, fistula, excessive mobility, sensitivity to palpation and percussion,

periapical radiolucency, color changes, persistent unresponsiveness to sensitivity testing, or nondevelopment of the root. Once the pulp has been diagnosed with certainty as necrotic, endodontic treatment should be instituted as soon as possible. The endodontic approach will be dictated by the stage of root development, type of injury, and time elapsed since the traumatic episode. Treatment often involves an apexification procedure (see further down in this chapter). All types of endodontic treatment should always be carried out with rubber dam isolation. It is not advisable to clamp the traumatized tooth but rather rely on clamping adjacent teeth or on using widgets or dental floss. 1. Endodontic Treatment of Necrotic Mature (closed apex) Teeth In decreasing order, the most severe injuries to the PDL and pulp are intrusion and avulsion, lateral luxation, extrusion, subluxation, and concussion. When there is little or no chance of pulp survival in mature teeth, endodontic therapy should be initiated between 7 and 10  days post-trauma in order to prevent the necrotic pulp from becoming infected [21, 24]. Endodontic treatment should not be started at the emergency visit for two reasons. Firstly, additional manipulation of the tooth soon after the injury could further traumatize the periodontal ligament [24, 140, 141]. Secondly, too early application of calcium hydroxide can have a detrimental effect on periodontal ligament healing [140–142]. Since a luxated or avulsed tooth may still be mobile 7–10 days after trauma, it is advised to start the endodontic treatment while the tooth is still splinted. The splint can be removed at the end of the appointment, if so indicated [21, 24]. Currently, the most widely accepted intracanal medicament is calcium hydroxide [Ca(OH)2] paste, either in premixed form or by mixing powder with sterile water or anesthetic solution [143–147]. It has been shown that if Ca(OH)2 is placed for 2  weeks into the root canal of a traumatized tooth prior to it becoming infected (i.e., within about a fortnight), the treatment outcome is favorable [104, 148]. If endodontic treatment is started later and an established infection exists prior to the placement of Ca(OH)2, it is recommended that the Ca(OH)2 remains in place for several months prior to the final root canal obturation. This is to reduce the risk of inflammatory root resorption [104]. 2. Endodontic treatment of necrotic immature (open apex) teeth As the pulp of immature teeth is needed for root development, it is of good clinical practice to monitor its status and consider the pulp as vital until there is clear evidence showing the contrary (at least two signs and symptoms indicating pulp necrosis and

403 Dentoalveolar Trauma of Children and Adolescents

infection). Only when a pulp is definitely diagnosed as necrotic should endodontic treatment be initiated. Several approaches exist: classical apexification, apical plug apexification or the so-called Regendo, or pulp space “revascularization” procedures. a. Classical apexification The classical apexification is a procedure where the root canal of an open apex tooth is cleaned and filled repeatedly with calcium hydroxide [Ca(OH)2] dressings to stimulate the formation of a natural hard tissue barrier at the apical portion of the root. After this biological calcified barrier has formed, it is possible to obturate the canal system without or with decreased risk of over extending the root filling material [149, 150]. It is a prerequisite to disinfect the canal space to create a suitable environment for stimulating apical barrier formation. Disinfection is achieved by thorough, but gentle, irrigation with sodium hypochlorite and by placing a relatively thin mixture (less than tooth paste thick) of calcium hydroxide powder mixed with anesthetic solution or saline solution. It is not recommended to use barium sulfate in the mixture because it prevents assessment of the calcium hydroxide placement in the canal space. The mixture is spun into the canal space. After 3 weeks, the patient is recalled, and the thin mixture irrigated out. At this time, a thick, almost dry, mixture of calcium hydroxide and sterile solution is packed to the full length of the tooth using pluggers or inverted gutta-­percha cones to seat it to the full length of the root. Once a radiograph indicates that the intracanal mixture is as dense as dentine all the way to the apex (. Fig.  16.56), a temporary restoration such as IRM® should be placed in the access cavity. The patient should then be recalled every 3  months and the density of the mixture evaluated radiographically. Currently, it is not recommended to replace the mixture if it appears to be intact at these recall appointments [24]. The time required to achieve the apical barrier formation varies between 6 and 24 months with an average of 1 year +/− 7 months [151]. Once the presence of the barrier has been confirmed both radiographically and clinically, the final root canal obturation can be done (. Fig. 16.57). b. Apical plug apexification In the last 20 years, the use of mineral trioxide aggregate (MTA™, Dentsply, Tulsa, OK, USA) as an artificial apical plug has gained popularity in order to allow root canal obturation sooner than with the classical approach [152]. However, it is important to note that MTA™ has minimal bactericidal effect on several bacterial species  

 

[153, 154]. Additionally, but only after its widespread use during many years, it was observed that MTA™ causes tooth discoloration. New bioceramic materials such as Biodentine® or Total Fill® have been suggested recently to replace MTA. As of today, there is neither enough data yet regarding outcome when these materials are used nor regarding the possibility that they may cause late discolorations. Given that bacteria are the single most important factor to maintain inflammatory root resorption, it is strongly advised to follow a two- to three-step apexification procedure when the canal space is likely infected. The protocol is to disinfect and medicate the canal for 7–14 days with a thin calcium hydroxide paste. Secondly, an artificial apical barrier is created by compacting the chosen apical plug material into the apical area (. Fig. 16.58). When MTA was used as the plug material, a wet cotton pellet needed to be placed in the canal for at least about 4 hours, so that the MTA could set. An extra treatment session was thus required. CollaCote™ or calcium sulfate can be placed apically beforehand to help preventing extrusion of the material in the apical area. The rest of the canal is then obturated. It is delicate to place the apical plug material correctly at the apex. An operating microscope is needed, as magnification and good lighting are essential. c. Pulp space revascularization of necrotic infected teeth (Revitalization or ‘Regenerative’ endodontics)  

a

b

Ca(OH)2 packing

Ca(OH)2 washout

..      Fig. 16.56  Calcium hydroxide placement and washout. Necrotic maxillary permanent right central incisor is very immature, and calcium hydroxide apexification is carried out. a Radiograph immediately after a dense packing of (barium sulfate free) pure Ca(OH)2 mixed with anesthetic solution or saline is placed in the whole canal length until the apex. Note that the canal “disappears” and takes the radiopacity of dentin. b After 3 months, some Ca(OH)2 washed out, and the wide diameter of the canal becomes visible again. If the apical barrier has not formed yet, a new dense Ca(OH)2 is placed again in the canal for 3  months. The final root canal obturation is performed when the natural apical calcified barrier has formed

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a

b

9m

c

..      Fig. 16.57  Calcium hydroxide apexification. a Pre-op radiograph of very immature maxillary permanent right central incisor with a wide-open apex and very thin root walls. Endodontic treatment had been started by another dentist. The canal is gently but thoroughly cleaned, irrigated, disinfected, and packed with Ca(OH)2. b, c After

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..      Fig. 16.58  Artificial apical plug apexification with MTA.  The material is placed apically, a wet cotton pellet is placed next to it, and the remaining root canal is obturated in a later treatment session

Until recently, it was thought that there was no possibility to promote regrowth of vital tissue into infected root canal spaces of teeth with open apexes [155–157]. Now it has been realized that under certain conditions, it is possible not only to heal periapical lesions associated with necrotic and immature teeth but also more interestingly to stimulate tissue growth inside the canal space of these teeth [158, 159]. This is accomplished by reducing the bacterial load, first by thorough irrigation and then by intracanal placement of either a dual or triple mix of antibiotics (metronidazole, ciprofloxacin, and possibly minocycline) or alternatively a Ca(OH)2 dressing for a few weeks [160–163]. Minocycline is not used anymore in the antibiotic mixtures because it causes tooth

9m

d

obtur

e

4 years

9 months of Ca(OH)2 protocol, an apical barrier has formed and is clearly visible. d Trial with a gutta-percha cone to check the apical stop. Full canal obturation is then performed. e At 4-year follow-­up. The tooth is asymptomatic and stable

discolorations. The key to success is to be able to disinfect the canal space and then to create a scaffolding for the ingrowing tissue [164]. Several teams worldwide are working on developing synthetic scaffolds to be placed within the canals. Presently, the scaffolding is created by allowing a blood clot to form at the second appointment, after the disinfecting paste has been washed out by irrigation. An endodontic instrument is then placed through the apex into the periapical tissues to induce bleeding within the root canal. Once a clot has started to organize itself, a double seal is placed in the access cavity, down close to the cervical area. Using a bioceramic material is recommended to cap the blood clot, and then a traditional restoration is placed on top [162]. The success rate of this procedure, where the root end continues to grow and/or mature, is reported between 27% and 55% and the survival rate of the teeth much higher [165–167]. If the tooth does not respond to treatment, then the traditional apexification procedure is still an option. It is important to remember that the response to this revascularization procedure can take months if not years to materialize [167]. Also, the vital tissue obtained so far, at least in animals, is rarely an authentic pulp tissue [92, 168]. That’s why the present procedures should rather be called “revitalization” than “regenerative” procedures (. Fig. 16.59). Post-endodontic considerations for immature traumatized teeth Non-vital immature teeth have thin roots with weak dentine walls and are especially at risk of root fracture at the neck of the tooth [105, 150, 169]. The cervical area of the tooth may be reinforced using etched and bonded composite resin, allowing space, if indicated, for a post [170, 171]. If little coronal tooth structure remains, a fiber  

405 Dentoalveolar Trauma of Children and Adolescents

a

b

c

..      Fig. 16.59  “Revitalization” of necrotic and infected immature tooth. a Pre-op radiograph. The incisor is very immature. b Aspect after the main treatment steps irrigation, disinfection of the canal with a dual antibiotic paste for 3 weeks, creation of bleeding to fill

the canal space, and placement of a hermetic access cavity restoration. c At 4-year follow-up. Some “revitalization” of the pulp canal space has occurred, with calcified tissue formation in some areas

post may be bonded into the root canal. Metallic posts should be avoided. Compared to metal posts, fiber posts have the advantage of some flexibility. If they fail, they are more likely to become decemented rather than cause a root fracture [172]. 3. Endodontic treatment in the presence of inflammatory root resorption As seen earlier in this chapter, calcium hydroxide as an intracanal medication has proven to be an effective method to halt the progression of external inflammatory root resorption (. Fig.  16.53) especially if detected early [104, 173]. Ca(OH)2 paste should be used in a thick, almost dry consistency. It should be renewed at 3  weeks and every 3  months because it may wash out. Treatment should be continued until all signs of inflammatory root resorption have healed and until a normal periodontal ligament width has reestablished. This can take anywhere from 6 to 24 months. The access of the tooth should be temporized with an appropriate restorative material such as IRM™ as it is of upmost importance to keep bacteria away of the canal space.

severe (i.e., in cases of avulsions and intrusions). Several older studies show this [94, 118, 174], and the current knowledge about factors affecting the survival of these teeth has considerably improved in recent years [85, 88]. In particular, teeth treated in compliance with today’s IADT’s Guidelines seem to have an even better chance of survival than those treated years ago [136, 175]. If proper emergency management is provided, as well as later treatment as deemed necessary on follow-ups (such as timely endodontic treatment), the prognosis of injured teeth turns out to be very good. In the case of avulsed teeth, for instance, the most important factor affecting prognosis, apart from extraoral dry time and timely endodontic treatment, has been reported to be the stage of root development. A better survival rate was observed for mature teeth [98]. Certainly, as seen earlier in this chapter, endodontic treatment of immature teeth is quite challenging when compared to mature teeth, but the main reason why their survival rate is reduced is their thin and fragile dentinal walls. Immature teeth tend to fracture easily even to minor impacts occurring repeatedly in everyday life, especially if they developed areas of resorption located cervically [105]. That’s why attempts should be made to prevent those resorptions. Some years ago, the long-­term use of calcium hydroxide has been blamed as a causative factor for immature teeth fractures. The study design of these in in vitro studies was far from ideal though [169]. It’s worth noting that calcium hydroxide apexification

 

16.4  Prognosis of Injured Teeth

Injured mature and immature teeth treated in an appropriate and timely fashion have a good chance of survival, up to 20 years or more and even if the injury was

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has been successfully used (97%) for decades in the treatment of injured teeth [105, 176]. In situations where the prognosis of an injured tooth is deemed dark due to developing ankylosis in a growing child, or due to high risk of tooth fracture (related to fragile dentinal walls or loss of tooth structure due to the presence of resorption areas), it’s advisable to check if the patient will need premolar extraction for orthodontic reasons. In the affirmative, one should consider the possibility of extracting the problematic traumatized incisor, rather than the healthy premolar. Autotransplantation of a premolar to replace the incisor might be a possibility. Proper overall treatment planning and coordination between different dental specialties is then needed (. Fig. 16.60) [177].

mild luxation injuries, such as concussion and subluxation, a 3-month observation time should be sufficient. In moderate to severe injuries, such as extrusion, intrusion, lateral luxation, and replantation of avulsed teeth, a minimum of 6 months to 1 year is advised. In root-fractured teeth, the recommended observation time is 1 year. In crown-fractured teeth, when the dentist is certain that no associated luxation injury occurred at the time of trauma, a 3-month observation time is still advised [179].

Eye Catcher

Traumatized teeth presenting root resorption before orthodontic treatment are at high risk of further resorption as a result of intense orthodontic force application [180]. Thus, no orthodontic treatment should be initiated on teeth presenting apical or lateral radiolucencies or signs of root resorption. The related pathologies should be treated first, usually with endodontic treatment. Only when healing is observed, orthodontic forces may begin to be applied but under careful and frequent clinical and radiographic monitoring every 3  months. Parents should be informed about possible contingencies happening during or after treatment of injured teeth, as complications may occur. Sometimes a treatment paucity or even total orthodontic treatment interruption is necessary for those teeth.

 

16.5  Orthodontic Management

of the Traumatized Dentition

16

The particular orthodontic management of intruded teeth, crown-root fractured, and ankylosed teeth is presented in this chapter within the specific injury types. Orthodontic treatment is so common nowadays, that it often involves movement of anterior teeth with a history of trauma. Before any treatment is initiated, the orthodontist needs to inquire with the patient and his parents if any dental injury occurred, both recently and in the past. Additionally, full mouth periapical radiographs should be taken, not only a panoramic radiograph, in order to make a thorough preoperative evaluation. The orthodontist also needs to take into consideration the impact of orthodontic treatment on long-term prognosis of such traumatized teeth [178]. Orthodontic treatment should always be interpreted as an added trauma to the teeth. Therefore, orthodontic forces should be light and short-acting and aimed at limited goals when moving previously injured teeth. Depending on the severity of trauma, it’s wise to wait before initiating orthodontic treatment. In the case of

a

b

..      Fig. 16.60  Autotransplantation of a premolar. a These avulsed and replanted maxillary central incisors were undergoing severe replacement root resorption at follow-ups. It was decided to use the patient’s premolars to substitute them. b Clinical view 2 weeks after autotransplantation of the immature second maxillary premolars and their splinting in the position of the extracted compromised

From a preventive perspective, increased overjet with protrusion of maxillary incisors is a common predisposing factor for dental injuries in the permanent dentition. It has been reported that an increase from 0–3 mm to 3–6 mm leads to twice as many trauma rates, while if protrusion exceeds 6 mm, incidence triples [14] (. Fig. 16.9). Insufficient lip coverage seems to play a role as well. Preventive consultation with an orthodontist is thus advisable for these patients.  

c

d

e

incisors. c Radiographic view of the premolars 2  weeks after the operation and after the splint had been removed. d One-year follow-­up radiographic examination showing sound progress in apical development. e Reshaping of the premolars into incisor crowns by palatal grinding and composite reconstruction after the end of orthodontic treatment. (Courtesy of Dr. Μ. Duggal)

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407 Dentoalveolar Trauma of Children and Adolescents

16.6  Prevention of Dentoalveolar Trauma

16.6.1  Mouth-guards

Accidents, including road accidents, are a major threat against the physical integrity and life of children. They are the top death cause during the first year of life and a major cause for hospital care and disability in industrially developed countries. Facial and dental trauma is due to various causes, many of which cannot be easily prevented. They happen more often during children’s leisure time and during play [11, 13]. In preschool years, and particularly in early infancy, when balance in movement and perception of danger are limited, there should be no obstacles on the ground, no stairs, furniture, or other hard objects with sharp angles in areas within which children move. Furthermore, athletic activities among children and adolescents have significantly expanded in recent years, particularly related to body contact sports. Injuries occurring during high speed and impact force sports, such as on ice or snow, result in more facial or skull trauma, which may be life-threatening, and require protective equipment, such as a helmet. Lower speed and impact force sports (e.g., basketball) result in dental trauma. Injuries in sports are more frequent than those due to fights or road accidents [181]. The need for educating children, parents, teachers, coaches, and owners of recreational venues in prevention and first-aid management of injuries is self-evident. In the permanent dentition, patients having proclined incisors with increased overjet and insufficient lip coverage tend to suffer more dental injuries. A preventive consultation with an orthodontist is thus advisable for these patients.

A dentist does not only provide treatment but can also assist in preventing trauma consequences by fabricating a mouth-guard. This is a sturdy functional device that protects against dental, periodontal, and supporting alveolar bone trauma. Depending on the sport and the level of involvement in it (professional, amateur), the appropriate type of mouth-guard should be used. A study investigating amateur athletes among newly recruited soldiers in the army, who were issued with free-­of-­charge type II mouthguards, showed that, although very few of them wore the device, users suffered milder dental trauma [182]. A mouth-guard has to meet numerous requirements: It should be resilient, comfortable, odorless, affordable, retentive, and properly fitting; its borders should be smooth and even, it should have the necessary thickness at critical regions, it should not prevent speech or breathing, it should not be cumbersome, and it should be easy to fabricate [183]. No type of mouth-guard fulfils all these requirements, and every type has its own pros and cons. In general, disadvantages have to do with difficulties caused to speech or breathing, with the effect on an athlete’s appearance, with the difficulty of their adaptability to various individuals, their volume, and their cost. The use of commercial mouth-guards prevents intense voluntary exhaling but has no negative consequences on pulmonary ventilation during the athlete’s training. There are three types of mouth-guards. Their advantages and disadvantages are presented in . Table  16.6 [184].  

..      Table 16.6  Advantages and disadvantages of the three basic types of mouth-guards based on Bourguignon and Sigurdsson [184] Advantages

Disadvantages

Type I

+Very low cost +Immediate placement

−Limited size numbers (small, medium, and large) −reduced fit −Lack of retention −Continuous occlusion/bite necessary −Obstruct athlete’s speech/breathing

Type II

+Relatively low cost +Better protection than Type I +Possibility of Refit + Immediate placement

−No absolute fit (better than type I) −Lack of retention, −Continuous occlusion/bite necessary −They are more cumbersome −They loosen easily with use

Type III

+ Good fit and stay in place + Sound retention +They cover the entire dentition +Less discomfort for breathing/speech +More acceptable to athletes +Choice of thickness

−High cost −Increased fabrication time

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55 Type I: Various, commercially available, prefabricated mouth-guards which cannot be adjusted to a specific individual, one or two sizes that are intended to fit most. Some have a “spring” fit and do cover both arches others require the athlete to clench to keep the mouth-guard in place. (. Fig. 16.61). 55 Type II: These are fabricated from a thermoplastic material. They are heat adapted to the teeth, albeit not ideal, by the athlete and can provide satisfactory protection. The right size of mouth-guard is selected and rendered relatively pliable, following the manufacturer’s instructions (by submerging it into very  

hot water). The mouth-guard is then transferred to the mouth, where it is adjusted and fitted while cooling (. Fig. 16.62). 55 Type III: One layer or multilayer custom-made mouth-guards, fabricated by a dentist. They allow any type of adaptation during their fabrication, taking into consideration regions of chronic trauma, dental-mandibular problems and the type of sport. An athlete can enjoy free flow of air during strenuous exercise, while teeth and mandible are protected. This type is ideal for athletes undergoing orthodontic treatment with fixed devices on both jaws (. Fig. 16.63).  

 

One of the most common materials for mouth-guard fabrication nowadays is ethylene-vinyl acetate (EVA). Mouth-guards can be fabricated using different devices and in various colors; this may also be useful, for example, in water polo sports, where, if lost, the mouth-­guards a

b

16

..      Fig. 16.61  Type I – Prefabricated mouth-guards. (With permission [184])

a

b

..      Fig. 16.63  Type III  – Custom-made mouth-guards require an impression. (With permission [184])

c

..      Fig. 16.62  Type II – Heat-adapted mouth-guards. (With permission [184])

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409 Dentoalveolar Trauma of Children and Adolescents

are easily visible at the bottom of the pool. Sound and hygienic maintenance is ensured by keeping the guards in a special case, by avoiding very hot water when cleaning them and by placing them, every so often, in an antiseptic solution. Furthermore, such guards should not be exposed to the sun or high temperatures to avoid warping [185].

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Developmental Defects of the Teeth and Their Hard Tissues Nikolaos Kotsanos, Petros Papagerakis, Haim Sarnat, and Agnès Bloch-­Zupan Contents 17.1

Disturbances in Tooth Number, Size, and Morphology – 416

17.1.1 17.1.2 17.1.3

 Short Introduction to Dental Development – 416 A Causes of Disturbances and Correlations with Overall Health – 420 Clinical Expression of Disturbances and their Treatment – 421

17.2

Malformations of Dental Tissue Structure – 430

17.2.1 17.2.2

T he Structure of Enamel, Dentin, and Cementum – 430 Clinical and Histological Appearance, Etiology, and Diagnosis – 432

17.3

Developmental Discoloration of Dental Tissues – 454

17.4

Conclusion – 456 References – 459

© Springer Nature Switzerland AG 2022 N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry, https://doi.org/10.1007/978-3-030-78003-6_17

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17.1  Disturbances in Tooth Number, Size,

and Morphology

17.1.1

 Short Introduction to Dental A Development

Primary teeth develop from oral ectoderm-derived cells, which differentiate into ameloblasts that form enamel, and cranial neural crest-derived mesenchyme cells, which differentiate into odontoblasts and cementoblasts forming dentin and cementum, respectively. These two cell types (epithelial and mesenchyme) interact to control the entire process of tooth initiation, morphogenesis, and cytodifferentiation [1]. Oral ectoderm-derived epithelial cells first form the dental laminae. Tooth formation begins with the thickening of the dental lamina and its ingrowth into the underlying cranial neural crest-derived mesenchyme at the sixth to eighth week in utero for the entire primary dentition. This folding of the epithelium along with a condensation of the adjacent ectomesenchymal cells leads to the formation of tooth germs or buds. Organized clusters of these cells are called the dental placodes. A very important transient structure named the enamel knot is derived from the dental placodes. The enamel knot functions as a signaling center of epithelial/mesenchymal interactions, which are responsible for tooth morphogenesis. In fact, the enamel knot’s signaling centers will determine the individualized crown shape for each tooth. This is done by controlling the appropriate size and number of cusps by complex mechanisms involving the differential expression of numerous genes including MSX for incisors, BARX-1 for molars, etc., and then going through the morphological cap and bell stages [2, 3] (. Figs. 17.1 and 17.2). Once morphogenesis is completed, the dental crown cytodifferentiation stage starts, during which neural crest-derived ectomesenchymal cells facing the enamel organ differentiate into odontoblasts and subsequently epithelial cells from the inner dental epithelium differentiate into ameloblasts. Both odontoblasts and ameloblasts produce extracellular organic matrix (dentin and enamel, respectively) in the space between them, as they move apart from each other. Almost simultaneously, mineralization of these two tissues with calcium phosphate (hydroxyapatite) starts at the cusps and then proceeds cervically [1]. The permanent teeth develop by further proliferative activity lingual to each primary tooth bud (anterior teeth and premolars) and backward extension (molars) of the dental lamina. Their budding (anlage) starts during the bell stage of primary tooth development, and their formation will begin later, at  

17

about the completion of primary tooth formation or its eruption. This means that formation of the first permanent tooth (first molar) begins at about the 20th week in utero and of the third molars at about the age of 5 years, but traces of mineralized tips of cusps cannot be seen radiographically before birth for the first and before year 8 for the third permanent molar [1]. Like the formation of other organs of the fetus, the histodifferentiation of ameloblasts, odontoblasts, and cementoblasts and the deposition of their matrix are regulated by complex mechanisms [1, 4]. Interaction between epithelial and mesenchymal cells, also between extracellular matrix and cells, and between different types of epithelial and mesenchymal cells is continuous and tightly regulated. The gene regulation of cell differentiation has been examined in animal studies using molecular biology. Advances in molecular genetics have allowed the identification of hundreds of genes that are related to dental developmental disorders. The regulating (signaling) molecules (growth factors) are peptides which are secreted and bind to specific receptors in adjacent cells. These molecules belong to specific families, like bone morphogenetic protein (BMP), fibroblast growth factor (FGF), hedgehog signaling routes, and Wnt families [2, 3, 5]. Their role has been studied in transgenic mice and shown that the inhibition of transcription activity inhibited odontogenesis [3]. In addition to growth factor signaling initially characterized in mice models, the last few years, direct DNA sequencing of patients with genetic traits has discovered an increasing number of genes involved in tooth number, tooth form, and dental structural anomalies (. Tables 17.1, . 17.2, and . 17.3). These genes include almost any type of proteins such as transcription factors, extracellular proteins, adhesion molecules, and even proteins with still unknown functions. Most of these newly discovered genes with key roles in tooth development play also key roles in different organs, but some are only expressed in dental tissues and have only tooth-specific phenotype such as amelogenin mutations causing amelogenesis imperfecta (AI). However, even amelogenin, the so-called “exclusive” enamel protein, might be present in other tissues and organs like the brain [28]. During the morphogenesis of the teeth including their root formation, the dental papilla constantly interacts directly and indirectly with the surrounding periodontal and bone tissues. During the eruption of the tooth, the surrounding cementum and bone tissues undergo continuous remodeling, with resorption in front of the erupting bud and apposition behind it, thus allowing for tooth eruption (see 7 Chap. 10).  

 

 

 

417 Developmental Defects of the Teeth and Their Hard Tissues

..      Fig. 17.1  Dental development from tooth bud stage through to enamel mineralization at cusp tips. (From Bekes K. (Ed) Pit and Fissure Sealants. 2018, Springer. By permission)

Placode

Bud

Signaling centers Wnt Shh BMP FGF Edar

..      Fig. 17.2  Epithelial-mesenchymal tissue interactions and epithelial signaling centers regulating tooth morphogenesis. Epithelial signaling centers express signals of four signal families and Edar, the receptor of ectodysplasin (Eda). The early signaling center in the placode regulates epithelial budding, while the primary enamel knot

Cap

Early bell

Mesenchymal centers

BMP FGF Activin

regulates the shift from the bud to cap stage and then to the bell stage. The secondary enamel knots regulate tooth cusp formation in molar teeth. Reciprocal signals (in green square) are expressed in mesenchyme. Arrows indicate signaling across the two tissues and within the epithelium [3]. (By permission)

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..      Table 17.1  Non-syndromic oligodontia: selected gene mutations responsible for non-syndromic variations in number and shape of teeth Gene

Mutation

Molecule type

Phenotype

MSX1 [6]

M61K and R196P (missense) S105X, Q187X, and S202X (nonsense)

Transcription factor (binds DNA through its homeodomain)

Hypodontia (AD or AR) Oligodontia (AD) Possible cleft palate

PAX9 [7]

K114X (nonsense) L21P, R26W, R28P, G51S, and K91E (missense) G73fsX316, R59fsX177, and V265fsX316 (frameshift)

Transcription factor (binds DNA through its paired domain)

Oligodontia (AD) Molar Hypodontia (AD) Peg-shaped laterals (AD)

AXIN2 [8]

Arg656Stop, 1994–1995insG (LOF)

Wnt signaling regulator

Incisor agenesis (unknown) Associated with Colorectal carcinoma

AD autosomal dominant, AR autosomal recessive

..      Table 17.2  Syndromic oligodontia (most common syndromes) Syndrome

Phenotype

Gene

Protein product

OMIM

Axenfeld-Rieger syndrome [9]

Oligodontia Eye and umbilical defects

PITX2/PAX6

Transcription factor

180,500

Hypohidrotic ectodermal dysplasia

Oligodontia Small peg-shaped teeth Hypoplastic teeth and glands

EDA EDAR EDARΑDD

Signal receptor Signal mediator Transcription factor

305,100 129,490 224,900

EEC syndrome

Ectodermal dysplasia Ectrodactyly Cleft palate

TP63

Transcription factor

129,900 604,273

CLPED syndrome

Ectodermal dysplasia Cleft lip/palate

PVRL1

Cell adhesion molecule (nectin-1)

225,060

Cleidocranial dysplasia

Supernumerary teeth Impaired eruption Deficient bone formation

RUNX2

Transcription factor

119,600

Tricho-dento-osseous syndrome (TDO)

Taurodontism Enamel hypoplasia Hair and bone defects

DLX3

Transcription factor

129,510

Autosomal dominant lacrimo-auriculo-dento-­ digital (LADD) syndrome (149730) [10] and autosomal dominant aplasia of lacrimal and salivary glands (ALSG; 180,920)

Microdontia Oligodontia Irritable eyes Dryness of the mouth Anomalies mainly affecting lacrimal glands and ducts, salivary glands and ducts, ears, teeth, and distal limb segments

FGF10 FGFR2 (176943) FGFR3 (134934)

Growth factor and receptors

602,115

Down syndrome [11]

Mental impairment Stunted growth Macroglossia Oligodontia (mainly in the lower incisors)

Trisomy 21

17

190,685

17

419 Developmental Defects of the Teeth and Their Hard Tissues

..      Table 17.2 (continued) Syndrome

Phenotype

Gene

Protein product

OMIM

ADULT syndrome [12]

Ectrodactyly Syndactyly Excessive freckling Broad nasal bridge Midfacial hypoplasia Lacrimal duct anomalies

TP63

Tumor protein

103,285

Limb mammary syndrome (LMS) [13]

Severe limbs anomalies, Mammary hypoplasia/aplasia Cleft palate and bifid uvula

TP63

Tumor protein

603,543

Ehlers-Danlos (type VII, dermatosparaxis) syndrome [14]

Severe skin and mucosal fragility

ADAMTS2

Proteinase

225,410

Incontinentia pigmenti [15]

Skin hyperpigmentation Peg-shaped teeth Delayed eruption and impaction

IKKα (NEMO)

Transcription factor activator

308,300

Witkop syndrome [16]

Nail dysgenesis

MSX1

Transcription factor

189,500

Apert syndrome [17]

Syndactyly Exophthalmia Hypoplastic midface Class III malocclusion

FGFR2

Growth factor receptor

101,200

Blepharocheilodontic syndrome [18]

Eyelid anomalies Bilateral cleft lip and palate Microdontia with peg-shaped teeth

CDH1 CTNND1

Adhesion molecules

119,580

Charcot-Marie-tooth disease type 2 [19]

Muscle weakness Sensory loss Grinding of the teeth

NEFL

Neuro-­ filaments

607,684

Ellis-van Creveld syndrome [20]

Short limb dwarfism Postaxial polydactyly Partial cleft lip Peg-shaped laterals Conical and microdontic teeth Enamel hypoplasia

EVC1 EVC2

Transmembrane proteins

225,500

Frontometaphyseal dysplasia [21]

Hearing loss Cleft palate Joint contracture

FLNA

Filamin A (actin-­ binding protein)

305,620

Hay-Wells syndrome [22]

Ankyloblepharon Ectodermal dysplasia Cleft palate and/or cleft lip

TP63

Tumor protein

106,260

Johanson-blizzard syndrome [23]

Small nose that appears “beak shaped” Microdontia

UBR1

Ubiquitin protein ligase

243,800

Kartagener’s syndrome [24]

Sinusitis Bronchiectasis Male infertility Enamel hypoplasia Missing lateral incisors

DNAI1 DNAHC11 DNAH5

Dynein protein complex

244,400

Williams syndrome [25]

Cardiovascular abnormalities Mental retardation Malocclusion Taurodontism Pulp stones

Deletion in the long arm of chromosome 7

189,500

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..      Table 17.3  Syndromic hyperdontia (most common syndromes) Condition

Mutation

Molecule type

Phenotype

Cleidocranial dysplasia (CCD)

RUNX2

Transcription factor

Bone dysplasia Defective development of the cranial bones and by the Complete or partial absence of the collar bones Supernumerary teeth

Apert [17]

FGFR2

Receptor

Premature fusion of certain skull bones (craniosynostosis) Syndactyly Supernumerary teeth

Sturge-weber [26]

GNAQ (G protein subunit alpha q)

G protein

Sturge-weber syndrome has three major features: a red or pink birthmark called a port-wine birthmark, a brain abnormality called a leptomeningeal angioma, and increased pressure in the eye (glaucoma) Supernumerary teeth

Crouzon

FGFR2

Receptor

Premature fusion of certain skull bones (craniosynostosis) Hearing loss Supernumerary teeth

Cleft lip

Multifactorial

N/A

Cleft lip Supernumerary teeth

Gardner syndrome (adenomatous polyposis of the colon) [27]

APC

Wnt signaling regulator

Multiple colorectal polyps and various types of tumors, both benign (noncancerous) and malignant (cancerous) Supernumerary teeth

17.1.2

17

Causes of Disturbances and Correlations with Overall Health

Tooth number, size, and shape are determined during the initiation and morphogenesis stages of odontogenesis. These disturbances of the teeth are associated and interrelated. Coexistence of missing (aplasia, agenesis) and small or even conical teeth is often reported in the same patient and his relatives and was termed “continuous variation” by Brook [29, 30]. It seems that an anomaly at an early stage of odontogenesis can lead to complete inhibition or restriction of the formation of the tooth. Such phenomena are often observed in the third molars, second premolars, and upper lateral permanent incisors and are termed “terminal reduction.” The epithelial buds of these teeth are formed last within their group of teeth (incisors, premolars, molars). This indicates that the aplasia is related to a quantitative deficit of the dental placode [31, 32]. The terms used for congenitally missing teeth are hypodontia (1–5 missing teeth), oligodontia (>5 missing teeth), and anodontia (complete agenesis), whereas additional teeth are described by the term supernumerary teeth or hyperdontia. Many of the disturbances in tooth development are attributed to local or systemic environmental causes, while there are some whose etiology remains unclear. Genetically regulated disturbances are caused by gene mutations, and thanks to advances in genetic research, many of these have already been identified [33]. The hereditary transmis-

●

..      Fig. 17.3  Example drawing of transmission pattern in autosomal dominant inheritance of a boy. □, male patient; ○, female patient; ■, affected

sion links of such anomalies need to be recorded at the initial consultation, and a pedigree should be designed as the example shown here (. Fig. 17.3). The majority of gene mutations that have been identified as causes of variations in the number and shape of teeth are related to genes responsible for the transcription of macromolecules of odontogenesis that act at very early stages summarized here for non-syndromic oligodontia (. Table  17.1) and syndromic oligodontia (. Table 17.2).  

 

 

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The main genes associated with tooth agenesis, regardless of the presence or not of a general syndrome, include the MSX1, PAX9, IRF6, AXIN2, WNT10A, EDA, EDAR, and EDARADD genes [3, 33]. As an example, the autosomal dominant trait of hypodontia is caused by gene mutation in MSX1 and PAX9, which are mediators in the interaction of epithelial/mesenchymal cells. Agenesis of the second premolars and third molars is almost always associated with mutations in MSX1. On the other hand, the etiology of hypohidrotic ectodermal dysplasia, which is characterized by severe oligodontia, small peg-shaped anterior teeth, and severe reduction of the hair, nails, sweat glands, and other epithelial appendages, is associated with the loss of function of ectodysplasin (EDA), the signaling molecule that together with the EDAR and EDARADD belongs to the family of tumor necrosis factors (TNF). However, these same genes (EDA, EDAR, EDARADD) are responsible for non-syndromic hypo−/ oligodontia and may not be associated with additional ectodermal symptoms. WNT10A gene, another mediator of the Wnt ­pathway, has also been suggested as a major cause of tooth agenesis. More than half of the patients presenting with non-syndromic oligodontia in a specialized center had bi- or monoallelic WNT10A mutations [34], which means that the mutations in this gene are the most common cause of these types of oligodontia [35]. Furthermore, WNT10A mutations have been identified in a large proportion of patients with oligodontia and mild phenotypes of ectodermal dysplasia. Significant differences are found among the ectodermal dysplasia phenotypes caused by the EDA and WNT10A genes. Those indicate that there are at least two different routes of occurrence [36]. In other cases of non-syndromic oligodontia, there may also be other genetic mutations, such as in AXIN2, an inhibitor of the Wnt signaling pathway [5]. Research has linked genetic background of dental agenesis of this pathway with some forms of cancer. The normal route of Wnt catenin shows such a relation. For example, a strong relationship has been found between the gene AXIN2, tooth agenesis, and the development of colon cancer, suggesting that tooth agenesis may in some cases be a sensitive cancer indicator [8]. This is particularly true for cases of oligodontia without ectodermal dysplasia, where the dentist should inform the physician, in order to suggest to the patient a genetic mutation test of AXIN2 to exclude the possibility of predisposition to cancer. It has also been reported that mutations in the APC gene, another “tumor suppressor gene” of the Wnt pathway, involved in tooth number variations, may be associated with polyps in the colon and osteomas

..      Fig. 17.4  Cleidocranial dysplasia. Supernumerary teeth, delayed eruption, and retention of the primary teeth

(Gardner syndrome) [37]. However mutations in AXIN2 and APC genes are rare. On the other hand, genetic mutations are also found in patients presenting supernumerary teeth as phenotypic traits (. Table 17.3). Among the most common syndromic conditions presenting numerous supernumerary teeth is cleidocranial dysplasia (cleidocranial dysostosis) which is inherited as an autosomal dominant trait on chromosome 6 p21 (. Fig. 17.4). Dysfunction in molecule RUNX2 significantly affects osteoblasts and bone remodeling and the epithelial/mesenchymal cell interactions during early odontogenesis [2]. Typically manifested by underdeveloped or missing clavicles, in severe cases the shoulders can be brought together in the midline. Other signs are delayed closure of the fontanelle, prominent forehead, hypertelorism, multiple teeth, delayed eruption, and retention of the primary teeth.  

 

17.1.3

 linical Expression of Disturbances C and their Treatment

Eye Catcher

The management of dental anomalies and associated rare diseases requires interactions with specialized dedicated centers with long term expertise. In Europe, per definition, rare diseases affect less than 1 in 2,000 persons. Among 7,000 rare mostly genetic diseases, 900 have orodental manifestations. These diseases affect 25 million people in Europe. Expert centers have been identified and certified by national health authorities and plans focused on rare diseases [33]. As examples, one could mention TAKO – Resource center for oral health in rare medical condition in Norway and the Rare disease reference center for rare oral and dental diseases O-Rares in Strasbourg France (see 7 https://www.­orpha.­net/ for a list of centers).  

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17.1.3.1

 ariations in Tooth Number: V Epidemiology and Clinical Phenotypes

In the primary dentition, the incidence of hypodontia is 0.6% and of supernumerary teeth is 0.3% or less. Both hypodontia and hyperdontia appear more frequently in the maxillary lateral incisor region [38], while oligodontia and anodontia occur very rarely in the primary dentition – mainly in cases of ectodermal dysplasia (. Fig.  17.5). Hypodontia in the primary dentition usually leads to missing corresponding permanent teeth [39]. In the permanent dentition, hypodontia is much more frequent, ranging from 2.6% to 11.3%, depending on ethnicity and sample characteristics. Terminal reduction is manifested and includes the third molar, second premolar, as well as the maxillary lateral incisor and mandibular incisors at a prevalence of 4% [40]. In a young Korean population with hypodontia in the high end of prevalence spectrum, mandibular incisors were missing about equally as frequent (34%) as the second premolars [41]. Hypodontia involves usually one to two teeth, is often symmetrical, and is rather more frequently found in girls than in boys [40]. Non-syndromic oligodontia is more rare, while anodontia occurs very rarely in cases of ectodermal dysplasia. Hypodontia and microdontia of the maxillary lateral incisors are related, and they are inherited as an autosomal dominant trait, but knowledge about the exact pathogenetic mechanism is limited [41] (. Fig. 17.6). There are more than 100 syndromes that include missing teeth. Information about these can be found in digital databases such as OMIM (Online Mendelian Inheritance in Man) and ORPHANET. The  

 

a

most common ones, in order of frequency, are Down syndrome, cleft lip and palate, and ectodermal dysplasia. Other less frequent are Rieger syndrome and incontinentia pigmenti (. Fig. 17.6). The prevalence of supernumerary permanent teeth not related to syndromes is about 1.5%. They are more frequently found in boys in the pre-maxilla, mostly near the midline and called mesiodens (see 7 Chap. 10) [42, 43]. They are sometimes multiple hypoplastic supernumeraries found in the form of compound odontomas (see later in this chapter). The presence of one or more forth molars is relatively rare (. Fig. 17.7). In children with cleft lip and palate, supernumerary as well as missing teeth at the cleft area are common. However, in cleft lip and palate, missing teeth may not concern solely teeth in the cleft area but also more distant teeth pointing toward a role of the responsible gene both in palate and tooth development [ 44].  

 

 

zz Treating Children with Missing Teeth

In the primary dentition, there is often no need for treatment, unless aesthetics or function (mastication) is significantly affected, as in cases of syndromic oligodontia. The problem then might also be social, and, for optimized integration of the child in society, prosthesis in the primary dentition would be considered from 3 years onward. Depending on the severity of the deficit, various types of partial dentures can be constructed once child cooperation can be achieved. In the permanent dentition, the treatment plan should have a long-term vision. Orthodontic assessment and treatment should come before any prosthetic solution, particularly in the anterior area. The most common problem is the agenesis

b

17

c

d

..      Fig. 17.5  a Congenitally missing primary mandibular canines resulting in diastemas. b The radiograph confirms their agenesis. c, d Agenesis of the right and a large (fused?) left maxillary primary inci-

e

sor. e Anodontia of a 5.5-year-old boy with ectodermal dysplasia. (e: courtesy Dr. E. Kotsiomiti)

423 Developmental Defects of the Teeth and Their Hard Tissues

a

b

c

d

e

f

..      Fig. 17.6  Agenesis of permanent teeth. a, b Hypodontia in a 10-year-old boy and his father. Both have aplasia of a permanent lower incisor. c, d Non-syndromic oligodontia of a 10-year-old girl. Agenesis

of 11 permanent teeth (8 premolars, maxillary canines, and right lateral). Microdontia of her left lateral incisor. e, f Syndromic oligodontia in a girl with incontinentia pigmenti. Clinical and radiographic appearance

of upper lateral incisors. One solution could be aligning the canine into the space of the lateral and then modifying the shape of the canine to mimic a lateral incisor [45] (. Fig. 17.8). However, if the orthodontic assessment requires maintaining the space of the lateral incisors (see 7 Chap. 11), an intermediate prosthetic solution can be offered by bonding an artificial lateral incisor in a removable appliance or directly onto the adjacent teeth (7 Fig. 13.50). An implant solution may follow growth  

 

 

..      Fig. 17.7  Panoramic radiograph of a 22-year-old with four supernumerary molars (fourth permanent molars). The patient complained of pressure during eruption of the third molars. (Courtesy Dr. V. Boka)

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a

b

..      Fig. 17.8  Shape correction by composite built-up of maxillary canines after orthodontic space closure. It was intended to mimic missing lateral incisors

completion in young adulthood. Because of limited evidence, these clinical options are currently based on case reports [46]. Severe oligodontia and conical anterior teeth are often part of different expressions of ectodermal dysplasia and contribute to a reduced height of the alveolar process. The appliance chosen for reinstatement of aesthetics and function will require adaptation to the growing oral structures. A multi-disciplinary approach including pediatric dentists, orthodontists, prosthodontists, periodontists, and others is of advantage. zz Treating Children with Supernumerary Teeth

17

In the primary dentition, there is usually no need for intervention, unless the treatment plan requires an extraction of the superfluous tooth/teeth. The timing of the extraction is of great importance, especially when it comes to extraction of a supernumerary permanent tooth. It depends mainly whether or not it is performed around the eruption time of the permanent tooth. Waiting for the supernumerary tooth to erupt can reduce the degree of difficulty of the extraction (. Fig. 17.9). Impacted supernumerary teeth that are not expected to erupt, such as inverted mesiodens, require exact localization with various radiographic means, such as CBCT.  Usually, a surgical flap is prepared under local anesthesia to carefully access and extract the tooth (. Fig. 17.10). In cases where surgical exposure of the tooth requires bone removal, care should be given to the  

 

..      Fig. 17.9  a The presence of two supernumerary primary maxillary lateral incisors. Extraction is only indicated for the one erupted in the palate. b Supernumerary primary maxillary incisor (mesiodens) aligned in the dental arch

periodontal tissues of adjacent teeth, because any minor damage might result in ankylosis (see also 7 Chap. 10).  

17.1.3.2

 ariations in Size, Shape, V and Morphology of Teeth

Eye Catcher

Tooth type, size, and morphology are genetically determined, but genetic factors may control mineralization, too, as seen, for example, in certain types of amelogenesis imperfecta. Environmental factors however may play their role in the morphology and shape of the teeth and beyond those importantly disturb their mineralization. Environmental factors can cause injuries to the developing tooth bud through direct trauma; deregulation of biological mechanisms by high fever, inflammation, drugs, and chemicals; radiotherapy of adjacent tissues; effect of cytotoxic agents; and other serious insults.

zz Variations in Size

Abnormal tooth size may be local or generalized. Microdontia is a relatively common finding. It may

425 Developmental Defects of the Teeth and Their Hard Tissues

a

b

d

c

e

..      Fig. 17.10  a Over-retention of the primary right central incisor in a 7.5-year-old girl is being investigated radiographically. b The presence of a mesiodens in a labio-palatal direction inhibits the successor’s eruption. c Eight months following surgical removal of the mesiodens, the impacted central incisor descent is slow, possibly

impeded by the already erupted lateral. This indicates its traction along with space regaining. d This is now possible with a partial wire arch. e A patient at a 3-year recall. No further orthodontic treatment was necessary

Teeth with microrrizia (short roots) occur rarely, e.g., in some cases of osteopetrosis or as a consequence of radiation or chemotherapy during root formation (. Fig.  17.13), and such cases need differential diagnosis from dentin dysplasia type I (rootless) or molar incisor malformation (MIM) described later in the chapter. Another type is known as short root anomaly (SRA), characterized by short roots, more so in the incisors. Other teeth may exhibit the abnormality, and, rarely, there are generalized cases. The root/ crown ratio may be 1:1 or lower with crown anatomy and periodontal tissues appearing normal. SRA was quite common (1.3%) in a young Finnish population [47]. There is a poorly understood genetic background. Patients with SRA did not exhibit a significant change of root length after orthodontic treatment when compared to controls [48].  

..      Fig. 17.11  Generalized mild microdontia of a 12-year-old girl, particularly prominent in the premolar area producing diastemata

affect a group of the teeth (. Fig. 17.11), but more usually individual teeth, mainly the maxillary lateral incisor (incidence 0.3% for primary and 1% for permanent ones) [8]. In this case the crown is narrower and often conical. Generalized microdontia is found in some syndromes, e.g., Down syndrome, pituitary short stature, and ectodermal dysplasia. Generalized macrodontia is found rarely associated with syndromes, e.g., KGB, otodental, or Ekman-Westborg-Julin (. Fig.  17.12). As an individual finding, if ever present, it may resemble a double tooth (gemination or fusion), which is a common dental anomaly.  

 

zz Variations in Shape/Morphology

Apart from the third molars, the permanent tooth that presents diversities in shape with greater frequency is the maxillary lateral incisor. Another variation that occurs in both dentitions, usually in the palatal surface of maxillary central incisors, is the talon cusp. This could appear as an isolated trait or be part of a syndrome, like the Rubinstein-Taybi, in which it represents a hallmark diagnostic trait. Depending on its size, a talon cusp may

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..      Fig. 17.12  a Generalized macrodontia in a 10.5-year-old boy with Ekman-Westborg-Julin syndrome. b Complete absence of space for the erupting canines. He needs orthodontic consultation for premolar extraction

a

b

a

b

..      Fig. 17.13  a Stunted root formation (at age 15). At age 8.5 years, the patient was diagnosed with leukemia and received chemotherapy. b A 12-year-old girl with generalized short root anomaly. The first

interfere with occlusion (. Fig. 17.14). The Carabelli’s cusp located on the palatal surface of the upper first permanent molars is very common causing little problems. Other extra cusps should be suspicious for dysplasia (. Fig. 17.15). Dens invaginatus is the result of the inner enamel epithelium submerging in the underlying mesenchyme. The folding of enamel within dentin has usually a tubular form which may be limited to the crown or might reach the root and create conditions for bacterial invasion and pulpal infection. It affects more often lateral incisors; possible suspicion from altered size, the presence of prominent palatal cingulum, or other surface defects is checked by tactile and radiographic examinations for diagnosis (. Fig.  17.16). Taurodontism may occur in both dentitions as a rare dental anomaly, it is however more commonly found in some syndromes. The underlying mechanism is related to late invagination of Hertwig’s epithelial root sheath, which is responsible for root formation. Radiographic examination shows long pulp chambers with their floor in a more apical position so that the short roots’ appearance resembles a bull’s head (. Fig. 17.17). The descriptive term “double teeth” includes the fusion of two or more tooth germs and the gemination of a normal with a supernumerary tooth or the incomplete division of a tooth bud (. Fig. 17.18). The

molars are unaffected, while maxillary laterals have near-­terminal root resorption

 

a

b

 

17

c

d

 

..      Fig. 17.14  a, b Talon cusps on the palatal surface of primary maxillary central incisors. During tooth eruption talon cusps may require periodic grinding. b Their radiograph shows particularly wide root canals. c Big talon cusps in the palatal surface of the permanent maxillary central incisors in a 10-year-old boy interfere with occlusion. d The radiograph confirms normal roots

 

 

i­ncidence of double teeth is more common in the anterior area of the primary dentition in Caucasians (0.7 to 1.6%), and there is a high probability (20–75%) of

427 Developmental Defects of the Teeth and Their Hard Tissues

a

b

c

..      Fig. 17.15  a One year after sealing this seemingly intact second permanent molar, the patient complains of pain at biting. b The radiograph shows apical periodontitis. c In drilling for endodontic

a

treatment, a large void in the dentin (arrow) is thought as infection channel prior to sealing. The anomalous mesio-buccal cusp should have raised suspicion

c

b

..      Fig. 17.16  a Invagination of mandibular lateral incisor with pulp necrosis and a fistula in a 10-year-old boy. b Lingual aspect. c The radiograph shows an anomalous wide root with enamel submergence

a

a missing permanent successor [49]. The crown may be twinned or simply very wide and thus be wrongly perceived as isolated macrodontia (. Fig. 17.19). The pulp chamber is usually one large, but in case of fusion, there may be two separate chambers. Differentiation between gemination and fusion and diagnosis of macrodontia and Talon cusp are carried out also by radiographic examination and comparison to the contralateral tooth. Dilaceration is a sharp angulation in the cervix, root, or crown of a permanent tooth. It is most commonly caused by trauma to the corresponding primary tooth, while the permanent one is about completing crown formation. Odontomas refer to the creation of a dental hamartoma or tumor of unknown etiology. It may be extra dental formation(s) or a traumatized developing tooth germ. It occurs mainly in the permanent dentition; their size varies from few millimeters to 1 or 2 centimeters and usually inhibits the eruption of one or more teeth. It appears in the form of compound odontoma composed of multiple smaller supernumer 

b

c

..      Fig. 17.17  a Taurodontism of primary mandibular molars in a 6-year-old with one successfully pulpotomized. Elongated pulp chambers in expense of root length and very late formation of successor premolars. b, c Taurodontism of the first permanent molars and maxillary primary molars in a 9-year-old with amelogenesis imperfecta

17

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N. Kotsanos et al.

a

b

c

..      Fig. 17.18  a Fusion of maxillary lateral with a supernumerary tooth in a 3-year-old boy, with advanced caries in the fusion line. b Radiograph showing the fused root ending in two apices. c Restora-

tion with composite inhibits further caries in the fusion line and improves aesthetics in the primary dentition

b

a

17

c

..      Fig. 17.19  a Abnormally wide left permanent maxillary central incisor of this 7-year-old appears as a macrodont. Its incisal edge has one more mamalon than usual. b The root does not reveal signs of fusion. c Wide mandibular central incisors in a 5-year-old boy. d Lin-

d

gual aspect reveals fusion with the respective supernumerary teeth. The course of cervical line and the exogenous pigmentation in the teeth “mid-line” support this diagnosis; a radiograph can verify it

429 Developmental Defects of the Teeth and Their Hard Tissues

..      Fig. 17.20  a, b Compound odontoma located palatally to maxillary central incisor of a 7-year-old girl, merely affecting its eruption path. c The eight surgically extracted supernumerary microdonts. d Complex odontoma in an 8-year-old girl prevents eruption of mandibular left first permanent molar. Its eruption occurred spontaneously after extraction of the odontoma with local anesthesia

a

b

c

d

ary teeth or in the form of complex odontoma, which is characterized by irregularly mixed hard dental tissues or a combination of both called composite odontoma (. Fig. 17.20). Many other very rare forms of dental anomalies have been described that it is not intended to present here, and their etiology may be unknown. Just an example is an exophytic hard dental tissue growth observed in otherwise well-formed mandibular incisors [50].  

a

zz Restoration of Dental Anomalies in Size, Shape, and Morphology

In many cases, teeth with size and shape variations may be modified by cutting and/or building with composite resin to restore or improve their shape. Peg-shaped lateral incisors are a typical example (. Fig. 17.21) just as was described earlier for altering the shape of maxillary permanent canines to mimic lateral incisors (. Fig. 17.8). In the case of talon cusp, which usually contains a pulp horn, grinding is done gradually, e.g., every 3 months, to allow the formation of reparative dentin and avoid pulp infection and necrosis. Drilling deep invagination should be carefully planned to avoid pulp exposure. The success of a possible endodontic treatment depends on the complexity of the invagination and the access to the root canal. Some cases are particularly difficult and end up in extraction. Early sealing of suspicious palatal pits of incisors may prevent carious complications. In case of asymptomatic double primary teeth, there is no need for any intervention apart from covering the dysplastic fissures for caries prevention. If there are symptoms, extraction is preferred. In case of permanent  

 

b

..      Fig. 17.21  a Hypoplastic “peg-shaped” lateral incisors of a 15-year-old girl. b Reshaping with composite resin restoration in a strip crown with no tooth preparation to meet her aesthetic demand

17

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N. Kotsanos et al.

double tooth, if the shape of the pulp chamber permits it, endodontic treatment is indicated, provided that an aesthetic restoration, either conservative or prosthetic, can follow. The sharp angulation in dilaceration often results in impaction of the tooth. If possible, the tooth is surgically exposed and guided into the correct position in the dentition [51] (. Fig. 17.22). Surgical removal of odontomas is usually carried out under local anesthesia. In young children, nitrous oxide inhalation or some other kind of sedation will aid child cooperation.  

17.2  Malformations of Dental Tissue

Structure

17.2.1

 he Structure of Enamel, Dentin, T and Cementum

Enamel, dentin, and cementum are three of the body’s mineralized tissues. Enamel is of epithelial origin and covers the crown of each tooth. In contrast, dentin and cementum are of mesenchymal origin. Dentin forms the bulk of the tooth and extends within both the crown and root. It is of yellowish tint, in contrast to the much whiter and harder enamel. Cementum is deposited only in the root area. Each tooth is anchored onto its socket (alveolar bone) by the periodontal ligament (PDL) that connects cementum to the alveolar bone through s­ pecialized made-of-collagen fibers [52]. Eye Catcher

17

Enamel, dentin, and cementum contain about 96%, 70%, and 50% (by weight) inorganic minerals, respectively, mostly calcium and phosphate salts, such as hydroxyapatite and others, as in other calcified tissues in the body [53]. Their organic matrices are different. The ameloblasts that are derived from ectoderm produce mainly amelogenin, enamelin, ameloblastin, kallikrein, and other proteins. The odontoblasts, originating from mesenchyme (ectomesenchyme neural crest), produce mainly collagen type 1 and some non-­ collagenous materials such as mucopolysaccharides. The apposition of the matrix occurs between the ameloblasts and odontoblasts as they keep retreating from the dentino-enamel junction. The ameloblasts end up at the surface of the rod-structured enamel they had produced. The odontoblasts having left behind the dentinal tubules (that contain their dentinal processes) remain at the periphery of the pulp and continue to function throughout the life of the tooth pulp, producing secondary and tertiary dentin depending on the stimuli [1] (. Fig. 17.23).  

At the formation of the organic substrate, mineralization plays an essential role with simultaneous incorporation of inorganic minerals at about 30%. Then, a period of maturation follows. This is a period of slower (lasting several months to a few years) completion of mineralization by removal of the remaining matrix proteins by proteases and replacement by minerals. The process advances from the cusps to the cervical margin of the tooth and right down the root. Cementum and periodontal ligament are essential for root formation and tooth eruption. Cementum is an avascular mineralized tissue that covers the entire root surface. It is the interface between the dentin and the periodontal ligament and contributes to periodontal tissue repair and regeneration after damage. The organic extracellular matrix of cementum contains proteins that selectively enhance the attachment and proliferation of cell populations residing within the PDL space [1]. All dental mineralized tissues are formed in a circadian rhythm, which in light microscope sections are seen as curved incremental lines, called after Retzius in enamel and von Ebner in dentin. In the enamel of primary teeth and sometimes also in the bucco-mesial cusp of the first permanent molar, an accentuated incremental line can be seen that corresponds to the time of birth which leaves a record of the change from intra- to extra-­uterine life – the neonatal line [54] (. Fig. 17.24). Its importance is that it helps estimate the timing of events in the child’s life. In forensics, it allows to decide if a child was born alive. Formation of enamel and dentin is circadian, characterized by daily repeated activity that controls cell morphology, gene expression, secretion, and degradation/removal of the proteins. All secretory, mineralization, and maturation stages are of vital importance for the final product and are regulated by relevant genes. As a result of differences in the circadian rhythm profile, the thickness and hardness of the enamel can vary greatly; this will affect the susceptibility of the tooth to caries, abrasion, and breakdown [53, 55]. Malformations in the structure of both hard tissues may occur due to disorders during tissue differentiation, formation, mineralization, and maturation stages. They are associated with many causative factors, environmental and/or genetic. A mild disturbance may be seen in light microscopy as an accentuated line or if more severe as a hypoplastic defect or opacity. These insults may be chronologically associated with possible causative events and assist diagnosis.  

17.2.1.1

Mineralization Chronology of the Teeth

Despite its variation, chronology of odontogenesis is always described as the mean average of observations and shown in . Fig.  17.25. The mineralization of the crown of the primary tooth starts from the cusps in the first half of the fourth month in utero until the middle  

431 Developmental Defects of the Teeth and Their Hard Tissues

b

a

c

d

..      Fig. 17.22  a Maxillary central incisor dilaceration in a periapical radiograph. b The CBCT gives a three-dimensional spatial relationship of the dilacerated incisor. c, d Traction through orthodontic

treatment made aligning possible [51]. (By permission from Am J Orthod Dentofacial Orthop)

of the fifth month in utero (second molars). The crowns are completed during the first year of life, during the first months for the incisors and the last months for the canines and second molars. The formation of roots is completed at the age of 1.5–3 years (. Table 17.4). The mineralization of the first permanent molars and incisors (excluding the upper lateral) begins roughly at birth,

while canines and the upper lateral incisors start to mineralize at the start and the end of the first year, respectively. Premolars and second molars mineralize between the age of 2 and 4 years (delays for the second premolars are frequent), and third molars between the age of 8 and 13 years (. Table 17.5). The completion of mineralization of the crown takes about 5–7 years, while the roots

 

 

17

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N. Kotsanos et al.

require about equal time, with the pace of mineralization and ultimately its duration being greater in the teeth formed later (like the second molars and premolars). Girls are usually about 6 months ahead of boys in completing mineralization of the teeth. The figure show-

a

b

ing the stages of the mineralization of the teeth in the panoramic radiograph is useful in calculating dental age. 17.2.2

Clinical and Histological Appearance, Etiology, and Diagnosis

A detailed clinical examination and history-taking help diagnose the type of dental defect and deliver appropriate treatment, possibly by multi-disciplinary approach with other health professionals if a systemic disorder is suspected (. Table 17.6).  

17.2.2.1 1 μm

..      Fig. 17.23  The start of enamel formation in a mouse tooth in the transmission electron microscope. a Ameloblast is located on the upper left side. Collagen fibers (CF) with characteristic vertical stripes. b Right below, enamel rods are in connection with collagen of predentin and the cellular membrane of the ameloblast, where mineralization is about to start [53]. (By permission)

a

 evelopmental Dental Defects D with Environmental Origin

Developmental defects of enamel can be manifested as reduced matrix formation, causing reduced quantity of enamel (hypoplasia), or as loss of its translucency (seen as opacity) and hardness. Both can be caused by systemic or local causes. The size and location of the defects will depend on the severity, duration, and time of the insult, i.e., the stage of enamel development at that time. If an

b

17

..      Fig. 17.24  a Photomicrograph of hard longitudinal tooth section showing the neonatal line (NNL) [54]. (By permission). b Drawing of human primary incisor showing the neonatal line (P pulp, D dentin, E enamel)

17

433 Developmental Defects of the Teeth and Their Hard Tissues

14 12 10 32 24 16 8 0

8

0 8 16 24 32

0

6 4 2 0

2 4

Permanent teeth (years)

Primary teeth (months)

..      Fig. 17.25  The chronology of the formation/mineralization of all teeth (except for the third permanent molars) appears on the left (in months) for primary teeth and on the right (in years) for permanent teeth (0 is birth time). The curved lines on the root relate to the root length at eruption. Tooth length is proportional to duration of its formation. Primary teeth are light blue in color. Tooth parts at the bottom signify the formation stage at birth time

6 8 10 12 14

..      Table 17.4  The chronology of mineralization and eruption of the primary teeth

Tooth

Start of mineralization (intrauterine week)

Crown completion (age in months)

Tooth eruption (age in months)

Root completion (age in years)

Maxilla

Mandible

Maxilla

Mandible

Maxilla

Mandible

Maxilla

Mandible

21/2

10

8

11/2

11/2

Central incisor

14th

14th

11/2

Lateral incisor

16th

16th

21/2

3

11

13

2

11/2

Canine

17th

17th

9

9

19

20

31/4

31/4

First primary molar

15th

15th

6

51/2

16

16

21/2

21/4

Second primary molar

19th

18th

11

10

29

27

3

3

..      Table 17.5  The chronology of mineralization and eruption of the permanent teeth Start of mineralization

Completion of the crown (age in years)

Eruption (age in years)

Completion of the root (age in years)

Tooth

Maxilla

Mandible

Maxilla

Mandible

Maxilla

Mandible

Maxilla

Mandible

Central incisor

3rd month

3rd month

4½

3½

7½

6½

10½

9½

Lateral incisor

3rd month

3rd month

5½

4

8½

7½

11

10

Canine

4th month

4th month

6

5½

11½

10½

13½

12½

First premolar

20 months

22 months

7

6¼

10½

10½

13½

13½

Second premolar

27 months

28 months

7½

7½

11

11½

14½

15

First permanent molar

32nd week in utero

32nd week in utero

4½

3½

6½

6

10½

10½

Second permanent molar

27 months

27 months

7½

7½

12½

12

15½

16

Third permanent molar

8 years

9 years

14

14

20

20

22

22

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N. Kotsanos et al.

..      Table 17.6  Hereditary dental hard tissues defects (most common) Condition

Phenotype

Gene

Protein product

OMIM

Amelogenesis imperfecta type IA [56]

Hypoplasia, hypomaturation dose dependent

AMELX (X-linked)

Amelogenin, enamel matrix protein

301,200

Amelogenesis imperfecta type IB

Hypoplasia Dose dependent Severe hypoplastic pitted enamel with grooves

ENAM (AD)

Enamelin matrix protein

104,500

Amelogenesis imperfecta type IIA1

Hypomineralized pigmented enamel

KLK4 (AR)

Maturation stage enamel proteinase

204,700

Amelogenesis imperfecta type IIA2

Hypomineralized pigmented enamel

MMP20 (AR)

Enamel proteinase (secretory stage)

612,529

Amelogenesis imperfecta type IIA3

Hypomaturation, grossly opaque enamel leading to discoloration and breakdown

WDR72 (AR)

Membrane trafficking protein (endocytosis)

613,211

Amelogenesis imperfecta type IIA4

Hypomaturation AI

C4ORF26 (AR)

May encode an extracellular matrix acidic phosphoprotein

614,832

Amelogenesis imperfecta type IIA5

Hypomaturation AI

SLC24A4 (AR)

Na/K exchanger

301,201

Amelogenesis imperfecta type III

Localized or generalized hypomineralized enamel Dose dependent

FAM83H (AD)

Not characterized

130,900

Amelogenesis imperfecta type IV; AI4

Hypoplastic AI with taurodontism

DLX3 (AD)

Transcription factor

104,510

Amelogenesis imperfecta and gingival fibromatosis syndrome

Generalized hypoplastic and failure of tooth eruption, gingival hypertrophy

FAM20A (AR)

Not characterized

614,253

Shields type I-DGI-I [57]

Osteogenesis imperfecta Brown to blue discoloration and attrition in both the deciduous and permanent dentitions Pulpal obliteration The degree of expressivity is variable

COL1A1 (AD) or COL1A2 Mutations can reduce the amount of collagen (less severe) or produce defective collagen (more severe phenotype)

Collagen

125,490

Shields type I-DGI-II [58]

Opalescent dentin Pulpal obliteration Bulbous crowns Discoloration in both dentitions

DSPP (AD)

Dentin sialophosphoprotein

125,420

Enamel

17

Dentin

17

435 Developmental Defects of the Teeth and Their Hard Tissues

..      Table 17.6 (continued) Shields type I-DGI-III (Brandywine isolate) [ 59]

Multiple pulp exposures in the deciduous teeth Bell-shaped permanent teeth Early abscess Shell teeth

DSPP (AD)

Dentin sialophosphoprotein

125,500

Dentin dysplasia type I (DD-I) [ 60]

Permanent and deciduous teeth crowns have normal shape and color in most cases Diminished root development with unusual mobility and early exfoliation Periapical radiolucencies in non-carious teeth

SMOC2 (AD)

–

125,400

Dentin dysplasia type II (DD-II) [61]

Dentin dysplasia II is distinguished from DGI-II because the permanent teeth are normal in color but show “thistle-tube pulp chambers” and pulp stones on radiographs

DSPP (AD)

Dentin sialophosphoprotein

125,420

Tricho-dento-­ osseous (TDO) syndrome [62]

Taurodontism Enamel hypoplasia Kinky, curly hair at birth Increased thickness and density of the cranial bones

DLX3 (AD)

Transcription factor

Amelogenesis imperfecta (type IV; AI4) [63]

Hypomaturation-hypoplastic AI type Taurodontism

DLX3 (AD)

Transcription factor

104,510

Cleidocranial dysplasia [64]

Supernumerary teeth Impaired eruption Deficient bone and cementum Formation

RUNX2

Transcription factor

119,600

Epidermolysis bullosa (several)

Enamel hypoplasia Cementum dysplasia Taurodontism

PLEC1 COL17A1; LAMA3; LAMB3; LAMC2; ITGB4

Intermediate filament-binding Components of hemidesmosomes

226,650 226,670 226,700 226,730

Hypophosphatasia [65]

Increased urine phosphoethanolamine bowing of long bone Bony fractures Cementum hypoplasia or aplasia Premature exfoliation of primary teeth (around age 3–4 years old)

ALPL

Membrane enzyme that converts pyrophosphate to phosphate

241,510

Gnathodiaphyseal dysplasia

Various amounts of cementum-like calcified mass are found in x-rays

ANOCTAMIN 5;(ANO5)

Cemento-osseous dysplasia

It is a benign condition of the jaws that may arise from the fibroblasts of the periodontal ligaments it is most common in African-American females

Unknown

Cementum hypoplasia

Cementum hyperplasia 166,260

436

17

N. Kotsanos et al.

insult occurs at the initial formation phase of the organic substrate of the enamel, it can cause hypoplasia, i.e., quantitative deficit of enamel. The enamel can be thinner or of relatively normal thickness but with pits or grooves. If it affects mineralization, either initial or late stage, the result would be hypomineralization or hypomaturation, respectively, i.e., qualitative defect of enamel with loss of its translucency. In hypomineralization there is usually a more severe deficiency in minerals than in hypomaturation resulting in softer less protective enamel. The opacities may be diffuse or well demarcated. Literally speaking, these terms are clinical as they are observed visually, while the terms hypomineralization and hypomaturation are histological ones despite they are often being used interchangeably. The DDE (Developmental Defects of Enamel) Index was proposed by the International Dental Federation (FDI) to distinguish and epidemiologically record these developmental defects of enamel, namely, 1) hypoplasia, 2) diffuse opacities, and 3) demarcated opacities. There are however other means or indices for classifying some defect entities like amelogenesis imperfecta or molar incisor hypomineralization (see later in the chapter). Histological examination with a polarizing microscope shows that the appearance of hypomineralized enamel under the microscope is not very different than enamel demineralized by the carious process, i.e., it is porous and opaque. Thus, other clinical characteristics like the topography are important for differential diagnosis. Hypomineralization opacities may be white or yellowish to brown. Discoloration may increase in time, due to degradation of the organic components and/or the influx of pigments from the oral environment. After tooth eruption, severely hypomineralized enamel may be broken down by mastication forces (post-eruptive breakdown). This is an acquired finding and may not be mistaken as hypoplasia. The distinction is based on the rounded defect boundaries in the case of hypoplasia. Opaque enamel adjacent to a hypoplastic defect is not uncommon and indicates more lasting disturbance, ­initiated at the formation stage of enamel. The medical history is important for diagnosis of developmental disturbances, i.e., maternal health during pregnancy, perinatal period events, and child health in the infantile period. Any disturbance, like high fever, sickness, or use of certain drugs, can be a contributing factor to the defect, if it disturbs ameloblast function and mineralization, so the child’s medical history should also be accurately recorded. Type of birth, full term or premature birth, whether intubation was necessary, complications during childbirth, breastfeeding, fluoride supplementation, and past serious illnesses or high fever are important notes of history-taking. Radiographic findings, other relevant findings in the hair or nails, and

searching for similar defects in first-degree relatives may be very useful for diagnosis [66]. A single-affected tooth usually signifies a local cause, a group of symmetric teeth affected a systemic environmental (chronological) one, and when whole dentitions are affected (primary and permanent) signifies a genetic cause. Systemic defects of environmental origin often involve the enamel as the ameloblasts are considered sensitive to low oxygen pressure and to high body temperature. At birth, for example, the normal but sudden change in diet and oxygenation is being recorded in enamel  – and dentin  – of primary teeth with the neonatal line. Difficult or premature birth/low birth weight of the infant might cause accentuation of that line [67]. Clinically apparent developmental dental defects caused by environmental reasons may occur throughout the course of tooth formation, before, during, and after birth. After the age of 7, mineralization and maturation of all crowns are expected to be complete, apart from the third molars (. Fig. 17.25). When the causes are systemic, there would usually be relatively symmetrical defects in all teeth developing during the time of the insult. When the causes are local, they involve a single region or a single tooth. If the cause, either systemic or local, acts for a given period, it may affect only a part of the crown of the tooth. Knowing the time of the formation of all teeth, a clinician can figure out the time and inquire for the specific cause.  

zz Molar Incisor Hypomineralization (MIH)

Molar incisor hypomineralization (MIH) affects the enamel of one or more first permanent molars and usually the incisors, too. MIH is the most common qualitative, developmental disorder of the enamel. The crown of the first permanent molar erupts with irregular, well-­ demarcated, opaque discolored areas (hypomineralized enamel). At the time of eruption, the tooth surface is believed to be intact. With time, depending on the severity of hypomineralization, progressive discoloration and/or post-eruptive breakdown (PEB) of enamel may occur [68, 69] (. Fig. 17.26). The consequent increased plaque accumulation often causes severe caries, leading to rapid crown destruction. In the past high caries era, molars with severe MIH became heavily carious very quickly, often resulting in extraction. Diagnosis was difficult and escaped attention (. Fig. 17.27), but, as the prevalence of dental caries in children and adolescents became significantly reduced, MIH came to be easily recognized. Epidemiology finds prevalence varying greatly throughout the countries between 3.5 and 40% with a mean world average of 14.2%, as suggested by a meta-analysis [70]. The highest has reported in countries of Northern Europe and Brazil, but this is constantly updated as new reports are increasingly published (. Fig.  17.28). Most cases  

 

 

437 Developmental Defects of the Teeth and Their Hard Tissues

are mild, and more severe forms of MIH with enamel breakdown accounted for 13% in 8-year-olds and significantly more, i.e., 35%, in 14-year-olds of all MIH cases in one of those studies [69]. a

b

The typical appearance of MIH involves mainly the first permanent molars and, in at least half of the cases, the permanent incisors. These 12 teeth are frequently mentioned as the index teeth for MIH.  The lesions in incisors cause mostly aesthetic concerns and present breakdown infrequently. Those in the molars can cause significant destruction, pain, and functional problems. Microscopically the pulp shows signs of hyperemia and mild inflammation, probably due to the invasion of bacteria and bacterial products through the porous enamel and via the dentinal tubules [71]. These histological findings in the pulp might explain the intense sensitivity of the affected teeth to thermal and osmotic stimuli, which tend to drive children to avoid brushing, reinforcing the vicious caries cycle, and are responsible for the difficulties in reaching adequate anesthesia levels during restoration.

c Eye Catcher

The appearance of MIH-type lesions in primary molars  – in the second one in particular, hence the acronym HSPM, hypomineralized second primary molar  – is quite common, about half the MIH ­prevalence. Its severe form has been recognized as the cause for the large, atypical, carious cavities of these teeth (. Fig.  17.29). The relationship between the occurrence of HSPM and MIH suggests a shared cause and indicates that clinically the first can be used as a predictor for the latter [72]. Usually less severe MIH-type defects may be found in any other permanent teeth with prevalence per tooth compared to that in incisors (. Fig.  17.30). While severe defects are rare, opacities often appear less well demarcated in premolars and second permanent molars [73].  

..      Fig. 17.26  Severity examples in MIH. a Demarcated opacity of white and brown color in a newly erupted molar (mild MIH but with the potential to become severe with time). b Severe MIH at newly erupted molar with breakdown becoming carious. c Demarcated white opacity (mild form) in a central incisor. MIH severity of the child is determined by the worst affected tooth

 

..      Fig. 17.27  Three mandibular molars of this 8-year-old with severe MIH have become heavily carious. The same is true for one of the hypomineralized second primary molars (HSPM)

17

438

N. Kotsanos et al.

..      Fig. 17.28  Histogram based on MIH prevalence reports in the literature until 2013. In some countries a second or third study (in red and green, respectively) had been conducted with the majority of studies being in European countries (left half of the horizontal axis) until that time

a

17

b

c

d

..      Fig. 17.29  a, b Hypomineralized primary molars and caries. Radiolucent dentinal lesions on both mandibular right molars are due to caries, but the clinical view suggests lesions are developed on a HSPM background. c Brown opacity (still mild MIH) in a maxil-

lary second permanent molar. d Mandibular second permanent molar with severe MIH-type lesion with breakdown-driven carious cavity while at an eruption process

Histologically, the lesions usually involve the entire thickness of the enamel (. Fig.  17.31). Therefore, unless very mild, they cannot be removed by superficial (micro-)abrasion. The hardness of the porous enamel is significantly reduced, with rods appearing thinner and with empty spaces between them in scanning electron microscope [74]. Despite the systemic nature of the disease, the lesions are not characterized by symmetry as they affect from one to four molars with defects of various sizes and in different tooth locations [68]. Considering the period of formation/mineralization of the enamel, causative factors of typical MIH should act mainly during the perinatal period or in the first year of life (. Fig. 17.32). The etiology is primarily environmental, and a proposed mechanism incriminates serum

albumin entrapment, which blocks normal enamel protein removal for uneventful replacement by mineral [75], but this is still open to further research. Causative factors have not been fully clarified. Among those implicated are premature birth and low birth weight, birth complications and cesarean section, mother illness at late pregnancy, early childhood diseases especially in the respiratory system in combination with high fever episodes, administration of amoxicillin, varicella, exposure to bisphenol A during pregnancy, and late introduction of gruel [76]. A genetic component involving gene expression during dental enamel formation or affecting the immune response cannot be ruled out, while no explanation has yet been offered for the asymmetrical clinical presentation of MIH.

 

 

17

439 Developmental Defects of the Teeth and Their Hard Tissues

..      Fig. 17.30  Per tooth prevalence and severity of MIH-­type opacities in all permanent teeth of 14-year-old adolescents. [73] (By permission)

140

White opacity poster uptive breakdown

120

yellow/brown opacity atypical restoration

atypical extraction

100 80 60 40 20 0

17

16

15

14

13

12

11

21

22

23

24

25

26

27

47

46

45

44

43

42

41

31

32

33

34

35

36

37

0 20 40 60 80 100 120 140

a

b

..      Fig. 17.31  a Longitudinally split surface of MIH molar. Areas of enamel hypomineralization are more opaque and extend in its full depth being absent in the cervical area. b Similar appearance of HSPM mainly in its occlusal enamel. [74] (By permission)

zz Restoration of Teeth with MIH

Older studies reporting MIH restorative outcomes reported that children with MIH had a tenfold chance of restorative needs in their first permanent molars and three times more chance of repeated treatment in the same teeth [77]. A treatment plan should respect the severity level; mild MIH may be treated by remineralization or sealants, and severe MIH requires restorations or crowns [77, 78]. Thus, in mild cases, monitoring and preventive programs are sufficient, including placing

sealants in occlusal fissures, despite the reduced retention expected in molars with MIH [79]. The application of 5% NaOCl rinse to remove part of the organic content of hypomineralized enamel before etching does not appear to increase the tag length of resin sealant [80], while the use of adhesive agents before the sealant application seems to increase its retention [79]. In cases where breakdown of severely hypomineralized enamel is observed or anticipated, the extent of its removal at cavity preparation poses a dilemma. A good clinical

440

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..      Fig. 17.32  Typical severe MIH in an 8-year-old boy. The mother had prolonged labor with full-term birth complications. It is remarkable that cusp tips of the first permanent molars – where mineraliza-

guide is to remove as much affected enamel as possible by means of a round steel bur in a low-speed hand piece only. Another conservative approach in hypomineralized fissure areas may be to extensively cover them with resin composite and thus prevent breakdown (. Fig. 17.33). Enamel opacity color bears relation to severity, with yellow/brown having more chance for breakdown than white opacities [81]. In selecting restorative material, resin composite bonding with sound adjacent enamel seems advantageous [82] and thus is preferred to amalgam, which is associated with further marginal fractures when its margins are not placed in entirely sound enamel [77]. As a medium-term solution to prevent rapid decay following the early breakdown of enamel until the full eruption of molars with severe MIH, or in fearful, apprehensive children, restoration with resin-modified glass ionomer cement (RMGIC) is proposed (. Fig. 17.34). Placing PMC in the first molars with severe multi-surface defects is a relatively easy and inexpensive option until adulthood and may then be followed by ceramic crowns or onlays. In very severe cases, extracting at an appropriate age (ideally 8–11  years with mandibular molars on the earlier range side) drives the second molars drift mesially and close the space spontaneously or with minimal orthodontic correction [83] (. Fig. 17.35). For the affected incisors, the use of a small amount of opaque

tion started prenatally – are more resistant to breakdown than the rest of the enamel. Incisors have a mild form, so far

a

b

 

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..      Fig. 17.33  a Minimal preparation with low-speed hand piece in the slightly broken down central fissures of recently erupted maxillary second permanent molar. b Successful survival of the overlaid composite restoration on occlusal and palatal surfaces in the 5-year recall

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..      Fig. 17.34  a Newly erupted maxillary second permanent molar with severe MIH (breakdown and caries). b Cavity protection with RMGIC and postponement of definitive restoration

441 Developmental Defects of the Teeth and Their Hard Tissues

a

b

..      Fig. 17.35  a, b An 11-year-old boy with severe MIH in the mandibular first molars, one with endodontic needs and normal relation of incisors. The recent formation of bifurcation of mandibular second permanent molars together with the existing developing third

and appropriate shade of resin composite produces usually good aesthetic results (. Fig. 17.36), while microabrasion with infiltration techniques may be options for very mild cases (. Fig. 17.37). Rarely if ever caries becomes an issue to anterior teeth with MIH.

c

permanent molars justifies a decision to extract the affected first molars. c Complete eruption of mandibular permanent teeth in 18  months. Persisting spaces may be managed with orthodontic treatment

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zz Molar Incisor Malformation

It was not until 2014 that severe root hypoplasia of the first permanent molars, coexistent in at least half of the reported cases with similar findings in primary second molars, crown hypoplasia of permanent incisors, and less often hypoplastic defects to other teeth, was reported [84, 85]. The term currently used is molar incisor malformation (MIM). The molar crowns seem normal clinically, while radiographically the pulp chambers appear very flattened. Their roots are anomalous in shape, thin or short, or are nearly absent (. Fig. 17.38). While no prevalence data are yet available, it does not seem to be a rare dental anomaly [86]. Systemic illnesses in the first year of life, more often involving neural structures, are present in the majority of MIM cases, and these possibly pose an insult to developing dental tissues. MIM pathogenesis is currently being searched more intensely. The anomaly seems to begin at about the formation of cervical enamel and dentin, severely affecting the integrity of the pulp chamber and canals and the Hertwig’s root sheath. The first permanent molars present usually with signs and/or symptoms of non-­cariogenic pulp inflammation or necrosis. These teeth often become mobile and lost early; if not, their malformed roots rarely can be successfully treated endodontically. No treatment other than their extraction seems appropriate, as MIM is typically seen early in panoramic radiographs when molar space closure is still possible.  

zz Enamel Fluorosis

Fluoride (F) has led to significant reduction in dental caries incidence in the previous decades world-

c

d

..      Fig. 17.36  a Maxillary lateral incisors of an 11-year-old girl, one with mild and one with severe MIH. b Restoration of the left one: partial removal of hypomineralized enamel in depth, but complete peripherally, with bevel in healthy enamel. c The final restoration with composite after placing a thin layer of opaque. d Case of severe MIH in a 25-year-old man. PMCs were placed in three first permanent molars 18 years ago. The effect of time is evident in the opacities and breakdown of lateral incisors, which had received no restoration

wide. When long-term accumulation of higher than the accepted doses of F occurs, it can cause incomplete enamel mineralization (hypomaturation), resulting clinically in diffuse opacities, which can be mild to very severe. The most porous areas, after tooth eruption, become strongly discolored, hence the old name mottled teeth (. Fig. 17.39). In mild to moderate cases, superficial enamel is worn away in time by occlusal forces. This may be mimicked in the dental clinic for aesthetic purposes. The fluorosis severity is classified into five to nine categories according to various existing indices (Dean, TSIF, TFI, etc.) [87]. The pathogenic mechanism of fluorosis also involves other factors such as matrix metalloproteinases (MMPs) mentioned also in the mechanism of amelogenesis imperfecta. Severe fluorosis occurs after chronic ingestion of water containing much higher than the desired  

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..      Fig. 17.37  a Maxillary incisors with demarcated white opacities. b The centrals were treated with microabrasion (scrubbing the affected areas with slurry of 18% hydrochloric acid and pumice) and additional resin infiltration in the right one

a

(0.7–1  ppm) fluoride ion concentration. This occurs naturally in certain areas of the world, for example, Tanzania, China, etc. Aesthetic restoration of these teeth is achieved by direct or indirect restorations and veneers or with porcelain or zirconia crowns. Mild to moderate forms of fluorosis may be found endemically in almost every country [87]. Mild forms of fluorosis can also occur, from drinking natural or even artificially fluoridated water, use of fluoridated water in baby formulas, or by prolonged ingestion of fluoride toothpaste around the age of 2  years (see “Toxicity of Fluoride” in 7 Chap. 12). The clinical picture is in the form of diffuse horizontal areas, which is the most common, and needs differentiation from other similar lesions, such as those of hypomaturation-­type amelogenesis imperfecta (see below). Histologically, in fluorosis, the porous lesion of enamel, in contrast to those observed in MIH, involves only the outer part, of a few hundred microns of the enamel. Therefore, with dental wear that occurs with age, or with micro-abrasion technique [88] applicable at the dental office, the white or discolored undesirable look of some of the lesions can be improved dramatically (. Fig. 17.40).  

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17.2.2.2

..      Fig. 17.38  a Panoramic radiograph of a 9-year-old girl with MIM involving all first permanent and second primary molars. b Her clinical presentation is as yet relatively normal. c A 13-year-old boy with MIM. All first molars have dysplastic roots with apical radiolucencies, while the second molars seem unaffected. In view of all third molar presence, he should have been treated as a 4X6 extraction case at a younger age

 namel Dysplasias Related E to Diseases or Drugs

Metabolic disturbances, drugs, and many other insults during tooth formation, if beyond the biologic threshold of the cell or the individual, can harm the sensitive ameloblasts and cause cessation of matrix formation (hypoplasia) or disturbed mineralization that will leave a mark on the surface of the tooth, as a developmental defect. The timing, duration, and intensity of the insult will determine the position, extent, and severity of the defect. Clinically, partial or total lack of enamel can be observed in a tooth or expressed as pitting, striations,

443 Developmental Defects of the Teeth and Their Hard Tissues

b

a

..      Fig. 17.39  a Mild enamel fluorosis of an adolescent (TFI = 1–2). Even in the recommended concentration of artificially fluoridated water, 10% of the children may present mild fluorosis. b Moderate fluorosis (TFI = 4–5) in a young woman after drinking water with

and fissures, single or multiple, with smooth edges. In systemic conditions, the lesions will be symmetrical or as generalized hypoplasia [89]. Some medical conditions can cause developmental dental defects, and the medical history of the child is important for linking with the etiology of the defect (. Fig. 17.41). Premature birth, serious chronic viral and bacterial infections, high fever, and conditions with a possible effect on calcium metabolism may be responsible, as well [68, 76]. Some conditions that may have that effect are listed below:

about 2  ppm fluoride during her preschool years. Points of breakdown are seen in the superficial enamel (TFI = 5), while the discoloration is acquired, attributed to pigment penetration (TFI, Thylstrup-Fejerskov index of fluorosis)

a

 

55 Toxic effect of drugs, chemical elements, or substances (fluoride, tetracycline, dioxins). 55 Severe malnutrition, neonatal hypocalcaemia, rickets from hypovitaminosis D, and jaundice. 55 Thyroid and parathyroid disorders and hyper-­ hemoglobinemia. 55 Mother’s diabetes, metabolic disorders of the infant (e.g., liver, kidney, or celiac disease), and others.

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zz Localized Defects from Environmental Causes

Traumatic intrusion of a primary incisor might destroy the ameloblasts of the bell stage tooth anlage and cause a hypoplastic defect in the crown of the permanent successor. A chronic abscessed primary molar might cause bone infection and injure the developing premolar tooth germ. The type and size of the damage in the permanent tooth depends on the stage of development of the tooth bud, as well as the intensity and duration of the insult [76]. Other reasons of localized hypoplasia or defect are radiotherapy: in the formation phase of some teeth, it may cause hypoplasia, microdontia, complete inhibition of the formation of some teeth, or stunting the growth of their roots. Hypoplasia of primary incisors is observed in some premature infants may be due to trauma from the metal laryngoscope intubation attempt (. Fig. 16.12). It has been suggested that such enamel defects of the primary dentition may be serious predisposing factors for severe ECC [89].  

d

..      Fig. 17.40  a Mild enamel fluorosis in a 10-year-old boy raised in Hong Kong with artificially fluoridated water (then 0.7  ppm). The possible cause was the additional ingestion of fluoride toothpaste during preschool age. b Appearance after micro-abrasion with Prema (Premier Dental Products) of right and with abrasion with composite polishing diamond bur of left incisors. The aesthetic result is similar. c Moderate enamel fluorosis in maxillary incisors of an 8-year-old. d Important aesthetic improvement after micro-­abrasion with Prema

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..      Fig. 17.41  a Severe enamel hypomineralization of a toddler aged 16  months with a history of premature birth at 25  weeks of pregnancy. b Chronological enamel hypoplasia of a 10-year-old with a history of hypoparathyroidism diagnosed soon after birth. c Chronological enamel hypoplasia of an 11-year-old girl with no recorded history. It is proposed that the insult occurred during the first year of life, and it did not affect the upper lateral incisors (intact left maxil-

lary canine is primary). d Chronological enamel hypoplasia of an 8-year-old girl with a history of meningococcal septicemia in the age of 10  months. e The unilateral full-depth enamel hypoplasia of a newly erupted second permanent molar could be attributed to the young patient’s medical history of severe respiratory infection at age 3 years

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17.2.2.3

 ental Defects with Genetic D Background

zz Amelogenesis Imperfecta (AI)

Amelogenesis imperfecta, the only known inherited malformation of the enamel, occurs with variable frequency of approximately 1:4000–14,000, but an extremely high (1:700) prevalence in a closed community of Sweden has been reported [90–92]. According to a current definition, AI is a group of heterogeneous genetic conditions or rare diseases that affect the structure and appearance of enamel of all or almost all teeth, inherited with different modes of transmission (autosomal dominant (AD), autosomal recessive (AR), X-linked). AI may rarely be associated with other morphological or biochemical lesions [93]. The autosomal mode of transmission involves about 95% of cases, and the sex linked 5%. AI manifests through a variety of phenotypes, and this has led to many attempts to build a classification [91–98], some of which add also mode of inheritance and eventually histological background. Additionally, the development of genetic research has contributed to the designation of specific genes to different types of AI [96] and thus arose classifications with molecular basis [97]. Most genetic defects are associated with the malfunctions of enamel proteins participating in the composition of the enamel matrix or in enamel maturation consisting in the replacement of the protein content by mineral to reach the optimal 96–98% mineralization. For example, lack of a guanine (nitrogen base) in exon 9 of ENAM causes premature termination of translation and synthesis of an enamelin protein with 276 amino acids instead of 1142 [99]. Among the genes that cause AI, FAM83H (AD) causes more and the most severe malformations (hypomineralized, yellowish brown) throughout the crown. However, the action mechanisms remain unclear. In . Table 17.7, a classification of 14 groups and AI subsets is presented, by Witkop [93] which is based on the phenotype and the mode of transmission. The hypoplastic type is characterized by reduction of the whole thickness of the enamel of all teeth in primary and permanent dentition. It may have pitted appearance (type 1A) or rarely vertical grooved enamel defects. Especially in 1D and 1E types, characterized by a very thin layer of enamel, teeth appear smaller and have no contact points (. Fig. 17.42). Although the prevalence of anterior open bite in the general population is 3.7%, in patients with AI, it varies from 24% to 60%, indicating a strong correlation between them [100, 101]. It is  

 

..      Table 17.7  Classification of amelogenesis imperfecta based on phenotype and the mode of inheritance, according to Witkop [93] Type 1. Hypoplastic

Enamel inheritance

1Α Hypoplastic, generalized pitted

Autosomal dominant

1Β Hypoplastic, localized pitted

Autosomal dominant

1C Hypoplastic, localized pitted

Autosomal recessive

1D Hypoplastic, diffuse smooth

Autosomal dominant

1E Hypoplastic, diffuse smooth

X-linked dominant

1F Hypoplastic, diffuse tough

Autosomal dominant

1G enamel agenesis

Autosomal recessive

Type 2. Hypomaturation 2Α diffuse pigmented

Autosomal recessive

2Β diffuse

X-linked recessive

2C snowcapped teeth

X-linked

2D snowcapped teeth

Autosomal dominant (?)

Type 3. Hypocalcified 3Α diffuse

Autosomal dominant

3Β diffuse

Autosomal recessive

Type 4. Hypomaturation-hypoplastic with taurodontism 4Α Hypomatured-hypoplastic with taurodontism

Autosomal dominant

4Β Hypoplastic-hypomatured with taurodontism

Autosomal dominant

probably multifactorial, and it is thought to be mainly a result of genetic effects. The future discovery of genes involved both in formation of the craniofacial complex, and amelogenesis may elucidate the relevant molecular mechanisms [102]. The types hypomatured and hypocalcified (old term for synonymous hypomineralized) are characterized by

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b

d

e

f

..      Fig. 17.42  Hypoplastic type of amelogenesis imperfecta. a Pitted (subtype 1A by Witkop [93]) in a 12-year-old girl. Tooth cusps present with milder hypoplasia. b Rare hypoplastic type with vertical striations that give wrinkled appearance in an 8-year-old girl (first described in Darling’s classification [94]. c The mandibular first molar of cases in B significantly lacks enamel requiring composite

restoration. d Hypoplastic subtype 1D by Witkop [93]. e, f More severe form of same subtype as in d, allowing for bonding of direct composite veneers in maxillary incisors. The super thin enamel can be observed in the radiograph leading to dental arch with spaces. PMCs were placed on permanent molars for maintaining vertical dimension

normal thickness of undermineralized enamel, which is porous and thus is relatively brittle with reduced resistance to masticatory forces (. Fig.  17.43). It is a qualitative and not a quantitative dental defect. The hypocalcified type presents with lower concentration of mineral salts, is subject to enamel wear, and coexists in a high percentage with anterior open bite and accumulation of plaque and calculus. In the hypomaturation type, open bite is also present but with lesser prevalence, with increased unaesthetic effect, due to oral pigment accumulation in the porous enamel and possibly increased tooth sensitivity. The hypomatured-hypoplastic with taurodontism [103] is less common and may coexist in certain syndromes. Its relationship with the tricho-dento-osseous syndrome (TDO syndrome: curly hair, AI, bone thickening particularly in the skull bones) is typical (. Fig. 17.44). However, taurodontism can coexist with hypoplastic and incomplete enamel maturation in the absence of the syndrome. Note that taurodontism is of ectodermal origin, as Hertwig’s sheath, which stimulates the formation of the root, is a product of the enamel organ. In this type, the enamel has a yellow/brown staining and is pitted (hypoplastic) especially on labial surfaces.

zz Dental Rehabilitation of AI

 

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c

 

The main problem and chief complaint of children and adolescents with any type of AI are the aesthetic appearance of the teeth and possibly pain as the teeth might be very sensitive. The form and color of the teeth become a very significant element in reducing the quality of life of people with AI, young as well as adult. AI has marked an impact on the psychosocial health of the affected people. Furthermore, there are other issues, such as orthodontic abnormalities, mainly open bite. Up to 60% of individuals have open bite in hypocalcified AI, as well as more dental caries, sensitivity to thermal stimuli, and difficulties in mastication. The multiplicity of treatment needs is best met by interdisciplinary approach [101]. Due to the nature of enamel, when restorations are needed, adhesive materials are preferred to amalgam. In more severe cases, PMCs may be placed in the first permanent and second primary molars, while, if preferred, aesthetic zirconia crowns are now available demanding more preparation efforts [112]. In the primary dentition however, the severity of AI is generally milder. Placing PMCs on molars helps primarily prevent attrition and maintain the vertical dimension of the face. Restorative options in the anterior area depend on the

447 Developmental Defects of the Teeth and Their Hard Tissues

a

c

b

d

..      Fig. 17.43  a, b Hypomineralized type of AI in a 12-year-old girl. All teeth present enamel worn/broken down to various degrees. c Young adult with severe hypomaturation type of AI. Enamel pres-

a

b

..      Fig. 17.44  a A 14-year-old Caucasian boy with TDO syndrome and characteristic curly light blond hair. b Wide pulp chambers and taurodontism are seen in permanent molars. c Hypoplastic enamel

ents intense post-eruptive brown discoloration and some breakdown. d Mild phenotype hypomaturation-type AI with little enamel breakdown

c

with severe tooth wear that soon led to pulpal complications and cervical root fracture which led to crown loss of left central incisor are evident in the maxilla

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Box  Gene Investigation and Correlation of AI with Other Diseases or Syndromes

17

Enamel formation depends on Ca2 + transport through the ameloblasts, namely, Ca2 + entry from the blood vessels and its exit from the opposite side of the ameloblast to form a hydroxyapatite. The recent identification of mutations in genes involved in the homeostasis of calcium ions such as STIM1 (encoding a protein that activates the transmembrane entry of Ca2 + to prevent depletion of its stocks into the endoplasmic reticulum) and SLC24A4 (Na +, K +, Ca2 + transporter), mutations which cause hypomaturation type AI, offered new insights into the molecular management of Ca2+ in ameloblasts [104]. Depletion of Ca2 + changes the structure of the protein STIM1, which is a calcium sensor located in endoplasmic reticulum [105]. STIM1 is then translocated close to the cell membrane where it is linked and activates Orai1, a cell membrane calcium channel. Once the STIM/Orai system is activated, they mediate the transport of Ca2 + from outside to inside the cell in many cell types, including T cells, muscle cells, and ameloblasts [106]. Mutations in Orai1 and STIM1 cause immunodeficiency 9 and 10, respectively, and predispose to congenital myopathy, ectodermal dysplasia, as well as enamel malformations [104]. The progressive fragmentation of proteins (degradation) which are secreted in pre-enamel and will be removed to make room for the prismatic hydroxyapatite crystals to increase in width and thickness during mineralization is caused by proteolytic enzymes. The most important of these is a metalloproteinase, the enamelysin MMP20. Mutations of MMP20 inhibit the smooth process of protein degradation and growth of crystals and cause hypomaturation type of AI, which is transmitted as an autosomal recessive disease [107]. The hypomatured enamel detaches relatively easily from dentin, while the yellowish discoloration is evident since tooth eruption and increases with time as pigments from the mouth enter porous enamel. The hypoplastic type of AI is mainly associated with mutations in amelogenin AMEL and enamelin ENAM genes, and, previously, it did not seem to have obvious association with syndromes. Mutations in FAM20A gene have been identified as causative agents of a syndromic type of hypoplastic AI with almost absent enamel. The enamel-renal syndrome (ERS) (combination of AI and nephrocalcinosis) and the AI-fibrous gingival hyperplasia are both associated with mutations in FAM20A gene and are allelic rare diseases [108] (. Fig.  17.45). FAM20A is a glycoprotein, a kinase phosphorylating extracellular matrix proteins involved in mineralization. Therefore, the hypoplastic type of AI, which is related  

..      Fig. 17.45  Hypoplastic-type AI and nephrocalcinosis. Complete lack of enamel associated with severe renal calcifications, associated with mutation in FAM20A gene

causally with mutation in FAM20A, is, at least partially, a result of an abnormal calcification process of phosphoproteins secreted into the enamel, probably by phosphorylation failure. Mutations of FAM20A are associated with erratic calcification traces in the gums, periodontal tissue, dental pulp, lungs, and kidneys. Clinical findings in patients presenting with FAM20A mutations include fibrous gingival hyperplasia, aggressive periodontitis, thin alveolar bone, secondary hyperparathyroidism, and nephrocalcinosis/nephrolithiasis. Nephrocalcinosis may be asymptomatic up to young adulthood. The first signs may be recurrent infections of the urinary system, pyelonephritis, renal colic, and excretion of kidney stones [109, 110]. The timely referral of juveniles with hypoplastic AI for kidney ultrasound may confirm early AI-renal syndrome, while a neglected nephrocalcinosis or nephrolithiasis would lead to significant morbidity. Therefore, cases of AI-fibrous gingival hyperplasia should be screened for FAM20A mutations and evaluated carefully for renal findings. FAM20C, a gene of the same family as FAM20A, presents interest, as its mutations are discovered in patients with Raine syndrome, a rare, autosomal recessive, fatal osseosclerotic bone dysplasia that has similar clinical findings as the ones observed in patients with FAM20A mutations, like fibrous gingival hyperplasia and ectopic calcification [111]. These are some examples of genetic research, and it is expected that many more genes, with unknown roles in amelogenesis, will be recognized in the future as causative of AI.

449 Developmental Defects of the Teeth and Their Hard Tissues

a

c

b

..      Fig. 17.46  a Direct minimal composite veneers in some incisors of hypoplastic AI of . Fig.  17.42b confirm clinically, after 3 years, the possibility of etching and adhesion to enamel. In both hypoplastic (b) and hypocalcified (c) AI types of . Fig.  17.42e  

 

type and severity of AI. In most case of hypoplastic and in some mild phenotypes of hypomineralized and hypomaturation type of AI, the enamel can be etched satisfactorily [113], so as to allow direct aesthetic composite veneers in the anterior teeth (. Fig. 17.46). These may require frequent repairs. Strip crowns have been used successfully for many years for restorations with composite of the crown of decayed anterior primary teeth. This clinical procedure requires only minimal preparation of the tooth. The long-term outcome of such direct restorations in permanent hypoplastic teeth after 10 years of follow-up was satisfactory in a retrospective study of 21 teeth; [114] however, more firm evidence is required [115]. Veneers and ceramic crowns as permanent restorations should be delayed until cervical margin becomes more permanent (. Fig. 17.47). The use of intraoral scanner and CAD-CAM technics may facilitate the use of veneers during teenage years. Enamel bonding issues complicate the, often necessary, orthodontic treatment, while the frequency of interventions and the long monitoring may have a burnout effect and discourage the patient, so a positive approach by the dentist is necessary.

and . Fig.  17.43b, maxillary anterior teeth (after canine further eruption) and premolars have received composite veneers on the vestibular ­surfaces, as a medium-term aesthetic solution. Regular observation is mandatory for possible composite detachments  

a

 

b

 

..      Fig. 17.47  a An 18-year-old young woman with mild phenotype of hypomaturation-type AI had direct composite veneers in anterior teeth for years and desires aesthetic improvement. b After the cementation of ceramic veneers. (Courtesy Dr. P. Gerasimou)

zz Dentinogenesis Imperfecta (DGI)

Dentinogenesis imperfecta is a hereditary dentin dysplasia divided in three types [116], Shields types I, II, and III, based on clinical, radiographic, and histologic findings. Except for a few cases of DGI type I, the hereditary malformations of dentin are transferred as dominant traits. The most frequent types are I and II with an overall prevalence of approximately 1:6000–8000. Type III has been described only in an isolated community of Brandywine Maryland, USA. DGI-Shields I is the dental expression of a generalized disorder of connective tissue, osteogenesis imperfecta (OGI). In 90% of OGI cases, mutations are found in genes encoding collagen type 1 (COL1A1 and COL1A2). Frequent findings in OGI are increased frequency of hypodontia, class III malocclusion, and posterior cross bite. In 50% of OGI patients, the teeth will show DGI characteristics clinically, but they will all present dentin defects if analyz-

ing the structure or ultrastructure of dentin under a microscope. In dentinogenesis imperfecta Shields II, the causative genetic defect is located in the long arm of chromosome 4 (4q21). DGI types II and III are basically dental conditions with no bone involvement. The genetic defect of almost all other heritable dentin dysplasias than DI involves dentin sialophosphoprotein (DSPP) encoding gene, which means that DGI types II and III are allelic conditions [115]. Furthermore, a study of patients with DGI and DSPP mutations concluded that they exhibited also enamel abnormalities, different from those of the dentin, indicating that DSPP may also participate in early stages of amelogenesis [117]. Histologically the abnormal dentin has few tubules with atypical direction (swirls) and many branches, with inclusions of cells and small blood vessels (. Fig. 17.48).  

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..      Fig. 17.48  a DGI: Pulp obliteration, histological section. Mantle dentin on the outside is normal, while the rest is globular, irregularly formed dentin. The enamel was lost in the preparation. b DGI-1 pathological dentin with large interglobular spaces, inclusion of cells and small blood vessels

a

..      Fig. 17.49  a DGI of a 5-year-old child in occlusion. Early eruption of mandibular permanent central incisors. b The occlusal view of mandible shows that the second primary molars still preserve almost completely their enamel. c DGI of his 38-year-old father. d The occlusal view of his mandible shows fractures, most severe in the posterior teeth

b

a

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c

d

zz Dental Rehabilitation in DGI

Over time the abnormal dentin accumulates to the point of pulp obliteration. Dentin mineralization is defective, with reduced hardness; dentin does not support the enamel, which detaches and exposes the softer dentin that will wear off quickly (. Fig.  17.49). In the permanent dentition, the production of abnormal secondary/tertiary dentin continues to fill the pulp chamber and canal, so that they appear radiographically fine as a thread (. Fig. 17.50). The support of the enamel is better, but it varies due to defects in the enamel-dentin junction [117]. The permanent teeth are much more resistant to occlusal forces than the primary teeth, but they have a characteristic brown-gray opalescent color. Radiographically the teeth show short roots, bulbous crowns that constrict at the cervix, and pulpal obliteration [117]. The main problems are the invasion of exposed dentinal tubules by bacteria-provoking pulp necrosis and subsequent untreatable periapical infections due to the disappearance of pulpal spaces related to anarchic dentin production; the aesthetics, mainly of the permanent dentition; and the abrasion of the primary and permanent teeth, often resulting in reduced vertical facial  

17

 

dimension. Therefore, PMCs should be placed early on primary molars and if possible aesthetic crowns with white facing on the maxillary primary incisors for psychological reasons. Therefore, early diagnosis and treatment are important. The first permanent molars usually show some wear, although to a much lesser degree than that of primary molars, yet regular monitoring is recommended from eruption. In cases of little abrasion, a layer of composite can be directly mounted on, although placing PMC may be preferred. When adolescence is over, ceramic crowns solve both problems, aesthetic and functional. The exclamation of the patient with DGI in . Fig.  17.50 after he received full mouth ceramic crowns was: “I can finally smile.”  

zz Dentin Dysplasia (DD)

It was first described in 1920 as “rootless teeth.” [118] DD type I presents with extremely short roots and small, almost obliterated coronal pulps, with often apical lesions appearing in the absence of caries (. Fig.  17.51). The teeth become mobile and are lost early, the treatment being only prosthetic rehabilitation of the oral cavity. There have been cases of DD I with autosomal dominant (SMOC2  

451 Developmental Defects of the Teeth and Their Hard Tissues

gene) transmission [119] associated with major microdontia, oligodontia, and tooth shape abnormalities. The prevalence is rare (1:100,000). DD type II may resemble DGI type II radiographically and clinically in the permanent teeth but with milder discoloration/opalescence. Subtypes of the two main types have even been proposed. It is suggested that type II is caused by mutations in DSPP, the largest member of SIBLING family of glycoproteins, or it is associated with a DGI type II allele gene [120].

eruption is usually delayed, or they do not erupt at all. Following eruption, local infections of the alveolar bone are frequently observed [122]. In favorable cases full coverage could prevent pulp inflammation. Otherwise, the management consists of surgical extraction of the dysplastic teeth and the placement of prosthesis, partial dentures in childhood, and implants/fixed following adolescence (. Fig. 17.52).

 ental Defects Unclassified D as to Etiology

There have been unerupted teeth, molars in particular, seen in routine radiographic examinations to have coronal dentin radiolucencies often reaching or involving the overlying enamel (. Fig.  17.53). They may be of non-­progressive or progressive nature, and, in the latter case, following eruption, these teeth may become cavitated and therefore not be recognized as such. The term used is pre-eruptive intra-coronal radiolucency/resorption (PEIR), suggesting that they are a result of resorption of as yet unexplained cause. In that sense they may not belong in developmental dental defects but are presented here until their etiology is clarified. Their presence has been associated with unfavorable tooth position or eruption path. Their prevalence is reported as about 3%, but this varies greatly in studies [123].

17.2.2.4

zz Regional Odontodysplasia

Regional odontodysplasia (ROD) is an uncommon dental anomaly with unclarified etiology. Recently, a suggestion of common genetic background with genes involved in tooth agenesis, namely, a codon mutation of the PAX9, has been put forward [121]. This disorder is characterized by severe malformation of all dental tissues of some teeth in a certain region, seemingly having affected the specific part of the dental lamina. It affects primary and permanent teeth in that side of the jaw, more often the maxilla, rarely crossing the midline and even more rarely affecting both jaws. The affected teeth have radiographically a “ghost tooth” appearance. Their

a

 

zz Intra-Coronal Dentin Radiolucencies

 

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 ystemic Diseases and Syndromes S with Dental Defects

Celiac disease is a condition of the small intestine caused by immunological sensitivity to gluten gliadin protein of wheat products. The prevalence is 3–8:1000, and there is a familial tendency, meaning a genetic component which so far has not been elucidated. Except for oral lesions mentioned in 7 Chap. 20, the enamel may have chronologic hypoplasia or hypomineralization defects, but usually only on the incisal third of the incisors, as the intolerance is diagnosed in infancy and its effects controlled by strict avoidance of all wheat sources [124– 126] (. Fig. 17.54). Rickets is caused by prolonged deficiency in vitamin D that is essential for calcium absorption and  

 

..      Fig. 17.50  a, b The radiographs of a 20-year-old man with DGI show pulp chamber and root canal obliteration in all teeth. c Their clinical side view with brown opalescent color

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..      Fig. 17.51  a Panoramic radiograph of adolescent with Dentin Dysplasia type I. Arrows show clinically caries-free molars with periapical radiolucencies. b, c Rootless teeth erupt and are shed soon

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..      Fig. 17.54  Zones of hypoplastic enamel as severe chronologic dental defects in the anterior teeth of a 9-year-old child with celiac disease history ..      Fig. 17.52  a Regional odontodysplasia (ROD) in all half of maxillary primary dentition. The affected teeth have erupted. b The permanent teeth have similar “ghost tooth” appearance radiographically. c After affected primary teeth extraction under general anesthesia, a partial denture was placed. d A rare case of ROD crossing the midline

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and, in the skeleton, it may cause kyphosis. The teeth appear with symmetrical enamel hypoplastic-hypomineralized defects, consistent with the period of hypocalcemia. Familial hypophosphatemia is a rare hereditary rickets resistant to vitamin D, usually X-linked (PHEX), affecting more severely boys. The low levels of phosphorus in the blood may be caused by dysfunction caused by renal over-reabsorption or perhaps by intestinal mal-­absorption or altered vitamin D metabolism in the kidneys. Dental findings are defective dentin formation with extensions of pulp horns that often reach the enamel. Moderate cusp wear of the teeth leads to microbial penetration and pulp inflammation, necrosis, and abscesses. Treatment is endodontic or full coverage of the molars with crowns to prevent pulp exposure, PMC in children, or ceramic later, but preventive sealing of all the fissures in primary and permanent molars and in premolars is also recommended [128]. Additional findings are class III occlusion, shorter cranial base, and mandibular ramus [129] (. Fig. 17.55). Hypophosphatasia is a metabolic disorder with low alkaline phosphatase activity and bone rickets findings, particularly in the legs. It is inherited as an autosomal dominant or recessive trait. It can be fatal in infancy, although many cases diagnosed prenatally have a good prognosis [130]. In milder types, delayed eruption and premature tooth loss, before 3 years of age, are observed, particularly in the anterior primary teeth (. Fig. 17.56). This is attributed to decreased and dysplastic cementum, while dentin is rather normal [131]. Similar dental findings have been recorded in young adults and may lead to loss of the teeth. Epidermolysis bullosa is a group of rare heterogeneously inherited diseases of mucosal and epidermal bonding to the connective tissue, which are gener 

..      Fig. 17.53  a Panoramic radiograph of a 13-year-­old girl at retention after orthodontic treatment. The radiolucencies of suprapulpal dentin observed in both unerupted second mandibular molars with unfavorable eruption paths (arrows) were not vissible at the radiograph taken pre-­orthodontically. b Large dentin radiolucency in an erupting mandibular first permanent molar in a 6-year-old girl with free medical history. Her mother had idiopathic very short stature. The tooth will be restored as soon as it erupts to prevent pulp complications

thus mineralization of bones and teeth [127]. Vitamin D is absorbed from food but needs sun exposure to the skin for its activation. Rickets affects children and adolescents. It is called osteomalacia in adults,

 

453 Developmental Defects of the Teeth and Their Hard Tissues

ally characterized by blister formation in response to mechanical trauma. In one of the three types in which it mainly manifests, generalized enamel hypoplasia is a common finding. Dental treatment is difficult with spe-

..      Fig. 17.55  A 9-year-old boy with hypophosphatemia and class III occlusion. Hypoplastic enamel is evident in all anterior teeth, permanent and primary, mostly noticeable in their incisal parts

cial precautions, as light pressure or tension on the lips or cheeks, for example, causes blisters. It is interesting to notice that genes involve in epidermolysis bullosa (AR) have also been reported as causative in hypoplastic AI when transmitted as an autosomal dominant disease [132]. Ehlers-Danlos syndrome is a group of connective tissue disorders; at least eight types are related to the synthesis of collagen, mainly transmitted as an autosomal dominant trait. The physical findings are loose joints (including TMJ) and super elastic skin, while dental findings include hypoplastic enamel, abnormal dentin and tooth roots with pulp stones, and also early loss of the teeth [133]. APECED (autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy, OMIM #240300) is a rare autosomal recessive autoimmune disease. It is due to a mutation in a single gene named AIRE in chromosome region 21q22.3. Among other ectodermal disorders, enamel defects in both primary and permanent dentitions appear to be common (. Fig.  17.57). Inherited developmental dental disorders are observed in many rare diseases or syndromes, for example, in tuberous sclerosis with pitted hypoplastic enamel [134], osteopetrosis with pitted hypoplastic enamel and oligodontia [135] (. Fig. 17.58), and others. The restoration of the anterior teeth with hypoplasia or hypomineralization defects has been discussed in 7 Chap. 13 and earlier in this chapter in the restoration of the teeth with MIH. Special attention is paid to removing discolored enamel and/or using an opaque composite color for camouflage toward a more aesthetic result. At the appropriate age, some cases will require porcelain veneers and other prosthetic solutions for better and more permanent aesthetics.  

 

 

..      Fig. 17.56  This 3.5-year-old boy with hypophosphatasia had three mandibular incisors shed already

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..      Fig. 17.57  A 10-year-old boy with APECED. a Enamel hypoplasia is evident in an erupting second premolar. b Drug-resistant tongue candidiasis

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..      Fig. 17.58  a, b Clinical view and panoramic radiograph of a 7-year-old girl with osteopetrosis and neglected mouth. c One of two mandibular first permanent molars removed because of infection

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..      Fig. 17.59  a Green discoloration of primary teeth of a 4-yearold girl (with manifest caries), which was operated for liver transplantation in the seventh month. The discoloration is due to

bilirubinemia. In the anterior teeth, it is evident only cervically because most of their crown had been formed and mineralized already. b The second primary molars suggest coexistence of HSPM

17.3  Developmental Discoloration

zz Tetracycline-Induced Discoloration

of Dental Tissues

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(under antibiotic coverage until prolonged bone healing) shows anomalous root with cementosis

Developmental discolorations are endogenous, and their clinical appearance is often modified after exposure to the oral environment and to daylight. They are mainly caused by: 55 Blood degradation products (e.g., congenital porphyria, atresia of the bile duct) [136] (. Fig. 17.59) 55 Incorporation of drugs or dyes during mineralization (e.g., tetracycline) 55 Hypoplasia/hypomineralization (e.g., some types of AI and DI)  

In these instances, the final tooth color is a combined result of internal and external discoloration. With societal norms demanding white smiles, children and especially adolescents are often concerned not only with discolored teeth but with the natural overall tooth color, all too often asking for “tooth whitening.”

Chronic intake of tetracycline, its hydrochloric salt in particular, causes brown-grey discoloration. This drug was prescribed in the past for the management of typhoid and cystic fibrosis, in young patients. Many children had subsequently yellow/brown or gray teeth, depending on the formulation that was administered [137]. That was because tetracycline has a strong tendency for binding to tissues in the mineralization phase, like dentin and bone. While staining of bones is lost in a few years due to its remodeling, it remains permanently in the dentin. When the teeth are exposed to light, the integrated tetracycline becomes darker and thus unsightly (. Fig. 17.60). When sections of the dentin are exposed to ultraviolet light, fluorescent characteristic lines are present corresponding to the dentin growth lines (mineralization fronts) during the days of intake (. Fig.  17.61). This allows dating the time of drug intake, as well as animal research on bone and tooth development. Histologically it seems that tetracycline does not color the enamel as much, but its transparency allows the discolored den 

 

455 Developmental Defects of the Teeth and Their Hard Tissues

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..      Fig. 17.61  a Longitudinal section of premolar tooth under fluorescence microscope of an adolescent who received tetracycline for 4 days during the mineralization phase of this tooth’s crown. They are obvious in the dentin (along von Ebner lines) and less so in enamel (along Retzius incremental lines). b Similar section of the first mandibular premolar suggesting multiple intakes of tetracycline for cystic fibrosis treatment in the 1970s [137]

..      Fig. 17.60  a The yellow zones in a young adult’s cervical area of maxillary incisors correspond to tetracycline intake at the age of 2–3  years of age. b Aesthetic improvement with direct composite veneers

tin to shine through. Several decades ago, since the side effect of tetracycline became known, their administration to children younger than 8  years and pregnant women has been replaced by other antimicrobial drugs, and the phenomenon is nowadays rare. A few cases are still seen in young people. As in other intrinsic discoloration cases, the aesthetic correction is made with veneers of opaque composite resin in children or with ceramic materials after the clinical cervical tooth margin has been finalized. zz External Bleaching of Discolored Teeth

The importance that many adolescents attribute to the appearance of teeth varies, and aesthetic views differ between dentists, parents, and children [138]. The sense

of normal color is very variable, but the final preferences should be left to the patient. As a health scientist, the dentist should not enforce his opinions regarding this subjective matter, and after taking into account possible different perceptions between parents and children, he should give satisfactory solutions within the framework of professional ethics. Tooth bleaching has become very popular. Techniques are based on the application of a composition of hydrogen peroxide (H2O2), while adding energy in the form of heat, light or laser radiation shortens the application time (. Fig. 17.62). Although successful use of the process has been reported even in children, the technique is recommended only after puberty and always taking precautions to avoid chemical trauma to the gums and pulp irritation [139, 140]. Some tooth sensitivity may at times appear after bleaching. Young people may also benefit from using “whitening” dentifrices. Discolorations due to developmental defects of dental tissues do not respond to bleaching, so other techniques are preferred, mainly by covering the discolored teeth, e.g., direct or indirect aesthetic veneers.  

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..      Fig. 17.62  Bleaching methods with trays. a, b At home (with carbamide peroxide 16% in transparent tray). c At the dental office (with hydrogen peroxide 35%) with the assistance of a ZOOM lamp. (Curtesy Dr. K. Giannakopoulos)

17.4  Conclusion

Dental anomalies have extremely complex causes and phenotypes making often clinical decisions very difficult for general, pediatric, and other dental specialists. It is imperative for dentists to acquire a good knowledge

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of the causes and differential diagnosis for each dental anomaly to precisely diagnose and be able to offer the optimal treatment to each patient. The attached table aims to contribute toward a successful differential diagnosis and provide useful clues for treatment (. Table 17.8).  

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..      Table 17.8  Differential diagnosis and clinical decision guidance for dental anomalies Abnormal tooth number Hypo−/oligodontia DDX Genotype/phenotype

Notes

Selected non-syndromic familial tooth agenesis

1. MSX1: No significant difference between the number of teeth missing on the left and right; the absence of maxillary first premolars is the most distinguishing feature of an MSX1 mutation [141] 2. PAX9: No significant difference between the number of teeth missing on the left and right; the absence of the second molars is the most distinguishing feature of PAX9 mutations 3. AXIN2: Incisor agenesis and colorectal cancer or precancerous lesions of variable types

The dentist is expected to order genetic tests: [142]   1. Defects are often first discovered by the dentist   2. Can be associated with cancer   3. The list of candidate genes is short: WNT10, LRP6…

Syndromic oligodontia (most likely candidates)

1. Ectodermal dysplasia (EDA, EDAR, EDARΑDD): Abnormalities of two or ectodermal structures such as the hair, teeth, nails, sweat glands, salivary glands, cranial-facial structure, and digits. Frontal bossing, longer or more pronounced chins, and broader noses are very common [143] 2. Achondroplasia (FGFR3): Disproportionate short stature, shortening of the proximal limbs, short fingers and toes with trident hands, and intelligence are generally normal [144] 3. Incontinentia pigmenti (IKBKG): Development of harder skin growths with grey or brown patches. Hair loss (alopecia), dental abnormalities, eye abnormalities that can lead to vision loss, and lined or pitted fingernails and toenails. Mainly affects males (X-linked) 4. Orofaciodigital syndrome-I (OFD1): Malformations of the face, oral cavity, and digits with polycystic kidney disease and variable involvement of the central nervous system. X-linked (males) [145] 5. Robin sequence (SOX9): A sequential chain of signs that start with micrognathia, followed by retraction of the tongue (glossoptosis) and upper airway obstruction. U-shaped cleft palate is very common [146] 6. Rieger syndrome (PITX2, FOXC1): Mild craniofacial abnormalities, and various abnormalities of the eye, especially glaucoma [147]

Because dental treatment is complex; a multi-disciplinary approach is best Children may need dentures as early as 2 years of age Multiple denture replacements are often needed as the child grows, and dental implants may be an option in late adolescence or adulthood, once the jaw is fully grown Orthodontic treatment may also be necessary

Supernumerary teeth/hyperdontia Non-syndromic supernumerary teeth

Mostly single or double supernumeraries, results in crowding, delayed eruption, diastema, rotations, cystic lesions, and resorption of the adjacent teeth

Rare in relation to syndromic

Syndromic hyperdontia (most likely candidates)

1. Cleidocranial dysplasia (RUNX2): Clavicles are poorly developed or absent so the shoulders are brought close together, supernumerary teeth, enamel-dentin hypoplasia, delayed teeth eruption, bone hypoplasia 2. Gardner’s syndrome (APC): Adenomatous polyps of the gastrointestinal tract which usually undergoes malignant change by the fourth decade. Mandibular lesion consisting of clumped toothlets [147–150]

There are several treatment strategies to treat CCD Dental practitioners’ awareness for clinical/radiological characteristics of Gardner’s syndrome; early detection of associated polyps could be lifesaving

AI variants

Type I (AMELX/ENAM): Hypoplastic, thin enamel. Enamel on the cervical 1/3 of the crowns is usually most severely affected, and horizontal groves of severely hypoplastic enamel could be evident Type II (MMP20/KLK4/WDR72/C4orf26/ SLC24A4): Hypomaturation, softer enamel with normal thickness. The enamel has a milky to shiny agar-brown color in newly erupted teeth but may become more deeply stained in contact with exogenous agents; it tends to chip away Type III (FAM83H): Hypocalcified. The enamel has a cheesy consistency and can be scraped from the dentin with a dental explorer. Newly erupted teeth are covered with a dull, opaque white honey-colored or yellow-­ orange-­brown enamel Type IV (DLX3): Hypomature hypoplastic enamel with taurodontism. Enamel has a variation in appearance, with mixed features from type 1 and type 2 AI. All type 4 AI have taurodontism in common

Subjects with AI regardless of the variant showed accelerated dental age [151] There is a sixfold increase in tendency of AI patients to show impaction of the permanent teeth and associated anomalies such as follicular cysts Forty-two percent of AI patients presented with skeletal and/or dental open bite compared to 12% in unaffected family members

Dental fluorosis

Mottled teeth: Early stage or mild (opaque, white spots, narrow white lines following the perikymata) and late stage or severe (enamel appears yellowish and pitted with white-brown lesions that look like cavities) [152]

Enamel defects

(continued)

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..      Table 17.8 (continued) Abnormal tooth number Hypo−/oligodontia DDX Genotype/phenotype

Notes

Molar incisor hypomineralization

Enamel opacities of the affected permanent molars and usually incisors (index teeth). They appear yellow, brown, cream, or white [153]. Other teeth may be involved

Multifactorial disease (perinatal illness, fevers, other unknown factors)

Syndromic enamel hypoplasia (most likely candidates)

1. Pseudohypoparathyroidism (GNAS): Short fourth and fifth metacarpals and rounded facies, tetany, enamel hypoplasia, interglobular dentin, delayed eruption [154] 2. Epidermolysis bullosa (PLEC1, COL17A1, LAMA3, LAMB3, LAMC2, and ITGB4, among others): Easy blistering of the skin and mucous membranes, enamel hypoplasia, cementum dysplasia, taurodontism 3. Vitamin D-dependent rickets type I and II (CYP27B1, VDR): Pitted type enamel hypoplasia [155] short stature, yellowish-to-brownish enamel 4. Vitamin D-resistant rickets (PHEX, CLCN5, DMP1, FGF23): Excessive pulp horn, interglobular dentin, “spontaneous” abscesses, bowed or knock-kneed legs, and a deformed chest and skull, with prominent frontal and parietal bones causing a distinctive “square headed,” taurodontism, poorly defined lamina dura, and hypoplastic alveolar ridge [156]

Alopecia is seen only in some vitamin D-resistant rickets

Dentin defects

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DD-I (dentin dysplasia type I)

Unknown gene: Rare autosomal dominant condition with clinically normal crowns and diminished root development. After an initial layer of normal dentin forms, there are repeated cycles of odontoblast death followed by new odontoblast recruitment leading to “cascading waterfall” histological appearance and pulp obliteration [157]

DGI-I/OGI (dentinogenesis imperfecta type I/osteogenesis imperfecta)

COL1A1 and COL1A2 mutation: Associated with osteogenesis imperfecta, primary teeth are more severely affected compared to the permanent dentition, commonly involving lower incisors and canines

DGI-II, DGI-III and DD-II

DSPP mutations: DGI-II, DGI-III, and DD-II are likely to be the same disease. No effect on bone. The effect of DSPP mutations on the protein may determine the severity of the clinical phenotypes: (1) DD-II, partial pulp obliteration and mild discoloration; (2) DGI II, complete pulpal obliteration and discoloration in both dentitions; and (3) DGI III, pulpal exposure and early abscess

Regional odontodysplasia

Non-hereditary: Ghost teeth appear more radiolucent than normal. These teeth are very brittle, and many of these teeth do not erupt [122]

Syndromic dentin hypoplasia (most likely candidates)

1. Ehlers-Danlos syndrome (ADAMTS2, PLOD1, TNXB…): Loose joints, stretchy skin and abnormal scar formation 2. Vitamin D-resistant rickets (mentioned in the enamel section) 3. Pseudohypoparathyroidism (mentioned in the enamel section) 4. Epidermolysis bullosa (mentioned in the enamel section)

Bisphosphonates – The nitrogen-­ containing in particular – Are being administrated to OGI patients to increase bone mass and reduce the incidence of fracture. Autosomal dominant or recessive inheritance

There is no predilection for race, but females are more likely to get regional odontodysplasia

Cementum defects Cementum hypoplasia (most likely candidates)

1. Hypophosphatasia (ALPL): Acellular and cellular cementum defect, excessive mobility of teeth, and premature exfoliation of teeth, usually missing the front teeth. Also present abnormal enamel (less severe in primary dentition), pulp chamber bigger 2. Epidermolysis bullosa (mentioned in the enamel section) 3. Cleidocranial dysplasia (mentioned in the hyperdontia section)

Cementum hyperplasia (most likely candidates)

1. Gnathodiaphyseal dysplasia (ANO5): Reduced bone mineral density (osteopenia, various amounts of cementum like calcified mass [158] 2. Cemento-osseous dysplasia (unknown): Benign, arise from the fibroblasts of the periodontal ligaments, periapical the lesion occurs in the mandibular incisors [159]

Lab tests for hypophosphatasia: Fasting serum ALP is lower 24 hr. urine PEA elevated Serum PLP will be elevated

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146. Selvi R, Mukunda PA. Role of SOX9 in the etiology of PierreRobin syndrome. Iran J Basic Med Sci. 2013;16(5):700–4. 147. Alhashimi N, Abed Al Jawad FH, Al Sheeb M, Al Emadi B, Al-Abdulla J, Al Yafei H. The prevalence and distribution of nonsyndromic hyperdontia in a group of Qatari orthodontic and pediatric patients. Eur J Dent. 2016;10(3):392–6. https:// doi.org/10.4103/1305-­7456.184162. 148. Singh K, Singh A, Kumar P, Gupta N.  Prosthodontic management of a patient with Gardner's syndrome: a clinical case report. Dent Res J (Isfahan). 2014;11(2):276–80. 149. Aletaha M, Fateh-Moghadam H. Gardner syndrome. J Ophthalmic Vis Res. 2012;7(3):257–60. 150. Öner AY, Pocan S. Gardner's syndrome: a case report. Br Dent J. 2006;200(12):666–7. https://doi.org/10.1038/sj.bdj.4813719. 151. Seow WK. Dental development in amelogenesis imperfecta: a controlled study. Pediatr Dent. 1995;17(1):26–30. 152. Ritter AV.  Talking with patients dental fluorosis. J Esthet Restor Dent. 2005;17(5):326–7. https://doi.org/10.1111/j.1708­8240.2005.tb00139.x. 153. Weerheijm KL, Jälevik B, Alaluusua S. Molar–incisor hypomineralisation. Caries Res. 2001;35(5):390–1. https://doi. org/10.1159/000047479. 154. de Nanclares GP, Fernández-Rebollo E, Santin I, GarcíaCuartero B, Gaztambide S, Menéndez E, et  al. Epigenetic defects of GNAS in patients with pseudohypoparathyroidism and mild features of Albright’s hereditary osteodystrophy. J Clin Endocrinol Metab. 2007;92(6):2370–3. https://doi. org/10.1210/jc.2006-­2287. 155. Kitanaka S, Kato S.  Vitamin D-dependent rickets Type I and Type II.  The genetics of osteoporosis and metabolic bone disease. Humana Press. 2000;95–110. https://doi. org/10.1007/978-­1-­59259-­033-­9_6. 156. Inoue Y, Segawa H, Kaneko I, Yamanaka S, Kusano K, Kawakami E, et al. Role of the vitamin D receptor in FGF23 action on phosphate metabolism. Biochem J. 2005;390(1):325– 31. https://doi.org/10.1042/BJ20041799. 157. Ye X, Li K, Liu L, Yu F, Xiong F, Fan Y, et al. Dentin dysplasia type I—novel findings in deciduous and permanent teeth. BMC Oral Health. 2015;15:163. https://doi.org/10.1186/ s12903-­015-­0149-­9. 158. Rolvien T, Koehne T, Kornak U, Lehmann W, Amling M, Schinke T, et al. A novel ANO5 mutation causing gnathodiaphyseal dysplasia with high bone turnover osteosclerosis. J Bone Miner Res. 2017;32(2):277–84. https://doi.org/10.1002/ jbmr.2980. 159. Alsufyani NA, Lam EW. Osseous (cemento-­osseous) dysplasia of the jaws: clinical and radiographic analysis. J Can Dent Assoc. 2011;77:b70.

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465

Tooth Wear in Children and Adolescents Nikolaos Kotsanos and Dowen Birkhed Contents 18.1

Various Types of Tooth Wear – 466

18.1.1 18.1.2

 ttrition and Abrasion – 466 A Erosive Tooth Wear – 466

18.2

Tooth Wear and Bruxism in Children – 467

18.3

Dental Erosion – 467

18.3.1 18.3.2 18.3.3 18.3.4 18.3.5

 revalence and Severity – 467 P Aetiology of Dental Erosion – 469 Examination and Diagnosis – 470 Prevention of Erosion – 471 Restoration of Erosive Lesions – 471

References – 472

© Springer Nature Switzerland AG 2022 N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry, https://doi.org/10.1007/978-3-030-78003-6_18

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There are different types of tooth wear, but in children and adolescents, dental erosion is the most common type. Since it relates to teeth lifetime and oral function, erosive tooth wear is usually lower in the primary than in the permanent dentition. The dentin of primary teeth can however be more rapidly exposed mainly due to thinner enamel than in corresponding permanent teeth [1]. Significant wear of young permanent teeth results in restorative needs and must therefore be diagnosed as early as possible and treated promptly. Dental erosion has increased during the last decades in many countries, and most studies relate this to an increased consumption of soft drinks and to changes of lifestyle [2, 3]. Erosive tooth wear is a cumulative multifactorial process starting from the eruption of the teeth. To some extent, it may be considered as a normal condition rather than an oral disease since the acid is of no pathological origin [4, 5].

18.1

Various Types of Tooth Wear

18.1.1

18

..      Fig. 18.1  The facets of lateral incisors in this primary dentition denote that attrition is involved in the tooth wear mechanism

a

Attrition and Abrasion

Both attrition and abrasion are related to mechanical wear, and acids are not involved as is in the case for dental erosion. Attrition is caused by tooth-to-tooth contact and is in most cases considered physiological. When it comes to “bruxism” (excessive teeth grinding), which is a more severe form of attrition, it often takes place during the night, which produces distinctive sound and is perceived by the patient’s environment. Abrasion is another form of mechanical wear induced by the interaction between teeth and foreign objects or substances. Both these two types of tooth wear (attrition and abrasion) are not always easily distinguishable. Pronounced occlusal wear has been found in skulls of past centuries and is attributable to chewing unrefined foods that act as a foreign substance. In bruxism, hard dental tissue micro-particles breaking off may act as an abrasive substance for the teeth [6]. Clinically, occlusal wear creates flat surfaces (facets) that fit each other in antagonist teeth (. Fig. 18.1). Similarly, attrition shortly leads to the flattening of the lobular cutting edge of newly erupted anterior teeth (. Fig. 18.2). Abrasion due to foreign objects may become apparent after intensive tooth brushing with toothpaste. Abrasion appears to be influenced by the frequency, duration and force of brushing [7] but is insignificant when brushing is carried out without toothpaste. Abrasion can be avoided by using toothpaste with low abrasivity and brushing with a gentle hand [8, 9]. On the other hand, toothpastes with whitening and stain removal properties often have high abrasivity [10].  

 

b

..      Fig. 18.2  a Uniform occlusal tooth wear of a 6-year-old girl. Notice the beginning of lobular incisal edge flattening of the newly erupted mandibular left central incisor. b Similarities in her mother’s dentition. There was no history connecting either of them with false dietary behaviours

Abrasion usually appears in adolescence as saucer-­ shaped cervical wear due to over brushing with incorrect horizontal movements, even worse when a hard bristle brush is used. Prevention is important because cervical abrasion can be more intense with increasing age and is often acquiring a wedge-shaped form combined with gingival recession (. Fig. 18.3).  

18.1.2

Erosive Tooth Wear

Dental erosion is defined as the loss of tooth structure by acid dissolution without the involvement of bacteria. It can be caused either by outer factors (drinks and

467 Tooth Wear in Children and Adolescents

understandably, does not correlate with age [17]. The most frequently affected tooth surfaces of attrition both in children and adults are the occlusal surfaces of molars and the incisal edges of anterior teeth by being the prime surfaces subject to the function of mastication (. Figs. 18.4 and 18.5).

a

 

b

Eye Catcher

..      Fig. 18.3  a Saucer-shaped erosive tooth wear of an 18-year-old male with overuse of lemons and juices. His gingival recession points to tooth brushing as a contributory factor. b Generalized erosive tooth wear modified by wedge-shaped abrasive wear in the posterior teeth due to his damaging brushing technique. (Courtesy Dr. C. Paximada)

The extent of synergy between attrition and erosive action cannot be easily estimated. Studies of sculls from past centuries reveal that the dentition was physiologically worn due to unrefined diets requiring much heavier mastication [18]. On the other hand, in modern populations, the ideal occlusion is represented by a dentition without wear, with a small (3–4 mm) overjet and vertical incisal coverage.

Observation of contemporary attrition patterns sugother acidic food products) or by inner factors (regurgi- gests that mandibular movement in sleep bruxism may tation and vomiting). It may appear on virtually plaque-­ be associated with current tooth attrition [19]. The prevfree tooth surfaces. Following dissolution of the outer alence of both self-reported and partner-reported sleep layer of enamel and/or dentin, the resulting surface is bruxism in young adults was found to be significantly more susceptible to mechanical wear of tooth brushing more common in the attrition group compared to the or mastication forces. Therefore, it is often a combina- controls [20]. The prevalence of bruxism in children is tion of dental erosion and abrasion. The primary tooth high, about 37% for preschool and 50% for first-grade enamel appears to be more prone to erosion than the primary school children in the USA, according to parenpermanent one in frequent consumption of acidic drinks tal records [20, 21]. In 4- to 9-year-old children with [11]. The salivary flow rate, buffering capacity and cerebral palsy, 70% of them exhibited bruxism [22]. In mucoprotein content affect the sensitivity-susceptibility 6-year-old children, bruxism resulted in greater wear of primary canines [23]. Significantly more attrition is of individuals to dental erosion [12]. Another type of tooth wear pathology, called abfrac- observed in young men than in women [24]. Significant attrition is often observed in dental tion, makes the enamel vulnerable to masticatory shear anomalies characterized by reduced tooth hardness, stress in the cervical area and is apparent in older age either developmental (e.g. molar incisor hypomineral[13]. All previously described types of wear can act ization, MIH) or inherited ones (e.g. dentinogenesis and simultaneously, but the morphology of defects may subamelogenesis imperfecta, . Fig. 18.6). Measures to prestantially vary depending on the predominant aetiologivent severely worn teeth in such children include restoracal factor [14]. The combination of these processes can tion of occlusal surfaces of primary or permanent teeth cause synergistic results (. Fig.  18.3), as the softer with composite or preformed metal crowns. enamel and dentin after an erosive acid attack are more prone to abrasion by an immediate brushing action [15]. Such effects are more obvious in some enthusiastic 18.3 Dental Erosion brushers in adolescence.  

 

18.2

Tooth Wear and Bruxism in Children

Physiological tooth wear (attrition) increases with age, and in modern societies, it is estimated that the acceptable wear rate of the posterior teeth is approximately 15–20 μm/year [16]. The severity of any type of pathological wear depends on parafunctional habits and,

18.3.1

Prevalence and Severity

Dental erosion seems to be the worst contemporary type of dental wear, and the dental community shows an increasing concern in the current century. Erosion began being recorded in Britain since 1993, and the prevalence had shown to increase within a few years [25]. There are more erosion prevalence studies in children and adoles-

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..      Fig. 18.4  a Tooth wear of a 5-year-old. b The occlusal and incisal wear is thought as owed to reported night bruxism, which, in combination to existing primary molar hypomineralization, led also to breakdown visible on the bucco-occlusal crest of first molar. c Occlusal wear of an Essix splint used at night verifies the action of attrition forces

a

b

18

..      Fig. 18.5  Severe occlusal wear extensively exposing the dentin in a 5.5-year-old with night bruxism. The greater wear in the anterior region is attributed to edge-to-edge type of occlusion. (Courtesy Dr. S. Papapetrou)

cents than in adults, which is mainly due to the ease of finding the respective study samples. A recent review of the global prevalence of erosive tooth wear shows a

c

mean prevalence in deciduous teeth between 30% and 50% and in permanent teeth between 20% and 45% [26]. The wide variation in prevalence has been attributed except for dietetic habits to the multiplicity of indices measuring tooth erosion. Some studies indicate a positive association between dental erosion and caries in teenagers [27, 28], while other reports find no such association. Concerning the primary teeth, erosion was found in 5.7% of preschool Chinese children, in 31% in Saudi Arabia and in 47% of 5-year-old Irish children [29–31]. A recent meta-analysis of all the studies published in the literature over the past three decades on the prevalence of dental erosion in preschool children showed that tooth wear into the dentin of deciduous teeth in children increases linearly with age [32]. A German study reported that the prevalence and risk factors of erosive tooth wear in 3- to 6-year-old kindergarten children increased from 2004–2005 to 2014–2015 [33]. In adolescence, prevalence data shows great variability, ranging from 37% to 100% in various European countries and the USA, and a variety of tooth numbers with erosive lesions [34, 35]. A Greek study, using a

469 Tooth Wear in Children and Adolescents

a

b

..      Fig. 18.6  Mandibular first molars of a 9-year-old odontogenesis imperfecta patient with worn out/disintegrated enamel casps exposing the defective dentin

newer index (BEWE, Basic Erosive Wear Examination, which does not evaluate wear depth but measures erosive tooth wear semi-quantitatively by its extent on tooth surfaces), recorded erosion in 65% of primary teeth of 8-year-olds and in 37% of permanent teeth of 14-year-olds [36]. 18.3.2

Aetiology of Dental Erosion

The aetiological factors for dental erosion can be divided into those of extrinsic and intrinsic origin. 18.3.2.1

Extrinsic Factors

1. Diet: The parameter of diet has been the most extensively studied factor regarding dental erosion. There are several reviews on the influence of diet on tooth erosion prevalence in children and adolescents [37– 39]. Overconsumption of acidic drinks (soft drinks and fruit juices), citrus fruits and lemon or vinegar is the most common aetiological factor (. Fig. 18.7). Despite the wide variation among populations  – in 1995 one in ten US students consumed at least four soft drinks daily [40] and in 2001 in Britain at least three soft drinks daily [41] – children generally consume more soft drinks and juices than adults. In Britain, 2/5 of fruit drinks are consumed by children up to 9 years old [42]. The soft drink consumption has been tripled in the USA in the last 20  years of the past century [43]. The acidity of some popular drinks aimed at young people ranges from pH = 2.6 (CocaCola, Sprite) and 3.0 (ice tea) to 3.4 (Red Bull) [44]. Except for the acidity, the erosive potential of a beverage depends on its inorganic content, its resistance to pH neutralization (buffer capacity) and possibly other chemical properties. At the same acidity levels, citric acid causes more erosion in  vitro than phosphoric acid [44], while the addition of calcium (and a  

..      Fig. 18.7  a Erosive tooth wear in a 15-year-old admitting overusing lemon in his diet. Maxillary central incisors present glossy surface with obvious enamel thickness reduction. b Incisal view of thinness

small amount of phosphate and fluoride) in juices may reduce their erosive potential [45]. 2. Medicines: Several studies have discussed the use of various medicines and their role for causing dental erosions in primary and permanent teeth [46–48]. One factor to take into consideration is the length of the treatment and the intake frequency of the drug. Thus, a causal relationship has been found for the frequent use of acetylsalicylic acid (aspirin) that is used in the treatment of juvenile rheumatoid arthritis as well as for ascorbic acid (vitamin C) [49, 50]. Both positive [51] and negative relationships [52] with erosion have been reported with asthma inhalation drugs. 3. Behaviour factors: There are some factors related to diet and particularly to drinking habits that can affect the erosion risk, such as swishing or retaining the soft drink, lemon or citrus fruits in the mouth before swallowing [53]. Other patient-­ related factors are intake frequency, lifestyle and oral hygiene [54]. It is not clear how socioeconomic status affects the prevalence of dental erosion. Most studies show a positive association with low socioeconomic status, but there are also some studies showing the opposite. A Chinese study in particular found that preschool children of higher socioeconomic status (higher parent educational level) drank more fruit juices daily [29]. When comparing factors potentially related to the occurrence of dental erosion in high- and low-erosion groups of young Saudi men, it was found that drinking habits was a significant factor [55]. Moreover, the contact time between the tooth and the acid may be a more important risk factor for dental erosions com-

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pared to frequency of dietary acid intake or frequency of tooth brushing [56]. Logistic regression of 392 Swedish adolescents showed predictive variables for high consumption of carbonated soft drinks, and thereby for dental erosion, to be unhealthy dietary habits, less physical activity, high BMI and long time spent in front of TV/computer [57]. 18.3.2.2 Intrinsic Factors kGastroesophageal Reflux Disease (GERD) and Vomiting

The hydrochloric acid (HCl) of the stomach reaches the mouth through vomiting or regurgitation and causes dental erosion especially in the palatal surfaces of upper anterior teeth, called perimylolysis (. Fig. 18.8). Lack of treatment of this condition results in the destruction of posterior teeth mainly their palatal cusps and occlusal surfaces. These acid-demineralized occlusal surfaces are less resistant to occlusal wear, and the result is a combination of chemical erosion and attrition. Erosion from chronic vomiting is uncommon in children. The vomiting may be spontaneous or induced and related with pathological conditions, e.g. irritable intestine syndrome, nausea or migraine and epilepsy [58]. Long-lasting emetic episodes starting from preschool age and continuing during child’s growth show a reduced frequency in adulthood suggesting a self-limiting condition. Vomiting is most common in the first 3 months of pregnancy. Vomiting is also sometimes self-induced by young women or even adolescents suffering from bulimia or anorexia nervosa [59, 60]. New-born babies often show GERD, but after the age of 1 year with the eruption of the first primary teeth, the frequency of this condition is reduced to 8% [61]. Moreover, a study in 2- to 16-year-old children with GERD showed no significantly increased dental erosion and concluded that perhaps the reflux of gastric acids in children is constrained in the esophagus [61]. Dentists however should keep in mind that children do not usually report this reflux because they consider it as normal.  

18

18.3.3

Examination and Diagnosis

The clinical examination includes inquiring for dietary habits, tooth brushing method, other habits, presence of GERD and estimation of salivary secretion rate and buffer capacity. Diagnosis is based on visual examination because all types of dental wear occur in clinically accessible surfaces. A relatively early finding of erosive tooth wear is the glossy appearance due to loss of surface structure (perikymata) of the enamel. A frequent later finding is an increased incisal edge transparency of the crown of anterior teeth (. Fig. 18.9). The most frequently affected sites are the occlusal surfaces of pri 

..      Fig. 18.8  An 18-year-old young man with GERD and severe erosion of the maxillary teeth (perimylolysis). Please observe that the palatal cusps of the premolars, especially the one on left side, are eroded and that the amalgam fillings, which are not affected of the stomach acid, are shiny and “stand out” on the palatal surfaces of the first molars and on the one of the premolars. The patient also has approximal caries in the anterior teeth, which is more noticeable because of the erosion of the palatal surfaces

a

b

..      Fig. 18.9  a Erosive tooth wear of an 18-year-old female with “sour taste preference” with pronounced incisal edge translucency of maxillary central incisors. b Erosion is complicated with incisal enamel breakdown of a 25-year-old male who likes to bite lemons

mary molars and palatal or labial surfaces of upper anterior teeth [34, 35]. This is associated with the predominant erosive factor, e.g. GERD or frequent consumption of acidic products. In advanced stages, dentin exposure can be observed (. Fig. 18.10). Depending on the prime aetiological and contributing factors, this may be in the palatal surface of anterior teeth or the occlusal surfaces of posterior teeth, starting with cupping in the cusp tips (. Fig.  18.6). Generally, the early stages of erosion are difficult to diagnose, especially before significant depth of enamel has been lost and dentin expo 

 

471 Tooth Wear in Children and Adolescents

a

proved wrong, revealing the difficulties in identifying true depth or lesions [65]. 18.3.4

b

c

..      Fig. 18.10  a Severe erosive tooth wear of the central incisors in a 20-year-old male with a history of 1.5lt daily consumption of cola drink. Note the minimal wear with stain deposited on the misaligned laterals’ labial surfaces. b Generalized wear of the palatal surfaces with exposed dentin in the lateral incisor. c Wear (and approximal caries) in his posterior maxillary teeth. (Courtesy Dr. C. Paximada)

sure and/or hypersensitivity is apparent, unless there is experience and specific interest in dental wear. Different index systems for grading dental wear severity in the clinical situation have been described. The most widely used tooth wear index is the one by Smith and Knight [62] using four grades – from 0 (no signs of dental wear) to 4 (pulp exposure or tertiary dentin). The number of such indices reported in the literature is extremely large amounting to dozens. The preferred index should be relatively simple so as to be used in epidemiological studies with large population samples, while it should be sensitive enough to accurately depict wear depth and extent on all tooth surfaces. Some indices like the “Basic Erosive Wear Examination” (BEWE) record only the most severely (regarding the surface area) affected tooth surface in each sextant of the dentition [63, 64]. Regarding the depth of erosive lesions, the comparison of clinical to histological assessments has shown that 1/3 of recordings of dentin exposure were

Prevention of Erosion

In the permanent teeth, dental erosion may develop early in life and may commonly be progressive [66]. Dentists should therefore be aware of this fact and perform regular screenings for erosion and recording of associated lifestyle factors [66]. Concerning the difficulty in early recognition of erosion, proper training of dental practitioners can help its diagnosis and prevention. Measures include [67–69]: 55 Detailed recording of diet for 4 continuous days (with 1–2 holidays), including the exact time, quantity and type of consumption, the time of brushing, evaluation of the erosive potential of acidic foods/ drinks and instructions to decrease them 55 Evaluation of GERD or vomiting reflexes and referral to a gastroenterologist if necessary. Chewing antacid tablets [70] or mouth washing with soda solution to neutralize acids 55 Brushing teeth with a soft tooth brush and low abrasivity toothpaste at a time that does not coincide with the presence of acidic pH in the saliva, e.g. at least 20  min after taking acidic food or drinks [71–73] 55 Personalized fluoride treatment (includes fluoride varnish or gel, brushing with high fluoride concentration toothpaste or stannous fluoride) [74] or possibly other enhancing agents 55 Instructions for inspection and possible improvement of saliva parameters, e.g. by chewing gum [54] 18.3.5

Restoration of Erosive Lesions

Eye Catcher

Just as with dental caries, restoring teeth with erosive lesions is not a causative treatment. It may however be useful for arresting their progression, for relieving possible hypersensitivity and for functional and aesthetic reasons. Restorative treatment does not replace preventive (causative) treatment, for the added reason that many restorative materials are affected by enamel erosion acids.

Composites are considered as the first choice of restorative treatment. Small to moderate occlusal lesions can be filled after using dentin bonding adhesives. In cervical lesions, glass ionomers are said to be inappropriate

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a

b

c

d

..      Fig. 18.11  a Erosive tooth wear of a young female needing restoration. b Initial reduction of labial tooth surfaces using a special bur with depth guide. c Near-final preparations for porcelain veneers. d

Final restorations of the six maxillary anterior teeth. (Courtesy Dr. P. Gerasimou)

because they are susceptible to erosion too [75, 76], although resin-modified glass ionomers are likely be more durable and suitable. In severely worn anterior teeth except for composite resin restorations with celluloid matrix (strip crown), porcelain veneers can be used at the end of adolescence (. Fig.  18.11). There is no data available about their longevity, other to limited evidence in teeth with caries or crown fractures. There have been many publications lately on the management of tooth wear with crowns and indirect restorations [77–81]. The conclusions from these literature reviews are that there is no strong evidence to suggest that any material is better than another. Direct or indirect materials may be feasible options to restore severely worn teeth. However, most of these reviews are focusing on rehabilitation of severely worn teeth in adults and very few on younger individuals.

 2. Carvalho TS, Lussi A, Jaeggi T, Gambon DL.  Erosive tooth wear in children. Monogr Oral Sci. 2014;25:262–78.  3. Johansson AK, Omar R, Carlsson GE, Johansson A.  Dental erosion and its growing importance in clinical practice: from past to present. Int J Dent. 2012;2012:632907.   4. Ganss C. Is erosive tooth wear an oral disease? Monogr Oral Sci. 2014;25:16–21.   5. Ganss C, Lussi A. Diagnosis of erosive tooth wear. Monogr Oral Sci. 2014;25:22–31.   6. Xhonga FA. Bruxism and its effect on the teeth. J Oral Rehabil. 1977;4:65–7.   7. Dyer D, Addy M, Newcombe RG. Studies in vitro of abrasion by different manual toothbrush heads and a standard toothpaste. J Clin Periodontol. 2000;27:99–103.   8. Addy M, Hunter ML. Can tooth brushing damage your health? Effects on oral and dental tissues. Int Dent J. 2003;53(Suppl 3):177–86.   9. Philpotts CJ, Weader E, Joiner A. The measurement in vitro of enamel and dentine wear by toothpastes of different abrasivity. Int Dent J. 2005;55:183–7. 10. Schemehorn BR, Moore MH, Putt MS.  Abrasion, polishing, and stain removal characteristics of various commercial dentifrices in vitro. J Clin Dent. 2011;22:11–8. 11. Hunter ML, West NX, Hughes JA, Newcombe RG, Addy M.  Erosion of deciduous and permanent dental hard tissue in the oral environment. J Dent. 2000;28:257–63. 12. Amaechi BT, Higham SM. Eroded enamel lesion remineralization by saliva as a possible factor in the site-­specificity of human dental erosion. Arch Oral Biol. 2001;46:697–703.

 

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References 1. Kreulen CM, Van't Spijker A, Rodriguez JM, Bronkhorst EM, Creugers NH, Bartlett DW. Systematic review of the prevalence of tooth wear in children and adolescents. Caries Res. 2010;44:151–9.

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13. Grippo JO.  Abfractions: a new classification of hard tissue lesions of teeth. J Esthet Dent. 1991;3:14–9. 14. Lussi A, Hellwig E.  Risk assessment and preventive measures. Monogr Oral Sci. 2006;20:190–9. 15. Attin T, Siegel S, Buchalla W, Lennon AM, Hannig C, Becker K. Brushing abrasion of softened and remineralised dentin: an in situ study. Caries Res. 2004;38:62–6. 16. Lambrechts P, Braem M, Vuylsteke-Wauters M, Vanherle G.  Quantitative in  vivo wear of human enamel. J Dent Res. 1989;68:1752–4. 17. Bartlett D, Dugmore C. Pathological or physiological erosion--is there a relationship to age? Clin Oral Investig. 2008;12(Suppl 1):S27–31. 18. Kaifu Y.  Changes in the pattern of tooth wear from prehistoric  to recent periods in Japan. Am J Phys Anthropol. 1999;109:485–99. 19. Okura K, Shigemoto S, Suzuki Y, Noguchi N, Omoto K, Abe S, Matsuka Y.  Mandibular movement during sleep bruxism assoc  ated with current tooth attrition. J Prosthodont Res. 2017;61:87–95. 20. Jonsgar C, Hordvik PA, Berge ME, Johansson AK, Svensson P, Johansson A.  Sleep bruxism in individuals with and without attrition-type tooth wear: an exploratory matched case-control electromyographic study. J Dent. 2015;43:1504–10. 21. Insana SP, Gozal D, McNeil DW, Montgomery-­ Downs HE.  Community based study of sleep bruxism during early childhood. Sleep Med. 2013;14:183–8. 22. Peres AC, Ribeiro MO, Juliano Y, César MF, Santos RC. Occurrence of bruxism in a sample of Brazilian children with cerebral palsy. Spec Care Dentist. 2007;27:73–6. 23. Rios D, Magalhães AC, Honório HM, Buzalaf MA, Lauris JR, Machado MA. The prevalence of deciduous tooth wear in sixyear-old children and its relationship with potential explanatory factors. Oral Health Prev Dent. 2007;5:167–71. 24. Seligman DA, Pullinger AG, Solberg WK. The prevalence of dental attrition and its association with factors of age, gender, occlusion and TMJ symptomatology. J Dent Res. 1988;67:1323–33. 25. Nunn JH, Gordon PH, Morris AJ, Pine CM, Walker A. Dental erosion - changing prevalence? A review of British National childrens' surveys. Int J Paediatr Dent. 2003;13:98–105. 26. Schlueter N, Luka B.  Erosive tooth wear  - a review on global prevalence and on its prevalence in risk groups. Br Dent J. 2018;224:364–70. 27. Isaksson H, Birkhed D, Wendt LK, Alm A, Nilsson M, Koch G.  Prevalence of dental erosion and association with lifestyle factors in Swedish 20-year olds. Acta Odontol Scand. 2014;72:448–57. 28. Mulic A, Tveit AB, Skaare AB. Prevalence and severity of dental erosive wear among a group of Norwegian 18-year-olds. Acta Odontol Scand. 2013;71:475–81. 29. Luo Y, Zeng XJ, Du MQ, Bedi R. The prevalence of dental erosion in preschool children in China. J Dent. 2005;33:115–21. 30. Al-Malik MI, Holt RD, Bedi R.  Erosion, caries and rampant caries in preschool children in Jeddah, Saudi Arabia. Community Dent Oral Epidemiol. 2002;30:16–23. 31. Harding MA, Whelton H, O’Mullane DM, Cronin M.  Dental erosion in 5-year-old Irish school children and associated factors: a pilot study. Community Dent Health. 2003;20:165–70. 32. Corica A, Caprioglio A.  Meta-analysis of the prevalence of tooth wear in primary dentition. Eur J Paediatr Dent. 2014;15:385–8. 33. Tschammler C, Müller-Pflanz C, Attin T, Müller J, Wiegand A. Prevalence and risk factors of erosive tooth wear in 3-6 year old German kindergarten children  – a comparison between 2004/05 and 2014/15. J Dent. 2016;52:45–9.

34. Jaeggi T, Lussi A. Prevalence, incidence and distribution of erosion. Monogr Oral Sci. 2006;20:44–65. 35. Provatenou E, Kaklamanos E, Kevrekidou A, Kosma I, Kotsanos N.  Erosive tooth wear and related risk factors in 8- and 14-year-old Greek children. Caries Res. 2016;50: 349–62. 36. Margaritis V, Mamai-Homata E, Koletsi-­Kounari H, Polychronopoulou A.  Evaluation of three different scoring systems for dental erosion: a comparative study in adolescents. J Dent. 2011;39:88–93. 37. Salas MM, Nascimento GG, Vargas-Ferreira F, Tarquinio SB, Huysmans MC, Demarco FF.  Diet influenced tooth erosion prevalence in children and adolescents: results of a meta-analysis and meta-regression. J Dent. 2015;4:865–75. 38. O'Toole S, Mullan F. The role of the diet in tooth wear. Br Dent J. 2018;224:379–83. 39. Lussi A, Jaeggi T, Zero D. The role of diet in the aetiology of dental erosion. Caries Res. 2004;38(Suppl 1):34–44. 40. American Academy of Pediatrics, Committee on School Health. Soft drinks in school. Pediatrics. 2004;113:152–3. 41. Al-Dlaigan YH, Shaw L, Smith A. Dental erosion in a group of British 14-year-old school children. Part II: influence of dietary intake. Br Dent J. 2001;190:258–61. 42. Rugg-Gunn AJ, Lennon MA, Brown JG. Sugar consumption in the United Kingdom. Br Dent J. 1986;161:359–64. 43. Cavadini C, Siega-Riz AM, Popkin BM.  US adolescent food  intake trends from 1965 to 1996. Arch Dis Child. 2000;83:18–24. 44. Lussi A, Jaeggi T.  Chemical factors. Monogr Oral Sci. 2006;20:77–87. West NX, Hughes JA, Addy M. The effect of pH on the erosion of dentine and enamel by dietary acids in vitro. J Oral Rehabil. 2001;28:860–4. 45. Barbour ME, Parker DM, Allen GC, Jandt KD. Human enamel erosion in constant composition citric acid solutions as a function of degree of saturation with respect to hydroxyapatite. J Oral Rehabil. 2005;32:16–21. 46. Lussi A, Carvalho TS. Analyses of the Erosive Effect of dietary substances and medications on deciduous teeth. PLoS One. 2015;10:e0143957. 47. Hellwig E, Lussi A.  Oral hygiene products, medications and drugs  - hidden aetiological factors for dental erosion. Monogr Oral Sci. 2014;25:155–62. 48. Scatena C, Galafassi D, Gomes-Silva JM, Borsatto MC, Serra MC. In vitro erosive effect of pediatric medicines on deciduous tooth enamel. Braz Dent J. 2014;25:22–7. 49. Sullivan RE, Kramer WS.  Iatrogenic erosion of teeth. J Dent Child. 1983;50:192–6. 50. Asher C, Read MJ. Early enamel erosion in children associated with the excessive consumption of citric acid. Br Dent J. 1987;162(10):384–7. 51. Al-Dlaigan YH, Shaw L, Smith AJ.  Is there a relationship between asthma and dental erosion? A case control study. Int J Paediatr Dent. 2002;12:189–200. 52. Dugmore CR, Rock WP. Asthma and tooth erosion. Is there an association? Int J Paediatr Dent. 2003;13:417–24. 53. Johansson AK, Lingström P, Imfeld T, Birkhed D. Influence of drinking method on tooth-surface pH in relation to dental erosion. Eur J Oral Sci. 2004;112:484–9. 54. Buzalaf MAR, Magalhães AC, Rios D.  Prevention of erosive tooth wear: targeting nutritional and patient-­related risks factors. Br Dent J. 2018;224:371–8. 55. Johansson AK, Lingström P, Birkhed D. Comparison of factors potentiall related to the occurrence of dental erosion in highand low-erosion groups. Eur J Oral Sci. 2002;110: 204–11.

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56. O'Toole S, Bartlett D. The relationship between dentine hypersensitivity dietary acid intake and erosive tooth wear. J Dent. 2017;67:84–7. 57. Hasselkvist A, Johansson A, Johansson AK.  Association between soft drink consumption, oral health and some lifestyle factors in Swedish adolescents. Acta Odontol Scand. 2014;72:1039–46. 58. O'Sullivan E, Milosevic A. UK National Clinical Guidelines in Paediatric Dentistry: diagnosis, prevention and management of dental erosion. Int J Paediatr Dent. 2008;18(Suppl 1):29–38. 59. Bartlett D.  Intrinsic causes of erosion. Monogr Oral Sci. 2006;20:119–39. 60. Osatakul S, Sriplung H, Puetpaiboon A, Junjana CO, Chamnongpakdi S. Prevalence and natural course of gastroesophageal reflux symptoms: a 1-year cohort study in Thai infants. J Pediatr Gastroenterol Nutr. 2002;34:63–7. 61. O'Sullivan EA, Curzon ME, Roberts GJ, Milla PJ, Stringer MD. Gastroesophageal reflux in children and its relationship to erosion of primary and permanent teeth. Eur J Oral Sci. 1998;106:765–9. 62. Smith BG, Knight JK. An index for measuring the wear of teeth. Br Dent J. 1984;156:435–8. 63. Mulic A, Tveit AB, Wang NJ, et  al. Reliability of two clinical  scoring systems for dental erosive wear. Caries Res. 2010;44:294–9. 64. Bartlett D, Ganss C, Lussi A. Basic Erosive Wear Examination (BEWE): a new scoring system for scientific and clinical needs. Clin Oral Investig. 2008;(Suppl 1):S65–8. 65. Ganss C, Klimek J, Lussi A.  Accuracy and consistency of the visual diagnosis of exposed dentine on worn occlusal/incisal surfaces. Caries Res. 2006;40:208–12. 66. Hasselkvist A, Johansson A, Johansson AK. A 4 year prospective longitudinal study of progression of dental erosion associated to lifestyle in 13-14 year-old Swedish adolescents. J Dent. 2016;47:55–62. 67. Amaechi BT, Higham SM. Dental erosion: possible approaches to prevention and control. J Dent. 2005;33:243–52. 68. Carvalho JC, Scaramucci T, Aimée NR, Mestrinho HD, Hara AT.  Early diagnosis and daily practice management of erosive tooth wear lesions. Br Dent J. 2018;224:311–8.

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69. Carvalho TS, Colon P, Ganss C, Huysmans MC, Lussi A, Schlueter N, et al. Consensus Report of the European Federation of Conservative Dentistry: erosive tooth wear, diagnosis and management. Swiss Dent J. 2016;126:342–6. 70. Lindquist B, Lingström P, Fändriks L, Birkhed D. Influence of five neutralizing products on intra-oral pH after rinsing with simulated gastric acid. Eur J Oral Sci. 2011;119:301–4. 71. Ganss C, Schlueter N, Friedrich D, Klimek J. Efficacy of waiting periods and topical fluoride treatment on toothbrush abrasion of eroded enamel in situ. Caries Res. 2007;41:146–51. 72. O’Toole S, Bernabé E, Moazzez R, Bartlett D. Timing of dietary acid intake and erosive tooth wear: a case-­control study. J Dent. 2017;56:99–104. 73. Lussi A, Lussi J, Carvalho TS, Cvikl B. Toothbrushing after an erosive attack:will waiting avoid tooth wear? Eur J Oral Sci. 2014;122:353–9. 74. Huysmans MC, Young A, Ganss C. The role of fluoride in erosion therapy. Monogr Oral Sci. 2014;25:230–43. 75. Jaeggi T, Grüninger A, Lussi A. Restorative therapy of erosion. Monogr Oral Sci. 2006;20:200–14. 76. Johansson A, Johansson AK, Omar R, Carlsson GE. Rehabilitation of the worn dentition. J Oral Rehabil. 2008;35:548–66. 77. Milosevic A. Clinical guidance and an evidence-­based approach for restoration of worn dentition by direct composite resin. Br Dent J. 2018;224:301–10. 78. Loomans BAC, Kreulen CM, Huijs-Visser HECE, Sterenborg BAMM, Bronkhorst EM, Huysmans MCDNJM, Opdam NJM.  Clinical performance of full rehabilitations with direct composite in severe tooth wear patients: 3.5 years results. J Dent. 2018;70:97–103. 79. Mesko ME, Sarkis-Onofre R, Cenci MS, Opdam NJ, Loomans B, Pereira-Cenci T. Rehabilitation of severely worn teeth: a systematic review. J Dent. 2016;48:9–15. 80. Mehta SB, Banerji S. The restorative management of tooth wear involving the aesthetic zone. Br Dent J. 2018;224:333–41. 81. Varma S, Preiskel A, Bartlett D.  The management of tooth wear  with crowns and indirect restorations. Br Dent J. 2018;224:343–7.

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Temporomandibular Disorders in Children and Adolescents Linda Van den Berghe and Louis Simoen Contents 19.1

 he Orofacial System: Principles of Occlusion T and Function – 476

19.1.1

 entric Positions of the Lower Jaw and  C Temporomandibular Joint – 476 Rest Position – 477 Eccentric Positions – 477 Eccentric Mandibular Movements – 477 Vertical Dimension in Occlusion – 477

19.1.2 19.1.3 19.1.4 19.1.5

19.2

Disorders of the Orofacial System – 478

19.2.1 19.2.2 19.2.3 19.2.4 19.2.5 19.2.6 19.2.7

E pidemiology – 478 Etiology – 478 Anamnestic Records – 480 Clinical Examination – 480 Imaging – 480 Diagnosis – 480 Treatment Strategies – 482

19.3

Summary – 482 References – 482

© Springer Nature Switzerland AG 2022 N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry, https://doi.org/10.1007/978-3-030-78003-6_19

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The content of this chapter is not intended to represent the extensive knowledge of the normal and pathological function of the temporomandibular system. The basic aim is to help the dentist understand the basic principles of normal functioning of the masticatory system [1, 2] and the extent, symptomatology, and etiology of temporomandibular disorders in children and adolescents, in order to enable general practitioners to contribute to treatment.

19.1

 he Orofacial System: Principles T of Occlusion and Function

The orofacial system (OFS) is the biological system of an individual where physiological functions of mastication, swallowing, speech, and breathing are performed. It consists of a number of elements and tissues that act together and form functional units. The components of the OFS are: (a) The temporomandibular joints (TMJs). (b) The maxilla or upper jaw and mandibula or lower jaw. (c) The teeth and periodontium. (d) The attached muscles of mastication. Functions of the OFS are neuromuscular driven, involving both the central and peripheral nervous system and muscles. What we accept as normal or efficient functioning of the OFS is not only determined by the mandibular movements but also by the proprioceptive control of the spatial positions of the lower jaw. Eye Catcher

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In the literature and in practice, the topic dental occlusion and its role in function or dysfunction of the masticatory system is often the subject of discussions and controversy. The variety of theories offering different specific guidelines for clinical approach is confusing and, moreover, often only based on personal clinical expertise or foundations and not always relying on actual scientific evidence [1, 2].

Maxillomandibular relationships exist as the positions or movements of the mandible with or without contacts of the occlusal surfaces of the teeth present in the oral cavity of each individual. The mandibular position with tooth contacts should be differentiated in a static position or occlusion and an eccentric or dynamic position or articulation. Without dental contacts the mandibular movements are generated with distinction between the eccentric or border movements, on the one hand, and the

functional movements, on the other hand. The rest position of the lower jaw is a variable position without tooth contacts, depending on the momentarily orofacial muscular tension status. These relationships should also be considered in the temporomandibular joint. The TMJ is often the subject of diagnostic failure of certain signs or symptoms in the masticatory system, due to incomplete or even absent “medical” knowledge concerning its anatomy and physiological functioning. It is a specific type of joint: it is a twin joint and contains an articular disc; it is about the strongest joint of the whole human body. Both units (condyles) move simultaneously according to their anatomic features and in harmony with the occlusal or dental configuration and enable functional luxation, generally throughout lifetime. 19.1.1

19.1.1.1

 entric Positions of the Lower Jaw C and Temporomandibular Joint Maximum Intercuspation

The maxillomandibular position also known as maximal occlusion represents the relation of both jaws with existing maximal contacts of opposing occlusal surfaces. The proprioceptive sense develops during infancy. Clinical reproducibility of this relation in the TMJs is doubtful and, therefore, it is never recommended to be used as a reference for dental reconstruction purposes. 19.1.1.2

Centric Relation/Centric Occlusion

Centric relation (CR) is known as the maxillomandibular relation in the TMJ where the hinge movement or rotation of the mandible takes place, around the so-­ called hinge axis, virtually connecting the center of both condyles. This determination is important as it is reproducible and therefore an important parameter in restorative dentistry, for instance, in youngsters with oligodontia or amelogenesis imperfecta or even in edentulous patients. The articular condyles effortlessly hold the rearmost, upmost, and midmost (RUM) position or centric relation in the TMJs. This position is individually determined and varies according to the personal anatomy of the condyles and the morphology of the glenoid fossa. The corresponding interocclusal contact between upper and lower jaws can be registered between antagonistic premolars and molars, not in the anterior region (canines and incisors), and is called centric occlusion (CO). According to the epidemiologic research, in a majority of individuals, there is indeed a difference between centric and maximal occlusions, the so-called long ­centric occlusion. Centric and maximal occlusion can be similar, always showing maximal intercuspation of all

477 Temporomandibular Disorders in Children and Adolescents

present teeth with the condyles in the reproducible RUM position, which is called the point centric occlusion [1, 2]. 19.1.2

Rest Position

Is a postural position of the mandible depending highly on the neuromuscular activation or state of the masticatory system. The mandible is suspended with an interocclusal distance, the freeway space, which is supposed to be maintained after dental reconstruction, but which is also able to adapt to minimal and slow changes in the equilibrium between elevator and depressor masticatory muscles. It cannot be considered as strictly reproducible and is mostly calculated by clinicians as an interdental space between 1 and 4 mm. It can be adversely affected by certain emotional conditions (anxiety, depression) and loss of teeth related to parafunctional habits or bruxism as these conditions can influence the neuromuscular balance in the masticatory system. 19.1.3

Eccentric Positions

Eccentric Occlusal Positions of the Mandible (Also Known as Articulation). These positions are static, with certain tooth contacts, depending on the occlusal or articulating type of the individual dentition. The ideal features in the adult dentition are: 1. Lateral excursion to the working side featuring only canines, called the canine guidance. 2. Lateral excursion to the working side with involvement of canines, premolars, and/or molars, called a group contact. 3. After lateral excursion, at the non-­working or balancing side, tooth contacts disappear and is called the unilateral clearance. 4. Maximal protrusion is reached with frontal or incisal guidance, involving incisors and/or canines with bilateral disocclusion or clearance between premolars and molars. During lifetime teeth can show continuous differentiation due to functional or natural loss of tooth substance, possibly enhancing or changing the eccentric positions of the lower jaw. 19.1.4

Eccentric Mandibular Movements

All mandibular movements can be traced and projected in the three spatial planes: the sagittal, the frontal or coronal, and the horizontal plane. When borderline,

these movements are reproducible, and within these limits, functional movements are developed. The latter are highly variable, depending on the neuromuscular status of the system. When recorded at the anterior teeth, a characteristic three-dimensional diagram is generated known as the Posselt envelope of motion: 1. In the horizontal plane, we distinguish maximal protrusion, maximal retrusion to centric relation, and maximal lateral excursions. 2. In the frontal or coronal plane, we distinguish maximal opening and closing in maximal intercuspation and maximal lateral excursions. 3. In the sagittal plane, we distinguish maximal protrusion, maximal retrusion to centric relation, and maximal opening and closing. When recorded at the TMJ: 1. In the horizontal projection, we distinguish the anterior-posterior translation and the lateral eccentric movements, at the working side, with the rotating condyle making the so-called Bennet movement or Bennet shift*, and at the non-working (balancing) side, with the translating condyle following the pathway of the Bennet angle. 2. In the frontal projection, we distinguish the opening movement and the lateral eccentric movements, with the Bennet shift* at the working side and the pathway of the Bennet angle at the non-working side. 3. In the lateral projection, we distinguish the opening movement with the condyle moving according to the condylar rotation around the hinge axis and followed by an anterior-inferior translation, following the pathway of the condylar plane, making an average angle of 30–35° with a reference horizontal line or plane. *The Bennet movement or shift of the working condyle is a bodily displacement and may be absent or very discrete. For extensive documentation of all these principles, see Dos Santos Jr. (2007) [2]. 19.1.5

Vertical Dimension in Occlusion

The vertical dimension is the morphologic facial height which can be measured with the teeth in maximum intercuspation. Theoretically it only changes three times throughout the human life evoked by enhanced bone growth. The first stage appears together with the eruption of the deciduous molars, the second stage between the ages of 6 and 8  years triggered by the start of the eruption of the permanent molars, and the third stage

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between the ages of 12 and 16  years during the last growth phase. During the function of the masticatory system (e.g., chewing, swallowing, speech), the feature of the mobile lower jaw or mandible and fixed upper jaw or maxilla, the organization of the dental arches and the dental anatomy (shape) determine the individual ability of the natural mandibular movements. In other words, harmony should exist between shape and function. Careful evaluation and registration of the individual determinants are mandatory in clinical practice, however without overestimation as well as oversimplification of the basic principles of occlusion. In biologic or anatomic absence of harmony or even installed disharmony (after restorative treatment), adaptation mechanisms derive in the majority of the human beings; in other words, disharmony not necessarily causes traumatic events, such as temporomandibular pain or dysfunction.

19.2

Disorders of the Orofacial System

Temporomandibular disorders (TMD, the term adopted in 1983 by the ADA) contain a number of problems involving the masticatory muscles, the TMJ, and associated structures. This term is synonymous with the term craniomandibular disorders (CMD) of the OFS.  The American Academy of Pediatric Dentistry (AAPD) accepts in its guidelines that TMD can also be observed in adolescents, children, or infants [3]. The role of the general dentist is regularly underestimated as it comes to observation, detection, differential diagnosis, and treatment strategies.

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and a lack of clinical reports on striking comorbidities in adults as well as in children and adolescents, e.g., sleep or sleep breathing disorders. Nevertheless in general, the signs and symptoms in children and adolescents are light and variable over time in the vast majority and can be characterized as mild or moderate [4–9]. Exceptionally, in some cases with rare diseases, such as juvenile idiopathic arthritis (JIA), it can progressively lead to severe functional limitations and pain [10]. Although at an early age (5–7 years) signs and symptoms of temporomandibular disorders are not usually found, some disorders can be detected in one third of children with primary teeth [4]. The existence of complaints (headaches, clicking TMJ), with some of them already known by the parents, is confirmed in 36% of children aged 7–14 years old, while 64% of those children apparently show also symptoms (mainly pain on palpation of the masticatory muscles) [11, 12]. In long-term studies, signs and symptoms show great variation in their appearance with the progress of time. Some findings, such as clicking, seem to come and go in an unpredictable way. Indeed, in a 10-year monitoring of children of 7, 11, and 15 years old, no significant proportion of unchanged signs or symptoms of TMD could be registered [13], while 20 years after the completion of the monitoring of the same individuals, not any recrudescence could be found within this remarkably long period of time [14]. 19.2.2

Etiology

In the majority of patients, temporomandibular disorders are of multifactorial origin. A long time ago, the dental profession associated occlusal relationships with temporomandibular pain and dysfunction. Unfortunately, 19.2.1 Epidemiology no or little scientific evidence can be found any longer for The prevalence of TMD signs in adults is estimated the majority of these associations as in the past only between 30 and 50% in general population samples. assumptions were made regarding the relationship They are the most common cause of pain of the non-­ between what is known, the principles of occlusion, and odontogenic origin in the orofacial system in about 5 to what was not known, the pathophysiology of pain. 12% of the patients seeking treatment. An important Mechanistic concepts can no longer be accepted as expladistinction should be made between signs and symp- nation or as therapy models for pain-related disorders. A possible etiologic factor, which can contribute to toms, on the one hand, and patients’ complaints, on the the occurrence of temporomandibular disorders in chilother hand. The occurrence of temporomandibular disorders in dren, is trauma. Lateral or bilateral intra-articular or children is much more difficult to map and tends to be epicondyle fractures are often the result of trauma to lower than in adults, with an increasing trend in the sec- the chin, after falling, which is a very common finding in ond and third decade of life. The variation in reports is childhood [15] and can eventually lead to ankylosis of mostly due to study design concerning, among others, the maxilla [16]. In isolated cases of condylar fractures study populations (general population or patient sam- in children, conservative treatment, using functional ples), examination methods, and discrepancies between orthodontic appliances as activator, may result in comdefinitions and variables. Important confounders are the plete recovery of the fracture and lead to the natural study methods and/or results from adult populations function of the TMJ and the OFS [17].

479 Temporomandibular Disorders in Children and Adolescents

Oral parafunctional behaviors such as lip, cheek biting, thumb sucking, and abnormal posturing of the jaw have no functional purpose, are common in all age groups, and occasionally can have some negative effects on the masticatory system. Nail biting and excessive chewing gum use on the contrary can cause more important overloading of the masticatory muscles and the TMJ, compared to the negative effects of bruxism. 19.2.2.1

Bruxism

In adults, bruxism is classified as either sleep bruxism, mainly characterized by tooth grinding, or awake bruxism, often characterized as tooth clenching. Both forms can be found in children and adolescents, with a global prevalence of 8–38% [18–21]. The etiology of bruxism cannot be explained by mechanistic concepts but is multifactorial. Its origin has to be searched in the central nervous system. Genetic but also peripheral environmental factors should be considered as the most evident influences nowadays. Tooth clenching while awake can lead to masticatory muscle fatigue and numbness (with difficulties to open the mouth widely or chewing hard food), clicking of the TMJ, and sometimes an uncomfortable occlusion. In other words, awake bruxism is a potentially higher etiologic risk factor for the emergence of myogenous or arthrogenous symptoms of TMD in childhood and adolescence [20]. Sleep bruxism will mostly do no harm in children concerning the teeth and the masticatory system, regardless the, sometimes, loud sounds produced and reported by the parents. They should always be informed about possible non-dental comorbidities. In fact, in the literature, sleep bruxism can be found to be associated with headache and sleep breathing disorders (snoring and obstructive sleep apnea), possibly resulting in growth disturbances of the maxilla and mandible [21], sleep disturbances, and behavioral disorders (e.g., hyperactivity, attention-deficit/hyperactivity disorder ADHD, fatigue, and attention deficit at school), but evidence is still insufficient to establish a cause-effect relationship [21]. The same lack of evidence exists about permanent damage to the dentition resulting from sleep bruxism during childhood. Tooth wear of primary teeth has a low predictive value for wear of the permanent dentition [22]. 19.2.2.2

Does Malocclusion Cause TMD?

Occlusal interferences, open bite, cross bite, and missing posterior teeth cannot be considered as etiologic risk factors for TMD [23]. Unilateral posterior cross bite (UPCB) is shown to be weakly associated with clicking of the TMJ and masticatory muscle pain [23, 24] but can on the other hand strongly be associated with facial asymmetry, disturbance of the masticatory cycle, reduced bite force, and masticatory muscle hypertrophy. Therefore

correction of UPCB is recommended in children to reduce the physiologic adaptation demands [23, 24]. 19.2.2.3

Does TMD Cause Malocclusion?

Structural and developmental changes and acquired and inflammatory disorders of the TMJ cause skeletal and dental changes and frequently lead to marked facial asymmetry. This is known for unilateral condylar hyperplasia and osteochondroma of the condyle, together with condylar asymmetry and open bite, but without the emergence of functional disturbances and TMD.  Idiopathic condylar resorption causes frontal open bite but in a majority of cases without functional limitations or risk of development of TMD [23]. On the contrary, idiopathic juvenile rheumatoid arthritis (IJRA) is known to involve the TMJs (50–78%) and to cause arthralgia, progressive limitation of jaw movements, destructive changes during mandibular growth, progressive class II, frontal open bite, and arthritic condylar changes (flattening and erosions) [23]. Recognition before the start of orthodontic therapy is mandatory (clinical and magnetic resonance imaging (MRI)) and should be confirmed with laboratory tests as it is an inflammatory disorder. 19.2.2.4

TMD and Orthodontics

If the patient shows signs or symptoms of TMD before the start of orthodontic therapy, a tailor-made treatment plan is mandatory and should consider the demand and preferences of the patient (even in adolescents, certainly in young adults) together with extensive information search. Timing and balance between function and esthetics are important issues. The relationship of the occurrence of symptoms of TMD with occlusal factors and orthodontic treatment in childhood has been the subject of controversy for a long time. Systematic reviews and meta-analyses especially from the last decade are reassuring concerning the risk for developing TMD during and after orthodontic treatment [23–28]. Orthodontic therapy performed during adolescence generally does not increase or decrease the chances of developing TMD later in life. Signs and symptoms of TMD occur also in healthy individuals and can increase with age, particularly during adolescence; thus, TMD originating during orthodontic treatment is mostly not related to that treatment [24]. Occlusal interferences are temporarily created, but in a majority of the patients, this will cause transient discomfort with a temporarily risk for increased muscle pain or clicking in the TMJ. Only in cases with a history of low adaptive capacity (bruxism, parafunctions) or occlusal hypervigilance, mandibular loading should be decreased, and conservative TMD management should be considered first.

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The extraction of the teeth as part of an orthodontic treatment plan does not increase the risk of developing TMD (e.g., extraction of premolars and the risk for condylar posterior displacement) [24–28]. There is no elevated risk for TMD associated with any particular type of orthodontic mechanics, although a stable occlusion is a reasonable treatment goal. Not achieving a specific gnathologic ideal occlusion does not result in TMD signs or symptoms [24]. No method of prevention for TMD has been demonstrated yet. Before, during, and after orthodontic therapy, always screen for TMD and for oral behaviors, and instruct the patient to avoid parafunctions. The psychological profile of the patient including his capacity of amplification of sensations (e.g., occlusal changes) has to be evaluated in advance and has to result in a customized treatment plan. 19.2.3

Anamnestic Records

Any dentist who works with children should include in the dental examination the TMJs and orofacial structures, being capable of evaluating related complaints, symptoms, or findings. The anamnestic record should include a dental as well as a medical part, and the patient should be asked about possible complaints such as headache, ear pain, or more extensive facial pain, clicking in the TMJs (. Fig. 19.1) [7]. Previous dental trauma and all the conditions causing, especially, chronic orofacial pain, with information on the origin, location, quality, intensity, and duration of pain, should be recorded. It is not always obvious to obtain the right answers to some questions; parents should be involved and informed extensively. The nature of the questions should certainly avoid confusion, as the same limitations can be experienced in adults as well. Adapted visual analogue scales like the Universal Pain Assessment Tool (UPAT) can be useful tools for TMD pain history-taking in youngsters (. Fig. 4.10) [29].

19.2.4

Clinical Examination

According to the Axis I examination protocol of the Diagnostic Criteria for Temporomandibular Disorder (DC-TMD) [30], the extraoral examination should include simultaneous bilateral palpation of the TMJ and the most palpable masticatory muscles, namely, the temporal and the masseter muscles (. Fig.  19.2). During examination so-called functional pain on (maximal) opening of the mouth (. Fig.  19.3) and lateral movements of the mandible, or possible irregular jaw deviations or TMJ sounds have to be recorded. Except for dental (e.g., tooth wear, caries) and periodontal (e.g., gingivitis, early-onset periodontitis) inspection, the intraoral examination for the presence of muscle pain on palpation is optional and not considered as mandatory any longer. The examination for the determination of the pain must be done very carefully, because the child can express any pressure on palpation as a pain experience. Children must be able to open their mouth maximally between 35 and 40 mm like adults. The lateral excursions of the mandible in children reach approximately 8–12  mm (each side), but the measurement is not reliable in very young children, due to the possible problem for them to follow instructions.  

 

19.2.5

Imaging

 

 

19

Questions for TMD history taking: • Do you feel pain in the face or jaw or the mandible? • Do you often suffer from headache? • Do you feel tired or pain when you chew? • Do you feel pain when you open your mouth too much? • Do you hear sounds from the TMJ and are they associated with pain? • Do you clench or grind your teeth? (also ask the parent) • Do you bite your nails or chew gum frequently? • What is the sleep position you prefer? ..      Fig. 19.1  Proforma for the dental record and the findings of possible TMJ disorders [7]

The panoramic radiograph is the recommended primary imaging tool to document the history and examination protocol in case of TMD in children as well as in adults. The obtained dental, periodontal, and TMJ information is in most cases sufficient to identify or confirm the presence or absence of structural pathology and rarely will affect the primary diagnosis and choice of baseline conservative therapy. Only in cases where there is injury, long-lasting pain, significant limitation of mobility, abnormal change of the occlusion, a progressive pathologic joint condition with facial asymmetry, numbness in the region of the mandible, a general joint disease (IRA), etc., further imaging of the TMJs is desired [31]. In these cases magnetic resonance imaging (MRI) and cone-beam computed tomography (CBCT) are the tools of choice nowadays. 19.2.6

Diagnosis

According to the worldwide scientifically approved diagnostic criteria of temporomandibular disorders (DC-­ TMD) [30], two major TMD entities should be distinguished: the pain-related and the non-pain-related disorders (defined as the temporomandibular dysfunctions). The pain-related disorders, regularly coexisting

481 Temporomandibular Disorders in Children and Adolescents

19

..      Fig. 19.2  a Palpation of the temporal muscle. b Palpation of the masseter muscle

..      Fig. 19.3  Maximal opening with location for palpation of the TMJ

in individuals, can be of muscular (myogenous) origin called myalgia, myofascial pain, myofascial pain with referral, or TMD-related headache, depending on the source(s) of pain situated in the masticatory muscles, or can be of arthrogenous origin, called arthralgia situated in the TMJ. Myogenous as well as arthrogenous pain is mainly the result of overloading of the masticatory system on the muscular and/or temporomandibular articu-

lation level. In isolated cases, it is the result of inflammatory processes including myositis or arthritis as in (juvenile) rheumatoid arthritis with involvement of the TMJ.  The non-pain-related disorders or dysfunctions of the masticatory system originate from intra-­ articular dysfunction and the TMJ disc dislocations with or without reduction, also called the internal derangements, or originate from TMJ hypermobility implications, defined as luxation or subluxation of the disc-condyle complex. The most typical characteristic of these dysfunctions is the TMJ clicking noise often experienced as disturbing or even threatening and may lead to certain levels of debilitation of mandibular movements [32]. Temporomandibular joint arthrosis due to degenerative processes and in most cases characterized by crepitation of the TMJ cannot be considered as a pain-related disorder, in its strict sense of existence. As already mentioned, the role of occlusal factors in the etiology of temporomandibular disorders in children is controversial. As mentioned before in this chapter (see 7 Sect. 19.2.2), the presence of a unilateral posterior cross bite (UPCB) is about the only parameter who should be taken into consideration and treated in youngsters as a risk factor on the long term, when relying on scientific evidence [23]. Differential diagnosis of TMD with some diseases such as dental pain, sinusitis, otitis, mastoiditis, Eagle’s syndrome, etc., is mandatory, and it is at least the task of the dentist to coordinate multidisciplinary investigations in case of the presence of such suspected non-­ dental pathologies or comorbidities.  

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19.2.7

Treatment Strategies

Children presenting with orofacial pain or dysfunctions show, in a majority, important and sometimes unpredictable fluctuations of their complaints and/or symptoms in time, individually as well as in general. Different issues should be taken into consideration: the transient and benign character of most of the signs and their origin, in the first place, and, in a minority but not less important, the coexistence of TMD with non-dental comorbidities such as sleep breathing disorders and headache (see 7 Sect. 19.2.2). Prophylactic early interventions such as extensive occlusal adjustment and orthodontic treatment, with exception of laterally forced cross bites (see 7 Sect. 19.2.2), to prevent TMD in children, are no longer supported scientifically. Simple conservative and reversible measures are strongly recommended as the latter have proven already for decades, effectiveness on the long term, in adults as well as in children. After history-taking and clinical examination, comprehensive explanation and information should be provided to the child but also to the parents or present accompanying person. Reassurance about the innocent character of the condition and the favorable prognosis of simple treatment is mandatory and possible in most cases. Treatment has to start with education about avoiding unnecessary loading of the masticatory system, such as nail biting, tongue thrusting, and excessive use of chewing gum, if present as oral parafunctional activities. Different small, take-home programs can be presented depending on the individual needs (in the presence of, e.g., clicking, fear for mobilization of the jaw in case of painful muscle splinting) can improve proprioceptive neuromuscular facilitation and offer sufficient pain management. Therapeutic exercises (e.g., careful stretching, mobilization of the lower jaw, opening, and lateral excursions with resistance) are an important part of physical as well as cognitive behavioral therapy and merit a place in the treatment of TMD in children and adolescents, depending on the understanding and compliance of the child.  

Only if the existence of a non-dental comorbidity is suspected with potentially severe consequences such as chronic fatigue, attention deficit, sleep apnea or hypopnea, and headache, the patient should be referred for specialized differential diagnosis. In these cases disturbing sleep bruxism in combination with snoring is often present, and it is recommended to refer to the ear-nose-­ throat (ENT) doctor or pneumologist, to exclude allergies or tonsillary obstruction of the upper airway. Other comorbid risks factors such as the use of psychoactive drugs, underlying stress-related factors, and neurologic diseases should be recognized by the dentist and are important reasons for referral.

 

19

>>Night Guards The use of night guards is controversial and should be considered with care in the deciduous and mixed dentition as they can have negative effects on physiologic growth and development patterns. Hard acrylic splints as used in adults for main protective reasons should be avoided even in the presence of sleep bruxism. In fact, it should be stressed that in children sleep bruxism tends to decrease at the age of 9 or 10 years and most of the children will not continue to grind their teeth during adolescence or adulthood [19, 20].

19.3

Summary

Temporomandibular disorders in children and adolescents are common and can mostly be characterized as mild and transient. Extensive history-taking in the presence of the parents or accompanying persons is mandatory, in order to try to exclude non-dental comorbidities as soon as possible (e.g., snoring, apnea, headache, ENT pathologies, rheumatoid arthritis). The latter should get priority for multidisciplinary differential diagnosis. Bruxism, occlusal discrepancies, and orthodontic therapy are no longer considered as primary or perpetuating etiologic factors for TMD. Careful functional examination should include recording of mandibular movements, extraoral palpation of the TMJ and informative masticatory muscles, and evaluation of the joint noises. Therapy has to start with extensive counseling adapted to the child’s age and maturity and should always be conservative and reversible like cognitive education and therapeutic exercises. The use of hard acrylic night guards should be avoided in the majority of youngsters with deciduous or mixed dentition. Similar as in adults, orthodontic therapy and orthognathic surgery are not the primary treatment options of choice for pain or dysfunction of the temporomandibular system in children or adolescents neither.

References 1. Ramfjord SP, Ash MM.  Anatomy and physiology of masticatory muscles and temporomandibular joints. In: Occlusion. In: W.B. Saunders; 1995. p. 4–23. 2. Dos Santos JJ. Maxillomandibular relations and movements. In: Occlusion. Principles and Treatment. Quintessence books; 2007. p. 1–37. 3. American Academy of Pediatric Dentistry. Guidelines on acquired temporomandibular disorders in infants, children and adolescents. Reference Manual 2012–2013. Pediatr Dent. 2012;34(6):258–3.

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4. Bonjardim LR, Baviao MB, Carmagnani FG, et  al. Signs and symptoms of temporomandibular joint dysfunction in children with primary dentition. J Clin Pediatr Dent. 2003;28(1):53–8. 5. Magnusson T, Carlsson GE, Egermark I. Changes in subjective symptoms of craniomandibular disorders in children and adolescents during a 10 year period. J Orofac Pain. 1993;7(1):76–2. 6. Magnusson T, Carlsson GE, Egermark I.  Changes in clinical signs of craniomandibular disorders from the age of 15 to 25 year. J Orofac Pain. 1994;8(2):207–5. 7. Magnusson T, Helkimo M.  Temporomandibular disorders. In: Koch G, Poulsen S, Espelid I, Haubek D, editors. Pediatric dentistry. a clinical approach. Wiley Blackwell; 2017. p. 309–15. 8. Nilsson IM.  Reliability, validity, incidence and impact of temporomandibular pain disorders in adolescents. Swed Dent J Suppl. 2007;183:7–6. 9. Toscano P, Defabianis P.  Clinical evaluation of temporomandibular disorders in children and adolescents: a review of the literature. Eur J Paediatr Dent. 2009;10(4):188–2. 10. Juvenile CR, Arthritis I. Overview and involvement of the temporomandibular joints, prevalence, systemic therapy. Oral Maxillofacial Surg Clinics. 2015;27(1):1–10. 11. Alamondi N, Farsi N, Salako N, Feteih R. Temporomandibular disorders among school children. J Clin Pediatr Dent. 1998;22:323–9. 12. Bertoli FM, Antoniuk SA, Bruck I, Xavier GR, Rodrigues DC, Losso EM. Evaluation of the signs and symptoms of temporomandibular disorders in children with headaches. Arq Neuropsiquiatr. 2007;65(2A):251–5. 13. Motegi E, Miyazaki H. Oqura I, et al. an orthodontic study of temporomandibular joint disorders. Part 1: epidemiological research in Japanese 6-18 year olds. Angl Orthodontist. 1992;62(4):249–6. 14. Verdonck A, Takada K, Kitai N, et al. The prevalence of cardinal TMJ dysfunction symptoms and its relationship to occlusal factors in Japanese female adolescents. J Oral Rehabil. 1994;21(6):687. 15. Kaban LB, Mulliken JB, Murray JE. Facial fractures in children: an analysis of 122 fractures in 109 patients. Plast Reconstr Surg. 1977;59:15–20. 16. Kaban L. Acquired abnormalities of the temporomandibular Joint. In: Kaban L, Troulis M, editors. Pediatric Oral and Maxilofacial Surgery. Philadelphia PA Saunders; 2004. p.340–376. 17. Chatzistavrou EK, Basdra EK.  Conservative treatment of isolated condylar fractures in growing patients. World J Orthod. 2007;8(3):241–8. 18. Barbosa Tde S, Miyakoda LS, Pocztaruk Rde L, et al. Temporomandibular disorders and bruxism in childhood and adolescence: review of the literature. Int J Pediatr Otorhinolaryngol. 2008;72(3):299–4.

19. Manfredini D, Restrepo C, Diaz-Serrano K, Winocur E, Lobbezoo F.  Prevalence of sleep bruxism in children: a systematic review of the literature. J of Oral Rehab. 2013;40:631–2. 20. Saulue P, Carra MC. Bruxism in children and adolescents. In: Laluque JF, Brocard D, d’Incau E, editors. Understanding Bruxism. Current Knowledge and Practice. Quintessence Publishing; 2017. p.63–71. 21. Carra MC, Bruni O, Huynh N.  Topical review: sleep bruxism, headaches and sleep-disordered breathing in children and adolescents. J Orofac Pain. 2012;26:267–6. 22. Nyström M, Könönen M, Alaluusua S, Evälahti M, Vartiovaara J.  Development of horizontal tooth wear in maxillary anterior teeth from five to 18 years of age. J Dent Res. 1990;69:1765–70. 23. Michelotti A, Iodice G.  The role of orthodontics in temporomandibular disorders. J Oral Rehab. 2010;37(6):411–7. 24. Sonnesen L, Bakke B, Solow B. Temporomandibular disorders in relation to craniofacial dimensions, head posture and bite force in children selected for orthodondic treatment. Eur J Orthod. 2001;23(2):179–92. 25. Mc Namara JA Jr, Seligman DA, Okeson JP.  Occlusion orthodontic treatment and temporomandibular disorders. A review. J Orofac Pain. 1995;9(1):73–90. 26. Vanderas AP, Papagiannoulis L.  Multifactorial analysis of the etiology of craniomandibular dysfunction in children. Int J Paediatr Dent. 2002;12(5):336. 27. Dibbets JM, van der Weele LT. Long-term effects of orthodontic treatment, including extraction, on signs and symptoms attributed to CMD. Eur J Orthod. 1992;14(1):16–20. 28. Kim MR, Graber TM, Viana MA. Orthodontics and temporomandibular disorders: a meta-analysis. Am J Orthod Dentofac Orthop. 2002;121:438–6. 29. Dugashvili G, Van den Berghe L, Menabde G, Janelidze M, Marks L. Use of the universal pain assessment tool for evaluating pain associated with TMD in youngsters with an intellectual disability. Med Oral Patol Oral Cir Bucal. 2017;22(1):88–4. 30. Schiffman E, Ohrbach R, Truelove E, et al. Diagnostic criteria for temporomandibular disorders (DC/TMD) for clinical and research applications: recommendations of the international RDC/TMD consortium network and orofacial pain special interest group. J Orof Pain Headache. 2014;28(1):6–27. 31. American Academy of Pediatric Dentistry. Treatment of temporomandibular disorders in children: summary statements and recommendations. J Am Dent Assoc. 1990;120:265–9. 32. Visscher CM, Ohrbach R, van Wijk AJ, Wilkosz M, Naeije M.  The Tampa scale for kinesiophobia for temporomadibular disorders (TSK-TMD). Pain. 2010;150:492–500.

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485

Oral Lesions in Children and Adolescents Stephen Porter and Alexandros Kolokotronis Contents 20.1

Common Oral Mucosal and Bony Abnormalities – 487

20.1.1 20.1.2 20.1.3 20.1.4

E rythema Migrans (Geographic Tongue) – 487 Palatal Torus (Torus Palatinus) – 488 Mandibular Torus (Torus Mandibularis) – 488 Cysts – 488

20.2

Reactive Overgrowths – 488

20.2.1 20.2.2 20.2.3 20.2.4 20.2.5

 yogenic Granuloma – 488 P Fibroepithelial Polyp – 489 Peripheral Ossifying Fibroma – 489 Peripheral Giant Cell Lesion – 489 Congenital Granular Cell Tumor (Congenital Epulis of the Neonates) – 490 Other Swellings – 490

20.2.6

20.3

Vascular Malformations (Hamartomas) – 490

20.3.1 20.3.2

 emangioma – 490 H Lymphangioma – 491

20.4

Oral Ulceration – 491

20.4.1 20.4.2 20.4.3

T raumatic Oral Ulceration – 491 Aphthous Ulceration and Related Disease – 492 Oral Ulceration Secondary to Systemic Disease of Childhood – 494

20.5

Infectious Diseases in Childhood – 495

20.5.1 20.5.2 20.5.3

 iral Infections – 495 V Bacterial Infections – 500 Fungal Infections – 502

20.6

Mucocutaneous Disease – 503

20.6.1 20.6.2 20.6.3

E rythema Multiforme – 503 Allergic Reactions – 504 Other Mucocutaneous Disease – 504

© Springer Nature Switzerland AG 2022 N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry, https://doi.org/10.1007/978-3-030-78003-6_20

20

20.7

Hematological Disease – 505

20.7.1 20.7.2 20.7.3

 ematological Malignancies – 505 H Disorders of Blood Cells – 506 Bleeding Disorders – 508

20.8

Salivary Gland Disease – 510

20.8.1 20.8.2 20.8.3 20.8.4

 ucocele – 510 M Ranula – 510 Sialolithiasis – 510 Acute Suppurative Sialadenitis (Suppurative Parotitis, Bacterial Sialadenitis, Bacterial Parotitis) – 511 Recurrent Parotitis of Childhood (Juvenile Recurrent Parotitis) – 511 Xerostomia (Oral Dryness) – 511 Drooling – 512

20.8.5 20.8.6 20.8.7

References – 512

487 Oral Lesions in Children and Adolescents

While the majority of child patients attending an oral health care service will have plaque-related oral disease such as caries and gingivitis, and more rarely congenitally driven disease of the teeth and/or jaws, a spectrum of disease can occasionally affect the mouths of children. In particular, a wide variety of disorders can affect the oral mucosa and more rarely the salivary glands. Such disease may reflect many different pathological mechanisms, and while most usually arise in adults, some such as the autoinflammatory disorder periodic fever, aphthous ulceration, pharyngitis, and adenitis (PFAPA) and recurrent parotitis of childhood seem to be almost unique to pre-pubertal individuals. Similarly, very occasionally children manifest disease expected of adulthood (e.g., lichen planus or Sjogren’s syndrome). Regardless of these trends, it is essential that clinicians managing the oral health of children have an awareness of the more common disorders and when to refer the patient to an appropriate specialist. Some of the disorders relevant to oral medicine that arise in children: 1. May be the first manifestation of significant systemic disease (e.g., ulceration or purpura of acute leukemias) 2. Can be the most troublesome manifestation of a systemic disease (e.g., oral ulceration of Crohn’s disease) 3. Can lessen the quality of life of the affected patients (e.g., oral ulceration of any cause) 4. May compromise the general health of child (e.g., failure to thrive due to loss of appetite caused by oral ulcers) 5. May reflect systemic disease that requires dental care to be particularly essential and/or modified The present chapter reviews the various disorders of the oral mucosa and salivary glands that may commonly arise in children. Detailed discussion of the many other diseases that may arise in childhood can be found elsewhere. 20.1  Common Oral Mucosal and Bony

Abnormalities

20.1.1

 rythema Migrans (Geographic E Tongue)

Erythema migrans is a common disorder, perhaps occurring in up to 3% of individuals and may often arise in childhood. It affects both genders and occurs in children of all ethnic groups [1, 2]. It manifests as discrete areas of erythema surrounded by a creamy white border on the dorsum of the tongue (. Fig. 20.1). The areas may  

..      Fig. 20.1  a, b Erythema migrans of the tongue  – often termed geographic tongue

..      Fig. 20.2  Erythema migrans of the buccal mucosa

change in site and appearance without an identifiable precipitant. Sometimes there is accompanying fissuring of the tongue, and rarely areas of erythema can arise on other oral mucosal surfaces (. Fig. 20.2). The areas of redness may sometimes, but not always, be painful, discomfort being brought on by a wide variety of agents that may include chocolate, cheese, and tomatoes. Similarly, the signs of erythema migrans can be precipitated or modified by different foods.  

Eye Catcher

The precise cause of erythema migrans is unknown although it may occasionally arise in patients with a history of atopic disease, cutaneous psoriasis, and possibly inflammatory bowel disease. There have been reports of erythema migrans arising in patients with SARS-2-Cov (COVID 19), but it is unlikely that this is a specific oral feature of this infection. The disease is a manifestation of mild localized acute inflammation.

Diagnosis can be based solely upon the clinical features, and there is no requirement for any additional investigations. The treatment of erythema migrans remains unsatisfactory and principally comprises avoidance of identified precipitants and local application of anesthetic agents such as benzydamine hydrochloride. There is no

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evidence of the long-term behavior of this disorder, but it is not potentially malignant and does not affect growth. 20.1.2

a

Palatal Torus (Torus Palatinus)

Palatal tori are common and arise in all genders and all ethnic groups [3]. They become more manifest as a child grows. They present as symmetrically enlarged, painless, bony enlargements of the vault of the hard palate. Tori do not warrant any treatment in childhood and do not seem to interfere in the use of removable orthodontic appliances. 20.1.3

Mandibular Torus (Torus Mandibularis)

Mandibular tori are less common than those of the palate and arise independent of the latter [4]. They tend to manifest as a child grows and present as painless bony enlargements on the lingual aspect of the mandible in the area of the permanent premolars. Mandibular tori have no systemic significance and do not warrant treatment in childhood. 20.1.4

b

Cysts

In total, 65–85% of newborn may present with small intraoral cysts and/or nodules. The term Epstein’s pearls refers to small cysts which are located on the junction of hard and soft palate, exclusively, in the middle line. They have a hemispherical shape and white color, and when their size extends over 3 mm, they may be visible at birth or a few days after. Similarly appearing swellings termed Bohn’s nodules are a single or multiple small cysts which are located on buccal or lingual aspects of the alveolar mucosae, more often the mandibular surface [5] (. Fig. 20.3).

..      Fig. 20.4  a Cyst of the incisive papilla in a 3½-year-old boy. b A relevant radiolucent lesion is distinguishable in the anterior occlusal maxillary radiograph

Both types of cysts contain keratin, and it is easy for the clinician to reach a diagnosis based on clinical signs with no further investigation. New cysts may continue to emerge for up to 2 months after birth, all of which are, eventually, self-limited and disappear spontaneously within a few days or up to 3 months after birth. Older children (with deciduous teeth and more often permanent teeth) can develop eruption cysts which are described in 7 Chap. 10 as eruption disorders [6]. There are a number of cyst types that may occur in childhood (e.g., cyst of the incisive papilla (. Fig. 20.4) or other odontogenic cysts), details of which are available in appropriate maxillofacial surgery textbooks.  

 

 

20.2  Reactive Overgrowths 20.2.1

20

..      Fig. 20.3  Bohn’s nodule on the buccal side of alveolar process of the maxilla in a 3-month newborn

Pyogenic Granuloma

Pyogenic granulomas are inflammatory lesions that usually manifest on the gingivae, particularly interdentally. They are not notably common in the first decade of life [7, 8]. They represent an overabundant local inflammatory reaction to plaque retention. They are thus typically associated with overhanging restorations, broken-down carious teeth, or other local plaque-­retaining factors. They manifest as sessile (i.e., broad-­based: red, purple, or occasionally yellow/brown) swellings that bleed easily with gentle pressure. They are usually painless with patients only reporting the presence of a swelling, local bleeding, or slight dysgeusia (. Fig. 20.5).  

489 Oral Lesions in Children and Adolescents

..      Fig. 20.6  Fibroepithelial polyp located at the mucosa of the lower lip

..      Fig. 20.5  Pyogenic granuloma before and after its excision. (Courtesy Dr. H. van Waes)

Pyogenic granulomas may sometimes resolve spontaneously but usually require excision together with correction of the underlying cause. They can arise in females in the second trimester of pregnancy and then enlarge as the pregnancy progresses. Following the birth of the child, these lesions often spontaneously regress, and, if not, then excision with removal of any plaque-retaining factors is warranted. Breast feeding does not prolong the presence of pyogenic granulomas. Such lesions can very rarely arise on the oral mucosae in response to physical trauma. The risk of such post-traumatic pyogenic lesions is possibly increased in patients receiving cyclosporin therapy and/or those with graft-versus-host disease (GvHD).

20.2.2

Fibroepithelial Polyp

These are common swellings that arise at sites of trauma. They are most likely on the buccal, labial, or lingual surfaces and are actually uncommon in children [9]. They manifest as sessile rubber-like swellings with either a normal overlying mucosa or less commonly a homogeneous white surface that reflects repeated local trauma (e.g., biting) (. Fig. 20.6). These lesions have no malignant potential but should be excised as they may hinder speech and/or eating and if repeatedly bitten may bleed or occasionally enlarge. Occasionally a long-standing  

..      Fig. 20.7  Clinical image of a peripheral giant cell granuloma

pyogenic granuloma may evolve into a fibroepithelial polyp (and are sometimes termed a fibrous epulis). 20.2.3

Peripheral Ossifying Fibroma

These are uncommon, exclusively arising on the gingivae, and have the clinical appearance of a fibroepithelial polyp but are found radiologically and/or histopathologically to have evidence of mild ossification [10]. They have no associations with systemic disease, are not potentially malignant, and warrant excision. They are unlikely to re-occur.

20.2.4

Peripheral Giant Cell Lesion

This tends to present as a sessile swelling of the gingivae and tends to arise in the first decade of life and particularly the mixed dentition period [11]. The lesions are single, sessile swellings that have a red, blue, or purple color (. Fig. 20.7). They are reminiscent of pyogenic granulomas, can be initiated by plaqueretaining factors, and can only be truly distinguished  

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by the differing histopathology – giant cell lesions contain multi-­nucleated giant cells, while pyogenic granulomas have no giant cells but have a polymorphonuclear leukocyte-­ dominating acute inflammatory picture. There is no erosion/destruction of the underlying bone. Treatment and indeed diagnosis require excision and subsequent histopathological examination of the lesions. Recurrence is possible when surgical excision is not radical. Peripheral giant cell granuloma is exclusively seen on gingivae (formerly giant cell epulis). Central giant cell granuloma is a bony lesion found especially in long bones and rarely in the mandible.

20.2.5

 ongenital Granular Cell Tumor C (Congenital Epulis of the Neonates)

 

Other Swellings

There is a wide spectrum of other causes of soft tissue swellings of the soft tissues of the mouth. These include benign or (very rarely) primary malignancies of the oral tissues, metastatic deposits (e.g., leukemic deposits (see later)), mucoceles, fibromas associated with tuberous sclerosis, hemangiomas of Sturge-Weber syndrome, neurofibromas in Neurofibromatosis or multiple endocrine neoplasia type 2B (MEN2B), and others [13]. a

The list of causes of soft tissue swellings is perhaps endless; hence perhaps the key factors to consider about any swelling are as follows: 1. Is the lesion enlarging quickly and/or destructive? 2. Does the swelling have a likely (i.e., easily identifiable) cause? 3. Are there any unusual features in the medical history? 4. Is the swelling interfering in normal oral function? If the answers to any of these are worrisome, it is advisable that the patient is investigated in a multidisciplinary manner with appropriate specialists.

20.3  Vascular Malformations (Hamartomas)

This, although not a reactive lesion, is a gingival overgrowth. It is a rare soft tissue anomaly that presents as a swelling or nodule of the alveolar ridge (typically the upper) [12]. The overlying mucosa is generally of normal appearance (. Fig. 20.8). It is present at birth and tends to resolve spontaneously over several months. These swellings have the potential to interfere in feeding (although rarely do). Surgical excision can be undertaken but is rarely warranted. 20.2.6

Eye Catcher

20.3.1

Hemangioma

Hemangiomas represent abnormal collections of normal non-arterial blood vessels [14]. They may be an isolated feature or part of a congenitally driven disorder such as Sturge-Weber syndrome. Hemangiomas manifest as solitary red, blue, or purple sessile swellings that typically blanche with gentle pressure (. Fig.  20.9). They usually arise on the tongue or buccal mucosae although if part of Sturge-Weber syndrome are extensive and follow the distribution of one or more divisions of usually one trigeminal nerve.  

Eye Catcher

Hemangiomas that manifest at birth often regress over the early years of life although some have a hamartous behavior – enlarging as the child grows. Most hemangiomas do not interfere in oral function, rarely if ever they bleed and hence rarely warrant complex investigation (e.g., radiology or histopathology) or treatment (e.g., removal or embolization).

b

20

..      Fig. 20.8  a, b Congenital granular cell tumors or congenital epulis of neonates

491 Oral Lesions in Children and Adolescents

a

b

..      Fig. 20.9  a Clinical image of a small hemangioma. b Picture of a large hemangioma of the lower lip in a 7-year-old girl. There were also hemangiomas at the right half of the tongue and the pharynx. c

20.3.2

c

The same case when the patient was aged 12 years. The expansion of the lower lip hemangioma is notable

Lymphangioma

Lymphangiomas are much more uncommon than hemagiomas [15]. They typically manifest on the tongue as minute brown, red, and/or purple swellings peppered across the dorsum of the tongue. Rarely large lymphangiomas can arise, usually on mobile surfaces of the mouth, and have a golden appearance that upon closer examination comprises small “bubble”-like swellings that have a blood-colored center – akin to frog spawn (. Fig. 20.10). Lymphangiomas are painless and do not usually interfere in oral function, although they may occasionally ooze a greasy fluid if bitten. Small lymphangiomas do not warrant investigation or treatment although the large ones may warrant investigation (e.g., lymphangiography/ultrasound scanning and/or histopathology) and occasionally treatment (e.g., excision or embolization).  

20.4  Oral Ulceration

..      Fig. 20.10  Lymphangioma of the dorsal surface of the tongue

may only affect the anterior aspects of the mouth, although if swallowed there will be ulceration and edema of the posterior aspects of the mouth and pharynx. Depending upon the cause and the time since injury, trauma to the oral mucosae and gingivae may actually have a spectrum of features that include erosions, ulcerations, swellings, petechiae, bruising bullae, and/or areas of hyperkeratosis (. Fig. 20.11). The diagnosis of most instances of traumatic ulceration is based upon the history of known injury and the clinical features. However, if there is a suspicion that the ulceration has been deliberately self-inflicted, there is a need to consider if the child is distressed and thus reflects their social circumstances.  

20.4.1

Traumatic Oral Ulceration

Oral and sometimes gingival ulceration due to trauma is common in childhood, particularly as young children often put items in their mouths for a wide variety of reasons, may fall while having an object in their mouths, or inadvertently drink chemicals, drugs, or detergents. The ulceration caused by trauma clearly depends upon the causative agent and what the child was doing at the time of the traumatic injury [16]. The site and extent of ulceration clearly depend on the cause of the injury. The ulceration may be superficial or deep but in general is localized. The trauma of injuries to the palate can be particularly severe if a child has fallen while biting in an object – there can be severe tearing of the palatal mucosa down to the level of the mucoperiosteum. The ulceration of trauma caused by the ingestion of chemicals is usually superficial but can involve several surfaces of the mouth [17]. If the child has spat the material out, the ulceration

Eye Catcher

The management of most traumatic ulceration usually comprises: 1. Ensuring that the cause is identified and further avoided 2. Placing an adherent paste (such as carboxymethylcellulose) over the area of ulceration 3. Use of an antimicrobial mouthwash to avoid any infection 4. Local application of an analgesic agent (e.g., benzydamine hydrochloride or lidocaine)

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The areas usually heal with little scarring; however, if there is extensive ulceration, as may occur with chemical injuries, scarring is possible and can lead to restricted mouth opening. The risk of subsequent restricted opening may be lessened with the use of splints (either custom made or simple wood sticks) and more rarely surgical removal of scars (. Fig. 20.12).  

20.4.1.1

 iga-Fede Disease and Riga-Fede R Granuloma

Riga-Fede disease and Riga-Fede granuloma are associated with the presence of neonatal teeth which can traumatize the oral mucosa of the newborns [18]. The former is characterized by a small area of ulceration on the ventral and/or dorsal surface of the anterior tongue. The ulcer may be covered by a whitish pseudomembrane without cervical lymphadenopathy (. Fig.  20.13). In instances where there is an epithelial hyperplasia, the  

a

term Riga-Fede granuloma is sometimes used as a descriptor. The treatment of these disorders is discussed in 7 Chap. 10.  

20.4.1.2

Chronic Mucosal Biting

Chronic oral mucosal biting is not uncommon in children and young adults who experience a stressful period, feel unsafe, or have psychological problems. The resulting clinical picture affects the buccal mucosa (. Fig. 20.14), the bilateral sides of tongue, or labial mucosa. The affected surfaces are rarely ulcerated but instead have areas of ragged white patches that represent hyperkeratosis. The lateral borders of the tongue may have homogenous white patches, while there may be more obvious, and white, occlusal lines of the buccal mucosae. The areas of white patch are localized to the areas that can be reached by the teeth and may be unilateral or bilateral. The disorder is painless and usually only detected during a clinical examination.  

Eye Catcher

Treatment of chronic oral mucosal biting is rarely required although there is a need to consider as to why the patient has developed this habit and occasionally consider the use of a soft occlusal splint to lessen any damage to the mucosal surfaces.

20.4.2 b

..      Fig. 20.11  a Traumatic ulcers on dorsal surface of a young patient’s tongue. b Clinical image of a chemical burn

a

b

 phthous Ulceration and Related A Disease

Recurrent aphthous stomatitis (RAS) is a common disorder characterized by recurrent episodes of superficial oral mucosal ulceration in otherwise well individuals. The ulcers are usually ovoid and have a yellow to brown center and surrounding erythematous halo [19]. Three types of clinical presentation may arise of which minor RAS (MiRAS) accounts for at least 80% of all presentations. Minor RAS is characterized by crops of about five ulcers of less than 1 cm in diameter that arise every few weeks on the non-keratinized surfaces of c

20

..      Fig. 20.12  a Electric burn on the lips due to biting an electrical cable. b Construction of a mobile device with flaps to aid ulcer healing without complications on the corner of the mouth. c Clinical view after healing

493 Oral Lesions in Children and Adolescents

a

..      Fig. 20.13  Clinical image of an infant with Riga-Fede disease due to injury by neonatal teeth

b

..      Fig. 20.15  a, b Clinical image of minor recurrent stomatitis in the buccal vestibule ..      Fig. 20.14  Chronic biting buccal mucosa in a teenage girl

the oral mucosa (. Figs.  20.15 and 20.16). The ulcers heal spontaneously over about 10–14  days and do not cause scarring. Major RAS (MaRAS) comprises larger but fewer ulcers than those of MiRAS, have an irregular outline, and arise on any mucosal surface. MaRAS heals spontaneously over several weeks and can cause some scarring (e.g., of the soft palate). A very rare type of RAS is termed (erroneously) herpetiform RAS (He RAS). This has no connection to herpetic infection and is characterized by 10s to 100s of 1 mm size on any oral mucosal surface. The small ulcers supposedly coalesce into larger irregular outlined ulcers  – but there are a few good descriptions of this.

a

 

b

Eye Catcher

Recurrent aphthous stomatitis usually arises in the second decade of life, but about 10% of the affected individuals develop disease younger than this. The cause of RAS is unknown and certainly does not reflect psychological distress, allergic reactions or foodstuffs, or viral or other infections.

There remains no effective means of stopping the emergence of the ulceration of RAS; hence the goal of treatment is to lessen the duration (and hence associated pain) of each episode [20, 21]. The present evidence suggests

..      Fig. 20.16  a Two minor aphthous ulcers on the lateral aspect of the tongue. b Clinical image of a major aphthous ulcer at a similar location

that there is no specific means of lessening the duration of ulcers, but typical strategies center upon topical corticosteroids such as fluticasone (given as a spray or mouthwash), betamethasone mouthwash, or prednisolone mouthwash. Painful symptoms may be lessened with benzydamine hydrochloride dabbed on areas of ulceration or used as a spray or, less appropriately, for children, as a mouthwash. Occlusive pastes such as carboxymethylcellulose-based agents can also be useful, but it is often dif-

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ficult for a child patient or their parent/guardian to achieve this. Systemic immunosuppressive therapies are only warranted when RAS is notably severe interfering in feeding, sleep, or lessening quality of life. Such immunosuppressive therapies are out with the practice of pediatric dentistry. Ulcers similar to MaRAS can arise in patients with anemia (e.g., secondary to gluten-sensitive enteropathy (coeliac disease (see below) or ileocecal Crohn’s disease) or neutropenias (e.g., in leukemias), but the affected individuals may have other oral or extra-oral features of these disorders (see below). Two disorders in which RAS-like ulceration is suggested to be particularly common are Behcet’s disease and FPAPA syndrome. Behcet’s disease, also called “Adamandiades-Behcet,” is an uncommon disorder that arises in adults and rarely in children. It is sometimes considered to be an autoinflammatory disorder (i.e., inflammation that arises spontaneously) clinically characterized by episodes of RAS-like ulceration that arises at least three times yearly, superficial genital ulceration that occurs at least once per year, ocular disease (posterior uveitis), skin rashes (various – including vesicular-type eruptions and erythema nodosum) as well as painful joints ­(arthralgia), and a spectrum of other possible manifestations. Behcet’s disease tends to arise in individuals with genetic origins associated with the Eastern Mediterranean (e.g., Turkey), across lower Asia and up to Japan (i.e., the old “Silk Routes”), suggesting perhaps an immunogenetic etiology [22]. With respect to pediatric dentistry, oral ulcers are akin to those of RAS although it is suggested that these may more commonly affect the hard palate and be MaRAS than with typical RAS disease. The management of BS is out with the specialty of pediatric dentistry but typically includes systemic immunosuppression strategies, including the use of biological disease-modifying drugs. 20.4.2.1

20

Systemic Autoinflammatory Disorders

Periodic fever, aphthous ulceration, pharyngitis, and adenitis (PFAPA, previously termed Marshall’s syndrome) is a rare systemic autoinflammatory disorder (SAID) characterized clinically by periodic episodes of fever, sore throat, cervical lymphadenopathy, and superficial oral ulceration [23] (. Fig. 20.17). The accompanying fever thus sets it apart clinically from RAS.  It represents a periodic release of IL-1β that then drives inflammation. The exact trigger for the episodes is not known although as the disease may abate following tonsillectomy there is a suggestion that it is bacterially driven. Present management is centered upon tonsillectomy and use of anti-IL1 monoclonal therapies.  

..      Fig. 20.17  Multiple aphthous-like ulcers during the onset of a febrile episode in a patient with PFAPA

20.4.3

20.4.3.1

 ral Ulceration Secondary O to Systemic Disease of Childhood Gastrointestinal Disease

A number of gastrointestinal disorders can give rise to oral ulceration and other manifestations in the mouth. 20.4.3.2

Crohn’s Disease

Crohn’s disease is a chronic bowel inflammatory disease, which may involve orofacial region in about 20% of cases. The etiology remains unknown. Frequently, the first manifestation occurs at the age of 14–15 years. Any part of gastrointestinal tract, i.e., from the mouth to the anus, may be affected. It, usually, occurs with mild abdominal pain, diarrhea, and slight weight loss [24]. When there are intraoral clinical signs during clinical examination, these may be the first or the only manifestations of the disease. These clinical signs vary. There may be diffuse or nodular swelling of oral and/or perioral tissue, giving the picture of granulomatous disease (e.g., granulomatous cheilitis) (. Fig. 20.18), ulcerative lesions which may resemble aphthous ulcerations, or large deep ulcers surrounded by mucosal tags which can be present on the buccal mucosae or the buccal vestibules. In addition, there may be swelling of the buccal and/or labial mucosa that is soft and termed “cobblestoning.” In some patients, there may be erythema migrans of the tongue (geographic tongue). A lower motor neuron palsy of the facial nerve is possible but extremely rare in children. In some individuals there may be pyostomatitis vegetans which is characterized by the development of multiple, diffuse small abscesses [24–27] (. Fig.  20.19). The management of the oral aspects of Crohn’s disease is out with the clinical practice of pediatric dentistry although as with all child patients affected individuals should be provided with appropriate advice to minimize the risk of plaque-­ related oral disease.  

 

495 Oral Lesions in Children and Adolescents

20.5  Infectious Diseases in Childhood

a

A number of infections can give rise to oral ulceration in childhood. The ulcers are typically superficial, but, unlike RAS, the affected patients are systemically unwell and the episodes of ulceration are not recurrent [31, 32]. Infections that give rise to white patches are considered in 7 Sect. 20.5.3, although consideration is also given in this chapter to “Human Papilloma Virus and Mumps.”  

b

20.5.1

Viral Infections

Viral infections caused by herpes simplex type 1 or Coxsackie viruses are by far the most common infectious causes of oral ulceration in childhood. 20.5.1.1 ..      Fig. 20.18  a Clinical image of labial swelling and angular cheilitis in a patient with Crohn’s disease. b Colonoscopy reveals ulcerative lesions within the intestinal mucosa

..      Fig. 20.19  Pyostomatitis vegetans

20.4.3.3

Gluten-Sensitive Enteropathy (Coeliac Disease)

Gluten-sensitive enteropathy (GSE) is an immunologically mediated disorder in which there is notable inflammation of the small bowel induced by wheat proteins such as gluten. It may arise in childhood and manifest with abdominal pain, altered bowel habit, failure to thrive, and many other features depending upon its severity. Oral ulceration similar in appearance to that of RAS is not uncommon and indeed may be the first clinically detectable sign of GSE. The ulceration arises as a consequence of hematinic deficiencies (e.g., folate and iron) secondary to the loss of small bowel function [13, 28–30]. Additionally, the affected children may also have enamel defects (see also 7 Chap. 17).  

Herpes Simplex

Herpetic infection can manifest as a primary (herpetic gingivostomatitis) or, rarely in childhood, secondary infection (herpes labialis). Primary herpetic gingivostomatitis arises about 7–10 days following initial exposure to herpes simplex (typically via oral secretions). The infection is typically caused by HSV-1, although HSV-2 can be causative (this not necessarily being related to oro-genital contact). Infection usually occurs in preschool years, although it can also occur in the teenage years and early 20s. In recent years there has been a shift away from the early age occurrence toward the later one – possibly reflecting improved hygiene within nurseries or schools. Primary infection commences with fever lasting 2–5 days, pharyngeal pain, and cervical lymphadenopathy with the later evolution to short-lasting vesicles that break down to form painful oral ulceration. The ulcers can arise on any oral mucosal surface, are superficial, and coalesce into large irregular areas of ulceration. The gingivae become erythematous, swollen, and ulcerated (and can be mistaken as acute necrotizing ulcerative gingivitis (ANUG). The affected patients have notable malaise, drooling, and anorexia. The ulceration and understandable poor plaque control may give rise to oral malodor. The clinical picture can thus be alarming to patients and their parents/guardians [33] (. Figs. 20.20 and 20.21). The clinical features are particularly distinct, the only differential diagnosis realistically being erythema multiforme (see below). There is a little need for any confirmatory investigations such as viral DNA identification or establishing a rise in anti-HSV antibody levels between the acute and convalescent phases.  

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The clinical features usually resolve over about 1  week, and treatment is generally directed toward reducing the pain and pyrexia with non-steroidal anti-­ inflammatory drugs (e.g., paracetamol or ibuprofen) and ensuring adequate fluid intake. Antiviral therapy is rarely warranted unless (1) the clinical picture seems to be notably severe at an early stage and/or (2) the child is known to be immunocompromised. The antiviral of choice is aciclovir (e.g., 15 mg/kg of body weight, 5 times a day for 5–7 days – although higher doses may be considered for immunocompromised patients). The prodrugs valaciclovir and famciclovir are sometimes used for immunocompromised children, and cidofovir is a possible option when aciclovir resistance (which is rare) is likely. Most children do not have later episodes of herpetic gingivostomatitis, this being most likely in some child patients with immunodeficiency states. Herpetic infection will have episodes of the secondary infection – herpes labialis. Herpes labialis (sometimes termed “cold sores”) is common and actually can arise in individuals who have no recollection of having had the illness of primary herpes simplex infection. Herpes labialis is rare in the first decade of life but becomes more likely after this age. It is

clinically characterized by episodes of infection, usually at the same site of the vermillion border of the lip that comprises a sequence of paresthesia, erythema, vesiculation, pustule formation, ulceration, and eventual healing. The cycle of clinical features occurs over about 5 days, and affected individuals do not have any other clinical features directly caused by the HSV infection. Episodes of herpes labialis usually have a precipitant that presumably causes a mild reduction in immunosurveillance and resultant viral replication within the trigeminal ganglion. Commonly reported precipitants include upper or lower respiratory tract infections, exposure to sunlight, pregnancy, and psychological distress. Many patients however report that they felt “run down” just prior to the onset of herpes labialis. The diagnosis of herpes labialis is based upon the clinical history and features. There is usually no justification for confirmatory investigations. Therapy that only reduces the symptoms and signs by 1–2 days can be topical aciclovir (5% cream) or topical penciclovir (1% cream). Each agent needs to be applied before the onset of vesiculation; otherwise clinical benefit is unlikely  – although it is suggested that penciclovir can still be of some benefit when applied late (as opposed to aciclovir). Eye Catcher

a

b

Children with herpes labialis do shed the virus from lesions, and presumably oral fluids, thus should not be in close contact with individuals who are not known to be immune to herpes simplex or elderly or immunocompromised persons.

20.5.1.2 ..      Fig. 20.20  a, b Clinical image of primary herpetic gingivostomatitis in a 16-month-old infant. Vesicles are observed on the perioral cutaneous region surrounded by a red halo, while mucosal inflammation and confluent vesicles may be seen intraorally

a

b

Herpes Zoster (Varicella Zoster)

Herpes zoster gives rise to a primary infection termed chickenpox and a secondary disorder called shingles. The virus is transmitted via the droplet route. ­Chickenpox occurs in early childhood and arises in waves of infecc

20

..      Fig. 20.21  a Typical clinical picture of primary herpetic gingivostomatitis. There are multiple vesicles surrounded by red halo. There also is coexisting, disease-specific, gingivitis together with a crusting

of the right labial angle of the young patient. b, c Cases of the same disease localized in the tongue and the palate, respectively

497 Oral Lesions in Children and Adolescents

tion in groups of children that typically arise in the winter months of a country. The affected children experience gradual onset of pyrexia, headache, and malaise followed by the emergence of a red vesiculopapular rash that gives rise to small pustules that ulcerate and heal. Complications such as meningitis and encephalitis are possible but rare. The complete clinical picture lasts about 7–10 days. Oral ulceration – usually just a small number of superficial ulcers – can occur alongside the cutaneous rash and should be managed symptomatically (. Fig. 20.22) [32, 34]. Shingles, the secondary infection of herpes zoster, is rare in childhood although it is more likely in children with certain primary or secondary immunodeficiencies. Shingles typically arises from the dorsal root nuclei of the thorax and abdomen and thus does not give rise to oral lesions. Oral ulceration can occur if there is reactivation of the virus in the trigeminal ganglion and manifests as superficial small ulcers that follow the distribution of one branch or division of the nerve (. Fig. 20.23). A rare feature of shingles is pain in a tooth that precedes the onset of the ulceration. The management of shingles in childhood is similar to that of primary herpetic gingivostomatitis although higher dosages of acyclovir are warranted. In view of the possibility that the shingles is a reflection of an underlying immune defect, it is important that the affected children are managed both by pediatric dentists and pediatricians.

a

 

b

 

20.5.1.3

Infectious Mononucleosis

Infectious mononucleosis (IN) is a type of glandular fever caused by Epstein-Barr virus (EBV). The majority of cases occur in the second and third decade and reflect salivary transmission, for example, via kissing. The infection has a long incubation period of 4–7 weeks [32]. Clinically IN commences with general symptoms onset. The first symptoms are malaise, headache, high

..      Fig. 20.22  Clinical image of mild varicella infection. On the perioral cutaneous region, there are a small number of erosive lesions (rash), while on the vermillion border of the lips, there are small erosions resulting from vesicular rupture (arrows)

..      Fig. 20.23  a Typical clinical picture of herpes zoster infection of the third branch of the trigeminal nerve in a 4-year-old patient. b The unilateral distribution of rash and mucosal lesions are distinctive characteristics of the disease

fever lasting 1–2  weeks, lymphadenopathy (predominantly cervical) and sometimes abdominal pain due to hepatosplenomegaly, and a pink macular skin rash. In the oropharyngeal region, the uvula, the fauces, and the tonsils are swollen, red, and painful. Sometimes there are multiple petechiae on the hard and soft palates and small numbers of superficial oral ulcers (. Fig. 20.24). The numbers of leukocytes in peripheral blood are, typically, moderately increased (10.000–15.000/mm3), but in some cases, they are intensely increased. There are also atypical lymphocytes. It is essential for the disease to be distinguished from acute leukemias since they share some similar clinical and laboratory features. The detection of antibodies to EBV (heterophile antibodies) is a specific laboratory examination called mono-test and previously the Paul Bunnell test. The normal course of the disease is self-limiting. Complications or recurrence is rare and only likely in those with immunodeficiency or immunosuppression. Because there are no specific therapeutic agents against the particular virus, the treatment of the patient is symptomatic – for example, with analgesics and/or antipyretics. Systemic corticosteroids have occasionally been used when there is severe pharyngeal edema.  

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a

b ..      Fig. 20.24  Petechiae and bruising on the border of soft and hard palate in a teenager with infectious mononucleosis

20.5.1.4

Hand Foot and Mouth Disease

This is caused by various types of Coxsackie virus. It tends to arise in school children in the first decade of life. The virus is transmitted from person to person by direct contact, and the incubation period of the disease ranges from 3 to 9 days. The disease begins with a fever, chills, rhinorrhea, and malaise. Almost simultaneously, there is a vesicular enanthema of the oral mucosa, which is usually located at the front of the oral cavity. The vesicles rapidly rupture to give rise to small erosions covered by whitish pseudomembranes and surrounded by red halo, which resemble minor aphthous ulcerations. The subjective symptoms are mild although there may be lymphadenopathy. In a very short time, a small number of vesicles may be observed on the skin of the upper and lower limbs (mainly the pulps of the fingers) and rarely on the buttocks or knees (. Fig. 20.25). There is no specific therapy for this disorder, lesions resolve within 7–10  days, and therapy should be directed toward lessening pain and any pyrexia [31, 32].

..      Fig. 20.25  Hand-foot-and-mouth disease. a The vesicular erythematous patches in the oral cavity are evident. b The vesicular rash on the fingers of the young patient

 

20.5.1.5

20

Herpangina

..      Fig. 20.26  Herpangina affecting the soft palate

20.5.1.6

Herpangina is caused by Coxsackie A viruses – in contrast to its name which suggests herpesvirus participation. Transmission of the virus occurs by direct contact, and the incubation time is 4–7  days [3]. Herpangina, normally, begins with high fever that lasts for 1–4 days, sore throat, difficulty in swallowing, rhinorrhea, weakness, muscle pain, and possibly vomiting and/or diarrhea. Almost simultaneously, there are a small number of vesicles which are typically found on the soft palate, uvula, faucal arches, and pharynx. Very quickly the blisters rupture, leaving erosions covered by whitish ­pseudomembranes, surrounded by red halo which are, clinically, similar to aphthous ulcerations (. Fig.  20.26). The normal course of the disease is self-limiting over about 8–12  days, and any treatment should be directed toward lessening symptoms [31, 32].  

Measles

Measles is caused by the homonymous virus. It affects mainly children of school age. It is transmitted by droplets, and the incubation period ranges from 10 to 12 days. The disease usually occurs in epidemics, which occur every 2–4  years. The clinical manifestations begin with general symptoms (fever, headache, malaise) rapidly followed by rhinorrhea and laryngotracheobronchitis manifesting as a cough. Almost simultaneously, asymptomatic intraoral lesions develop which are located mostly on buccal mucosa. They are consisted by small whitish confluent spots (Koplik spots, similar to chips of chalk), which are based on an erythematous base and disappear after 2–3  days. Moreover, local lymphadenopathy coexists. A few hours later, a maculopapular rash takes place. Typically, the disease manifests firstly behind the ears and extends to the neck, cheeks, chest, upper limbs,

499 Oral Lesions in Children and Adolescents

and then the body and lower limbs. After the fever which, usually, lasts 6–9 days, the rash starts to diminish and after a week resolves [32]. Concerning the defense against measles, there is a preventive vaccination, which protects young people around 90%. Usually the measles vaccine is applied along with that for mumps and rubella (MMR vaccine), in two doses. 20.5.1.7

Mumps

20.5.1.8

In view of the wide availability of effective vaccination, mumps should now be considered a disorder of the past – nevertheless not all children receive this vaccine; hence, a small number of children and adults may still manifest this disease. Mumps is an acute generalized paramyxovirus infection of children and young adults. Mumps typically affects the major salivary glands, although involvement of other structures can occur including the pancreas, testes, ovaries, brain, breast, liver, joints, and heart. Mumps is transmitted via the droplet route and has an incubation time of approximately 14–18  days. Patients present with initial pyrexia, chills, and facial pain. The parotids are typically bilaterally enlarged, although this may initially be unilateral. There is often swelling of the submandibular glands together with lymphadenopathy, giving rise to profound facial and neck swelling (. Fig. 20.27). Rarely sublingual swelling may be so profound as to cause elevation of the tongue and dysphagia and dysarthria. The salivary swelling tends to diminish after approximately 4–5 days and may precede more complicated aspects of the illness. Affected patients may be unwell for about 1  week, but complications can include orchitis (infection of the testes – usually in post-pubertal years), mild pancreatitis, and viral meningitis or encephalitis. Cardiac, hepatic, and joint infection can occur, and they are rare and do not generally cause notable complications. However long-term neurological damage, including deafness, is rarely possible [35].  

a

There is no specific treatment for mumps, analgesia and appropriate fluid intake being the mainstays of therapy. It has been suggested that corticosteroids may be effective for severe parotitis, but generally these are not required unless the patients have other systemic symptoms such as orchitis. Mumps can generally be prevented with appropriate vaccination (mumps/measles/ rubella (MMR)) [36].

Human Papilloma Virus Infections

Human papilloma virus (HPV) is a DNA virus that comprises about 200 different genotypes that infect epithelial cells. They may be classified as cancer-causing (i.e., oncogenic types) and non-cancer-causing (i.e., non-­oncogenic types). The virus is transmitted by close contact. Oral infection with HPV in children is almost always is with non-oncogenic types. The exact route of acquisition of HPV in children is rarely identifiable although presumably some children bite warts of their fingers and hence transfer the virus to the mouth. There is no good evidence that pediatric oral HPV infection is a consequence of abuse of any kind [13]. 20.5.1.9

 ommon Warts (Verruca Vulgaris, C Squamous Papilloma)

This is the most presentation of HPV infection of the mouth. These manifest as slow-growing, solitary raised white nodules that have a cauliflower-like appearance (. Fig. 20.28). They can arise on any oral mucosal or gingival surface and are painless. They have no malignant potential and should be removed by scalpel excision (which allows histopathological confirmation of the diagnosis) or less commonly by laser ablation or thermocoagulation. In general these lesions do not recur. Occasional children with immunodeficiencies such as HIV disease may have multiple or recurrent oral  

b

..      Fig. 20.27 Mumps. a Bilateral swelling of the major salivary glands. b Unilateral swelling of the right parotid gland

..      Fig. 20.28  Wart of the vermillion border of the upper lip in a 17-year-old patient (arrow)

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is not itself a common feature of HIV infection of childhood. The most likely features of undiagnosed or poorly controlled HIV infection are: kPseudomembranous candidiasis (thrush)

See 7 Sect. 20.5.3.  

kOral hairy leukoplakia

..      Fig. 20.29  Multifocal epithelial hyperplasia (or Heck’s disease)

warts that will lessen if the underlying immune dysfunction can be corrected. 20.5.1.10

 ultifocal Epithelial Hyperplasia M (MEH, Heck’s Disease)

This is a very rare disorder that usually arises in early childhood and manifests as multiple flat or nodular/ popular warts affecting any oral mucosal or gingival surface (. Fig.  20.29). There are often so many warts that can become large, such that speech and/or eating can become difficult as patients incidentally bite the lesions. The exact route of acquisition of the infection is unknown although suggested routes have been via the vaginal tract during child delivery or via utensils [37]. The disorder is said to be most common in individuals of Inuit (i.e., American-Indian) genetic origin and hence likely in children living in Greenland and Central America (although it can arise in children without such ethnicity/residency). The disorder tends to spontaneously resolve in the late second decade, but before this therapy is difficult as the only reliable means of treating the warts is by scalpel or laser excision or thermocoagulation. Topical imiquimod or interferon alpha have been used by there are no good data to suggest that they are reliably effective.  

20.5.1.11

20

Human Immunodeficiency Virus (HIV)

Pediatric HIV disease still arises across the globe although the number of children becoming infected is falling. Children typically have become infected either in utero or less commonly during birth or very rarely as a consequence of breastfeeding. The fall in new pediatric infection reflects the availability of anti-retroviral therapy (ART) although, unfortunately, not all children with HIV are identified and hence are not receiving ART. In the past, when ART was not notably effective, children with HIV infection could develop a wide range of infections as well as Kaposi’s sarcoma (KS) and non-­ Hodgkin’s lymphoma (NHL) reflecting the progressive loss of cell-mediated immunity [38, 39]. The present discussion focuses upon the most common oral manifestations of pediatric HIV disease – although oral ulceration

This manifests as painless adherent white patches of the tongue and/or floor of the mouth. It is caused by Epstein-Barr virus (EBV) and is not potentially malignant. The extent of the OHL usually reflects the degree of the patient’s immune dysfunction – indeed if ART is effective, any pre-existing OHL may melt away only returning if ART (now rarely) becomes ineffective. Confirmation of the diagnosis of OHL requires histopathological examination of lesional tissue together with the identification of EBV proteins or DNA within the tissue. There is no specific therapy for OHL, and indeed as the lesion is painless and not potentially malignant, there should never be a need to consider any therapy such as acyclovir [40]. kKaposi’s sarcoma

This only arises in HIV disease when there is severe immunosuppression. This is a tumor of blood vessels caused by human herpes virus-8 (HHV-8). It manifests as a red, blue, or purple macule, papule, or nodule typically on the hard/soft palate of one side of the mouth although another common site is the upper gingivae. It is locally destructive and hence can cause ulceration and possibly bony destruction. The management of Kaposi’s sarcoma of the mouth is usually undertaken by oncology teams but may include local radiotherapy or systemic chemotherapy as well as treatment of any undiagnosed or poorly controlled HIV disease [31, 32]. kOther features

As noted above, a plethora of other oral disorders can arise in children with HIV disease. These may include ANUG, severe HSV, and occasionally VZV infection, systemic mycoses, unusual bacterial infections (e.g., Borrelia henselae), as well as large oral or pharyngeal ulcers of unknown cause. All unusual features of HIV disease should be managed by appropriate specialists.

20.5.2 20.5.2.1

Bacterial Infections Impetigo

Impetigo is a cutaneous disease. It does not affect the oral mucosa but gives rise to golden-colored vesicles or small blisters of the perioral or perinasal skin – although

501 Oral Lesions in Children and Adolescents

a

b

and spreads to the rest of the body. It is characteristic that the rash is absent from the perioral and paranasal region (Filatoff sign). In the oral cavity-intensive inflammatory, mucosal erythema and white tongue coating can be present from the initial stages of the disease. The tip and the lateral borders of the tongue are intensively erythematous. During the third to fifth day of the disease, the white coating of the tongue is gone, and the tongue is intensively erythematous with swollen fungiform papillae and is called raspberry tongue. The disease results in permanent immunity to erythrogenic toxin but not to streptococci. Penicillins are typically effective. 20.5.2.3

..      Fig. 20.30  a, b Bullous impetigo of the perioral area skin affecting a male and a female teenager. In such cases differential diagnosis from herpetic infections is important

in extreme cases, it can affect several other sites of the face. It tends to arise in young infants and early-year school children without any pre-existing skin disease, although it may complicate disease such as eczema or arise the following simple injuries such as cuts and grazes. Children with diabetes mellitus may be at increased risk of impetigo. It is usually caused by Streptococcus pyogenes and/or Staphylococcus aureus. There are two types of impetigo: bullous impetigo (usually caused by Staphylococcus), which affects neonates, infants, and toddlers, and the non-bullous impetigo, which affects more often school-age children (. Fig. 20.30). The prognosis is generally good, and the treatment includes administration of antimicrobial drugs usually topically or/and systemically [41]. ­Effective topical antimicrobials include mupirocin and fusidic acid 2%. These agents are commercially available as ointments and should be applied to the lesions two to four times daily for 7–10 days.

Tuberculosis

Tuberculosis (TB) is caused by Mycobacterium tuberculosis usually acquired via the droplet route from someone with open pulmonary TB.  It can be acquired via other routes, but this is most unusual. TB remains a significant health problem in countries with poor economies where there is social poverty, malnutrition, and lack of health care resources. However, in view of migration and travel, children and adults living in high-­ resource countries can present to clinics with clinically detectable TB.  In addition, undetected HIV disease increases the risk of TB [42]. In childhood and adolescence, the disease appears more often as chronic submandibular or cervical lymphadenopathy which is called scrofula (. Fig. 20.31). Oral ulceration – usually single ulcers – or labial enlargement can be features of TB but are remarkably rare. Although highly unlikely in children, TB can cause destruction of  

 

20.5.2.2

Scarlet Fever

The cause of scarlet fever is the Streptococcus pyogenes erythrogenic toxin. The infection is transmitted through inhalation of droplets, and the mean incubation time is 2–4  days [1]. The clinical expression of the disease includes initially pharyngotonsillitis, painful bilateral regional lymphadenitis, and general symptoms (fever lasting usually 5–6  days, severe headache, weakness, etc.). The typical micro-macular rash appears soon in the great folds of the body (axillae and inguinal region)

20

..      Fig. 20.31 Tuberculosis-associated cervical lymphadenitis (scrofula) in a young patient. The fistula opening and the erythema of the overlying skin are obvious

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the adrenal cortex and the later development of hyperpigmentation of the buccal mucosae (“Addisonian pigmentation”). The diagnosis of TB is out with the clinical practice of pediatric dentistry but typically requires identification of the causative organism via molecular analyses – culture is now considered to be a second line for the identification of TB. The management of TB is typically undertaken by infectious disease specialists. Protection from TB is achieved with BCG vaccination – hence why all healthcare providers must receive this prior to commencing clinical work. 20.5.2.4

 cute Necrotizing Ulcerative A Gingivitis

The diagnosis and general therapy are outlined in 7 Chap. 15. Very rarely acute necrotizing ulcerative gingivitis can extend to the periodontal tissues (necrotizing periodontitis) and/or the oral mucosa (necrotizing stomatitis), and in such instances, the treatment is the same as above although systemic antibiotics are essential.  

Eye Catcher

Children with severe malnutrition are at risk of acute necrotizing ulcerative gingivitis necrosis spreading to the underlying muscle and indeed facial skin in which case the disorder is termed NOMA.  This disorder tends to arise in geographic areas with extreme poverty (e.g., some African countries). Then malnutrition is the consequence of a poor economy brought on by political unrest and sometimes warfare. NOMA can have a devastating impact upon the facial growth of children and may result in lifelong facial disfigurement that requires many, often complex, surgical procedures to overcome [43, 44].

20.5.2.5

20

Other Bacterial Infections

A wide range of other bacterial infections of the mouth, most giving rise to oral ulceration, can arise in children, but these almost always arise in severely immunocompromised states such as undiagnosed late HIV disease, primary immunodeficiency, or hematological malignancy [31]. 20.5.3

Eye Catcher

White patches of the mouth can be subgrouped into adherent (i.e., do not easily wipe off) and non-­ adherent. Except for thrush, non-adherent white patches may usually be just food debris. They may also be found as necrotic tissue in oral mucositis secondary to local radiotherapy or systemic chemotherapy [13]. Adherent white lesions may be seen in congenital rare disorders, such as dyskeratosis congenita and pachyonychia congenita.

20.5.3.1

Pseudomembranous Candidiasis (Thrush)

This manifests as gelatinous white to yellow, curd-like white patches that are easily wiped off to leave areas of erythematous erosion. It tends to present on the soft palate, fauces, or posterior buccal mucosae but can occur anywhere in the mouth (even on the gingivae) (. Fig. 20.32) [45]. The presence of thrush always reflects a local and/or systemic cause that requires acknowledgment or identification. Common causes are the present or recent use of broad-spectrum antibiotics (e.g., amoxicillin or tetracyclines) or corticosteroids (particularly inhaled or administered systemically). Long-standing oral dryness may cause thrush, but this would be rare in children. Of importance however, thrush can be an early feature of immunodeficiency (e.g., due to HIV disease, leukemia, or undiagnosed/poorly controlled diabetes mellitus). Hence, it is essential that the cause of thrush is always identified. Thrush is caused by the superficial mycotic infection candida. Candida albicans is the usual infecting species although many other candida types may also give rise to this clinical disorder. The management of thrush principally rests upon the identification and management (where possible) of any underlying cause. In some instances the thrush will resolve spontaneously, for example, following comple 

Fungal Infections

The most common oral fungal infection in childhood is oral candidiasis, especially the acute pseudomembranous candidiasis (thrush), appearing in the form of ­non-­adherent white patches.

..      Fig. 20.32  Pseudomembranous candidiasis

503 Oral Lesions in Children and Adolescents

tion of courses of antibiotics or systemic corticosteroids, while with some patients, it is impossible to remove any underlying cause  – for example, corticosteroid inhaler use for asthma. In such instances there may be no need to provide therapy as thrush is usually not symptomatic and is not known to have any malignant potential. Where therapy is required, topical agents such as nystatin suspension may be useful, and when disease is severe, does not resolve with nystatin, and/or is symptomatic, there may be a need for systemic fluconazole therapy. Topical anti-fungal gels such as those with miconazole or clotrimazole may be alternative therapies, but they are unlikely to be easy to apply. There is rarely any requirement to confirm the diagnosis of thrush by microbiological means (e.g., culture): (1) candida is a common commensal of healthy persons and (2) the candida load (or count) does not predict disease severity or likely response to therapy. Long-term use of anti-fungals can increase the risk of the emergence of anti-fungal resistance, but this is only a concern in patients who are severely immunocompromised. Candida can give rise to a number of clinical presentations other than thrush and they include the following: kDenture-associated stomatitis

In children, a red appearance beneath the acrylic plate of a prosthetic or a removable orthodontic appliance. This is painless, and therapy is directed to improving appliance hygiene and occasionally placing miconazole gel on the fitting surface of the appliance. kChronic erythematous candidiasis

A red patch in the center of the dorsum of tongue. This is painless and may arise in children using corticosteroid inhalers for long periods. A similar patch may occasionally also arise on the hard palate (sometimes termed chronic erythematous candidiasis). This rarely warrants any therapy (i.e., anti-fungals) as it is painless, is not potentially malignant, and in any case is unlikely to resolve if the patient continues to have corticosteroids. kAngular cheilitis

Red patches at the corners of the mouth. This is rare in children and if present may be associated with severe anemia or immunodeficiency (e.g., HIV disease). The lesions can be painful and are infected with Candida and/or Sstaphylococcus aureus. Treatment should be principally directed toward resolving the underlying cause, although nystatin suspension plus local application of miconazole gel may hasten healing. kChronic hyperplastic candidiasis

This manifests as adherent white or speckled (i.e., red and white) patches of the oral mucosa. It is very rare in

children, can only be diagnosed by histopathological examination of lesional tissue, and if present may be a sign of known or unknown long-standing immunodeficiency (e.g., worsening HIV disease, congenital defects of cell immunity, or chronic mucocutaneous candidiasis) (see below). Topical or systemic anti-fungal agents may lessen or resolve such disease, but there is little good data on effective therapy, and in any case, there should be a focus upon identifying and where possible resolving any underlying cause. kChronic mucocutaneous candidiasis (CMC)

This is a group of rare disorders that reflect a number of defects of cell-mediated immunity [46]. They are collectively characterized by recurrent candida infection of mucosal surfaces and/or skin. Oral disease can manifest in childhood and presents as recurrent episodes of any of the above clinical presentations of candida infection of the mouth. The most significant CMC type is autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) characterized by autoimmune destruction of the endocrine tissue (e.g., parathyroid, adrenal cortex, pancreas, ovaries, testes) such that the affected children may have enamel hypoplasia or hypocalcemia of the developing teeth and Addisonian pigmentation [46, 47]. CMC is sometimes accompanied by an iron deficiency; hence, children may have oral ulceration angular cheilitis and/or glossitis (i.e., a smooth tongue). The management of CMC is out with the practice of pediatric dentistry although clearly enamel anomalies in APECED may warrant treatment. Except for candidiasis, there are some systemic mycotic infections such as mucormycosis, aspergillosis, histoplasmosis, and blastomycosis, which may cause ulceration in immunocompromised children. 20.6  Mucocutaneous Disease

Immune-mediated mucocutaneous disease that may affect the mouths of children is extremely rare. Pemphigus types have been reported in children (erosions/ulcers), but perhaps the most common, although rare, of these disorders to arise in children would be erythema multiforme. 20.6.1

Erythema Multiforme

Erythema multiforme (EM) very rarely arises in children. This is an unusual hypersensitivity disorder that may arise in response to medication and occasionally infection (e.g., HSV or Mycoplasma pneumoniae. The more different drugs that an individual is receiving, the greater

20

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S. Porter and A. Kolokotronis

Eye Catcher

a

Allergic reaction is a most severe adverse effect; hence, there is always a need to review the medical history of child patients before prescribing penicillin or indeed any systemic medication. The management of possible angioedema and anaphylaxis varies across the globe, but the major principles (regardless of the precipitant) are as follows: 1. Removal of the potential cause (usually impossible – it is too late) 2. Call for professional support 3. High flow oxygen 4. Repeated intramuscular adrenaline (every 5 minutes) until professional support arrives

b

..      Fig. 20.33  a Clinical image in Stevens-Johnson syndrome. b In Steven-Johnson syndrome, ulcerative lesions often arise on the vermilion borders of the lips

the likelihood of EM. This disorder comprises four clinical presentations: erythema multiforme minor, EM, major, Steven’s Johnson syndrome (SJS) (. Fig. 20.33), and toxic epidermal necrolysis syndrome (TENS). The minor type comprises ulceration of a mucosal surface or less than 10% of the skin, while the other types involve more extensive mucocutaneous ulceration with TENS giving rise to more than 30% of the skin being affected [48, 49]. Mucosal and/or cutaneous disease may sometimes, but not always, be accompanied by target lesions (concentric rings of white and red) that may affect any cutaneous surface but particularly the palmar and plantar surfaces. A detailed discussion of EM is out with the scope of this chapter, but if EM is suspected, it is essential that patients are rapidly referred to appropriate specialists.  

20.6.2

20

Allergic Reactions

Allergic reactions, i.e., hypersensitivity responses in response to oral healthcare procedures, are very rare. The most common allergic reaction that is likely to arise is a type 1 reaction (i.e., immediate hypersensitive) to penicillin. This is clearly most likely when a patient with known allergy to penicillin is mistakenly prescribed this drug. The clinical presentation of penicillin allergy varies from mild urticaria (i.e., skin rash) to angioedema (swelling of the lips, tongue, pharynx, and larynx) and anaphylaxis (urticaria, asthma, angioedema, anoxia, and possible death).

Hypersensitivity reactions to a wide range of other agents used in pediatric dentistry are possible and include natural elastic gum (latex, e.g., gloves, rubber dam) (. Fig.  20.34) and, in rare cases, after contact with materials which do not contain latex (e.g., various metals, such as nickel which is used in orthodontic materials [50, 51]) (. Fig.  20.35). The reactions to these agents vary in severity and timing; some may be rapid (within a few minutes, e.g., angioedema in response to an impression material) or slow (within 48–72  hours, e.g., perioral rash with some instruments) [50–53]. Reactions to local anesthetics are almost unheard of although some patients or their parents report that they are “allergic” when in fact upon closer discussion they are found to have possibly fainted or just “felt unwell” or “tired.” If a genuine allergy to components of local anesthetic solutions is suspected, then it is important that the patient is referred to a suitable specialist for detailed evaluation.  

 

20.6.3

Other Mucocutaneous Disease

Unlike adults, children are not liable to develop autoimmune disease such as immunobullous disease nor oral lichen planus, although clearly these can occasionally arise in children or young adults. A detailed discussion of these is out with the scope of this book. However, it must be borne in mind that oral lichen planus-like disease can arise in children with graft-versus-host disease. Graft-versus-host disease (GvHD) arises in children who receive a bone marrow allograft (e.g., in the management of leukemia) in which, as the term suggests, the graft exerts a cytotoxic response upon the host. The oral consequences of GvHD include early oral superficial ulceration and later the emergence of white patches, erosions, and ulcers on the mucosae and/or gingivae that mimic those of oral lichen planus. Other features include

505 Oral Lesions in Children and Adolescents

20

loss of salivary gland function (hence xerostomia), multiple mucoceles, and pyogenic granulomas (that may be driven by cyclosporin). This immunosuppressant may also cause gingival enlargement [54].

a

20.7  Hematological Disease

There are a vast array of hematological disorders of childhood that may give rise to oral manifestations and/ or have the impact upon the acute care of pediatric dentistry. The present discussion is not intended to be definitive but to provide an overview of relevant aspects of hematological disease. Hematological disease reflects either altered cellular number or function of cells derived from bone marrow (i.e., reticulocytes, white blood cells, and platelets) or the proteins of the coagulation pathways. Hematological disease also includes non-solid (e.g., leukemias) and solid (e.g., lymphomas and tumors of Langerhans cells).

b

c

20.7.1 20.7.1.1

..      Fig. 20.34  Three images demonstrating the progress of a probable allergic reaction to rubber dam latex. a Edematous reaction of the left buccal area 2 hours after the dental treatment. b Exanthema after 3 days. c The same region 15 days later

a

b

Lymphomas

Lymphomas are hematological solid tumors. They broadly split into Hodgkin’s disease (HD) and non-­ Hodgkin’s lymphoma (NHL). Hodgkin’s disease usually arises from nodal lymphoid tissue and spreads locally from one group of nodes to another (and can include the liver and spleen); a characteristic histopathological feature of HD is the presence of Reed-Sternberg cells. In contrast NHL usually commences in extra-nodal sites (e.g., tonsils, Peyer’s patches, brain, viscera), spreads erratically, and is histopathologically dominated by abnormal lymphocytes (usually). The cause of most lymphomas is unknown although some NHL may be caused by EBV or Helicobacter pylori. Lymphomas are in general uncommon in children although some NHL are more common in children than adults. 20.7.1.2

..      Fig. 20.35  a Unusual allergic reaction (type IV-delayed hypersensitivity), which arose during orthodontic treatment of a young female. Diagnostic evaluation by an allergist revealed hypersensitivity to nickel (degree ++++). b Complete clinical signs of remission after the removal of the brackets. The orthodontic treatment was completed by using nickel-free brackets. (Courtesy by Dr. O. Kolokitha)

Hematological Malignancies

Hodgkin’s Disease

Hodgkin’s disease arises in young individuals (15– 30 years old). Initially there is painless swelling of one or few lymph nodes belonging to one group – and of note the cervical group is often the first to be affected. Patients can develop “B” symptoms of weight loss, pyrexia, and lethargy. Involvement of the mouth is very rare [55] although if disease affects the bone marrow patients will be liable to opportunistic infection (e.g., acute pseudomembranous candidiasis) or have features of thrombocytopenia. Gingival swelling due to HD has been reported, and there are occasional reports of bone involvement (manifesting as radiolucencies). Hodgkin’s

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disease is managed by hematological oncology teams and usually has a good prognosis. 20.7.1.3

Non-Hodgkin’s Lymphoma

This is a notably broad group of malignancies. Children are rarely affected although Burkitt’s lymphoma tends to arise in children and usually affects the jaw bones manifesting as large bony swellings, gingival enlargement, tooth mobility, and possible pathological fracture. NonHodgkin’s lymphoma can arise in the mouths of children with severe HIV disease and may manifest as large areas of necrotic ulceration of the gingivae and/or oral mucosae. As with HD, such disease is managed by hematology oncologists, but unlike HD, it has a variable prognosis [56–58]. 20.7.1.4

Langerhans Cell Histiocytosis

This comprises a group of rare tumors of myeloid dendritic cells. Although uncommon it can give rise to notable oral features and by virtue of its systemic effects has the possibility of complicating the care of children requiring pediatric dentistry [59, 60]. It comprises three clinical presentations: eosinophilic granuloma, Hand-­ Schüller-­Christian syndrome, and Letterer-Siwe disease. The terminology is sometimes variable such that the non-localized form of eosinophilic granuloma is termed histiocytosis X. These disorders tend to arise in children and young adults.

Eosinophilic Granuloma This is usually a localized disease that arises in late childhood. The skull and often the jaws, especially the mandible, are common sites of involvement. Jaw disease can cause mobility of the teeth in the affected area, and pathological fracture (of the mandible) can rarely occur. Radiology can reveal radiolucent areas that are observed, and the teeth may have the appearance of floating on the top of the radiolucency. Usually, the overlying oral mucosa may be ulcerated. The jaws can be affected in  localized multisystem disease (that can involve the lungs, liver, spleen, bone marrow, or CNS) [61].

20

Letterer-Siwe Disease This is rare but the most severe type of Langerhans cell histiocytosis and tends to arise in young children (e.g., 2 years of age). Affected children develop a seborrheic rash, ear discharge, and features of severe multisystemic disease including anemia, thrombocytopenia, neutropenia, lymphadenopathy, and/or hepatosplenomegaly is the most severe type of Langerhans cell disease. The oral manifestations can be those of eosinophilic granuloma, but in addition there may be features of anemia (e.g., superficial ulceration), neutropenia (e.g., candida infections), and thrombocytopenia (e.g., petechiae and ecchymoses) [63].

Leukemia

20.7.1.5

Leukemias are hematological non-solid tumors in which there are clones of neoplastic, immature, or mature lymphocytes or granulocytes. They are principally divided into four main types: • Acute myelogenous leukemia (AML) • Acute lymphoblastic leukemia (ALL) • Chronic myelogenous leukemia (CML) • Chronic lymphocytic leukemia (CLL) Apart from these four major types, there are also various (and many) subtypes. Children and young adults tend to have a greater risk of acute than of chronic leukemias. Acute lymphoblastic leukemia is the most common type in childhood. Further details of the implications of leukemia for pediatric dentistry are provided in 7 Chap. 21; however, in general, the oral manifestations encompass those of loss of bone marrow function, complications (both short- and long-term) of therapy, leukemic deposits (as with acute lymphoblastic leukemia), and gingival deposits of acute myeloid leukemia that manifests as gingiva enlargement [64].  

20.7.2

Disorders of Blood Cells

The majority of red cell defects in children center around anemia (i.e., a reduction in hemoglobin and red cells).

Anemia

Hand-Schüller-Christian Disease

20.7.2.1

This is a variant of disease that includes the clinical triadof: (a) Osteolytic lesions (in 100% of the affected individuals) (b) Diabetes insipidus (reflecting destruction of the posterior pituitary gland (50%) (c) Exophthalmos (10%)

Anemia in adults tends to reflect a deficiency of one or more of the hematinics (iron, vitamin B12, and folate (folic acid)), and certainly, for example, children with undiagnosed gluten-sensitive enteropathy are at risk of this. Young adults with bulimia nervosa and/or anorexia nervosa may be at risk of anemia due to a lack of intake of folic acid or iron. Anemias cause oral ulceration, a red smooth dorsum of the tongue (“atrophic glossitis”), and angular cheilitis. Vitamin B12 deficiency (e.g., in Crohn’s disease) may also cause a soreness of the tongue. Anemias must be managed by appropriate specialists [65].

However, these features do not arise simultaneously, and there may be lymphadenopathy, cutaneous rashes, and hepatosplenomegaly. The jaws can be affected in the same way as eosinophilic granuloma [62].

507 Oral Lesions in Children and Adolescents

The dominating anemias of childhood and in particular certain parts of the globe are the hemolytic anemias due to hemoglobinopathies  – thalassemia and sickle cell disease. 20.7.2.2

Thalassemia

Thalassemias are a group of hemolytic inherited (following the autosomal recessive pattern) diseases which are caused by hemoglobin composition disorders and particularly by reduced production of α (α-thalassemia) or β (β-thalassemia) hemoglobin A (HbA) peptide chains. In the Mediterranean there are in general three following forms of β-thalassemia; other thalassemias are much less common and indeed can be life-­ threatening. kβ-Thalassemia major

55 This manifests in the first few months of life and is characterized by severe hemolytic anemia, delayed body development, recurrent infections, and splenomegaly. Affected individuals have features of anemia. With time bony enlargement can arise as a consequence of extra-medullary bone marrow expansion, and this particularly affects the long bones and skull. Radiologically there may be expansion of the diploic space with trabeculae having a “hair on end” appearance [66–69] (. Fig.  20.36). Enlargement of the mandible and more commonly the maxilla can give rise to a liontine (“lion-like”) appearance. The oral features of thalassemia are now rare in children in view of the advances in treatment – indeed bone marrow transplantation is now sometimes undertaken.  

kβ-Thalassemia intermedia

This may be caused by double heterozygosity (combination of α- and β-thalassemia). It is rare and presents almost the same clinical picture of with thalassemia major – but is milder. kβ-Thalassemia minor

55 This rarely gives rise to severe anemia or the features of major disease. 20.7.2.3

20.7.2.4

..      Fig. 20.36  Lateral skull radiograph of a child with thalassemia major. The “hair-on-end” skull is depicted

Sickle Cell Disease

The sickle cell diseases reflect a defect in the structure of the globin chain  – i.e., there are a normal number of chains (unlike thalassemias), but the structure and function are defective. When there is a reduction in blood oxygenation, the reticulocytes become sickle in shape, do not pass along small blood vessels with ease, and may cause obstruction of vessels. Sickle cell disease has some notable racial (hence geographical) variation being most likely in individuals of a Black Africa decent. Affected individuals are prone to hemolytic anemia and intermittent vaso-occlusal disease. The abnormal red blood cells become sequestered in the spleen, and with severe disease, there is a loss of splenic function and risk of pneumococcal infection. The vaso-occlusal disease varies in presentation between patients but in its most severe form can cause acute pain crisis that may be precipitated by infection, extreme temperature, hypoxia, dehydration, psychological or physical stress, or even menstruation [70, 71]. A detailed discussion of sickle cell disease is out with the scope of this chapter but key issues relevant to pediatric dentistry include effective preventative care to avoid a risk of periapical infection precipitating a painful crisis, the need for general anesthesia, avoidance of the use of agents likely to suppress respiratory function, avoidance of non-steroidal anti-inflammatory drugs in patients with possible or known renal disease, and awareness that patients with severe sickle cell anemia can develop pain in single non-carious teeth that is a manifestation of a pulpal infarct.

Neutropenia

Neutropenia reflects a reduction in the number of polymorphonuclear neutrophils. In children this can reflect congenital disease such as chronic neutropenia and cyclic neutropenia or be a consequence of bone marrow failure (e.g., with leukemias and lymphomas) or due to a reduction in bone marrow function due to drug therapy (e.g., cytotoxics or immunosuppressives). Rarely autoimmune disease may cause an autoimmune neutropenia [72, 73]. In general, neutropenias increase the risk of recurrent infections of the respiratory and urinary tracts and skin, and children may have recurrent episodes

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of pyrexia of unknown cause. Depending upon the cause and hence severity of the neutropenia, the oral cavity can be greatly affected. Common features are deep ulceration of the mucosae or gingivae (these are sometimes said to lack an inflammatory halo), profound gingivitis, and cervical lymphadenopathy. Oral pseudomembranous candidiasis can also arise. In long-­standing profound anemia, there is a risk of aggressive periodontitis with resultant tooth mobility and even early loss of the primary dentition. In cyclic neutropenia the neutrophil count tends to spontaneously reduce about every 3–4 weeks such that patients develop all of the above features in a cyclical manner.

tures may include the risk of brain abscess, hemorrhagic stroke, hepatic failure, and risk of high-output cardiac failure. Aside from its oral manifestations, the implications of HHT for pediatric dentistry center upon the need for effective preventative dental care to avoid the need for general anesthesia, careful nasal intubation (if essential) to avoid epistaxis, and cessation of spontaneous bleeding of oral telangiectasias with chemical cauterization and post-surgical (e.g., post-extraction) bleeding with chemical cauterization and/or tranexamic acid [76]. 20.7.3.2

Eye Catcher

There are a wide range of rare disorders in which neutrophil function (e.g., adherence, chemotaxis, phagocytosis, or killing) can be defective. In general, these disorders increase the risk of aggressive periodontitis although some may also cause orofacial granulomatosis-­type disease.

20.7.3

Bleeding Disorders

Cessation of bleeding rests upon vasoconstriction, the formation of the primary platelet plug, and the subsequent establishment of a clot. Defects of any of these elements have the potential to increase the risk of post-­injury bleeding and in severe disease cause spontaneous bleeding. The present discussion focuses upon the more common or well recognized of this group of disorders. 20.7.3.1

20

Hereditary Hemorrhagic Telangiectasia (HHT, Osler-Weber-Rendu Syndrome)

This is an uncommon autosomal dominant disorder of blood vessel formation characterized by mucocutaneous telangiectasias and arteriovenous malformations in various internal organs (e.g., lungs, liver, and brain). The telangiectasias have a high likelihood to occur in the nose, mouth, and gastrointestinal tract; they bleed easily causing, for example, repeated and/or severe epistaxis and unknown gastrointestinal bleeding leading to anemia [74, 75]. Affected children and adults may have multiple small 1–3-mm-diameter telangiectasias on the face, periorally, on the lips, and on any oral mucosal of gingival surface. Patients may also have oral signs of anemia. Other fea-

Thrombocytopenia

Thrombocytopenia – reduced platelet count – is uncommon in childhood although when present it has many causes that range from autoimmune disease such as idiopathic thrombocytopenic purpura (ITP) and systemic lupus erythematosus (SLE), viral infection (when there is usually a short-term fall in platelet count), congenital disease (e.g., Wiskott-Aldrich syndrome and Fanconi anemia), malignancy (e.g., leukemias or other tumors of the bone marrow), or loss of bone marrow function due to radiotherapy, chemotherapy, or immunosuppressives. As detailed previously the oral features of thrombocytopenia comprise a variable number of petechiae and/ or ecchymoses. The petechiae (small red-to-purple flat dots that when larger are termed purpura) can arise on any oral mucosal and/or gingival surface, while the ecchymoses (large bruises) are more likely at sites of trauma such as the palate and buccal mucosae. When there is a severe reduction in platelet numbers (e.g., below 20,000/mm3), there may be spontaneous gingival bleeding. Cleary children with severe thrombocytopenia will have cutaneous purpura and bruising and be liable to epistaxis and gastrointestinal tract bleeding. Bleeding within viscera is uncommon. The management of thrombocytopenia clearly depends upon the severity of the platelet deficiency and the underlying cause. Aside from its oral features, the implications of thrombocytopenia center upon avoiding bleeding with infiltrations (in general the platelet count should be above 20,000/mm3) or regional blocks (the count should be above 50,000/mm3), ensuring effective post-surgical hemostasis and avoidance of drugs likely to increase bleeding (e.g., NSAIDs), and considering any interaction between dentistry and the underlying disease or its treatment (e.g., possible corticosteroid cover for children receiving long-term corticosteroids). Finally, there should be a focus upon the prevention of childhood dental disease – hence avoiding the need for any invasive dental treatment [77].

509 Oral Lesions in Children and Adolescents

There are a number of disorders in which platelet numbers are normal but their function abnormal (thrombasthenias). In general patients with such disease should be managed with the similar considerations as for thrombocytopenia. 20.7.3.3

AIDS.  Similarly, HCV transmission occurred in some instances. It is now highly unlikely that any child or young adult who has received factor concentrates in recent years will be infected with HCV and certainly not HIV [77–80].

Coagulopathies

There is a wide spectrum of defects of the clotting mechanism. These may be of congenital defects of the clotting factors (e.g., the hemophilias) or secondary to hepatic or gastrointestinal disease (e.g., vitamin K deficiency secondary to gluten-sensitive enteropathy) or the use (all be it rarely in children) of anti-coagulants – especially coumarin agents such as warfarin. The present discussion will center upon more well recognized congenital clotting factor deficiency disorders.

Hemophilia A Hemophilia A is an X-linked (i.e., the affected gene lies on the chromosome X) recessive inherited disease that gives rise to a reduction or absence of Factor VIII. As an X-linked recessive disorder, females may be carriers or very rarely affected, while males are at risk of having the disease. Hemophilia A accounts for 85% of all instances of hemophilia and has an incidence of about 1:5000 live births. Depending upon the level of the Factor VIII deficiency, there are three forms: severe (when levels are 100,000/ml), although in a few cases, they may be within normal limits or decreased (under- or non-­ Mucositis, ulcerations, and infections  Mucositis of the mouth and throat appears in 50–80% of children underleukemic forms). going cancer therapy (. Fig. 21.2). Symptoms are felt by the first week of radiotherapy or chemotherapy and Eye Catcher retract after the end. Mouth rinsing four to five times a day with a 3% H2O2 or soda solution relieves mild mucoBoth radiotherapy and chemotherapy cause serious sitis symptoms. In more severe forms, anti-inflammatory oral complications in children at a greater frequency and anesthetic preparations are used. There is also encourthan in adults [6]. The chemotherapeutic drugs and aging evidence supporting that low-­level laser irradiation radiotherapy target cells with high mitotic activity, therapy reduces significantly the duration of the mucositis which is high also in normal cells of children in comcaused by chemotherapy [9]. parison to adults. The levels of leukocytes are affected Oral infections from fungi, viruses, and bacteria are and fall 5–7  days after each cycle of chemotherapy, the result of immunosuppression, dry mouth, and/or lasting for 14–21 days. A few days after the leukocyte mucous membrane lesions. The most common infection number recovery, the next cycle of chemotherapy is candidiasis (thrush), for which the antifungal drugs could follow. nystatin, miconazole, etc., are administered. For the Chemotherapeutics affect drastically the renewal healing of ulcers, topical application of iodine solution of the cells of the oral epithelium and may cause or cetylpyridinium chloride three to four times daily problems such as ulcers (71%), lip lacerations (38%), gives satisfactory results. Younger patients undergoing dry mouth (11%), mucositis (9%), lymphadenopathy antineoplastic treatment are more prone to infections (7%), candidiasis (4%), and other infections (4%) [7]. associated with the herpes virus. The infection can be In some cases, disturbances appear in the craniofacial localized (cold sores) or display severe herpetic gingivodevelopment or the formation of the teeth. stomatitis (see 7 Chap. 20). The severity of the infection depends on the size of immunosuppression.  

 

 

Dry mouth  Dry mouth, caused by radiotherapy due to

Dysgeusia and eating disorders  Dysgeusia (foul taste)

dramatic decrease of saliva production from the salivary glands, increases the likelihood of infections in the mouth and affects speech, chewing, and swallowing. Dry mouth is accompanied by a feeling of burning tongue and thirst. For children these symptoms are usually temporary, either

can be a lasting symptom in young patients undergoing chemotherapy or radiotherapy and affects especially the taste of bitter and acidic, while that of salt and sweet is not seriously affected. It can be treated by the administration of zinc sulfate during meals. These changes are due to

..      Fig. 21.1  a, b Commercial preparations as saliva substitutes to reduce the dry mouth sensation. c Chewing gum with xylitol

b

a

c

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518

A. Arhakis and N. Kotsanos

21.1.2

a

Dental Care Protocol

Before starting antineoplastic therapy, it is very important for minimizing oral complications to begin with prophylaxis and care of the existing dental needs. This includes adopting the right dietary habits and brushing with a soft toothbrush and fluoridated toothpaste. Complementary use of fluorides (described in 7 Chap. 12) may be required for children at high caries risk, with dry mouth, and those undergoing head and neck radiation [6]. When there is no time for complete dental rehabilitation before the start of the antineoplastic therapy, dental infections should at least be removed, e.g., by extractions and periodontal therapy, because they can lead to systemic infections when the patient will become immunocompromised [12]. In primary teeth, extraction is a safer treatment option to endodontic treatment, while in permanent dentition, the latter is acceptable if it could be completed and allow at least a week for assessing a successful outcome [7]. Tooth extractions, after platelet and blood neutrophil counts, can be performed at least 10 days beforehand, to allow time for wound healing. Fixed orthodontic appliances are removed if patient do not apply adequate oral hygiene or if there is a severe mucositis. During antineoplastic therapy toothbrushing is regularly performed despite the reduction of platelets [6], if necessary with extra soft toothbrush respecting the sensitive soft tissues. Dental treatment is done only in emergency situations, in cooperation with attending physician [7, 12]. After the end of antineoplastic therapy, any unfinished dental treatment could be completed and a recall program followed, as in healthy children. In those suffering from severe mucositis, the remaining mucosal lesion is taken care of and examined histologically if needed. Compliance in preventive program is often poor because of both children and parents’ fatigue, after a long demanding process of therapy. Burnout by cancer treatment is usually greater by adolescents than children [13].  

b

..      Fig. 21.2  a An improved stage of mucositis following chemotherapy of a patient with leukemia at ages 4 and 6 years. b His panoramic radiograph at age 14 years shows several teeth with short roots

swelling of the taste buds, becoming normal 6–12 months after therapy [10]. Eating disorders are associated with the disease itself, while anorexia may be related to complications of antineoplastic therapy such as mucositis, dry mouth, and loss of taste or nausea. Abnormalities of teeth and jaws  Children being at the

growth period are subject to developmental abnormalities. These may be related to dental and/or skeletal development, like maxillary or mandibular hypoplasia or dental root growth (short roots, early root completion) (. Fig.  21.2), oligodontia, enamel hypoplasia, and disturbance of tooth eruption time, all dependent on the radiotherapy or chemotherapy time and duration [10].  

Neurotoxicity  Neurotoxicity is a side effect resulting

from certain types of chemotherapy drugs such as alkaloids and vincristine. The resulting facial pain is continuous and dull but may be reported by the young patient as toothache. Usually the symptoms subside a week after the end of chemotherapy [11]. Rampant caries  Particularly, in those patients undergo-

21

ing head and neck radiation therapy, there is the risk of a rampant form of dental caries within months after therapy, as a result of a combination of dry mouth and negligence of undertaking preventive measures, i.e., very good oral hygiene and use of fluoride (. Fig.  21.3). Extractions and minor surgical interventions can be done under prophylactic antibiotic chemotherapy without fear of necrosis or infection, if they are least traumatic [6, 11].  

21.2

Cardiovascular Diseases and Chemoprophylaxis

Heart diseases in infants and children are among the most frequent chronic diseases of childhood and are divided into congenital and acquired forms. Congenital heart diseases, owed to malformation of the heart and/ or large vessels, have a prevalence of five to eight cases per 1000 live births. The time of occurrence and the severity vary. Almost half of them are diagnosed in the first year of life, while others may remain undetected for years. Cardiomyopathies and some types of arrhythmias usually coexist with other congenital anomalies of the heart or occur as a complication of the surgical correc-

519 The Young Dental Patient with Systemic Disease

a

b

c

d

e

f

..      Fig. 21.3  a, b Dental treatment needs of a 4-year-old boy with acute lymphoblastic leukemia. All needs were met before chemotherapy. c New caries in primary molars and burnout neglect of oral hygiene following a 3-year miss of recalls. d Extensive hypomineral-

ization of permanent incisors, visible after new supervised oral hygiene. e Juice-drinking abuse and bruxism have contributed to additional erosive wear. f The 18-month recall shows arrest of caries lesions as a result of the reinstituted preventive program

tion. Acquired heart diseases are rare in infancy. These include endocarditis, myocarditis, Kawasaki disease, pericarditis, and acquired arrhythmia. Some of these can be fatal or lead to disabilities.

A small number of incidents have been directly correlated with previous dental treatment [15]. Microorganisms  – especially virulent streptococci  – cause endocarditis typically associated with the normal flora of the mouth. Colonization occurs at irregularities of cardiovascular endothelium due to anatomical defects, disease, or foreign body. The real cause is considered to be consecutive bacteremia episodes and not isolated incidents, e.g., tooth extraction or the placement of rubber dam and matrix with wedge [16]. Thus, the most important bacterial endocarditis prevention measure in high-risk individuals is daily oral hygiene, since the extent of bacteremia (the number of bacteria entering the blood flow) is related to the severity and extent of the already existing gingivitis [17]. Preventing bacterial endocarditis is not only by chemoprevention, but is supported by the treatment of any infection that could lead to bacteremia [14].

21.2.1

Microbial Endocarditis and Dental Care

Endocardial microbial infection is characterized by formation of shoots, mainly in heart valves, and has a high mortality rate if not treated promptly (. Fig.  21.4). Chemoprophylaxis recommendations along with the views on morbidity causes for bacterial endocarditis have undergone many changes over time. Theoretical risk prevalence is very low (1:150,000 for adults at high risk who received chemoprophylaxis and three times higher for those who did not) [14].  

21

520

A. Arhakis and N. Kotsanos

..      Fig. 21.4  A schematic representation of a longitudinal heart section with possible sites of bacterial endocarditis vegetations

21.2.2

 revention Protocol for Dental P Patients

The protocol adopted by the European Academy of Paediatric Dentistry for the prevention of bacterial endocarditis in children with an increased risk is as follows: amoxicillin, 50  mg/kg body weight (maximum dose of 2 gr) as a single dose per os 1 hour before dental surgery. In case of allergy to penicillin, clindamycin is selected, 20  mg/kg body weight (maximum dose of 600 mg). In case of intramuscular or intravenous administration, the above is proposed to be done, half an hour before the dental treatment: ampicillin 50  mg/kg body weight (maximum dose of 2 gr). In case of allergy to penicillin, clindamycin is administered, 15 mg/kg body weight (maximum dose of 600 mg) [15]. >>Important Patients proposed to take chemoprophylaxis are classified into two groups

21

High risk. Patients with a history of bacterial endocarditis, congenital cyanotic heart diseases (e.g., transposition of the great vessels, tetralogy of Fallot), and iatrogenic arteriovenous communications in systemic or pulmonary circulation. Patients with cardiac implants who develop cardiac valvular diseases. Congenital heart defects, which are fully treated, surgically or using a catheter, requiring antibiotic coverage in the first 6 months after surgery. Medium risk. Patients with congenital heart defects, acquired valve dysfunction, hypertrophic cardiomyopathy, mitral valve prolapse with valvular regurgitation, and/or thickening of the leaflets.

>>Important Dental treatments for which chemoprophylaxis is proposed • Tooth extraction or any other surgical procedure • Periodontal treatment, root scaling, and pocket depth measurement • Implant placement or avulsed tooth re-implantation • Chemo-mechanical root canal preparation, if exceeding root apex • Subgingival placement of antimicrobial fibers or films • Orthodontic band placement • Intraligamentary local anesthesia • Scaling and tooth or peri-implant prophylaxis

Studies have shown that, in children who had recently received chemotherapy (antibiotics), colonization of strains resistant to the antibiotic administered was more frequent [18]. The British Society for Antimicrobial Chemotherapy proposes revision of the current protocol, by administering preventive chemoprophylaxis only in high-risk patients for endocarditis as well as in those with high mortality risk when ill. Generally, there is a worldwide debate and frequent revisions on chemoprophylaxis necessity for various patient categories. For patients who require multiple appointments for dental treatment, an interval of at least 14  days between sessions is proposed, in order to reduce the risk of developing resistant strains of the administered antimicrobial for chemoprophylaxis. Furthermore, mouthwash with chlorhexidine 0.2% solution for 1 minute prior to dental treatment, if possible, is proposed.

521 The Young Dental Patient with Systemic Disease

21.3

Diabetes Mellitus

Diabetes is characterized by elevated blood sugar levels due to reduced production of insulin by the beta cells of the islets of Langerhans in the pancreas. Diabetes is divided in type I (insulin-dependent or teenage) and type II (non-insulin-dependent or adult) form. The incidence of diabetes is low in infants, increases in school age children, and reaches the rate of 1:500 among children at the age of 17, in Europe. Diagnosis is made by medical history, clinical presentation, and laboratory urine and blood tests. Originally, a child suffering from this disease has symptoms such as polyuria, polydipsia, drowsiness, anorexia, weight loss, and constipation. Regarding the treatment, monitoring blood sugar is needed as well as suitable diet and daily insulin administration. Three meals and two to three sugar-free between-meal snacks, low fat and rich in fiber, are required [19, 20].

Dental Findings and Treatment

21

Eye Catcher

Diabetes’ implications on a young patient could be: 1. Hypoglycemic coma: Chills and cold skin, fast pulse, stress, confusion, convulsions, and coma. If the patient retains his/her senses, sugar or honey through the mouth must be given. The patient recovers usually within 5–10 minutes. If they lost their senses, 1 mg of glycogen intramuscularly or 10–20  ml 20–50% dextrose is intravenously injected [19]. 2. Hyperglycemic coma: (Due to lack of insulin) dry mouth and skin, fast and weak pulse, low blood pressure, and tendency to vomit. Immediate intravenous administration of fluids (bicarbonate salt 8.4%) and direct communication with the physician or hospital for insulin are required [19].

21.4

Asthma

Asthma is a chronic inflammatory condition of the airways, characterized by recurrent episodes of wheezing, Flow rate of saliva in diabetic children is reduced due to breathlessness, retrosternal (back of chest) dull pain, the dehydration associated with polyuria, but caries and coughing, particularly at night and early morning index is not affected, probably due to low frequency of [23]. More severe bronchial obstruction leads to difficarbohydrate intake. Only in uncontrolled diabetes and culty in breathing and tachycardia [24]. Asthma is a heterogeneous disease, especially in early childhood, and is uncontrolled diet a child can be considered as high carcaused both by endogenous and environmental factors. ies risk [19]. More correlation has been established The most common of the latter is exposure to allergens, between diabetes and periodontal disease, especially in infections, and airway exposure to nonspecific stimuli adults. The longer the diabetes history, the more serious such as cigarette smoke. Activity at low temperatures are the periodontal problems, particularly in non-­ causes symptoms in 80% of children with asthma. The insulin-­dependent diabetes and uncontrolled one [21]. emotional state and stress may also trigger an asthma When blood glucose is elevated, increased amounts of attack [25]. glucose are found in the saliva and gingival fluid. The best time for dental treatment is during morning Eye Catcher hours, when blood sugar is stable. Before treatment the dentist is necessary to consult the pediatrician for the Asthma affects 5–10% of children. Depending on the patient’s dosage, and frequency of insulin administrafrequency and intensity of symptoms and the need for tion, diet, blood glucose level, and any other problem medication, it is classified into four categories: mild, may coexist. Low resistance of diabetic children to moderate, severe, and very severe. Three quarters infections has to be always in mind. Orofacial infections belong to the mild category with little daily episodes or short-term crises [26]. The majority (60%) of chilmust be treated immediately as they can trigger the dren with asthma show no symptoms until the age of appearance of ketosis. Conducting ordinary dental 6 years. treatment and minor surgical procedures under local anesthesia does not require special precautions. In more extensive surgical procedures, special attention has to be Medicinal treatment of chronic asthma in children given to avoid hypoglycemia, in order to prevent a pos- includes two main groups of drugs, bronchodilators, sible delay in healing because of impaired phagocytosis. and anti-inflammatory. Mild asthma is usually treated Adrenaline contained in  local anesthetics does not by inhaling beta-2 agonists alone, usually every increase the blood glucose levels [22]. 4–6  hours. In patients with moderate asthma, anti-­ 21.3.1

522

A. Arhakis and N. Kotsanos

a

b

c

d

..      Fig. 21.5  a Fixed-dose inhalation apparatus for asthma. b In very young children, it is used with chamber and mask covering both the mouth and nose. c, d MIH-type mild and severe molar hypomineralization of MIH appearance, respectively, in a young boy with asthma. (Courtesy Dr. G. Vadiakas)

inflammatory drugs are sometimes given proactively, but not for treating an acute episode [27, 28]. Inhaled steroids administered per os two times a day provide good control. In acute severe asthma, the usual treatment is a short-acting beta-2 antagonist [27, 28]. The latter is applied by a nebulizer or fixed-dose device in a hospital (. Fig. 21.5). Systemic administration of corticosteroids is also proposed [28].  

21.4.1

21

Dental Findings and Treatment

Although there is no general agreement, caries indices seem to increase with the severity of asthma and while the patient is under medication [29]. The presence of fermentable carbohydrates, such as lactose, to ensure a more tolerable taste of the inhaled medications may be responsible. It is reported that up to 80% of inhaled medication stays in the mucosa remaining in the oral cavity. In children with asthma, increased dental erosion was observed. This was ascribed to more frequent carbonated and/or low pH fluid intake – according to preference styles of adolescents – due to dry mouth sensation caused by commonly observed oral breathing [30]. Some reduction in the flow rate of saliva is expected from the activity of beta-2 blockers, and more plaque and gingivitis have been found [31]. Increased calculus is observed, possibly related to high calcium and

phosphate levels in the saliva secreted by the submandibular salivary and parotid glands [29, 30]. The respiratory function of the patient may improve if the dental chair is placed in a less inclined position. It is appropriate to use a rubber dam and high-volume suction for minimizing aerosols. Dental visits should be as short as possible to prevent the child feeling fatigue. Aspirin and other non-steroidal anti-inflammatory medications are to be avoided [27]. Erythromycin should not be administered in patients receiving theophylline, because the former interferes in the metabolism of the latter, thereby increasing blood theophylline to possibly toxic levels. Inhalation sedation with N2O/ O2 for dental treatment can be helpful, as it does not irritate the lung epithelium and may prevent asthmatic attacks [32]. In the event of an asthmatic attack, dental treatment is discontinued; the patient is placed in a comfortable position, sitting or standing, and an inhaled beta-2 blockers is administered directly. If there is no improvement, the patient is given corticosteroids and epinephrine subcutaneously at a dose of 0.01 mg/kg of a 1:1000 (maximum dose 0.3 mg), while medical assistance is sought [33].

21.5

Chronic Renal Failure

Chronic renal failure is progressive bilateral destruction of nephron function, which results in the kidneys being unable to maintain the internal environment balance for which they are responsible [34]. Before the age of 5, the disease is caused by genetic abnormalities in the kidneys, such as hypoplasia, and in the urinary tract, manifested by vesicoureteral reflux. At age 5–15 years, the disease is usually caused by lesions of the glomeruli (e.g., glomerulonephritis) or hereditary kidney diseases (cystic fibrosis, nephrotic syndrome). The degree of dysfunction of the kidneys determines the symptoms the child exhibits. Initially it complains of malaise, headache, vomiting, anorexia, polyuria, and polydipsia. Later there is a progressive disorder of electrolytes and dehydration after metabolic acidosis, increased pressure, heart failure, and uremia. Younger patients suffering from the disease have some physical growth retardation and muscular weakness, while their skin color is pale with a brown hue [34]. It is ranked the fourth most serious illness in the USA, with attack frequency of urinary tract infection at 1% for boys and 3% in girls before the age of 10 years. Diagnosis is made by medical history, clinical examination, and laboratory tests. Depending on the severity of the disease and the stage of development, the treatment is divided into three categories: conservative treatment, dialysis, and kidney transplantation [35].

523 The Young Dental Patient with Systemic Disease

21.5.1

Dental Findings and Treatment

The oral manifestations of the disease depend on the age at which the disease occurs, the duration, severity, and the cause. Changes are observed in both the soft and the hard tissues. One of the most important findings in the soft tissue is pale mucosa from anemia which is due to decreased secretion of erythropoietin by the kidney [36]. Intraoral hematomas and ecchymosis and mild coagulation problems are due to the sensitivity of the walls of the capillaries and the reduced energy of the plasma II agent. Dental Findings at Chronic Renal Failure

The teeth and bones of the jaws are affected when kidney failure occurs during tooth formation/mineralization (chronologic enamel hypoplasia/hypomineralization) or in critical periods of bone growth, possibly leading to orthodontic anomalies [37]. The uremia affects the bone remodeling causing disappearance of lamina dura and creating bone lesions which histologically resemble giant cell tumors, as in hyperparathyroidism [36]. Despite the disappearance of the lamina dura, if there are no other bone lesions, mobility of the teeth is not usually observed. Discolored teeth have been reported from deposition of blood pigments due to uremia or by prolonged use of tetracyclines [38]. Reduced dental caries and increased deposition of calculus are also reported [39].

Dental treatment varies depending on the child’s medical condition and its treatment phase. Routine dental treatment should be avoided when the serum urea nitrogen is >60 mg/dl and the rate of creatinine is >1.5 mg/dl. Arterial blood pressure and hemorrhagic tendency of the patient should be monitored. Aspirin should be avoided, and the responsible physician contacted before administering any medication, because of the limited ability of the kidneys to metabolize and excrete it. Antibiotics are not considered necessary, unless there is active inflammation. If herpetic gingivostomatitis occurs in very young children, total liquid intake is monitored to ensure electrolyte balance [40]. A child who is receiving hemodialysis needs some extra precautions. Before any dental restoration is undertaken in patients with surgically inserted artificial anastomosis, chemoprophylaxis is necessary. The hand or foot on which the anastomosis is mounted should not be used to administer drugs and be free to move for preventing blood clotting. Many of these children are taking anticoagulants (coumarin) to prevent blood

clots. Their administration should be stopped 48 hours, in order for normal hemostasis to be achieved if hemorrhagic dental procedures are anticipated [41]. The number of transfusions these children undergo because of blood loss classifies them at high risk for hepatitis. The dentist should therefore take the necessary precautions. For a patient who has had a kidney transplant, further precautions are needed, because of taking corticosteroids and immunosuppressants to prevent foreign body expulsion. One of the side effects of these drugs is that they cover the symptoms of inflammation so that infections become a frequent cause of death in these patients. Therefore, it is vital to communicate with the attending physician for antibiotic coverage before any dental procedure, for minimizing inflammation chances [37].

21.6

Gastroesophageal Reflux Disease

Gastroesophageal reflux disease (GERD) is the entrance of gastric or intestinal contents into the esophagus with or without vomiting [42, 43]. About 7–8% of infants and toddlers manifest daily episodes of GERD of short duration (>Important Patient/parent interactions –– Delayed presentation of injury –– History of any injury inconsistent with clinical findings –– Withdrawn child –– Lack of parental empathy –– Inappropriate comments Physical signs –– Failure to thrive (low body mass index) –– Dirty and smelly –– Inappropriately dressed –– Untreated head lice or other infections (e.g. impetigo) –– Multiple bruises, of different vintage –– Unusual injuries, bites, burns, pinch marks Family risk factors –– History of drug/alcohol dependency –– History of domestic violence –– Parent subject to abuse as a child

557 Child-Centred Dentistry: Engaging and Protecting Children

–– Low socioeconomic status –– Chaotic and lifestyle stressors, multiple children from different fathers –– Unemployment, financial stress –– Frequent past attendances at emergency departments –– Child not attending school

This is an area that clinicians find particularly difficult, with many reported barriers to addressing potential abuse, including lack of training, concern about how their questioning may be received by the family and worry that they may make things worse for the child. Support and resources should be available to support clinicians in this challenging area. Furthermore, mandatory training in safeguarding should be undertaken by all dental health professionals. It is also important that the dental team receive regular updates on wider issues such as female genital mutilation and child trafficking, as intelligence about these practices continues to grow. Physical abuse may be more readily identifiable than neglect per se, which may therefore remain unchallenged. The question has to be asked as to whether severe dental caries, which is ubiquitous in some populations, in itself constitutes neglect and thus warrants social care referral and intervention. The general consensus is that dental neglect is a ‘persistent failure to meet a child’s basic oral health needs, likely to result in the serious impairment of a child’s oral or general health or development’ [24]. It may also be a manifestation of general neglect. The scenario of a parent failing to bring their child for a scheduled general anaesthetic appointment for necessary dental extractions, following a previous presentation of pain and/or infection, has to be viewed seriously and neglectful of the child’s basic oral healthcare needs. The wider issue of failed dental/medical attendances is also debated within the safeguarding arena. The term ‘was not brought’ has been proposed by some as a more appropriate terminology than other descriptors, such as ‘did not attend’ or ‘failed to attend’ [25]. Conceptually, children are mostly reliant on an adult to bring them to their dental appointments, and therefore they themselves should not be labelled as ‘non-attenders’. Every clinician should adhere to an agreed local/national protocol for following up on children who were not brought to their scheduled dental appointments. This will ensure that children who are known to be ‘at risk’ are not over-

23

looked and a clear pathway is identified for subsequent information sharing, multiagency support and social care referral where necessary.

23.5

Service Evaluation

There are currently around 2.2 billion children in the world, representing a large sector of health service users. Thus one can readily see the argument for greater child representation, as key stakeholders, in consultations about quality assurance and planning of healthcare ­services. An example of this commitment to involve children comes from a 2016 survey of the quality of care received by British children during their hospital admission (see 7 http://www.­cqc.­org.­uk/sites/default/files/20171128_ cyp16_statisticalrelease.­pdf). Questionnaires were completed by almost 35,000 children aged 8–15  years and provided important feedback about good practice and where things could be further improved.  

23.5.1

PROMs and PREMs

Many healthcare sectors routinely employ patient-­ reported outcome measures (PROMs) and patient-­ reported experience measures (PREMs) as part of ongoing overall service evaluations [26]. Whereas PROMs tend to measure the impact of a clinical intervention in improving a patient’s perceptions of their own health, PREMs capture a patient’s objective experience of specific aspects of healthcare (e.g. were they seen on time, were the staff friendly). Within children’s oral health, the use of PROMs and PREMs is still emerging as highlighted by a systematic review on child-reported outcomes for cleft lip and palate care [27]. The management of traumatic dental injuries is another key area where the need for standardised patient-reported outcome measures has been recognised [28]. Child OHRQoL questionnaires, as described previously, are probably the most frequently used PROM within clinical research, including clinical trials, with the aim of measuring the effectiveness of an intervention from the child’s perspective [29]. Picker (7 www.­picker.­org) is an international charity, established in 2000, that provides expertise for developing effective tools to capture patients’ experiences, thereby improving the quality of health and social care.  

558

Z. Marshman and H. Rodd

Tip

The ‘Children’s Friends and Family Test’ is one of the freely available resources that can be used to measure children’s experiences of healthcare (access at 7 http:// www.­p icker.­o rg/wp-­c ontent/uploads/2015/04/ BIG_6260-­P 2778_CYP-­F FT-­Q uestion-­Form_CW_ TD-­_No-­Online_050215_FINAL_A4.­pdf).  

It was developed following wide consultation with children themselves, who were able to comment on the wording, response format and overall design. This is considered an exemplary child PREM, which can be completed as a hard copy or online via a smartphone app or website.

23.6

Oral Health Research and Ethics

23.6.1

23

The Rationale for Child Engagement

Children can be enthusiastic and reliable research participants, offering unique insights to investigators. A key driver to greater child engagement has come from the social sciences where research practice has shifted from being ‘on’ children to ‘with’ children and acknowledges them as experts in their own lives [30]. It is paramount that young people are given the opportunity to contribute to clinical research in order to improve future healthcare services and to promote greater understanding of childhood conditions. With appropriate approaches, children of all ages and abilities can be involved throughout the research process. Even prior to study commencement, children can be consulted to prioritise the research topic and suggest questions to be posed, thereby ensuring that the research is actually relevant to them. They can also provide invaluable advice on the study design and recruitment and retention of participants [31, 32]. Interestingly, there has been a fundamental shift in the priorities of many funding bodies, who now stipulate that there must be evidence of significant patient and public involvement within a proposed research programme. As well as recruiting children to oral health research, it is important that the findings of such research are conveyed in such a way that children can readily access and understand them. Over the last decade, the contribution of children to oral health research has become much more transparent. Previously, however, there was a paucity of dental research that actively involved children, as highlighted in a 2006 systematic review [33]. This enquiry was

repeated in 2014 and evaluated all child-related dental studies, published between 2006 and 2014, with the aim of determining to what degree children had been actively involved [34]. Children’s participation was classified according to the following four categories: 1. Children fully engaged, contributing to the research process or having their own words used. 2. Children as research subjects, completing measurers designed by adults. 3. Children’s input sought via a proxy, parent or clinician. 4. Children seen simply as objects with no engagement at all. The key finding was that, although only 20% of the contemporary literature involved children fully as active participants, this was a considerable improvement on the 7% engagement identified by the previous review. It is encouraging, therefore, to see how child dental research has continued to move towards greater participation in recent years. There are still missed opportunities, however, particularly within more ‘traditional’ research areas, such as clinical trials. 23.6.2

Methodological Considerations

Broadly speaking, children can be engaged in oral health research through quantitative or qualitative approaches or a combination of the two [35, 36]. Quantitative methods essentially seek to measure or define something. They rely on the use of questionnaires or scales, potentially providing a vast amount of numerical data, usually from large cohorts, which are conducive to statistical analyses and interpretation. With today’s modern technologies and social media explosion, the burden of administration and analysis can be greatly reduced by using online surveys. Caution does have to be exercised, however, when using non-validated questionnaires for research purposes, as these could undermine the reliability of the data. However, the stages involved in developing and validating a child-centred questionnaire are complex and time-consuming. Another caveat relates to the ‘adaptation’ of adult questionnaires for use with children, as the meaning of words and response formats may be entirely inappropriate. Furthermore, items of importance to young people may have been omitted altogether. Qualitative enquiries, on the other hand, do not seek to measure things, but rather to describe things through people’s own accounts. As such, they can gain more meaningful insights into behaviours, opinions and motivations. A wide variety of approaches can be employed

559 Child-Centred Dentistry: Engaging and Protecting Children

..      Fig. 23.3  Two young sisters engaged in a participatory activity relating to genetic research about amelogenesis imperfecta, drawing their ‘family trees’

including interviews, focus groups, film-making, video or written diaries. These techniques can also be supported by participatory activities such as drawing, model-making or role play (. Fig.  23.3). Qualitative methods offer some advantages to quantitative approaches in that they facilitate participation of younger children or those with specific learning or language disabilities. They also allow a deeper insight into a topic as children are generally given the opportunity to say what they like, without being too restricted by the researcher’s agenda. Conversely, this approach may provide data that are irrelevant or difficult to analyse and interpret. Assuring the quality of qualitative research remains equally as important as for quantitative research.  

23.6.3

Ethical Issues

Alongside considerations for meaningful research participation comes the requirement for ethical research conduct. In addition to the general principles that govern ethical research practice as whole, there are some special considerations that relate to children’s participation. A valuable resource for those undertaking research with children is the comprehensive 2015 report produced by the Nuffield Council of Bioethics, entitled ‘Children and clinical research: ethical issues.’ Over 500 children, parents, clinicians and researchers were consulted to make proposals as to how children and young people

can be ethically be involved in research as well as identifying roles and responsibilities of all involved. Tip

The accompanying website provides excellent films, animations and other resources for involving children in health research (accessed at 7 http://nuffieldbioethics.­ org/project/children-­research).  

It is imperative that children are protected from any emotional or physical harm as a result of their research participation. Clearly the research must be well justified, in terms of addressing an important question and the need to be conducted with children specifically. Any risks and burdens of participation must also be as low as possible. Children (as well as their parents/carers) should be provided with information about the proposed study in a clear and easy-to-understand format, so they can make up their own mind, with no time pressure as to whether or not they would like to participate. The associated assent or consent forms should also be easy to comprehend. It is important that there is not seen to be a power imbalance between the researcher and the child. So, for example, the person doing an interview should be independent and not someone who is actually providing the child’s treatment, as children may not feel comfortable saying what they really think. Finally, although confidentiality is key to research governance, children

23

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Z. Marshman and H. Rodd

should be made aware that if they disclose something that concerns the research team from a child protection point of view, the researcher may have to share this information.

23.7

Conclusion

Paediatric dentistry, by the very nature of the specialty, has always striven to be patient-centred. However, continued transformation within social, educational and health policy has driven more robust and evidence-based approaches to the way in which children are engaged within dentistry.

References

23

1. The United Nations International Convention on the Rights of the Child. https://downloads.unicef.org.uk/wpcontent/ uploads/2010/05/UNCRC_united_nations_convention_on_the_ rights_of_the_child.pdf. Accessed 11.2.21. 2. Lenton S, Ehrich J. Approach to child-friendly health care--the Council of Europe. J Pediatr. 2015;167:216–8. 3. Yang C, Crystal YO, Ruff RR, Veitz-Keenan A, McGowan RC, Niederman R.  Quality appraisal of child Oral health-related quality of life measures: a scoping review. JDR Clin Trans Res. 2020;5(2):109–17. 4. Gilchrist F, Rodd HD, Deery C, Marshman Z. Development and evaluation of CARIES-QC: a caries-specific measure of quality of life for children. BMC Oral Health. 2018;18:202. Published online: https://doi.org/10.1186/s12903-018-0662-8. 5. Jokovic A, Locker D, Stephens M, Kenny D, et  al. Measuring parental perceptions of child oral health-­related quality of life. J Public Health Dent. 2003;63:67–72. 6. Li YJ, Gao YH, Zhang Y. The impact of oral health status on the oral health-related quality of life (OHRQoL) of 12-year-olds from children's and parents' perspectives. Community Dent Health. 2014;31:240–4. 7. Dantas-Neta NB, Moura LF, Cruz PF, Moura MS, et al. Impact of molar-incisor hypomineralization on oral health-related quality of life in schoolchildren. Braz Oral Res. 2016;30:e117. 8. Reissmann DR, John MT, Sagheri D, Sierwald I.  Diagnostic accuracy of parents' ratings of their child's oral health-related quality of life. Qual Life Res. 2017;26:881–91. 9. Eckstein DA, Wu RL, Akinbiyi T, Silver L, Taub PJ. Measuring quality of life in cleft lip and palate patients: currently available patient-reported outcomes measures. Plast Reconstr Surg. 2011;128:518e-26e. 10. Zaror C, Martínez-Zapata MJ, Abarca J, Díaz J, et al. Impact of traumatic dental injuries on quality of life in preschoolers and schoolchildren: a systematic review and meta-­analysis. Community Dent Oral Epidemiol. 2018;46(1):88–101. 11. Knapp R, Gilchrist F, Rodd HD, Marshman Z. Change in children's oral health-related quality of life following dental treatment under general anaesthesia for the management of dental caries: a systematic review. Int J Paediatr Dent. 2017;27:302–12. 12. Hasmun N, Lawson J, Vettore MV, et al. Change in Oral healthrelated quality of life following minimally invasive aesthetic treatment for children with molar incisor Hypomineralisation: a prospective study. Dent J (Basel). 2018;6(4):61. https://doi. org/10.3390/dj6040061.

13. Aimée NR, Damé-Teixeira N, Alves LS, et al. Responsiveness of Oral health-related quality of life questionnaires to dental caries interventions: systematic review and Meta-analysis. Caries Res. 2019;53(6):585–98. 14. Hall M, Gibson B, James A, Rodd HD. Children's experiences of participation in the cleft lip and palate care pathway. Int J Paediatr Dent. 2012;22:442–50. 15. Patient Information Forum. Guide to Producing Health Information for Children and Young People. 2014. https://www.pifonline.org.uk/ wp-content/uploads/2014/11/PiF-Guide-Producing-Health-Information-Children-and-Young-People-2014.pdf. Accessed 11.2.21. 16. Wyatt KD, List B, Brinkman WB, Prutsky Lopez G, et al. Shared decision making in pediatrics: a systematic review and Metaanalysis. Acad Pediatr. 2015;15:573–83. 17. Marshman Z, Eddaiki A, Bekker HL, Benson PE. Development and evaluation of a patient decision aid for young people and parents considering fixed orthodontic appliances. J Orthod. 2016;43:276–87. 18. Hulin J, Baker SR, Marshman Z, Albadri S, Rodd HD. Development of a decision aid for children faced with the decision to undergo dental treatment with sedation or general anaesthesia. Int J Paediatr Dent. 2017;273:44–55. 19. Nunn J, Foster M, Master S, Greening S. British Society of Paediatric Dentistry: a policy document on consent and the use of physical intervention in the dental care of children. Int J Paediatr Dent 2008;Suppl 1:39–46. 20. Peretz B, Gluck GM.  The use of restraint in the treatment of paediatric dental patients: old and new insights. Int J Paediatr Dent. 2002;12:392–7. 21. Welbury RR, Murphy JM. The dental practitioner's role in protecting children from abuse. 2. The orofacial signs of abuse. Br Dent J. 1998;24(184):61–5. 22. American Academy of Pediatrics Committee on Child Abuse and Neglect; American Academy of Pediatric Dentistry; American Academy of Pediatric Dentistry Council on Clinical Affairs. Guideline on oral and dental aspects of child abuse and neglect. Pediatr Dent. 2008-2009;30(7 Suppl):86–9. 23. Harris C, Welbury R.  Top tips for child protection for the GDP. Dent Update. 2013;40:438–40. 24. Bhatia SK, Maguire SA, Chadwick BL, Hunter ML, et al. Characteristics of child dental neglect: a systematic review. J Dent. 2014;42:229–39. 25. Powell C, Appleton JV.  Children and young people's missed health care appointments: reconceptualising 'Did not Attend' to 'Was not Brought' – a review of the evidence for practice. J Res Nursing. 2012;17:181–92. 26. Weldring T, Smith SMS. Patient-reported outcomes (PROs) and patient-reported outcome measures (PROMs). Health Serv Insights. 2013;6:61–8. 27. Ranganathan K, Vercler CJ, Warschausky SA, MacEachern MP, et  al. Comparative effectiveness studies examining patientreported outcomes among children with cleft lip and/or palate: a systematic review. Plast Reconstr Surg. 2015;135:198–211. 28. Sharif MO, Tejani-Sharif A, Kenny K, Day PF.  A systematic review of outcome measures used in clinical trials of treatment interventions following traumatic dental injuries. Dent Traumatol. 2015;31:422–8. 29. Gilchrist F, Marshman Z. Patient-reported outcomes (PROs) in clinical trials in paediatric dentistry. Int J Paediatr Dent. 2020;31(Suppl 1):31–7. 30. Clark A, Flewitt R, Hammersley M, Robb M (eds). Understanding Research with Children and Young People (published in association with The Open University). 2013. Sage publications ltd, London (ISBN: 9781446274934).

561 Child-Centred Dentistry: Engaging and Protecting Children

31. Marshman Z, Innes N, Deery C, Hall M, et al. The management of dental caries in primary teeth - involving service providers and users in the design of a trial. Trials. 2012;22;13:143. 32. Weintraub JA, Breland CE. Challenges, benefits, and factors to enhance recruitment and inclusion of children in pediatric dental research. Int J Paediatr Dent. 2015;25:310–6. 33. Marshman Z, Gibson BJ, Owens J, Rodd HD, et al. Seen but not heard: a systematic review of the place of the child in 21st-century dental research. Int J Paediatr Dent. 2007;17:320–7.

34. Marshman Z, Gupta E, Baker SR, Robinson PG, et al. Seen and heard: towards child participation in dental research. Int J Paediatr Dent. 2015;25:375–82. 35. Marshman Z, Hall MJ. Oral health research with children. Int J Paediatr Dent. 2008;18:235–42. 36. Gilchrist F, Rodd HD, Deery C, Marshman Z.  Involving children in research, audit and service evaluation. Br Dent J. 2013;214:577–82.

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Supplementary Information Index – 565

© Springer Nature Switzerland AG 2022 N. Kotsanos et al. (eds.), Pediatric Dentistry, Textbooks in Contemporary Dentistry, https://doi.org/10.1007/978-3-030-78003-6

565

Index A Abfraction 467 Abrasion 466 Actinomyces sp.  348 Active immobilization  71, 72 Acute fluoride toxicity  266–267 Acute hyperplastic inflammatory  355 Acute lymphoblastic leukemia  516 Acute necrotizing ulcerative gingivitis (ANUG)  495, 502 Acute orofacial infections  323 Acute suppurative sialadenitis  511 Acute ulcerative gingivitis  357–358 Adamandiades-Behcet 494 Aesthetic restorative materials  3 Allergic reactions  504, 505 Alveolar bone fracture  375 Amelogenesis imperfecta (AI) –– definition 445 –– dental rehabilitation  446, 449 –– gene investigation and correlation  448 –– hypomatured-hypoplastic with taurodontism  446, 447 –– hypoplastic type  445, 446 –– masticatory forces  446, 447 –– mechanisms 445 American Academy of Pediatric Dentistry (AAPD) guidelines  3, 62, 259 Analgesia  138, 511 Anamnestic records  480 Anemia 506 Anesthesia 138–140 Angle Class II malocclusion  225, 235, 243 Angle Class III malocclusion  226, 235 Angle Class III molar relationship  237 Angular cheilitis  503 Ankyloglossia 359 Ankylosed primary molars  239 Ankylosis 190–193 Anorexia nervosa  538 Anterior cross bite  227 Anterior middle superior alveolar nerve block (AMSA) injection  119 Anterior open bite  234, 243 Anteroposterior discrepancies  224 Anxiolysis –– antihistamines 144 –– benzodiazepines  143, 144 –– definition 137 –– evaluation 145 –– nitrous oxide/oxygen mixture –– adverse effects  142 –– breathing practice  140 –– contraindications  141, 142 –– in COVID-19 era  142 –– informed consent  140 –– inhalation sedation  137–140 –– monitoring 141 –– personnel safety  142 –– rapid induction technique  141 –– rubber dam  141 –– standard titration technique  141 –– patient history  144, 145

Apexification technique  338–339 Aphthous ulceration  492–494 Apical plug apexification  403 Arch length discrepancy  209 Arch space anomalies  218–223, 229–233 Artificial apical plug apexification  404 Aspirin 522 Association for Dental Education in Europe (ΑDΕΕ)  133, 134 Asthma  521, 522 Atraumatic restorative technique (ART)  285 Attention deficit hyperactivity disorder (ADHD)  352, 535–537 Attrition 466 Autism spectrum disorders (ASD)  534–536 Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED)  453, 503 Autotransplantation of premolar  406 Avulsion 375

B Bacterial infections –– acute necrotizing ulcerative gingivitis  502 –– impetigo  500, 501 –– scarlet fever  501 –– tuberculosis  501, 502 Bacteriotherapy 267 Basic erosive wear examination (BEWE)  471 Basic life support (BLS) training  135 Behavior guidance –– ask-tell-ask aims  65 –– classification 62 –– definition 62 –– demanding behavior problems –– emotional immaturity and language problems  75, 76 –– gag reflex  75 –– intense fear of dental injection  74, 75 –– directed breathing  69 –– distraction  66, 67 –– ethical, legal issues and parental consent  76, 77 –– guided imagery  69 –– humor 69 –– hypnosis 69 –– memory restructuring  69 –– modeling 67 –– outcomes 71 –– parental presence  68, 69 –– positive reinforcement  66 –– protective stabilization –– active immobilization  71, 72 –– passive immobilization  72–74 –– providing control  65 –– routine dental treatment –– initial examination  70 –– restorative treatment  70, 71 –– rubber dam and accessories  70 –– sound analgesia  69 –– ‘Tell-show-do’ technique  63–65 –– time structuring  69 –– voice control  68

A–B

566

Index

Behavior management –– classification 62 –– and guidance  2 –– techniques 107 Behavior observation  81 Behaviour factors  469, 470 Behcet’s disease  494 Benzodiazepines  143, 144 Bioactive Endodontic Cements (BECS)  336 Biodentine® 384 BiodentinTM cement  337 Bisphenol-A (BPA)  306 Bisphosphonates (BP)  545, 546 Bite wing radiograph  294 Bleeding disorders –– coagulopathies 509 –– HHT 508 –– thrombocytopenia  508, 509 Blood cells –– anemia  506, 507 –– neutropenia  507, 508 –– sickle cell diseases  507 –– thalassemias 507 Bottle-feeding associated S-ECC  283 Bulimia  538, 539

C Calcium hydroxide  326 Calcium hydroxide apexification  404 Canavan disease  549 Candida albicans 502 Capnocytophaga sp. 348 Cardiovascular diseases –– microbial endocarditis and dental care  519 –– prevalence 518 –– prevention protocol  520 Cariogram pie graph  261 Carpenter syndrome  549 Casein phosphopeptide  267 Casein phosphopeptide-amorphous calcium phosphate (CPP-­ ACP) 267 Castillo-morales palatal plate  541 Cavity lining/base materials  301–302 Cavity matrices  301 Celiac disease  451 Central nervous system (CNS) injuries  367 Centric relation (CR)  476, 477 Cephalometric radiograph  102 Cephalometrics 170–172 Cerebral palsy  530–532 Cervical pulpotomy  337, 385, 386 Cervical resorption  401 Cervical root resorption  400 Charge-coupled device (CCD) technology  256 Chemoprophylaxis –– microbial endocarditis and dental care  519 –– prevalence 518 –– prevention protocol  520 Child engagement  558 Child oral health –– airborne Covid-19  6 –– appointment delays  6 –– dental auxiliary personnel  5 –– dental caries  4

–– endodontic treatment  4 –– evidence-based dental care  3 –– fluoride use  4 –– future trends  6 –– interventions 5 –– oral health care demands  5 –– orthodontic treatment  5 –– preschool children report  4, 5 –– prevalence and severity  4 –– smile aesthetics  5 –– special care needs children  5 Child Oral Health Impact Profile (COHIP)  554 Child Perceptions Questionnaire (CPQ)  554 Child-centred dentistry –– consent 556 –– decision-making  555, 556 –– ethical issues  559, 560 –– oral health research  558, 559 –– oral health-related quality of life  554, 555 –– principle 554 –– safeguarding  556, 557 –– service evaluation  557 Childhood caries –– age up to 3 years –– ART 285 –– ECC 283–285 –– S-ECC 283 –– age 3 to 6 years –– PMF 287–289 –– primary molar restorations  286–287 –– restoring anterior primary teeth  290–291 –– age 6 to 12 years –– molar incisor hypomineralization  294 –– pit and fissure caries  291–293 –– proximal surfaces of permanent teeth  293–294 –– age 12 to 18 years –– alternative options for isolation  300–301 –– cavity lining/base materials  301–302 –– cavity matrices  301 –– class II cavities  296–297 –– dental amalgam  307 –– dental materials  310–311 –– enamel and dentine adhesives  302, 303 –– equipment 299–300 –– failure and repair of restorations  309–310 –– glass ionomer cements  303, 304 –– permanent molars  308 –– preformed metal crowns  307 –– preparation and placement  300 –– proximal and smooth surface caries  294–296 –– resin based composites  305–307 –– veneers and prosthetic appliances  308–309 Children’s Fear Schedule Survey–Dental Subscale (CFSS-DS)  47 Children’s participation  558 Children's rights  6, 7 Chin blow  365 Chlorhexidine 267 Chronic erythematous candidiasis  503 Chronic generalized gingivitis  349 Chronic gingivitis  348 Chronic hyperplastic candidiasis  503 Chronic mucocutaneous candidiasis (CMC)  503 Chronic mucosal biting  492, 493 Chronic periodontitis  353–356 Chronic renal failure  522, 523 Chronic respiratory disease  80, 542

567 Index

Class I amalgam restorations  307 Class II cavities  296–297 Class II malocclusion  212–214, 218 Class II RMGIC restoration  310 Class III malocclusion  213 Classical apexification  403 Clefts  544, 545 Cleidocranial dysplasia (CCD)  183–185, 239 Coagulopathies 509 Coeliac disease  495 Cognitive development –– children’s thought process  12 –– concrete operational stage  12, 17, 18 –– formal operational thought  12, 18, 19 –– preoperational stage  12, 15–17 –– preventing dental fear  20, 21 –– sensorimotor stage  12–15 –– short-and long-term goals  12 –– tailoring oral messages  21, 22 Colony-stimulating factor-1 (CSFL1)  180 Communication –– aspects 52 –– with children  54 –– empathy and  55, 56 –– nonverbal communication  52, 53 –– with parents  53, 54 –– verbal communication  53 –– written information  54 Complicated crown fracture  383–386 Computer controlled administering of anesthesia (C-CLAD)  114, 115 Concussion 372–373 Cone beam computed tomography (CBCT)  102–104, 388 Cone beam tomographic examination (CBCT)  398 Congenital granular cell tumor  490 Congenital heart disease  81, 540 Consent 556 Contemporary attrition  467 Cotton wool pellet  335 COVID-19  6, 142 Coxsackie virus  498 Craniofacial anomalies  546–548 Craniomandibular disorders (CMD)  478 Crohn’s disease  494, 495 Crouzon and Apert syndromes  546, 547 Crowding 229 Crown angulation  379 Crown dilaceration  379 Crown-root fracture  366, 370, 386, 387 Cvek’s partial pulpotomy  385 Cystic fibrosis  542, 543 Cystic fibrosis transmembrane conductance regulator (CFTR)  542

D Decision-making  555, 556 Dental amalgam  307 Dental anxiety  40 Dental caries  85 –– caries risk assessment  259–261 –– chlorhexidine 267 –– clinical manifestation  252–253 –– CPP-ACP 267 –– dental plaque removal –– depth and morphology of pits and fissures  270–273

–– tooth brushing  268, 269 –– diagnosis and record keeping –– detection of early caries  255 –– DIFOTI 256 –– digital radiography  257–259 –– direct visualization  255 –– laser/light fluorescence  256 –– non-operative diagnostic methods  255 –– QLF 257 –– radiographic examination  255 –– tactile sensation  255 –– diet 273–274 –– epidemiology and treatment  252 –– fluoride gels  264 –– fluoride rinses  264 –– fluoride tablets and drops  263 –– fluoride toxicity  266–267 –– fluoride varnish  265 –– mechanism of action  262–263 –– milk fluoridation  263 –– pathogenesis of –– caries microbiology  248–250 –– dental appliances and restorations  250–251 –– fermentable carbohydrates  248 –– hereditary (genetic) factors  251 –– physico-chemical process  248 –– salivary flow  250 –– socio-economic status  250 –– thickness/maturation of dental plaque  248 –– tooth morphology and structure  250 –– patient motivation  274–277 –– presence of black stains  261 –– prevention and control of   262 –– probiotics 267–268 –– recall visit  277 –– silver diamine fluoride  265 –– toothpaste 264 –– treatment strategy of   261 –– water fluoridation  263 –– xylitol 267 Dental education  2 Dental erosion –– abfraction 467 –– clinical examination and diagnosis  470, 471 –– definition 466 –– extrinsic factors  469, 470 –– intrinsic factors  470 –– prevalence and severity  467–469 –– prevention 471 –– restoration  471, 472 Dental fear –– behavior rating scale  47, 48 –– child misbehavior  39–41 –– classical conditioning  41, 42 –– cognitive vulnerability  43 –– communication –– aspects 52 –– with children  54 –– empathy and  55, 56 –– nonverbal communication  52, 53 –– with parents  53, 54 –– verbal communication  53 –– written information  54 –– definition 40 –– dental environment  56, 57 –– family stressors  44

B–D

568

Index

Dental fear (cont.) –– genetic bases  44 –– helplessness and loss of control  43 –– issues with adolescents  50–52 –– pain threshold and experience of pain –– attention to children  48 –– dental check-up visits  49 –– graphic scale  48 –– information providing  49 –– pain tolerance  47 –– sense of loss of control  49 –– parental dental fear  46 –– parenting styles  45, 46 –– physiological changes  46 –– self-management –– age and maturity  50 –– child crying and coping behavior  50 –– therapeutic management  50 –– self-report measures  46, 47 –– social learning theory  42, 43 –– temperament  44, 45 –– uncooperative child behavior  39 Dental floss  270 Dental fluorosis  267 Dental health  3 Dental history  81 Dental knowledge  7, 8 Dental radiographic examination –– criteria for  87, 88 –– extra oral radiographs –– CBCT 102–104 –– cephalometric radiograph  102 –– ghost images and distortions  100–101 –– oblique lateral radiograph  103, 104 –– panoramic radiography  101, 102 –– guidelines 86 –– intraoral radiographs –– bitewing radiographs  91, 93–95 –– collimation  90, 93 –– image detector holders  89, 92 –– image detectors  86, 88–91 –– imaging techniques  86, 89, 90 –– periapical radiograph  95–97 –– protective apron/thyroid gland shield  91 –– standard occlusal radiograph  97–100 –– patient radiation doses  86, 88 –– potential risks  86 Dental spacing  233–234 Dentin dysplasia (DD)  451 Dentinogenesis imperfecta (DGI)  449–451, 545 Dentist-child communication  139 Dentoalveolar trauma –– classification 364 –– definition of   364 –– dental trauma history  368 –– epidemiology 364–366 –– etiology of   366–367 –– extraoral examination  368 –– IADT guidelines  369 –– intraoral examination  368 –– medical history  367 –– orthodontic management  406 –– permanent teeth (See Permanent teeth) –– prevention of   407–409 –– primary teeth –– follow-up and complications of   376–377 –– fractures of   370–372

–– luxation injuries  372–375 –– traumatic injuries  377–380 –– prognosis of injured teeth  405–406 –– radiographic examination  369 Dentosafe® 395 Denture-associated stomatitis  503 Developmental dental defects –– developmental discolorations  454–456 –– differential diagnosis and treatment  456–458 –– tissue structure malformations –– enamel, dentin and cementum  430, 432, 433 –– environmental developmental defects (See Environmental developmental defects) –– tooth number, size and morphology disturbances –– causes and correlations  418–421 –– dental development  416–420 –– epidemiology and clinical phenotypes  422, 423 –– expert centers  421 –– supernumerary teeth  424, 425 –– syndromic oligodontia  422, 424 –– variations 424–431 Diabetes mellitus  357 –– definition 521 –– dental findings and treatment  521 DIAGNOdent (KaVo Dental Co)  256 Diet  273–274, 469 Digital image fiber-optic trans-illumination (DIFOTI)  256 Digital radiography  257–259 Direct pulp capping (DPC)  325–327, 336–337, 383 Disabilities –– access and design  528 –– cerebral palsy and physical disability  530–532 –– classification 529 –– cognitive development  532, 533 –– dental treatment  529, 530 –– prevalence and preventive care  529 –– sensory –– hearing problems (deafness)  533, 534 –– visual impairment blindness  533 Distal step occlusion  225 Disto-occlusal cavity  286, 287 Double teeth  426 Down syndrome  532 –– clinical features  540 –– dental findings and treatment  540–542 –– incidence 540 Drooling 512 Dry mouth  517 Duchenne muscular dystrophy  543 Dysgeusia 517

E Early childhood caries (ECC)  283–285 Eating disorders  517 Ecological plaque hypothesis  248 Ectodermal dysplasia  541, 542 Ectopic eruption  209, 238 Ehlers-Danlos syndrome  453, 548 Enamel and dentine adhesives  302, 303 Enamel fracture  381 Enamel hypoplasia  378 Enamel-dentine crown fracture  370, 382 Endocardial microbial infection  519 Environmental developmental defects –– amelogenesis imperfecta –– definition 445

569 Index

–– dental rehabilitation  446, 449 –– gene investigation and correlation  448 –– hypomatured-hypoplastic with taurodontism  446, 447 –– hypoplastic type  445, 446 –– masticatory forces  446, 447 –– mechanisms 445 –– dentin dysplasia  451 –– dentinogenesis imperfecta  449–451 –– enamel dysplasia  442–444 –– enamel fluorosis  441–443 –– histological examination  436 –– hypomineralization and hypomaturation  436 –– intra-coronal dentin radiolucencies  451, 452 –– medical history  436 –– MIH 436–442 –– mineralization and maturation  436 –– molar incisor malformation  441, 442 –– ROD  451, 452 –– systemic diseases and syndromes  451–454 –– systemic/local causes  432, 434–435 Eosinophilic granuloma  506 Epidermolysis bullosa  453 Epilepsy 537 Epstein Barr virus (EBV)  497 Er:YAG laser  287 Erythema migrans  487, 488 Erythema multiforme (EM)  503, 504 Eudomembranous candidiasis  502 European Academy of Pediatric Dentistry (EAPD)  62 Ewing’s sarcomas  516 Extraoral examination  81, 83, 84 Extra oral wound  364 Extrusive luxation  374, 393–395

F Facemask 213 Facemask treatment  217 Familial hypophosphatemia  452 Familial mediterranean fever  544 Family and social history  80 Ferric sulphate  331 Fibroepithelial polyp  489 Fluoride 471 Fluoride gels  264 Fluoride rinses  264 Fluoride tablets and drops  263 Fluoride toxicity  266–267 Fluoride varnish  265 Formocresol 331 Fragile X chromosome syndrome  546 Frankel applian  213 Frankl rating scale  47, 48 Frenum pull  358–359 Functional posterior crossbite  229 Fungal infections  502, 503 Furcation bone infection  322

G Gastroesophageal reflux disease (GERD)  470, 523 Gastrointestinal disease  494 Gene mutations  539 General anesthesia (GA)  285 –– admission to hospital  145, 146

–– contraindications 145 –– dental treatment  146–149 –– indications 145 –– induction 146–148 –– operating room procedure  146 –– oral rehabilitation goals  145 –– patient history  150 –– pre-operative evaluation  145, 146 –– safety 151 –– stages  139, 140 Genetic diseases –– clefts  544, 545 –– cystic fibrosis  542, 543 –– down syndrome  540–542 –– ectodermal dysplasia  541, 542 –– familial mediterranean fever  544 –– muscular dystrophy  543, 544 –– osteogenesis imperfecta  545, 546 –– syndromes and craniofacial anomalies  546–550 Gingival health  3 Gingival hyperplasia  351, 352 Gingival index (GI)  83 Gingival recession  358 Gingivitis 348–350 Glass ionomer cements (GIC)  303, 304 Gluten-sensitive enteropathy (GSE)  495 Graft-versus-host disease (GvHD)  504, 505 Growth –– area relocation  160, 161 –– bone age  27, 30 –– bone and cartilage  162, 163 –– cephalometrics 170–172 –– childhood growth  26 –– dental age  27, 30 –– growing face features  156, 157 –– growth fields  160 –– infantile growth  26 –– IUGR 30 –– malocclusions 172–175 –– mandible –– lingual tuberosity  168 –– mandibular condyle  168, 169 –– ramus  167, 168 –– ramus uprighting  169, 170 –– mandibular condyle  160, 161 –– MPH/target height  27 –– nasomaxillary complex –– arch lengthening  165 –– maxillary tuberosity  165, 166 –– palatal remodeling and alveolar development  166 –– primary displacement  167 –– neurocranium –– basicranium  164, 165 –– calvaria 164 –– palate inferiorly relocation  161 –– prenatal facial growth and development –– characteristic postnatal resorptive fields  160 –– cranial nerve  157, 158 –– eyes location  157, 158 –– hyoid arch  158, 159 –– interorbital dimension  157, 158 –– mandibular arch  158, 159 –– oral and paired nasal chambers  159 –– prenatal growth  26 –– primary displacement  161–163, 165 –– process 26 –– pubertal growth  26

D–G

570

Index

Growth (cont.) –– puberty –– delayed puberty  35 –– development 34 –– environmental, metabolic and genetic factors  34 –– precocious puberty  34, 35 –– rate of growth  26 –– secondary displacement  161 –– SGA 30 –– short stature  30–34 –– tall stature  32, 34 –– velocity  27, 30 –– weight and height measurement  26–29 Growth hormone deficiency  32

H Hall technique  289 Hamartomas  490, 491 Hand-foot-and-mouth disease  498 Hand-Schüller-Christian disease  506 Hank’s Balanced Salt Solution (HBSS)  395 Hearing problems (deafness)  533, 534 Heck’s disease  500 Hemangiomas  490, 491 Hematological disease –– anemia 506 –– bleeding disorders –– coagulopathies 509 –– HHT 508 –– thrombocytopenia  508, 509 –– Hodgkin’s disease  505 –– langerhans cell histiocytosis  506 –– leukemias 506 –– lymphomas 505 –– neutropenia  507, 508 –– NHL 506 –– sickle cell diseases  507 –– thalassemias 507 Hemophilia A  509 Hemophilia B  509 Hemorrhagic pulp  335 Hereditary gingival fibromatosis (HGF)  352 Hereditary hemorrhagic telangiectasia (HHT)  508 Herpangina 498 Herpes labialis  496 Herpes simplex  495, 496 High molecular weight lipopolysaccharide (HMWLPS)  355 Hodgkin’s disease (HD)  505 Human herpes virus-8 (HHV-8)  500 Human Immunodeficiency virus (HIV)  500 Human papilloma virus (HPV)  499 Hydrochloric acid (HCl)  470 Hydroxyethylmethacrylate (HEMA)  303 Hyperglycemic coma  521 Hypersensitivity reactions  504 Hypoglycemic coma  521 Hypohydrotic ectodermal dysplasia  184 Hypomineralized second primary molars (HSPM)  253 Hypophosphatasia 452 Hypoplasia 370 Hyrax-type RME  212

I Idiopathic juvenile rheumatoid arthritis (IJRA)  479 Impetigo  500, 501

Incontinentia pigmenti syndrome  549, 550 Indirect pulp capping (IPC)  323, 325, 335–336 Inequalities  4, 5 Infectious mononucleosis (IN)  497, 498 Inferior alveolar nerve (IAN) block  117, 118, 120 Inflammatory root resorption  401 Informed consent  7 Intellectual quotient (IQ)  532 Intelligence quotient (IQ)  540 Interdental brushes  270 Interim therapeutic restorations (ITR)  286 Internal resorption  400, 402 International association for disability and oral health (iADH)  528 International Association of Dental Traumatology (IADT)  369 International caries detection and assessment system (ICDAS)  254 International classification functionality, disability and health (ICF) 528 Intraligamental anesthesia (ILA)  121, 122 Intraoral examination –– dental occlusion  84, 85 –– hard dental tissues  83–85 –– pathology 81 –– periodontal tissues  83 –– soft tissue  83 Intraosseous anesthesia  120, 121 Intrapulpal anesthesia  122 Intraseptal anesthesia  120 Intrauterine growth retardation (IUGR)  30 Intrusion of maxillary primary left central incisor  375 Intrusive luxation  373, 391, 393

J Jet injection technique  115, 116 Juvenile idiopathic arthritis (JIA)  524

K Kaposi’s sarcoma  500

L Labial ectopic and delayed eruption  380 Langerhans cell histiocytosis  506 Laser/light fluorescence  256 Lateral luxation  373 Lateral root bending  379 Left-side unilateral posterior crossbite  212 Leptotrichia sp.  348 Lesch-Nyhan syndrome  549 Letterer-Siwe disease  506 Leukemias  356, 506 Lingual holding arch  224 Lip jewelry  359 Lip sucking  243–244 Local anesthesia –– behavior guidance –– administration 123–125 –– fear of needles  122 –– patient preparation  122 –– C-CLAD  114, 115 –– craniofacial complex of children  115–118 –– dosage  113, 114 –– IAN block  117, 118, 120 –– ILA  121, 122 –– injected solution

571 Index

–– rate/speed 114 –– temperature 114 –– injection within bone –– intraseptal anesthesia  120 –– IO anesthesia  120, 121 –– injectors and needles  112, 113 –– intrapulpal anesthesia  122 –– jet injection technique  115, 116 –– local complications –– cheek, lip/tongue injury  125, 126 –– edema 125 –– hematoma 125 –– needle breakage  125 –– pain and sense of burning  125 –– paraesthesia 125 –– trismus 125 –– vasoconstrictors  125, 127 –– local infiltration anesthesia  116–119 –– palatal techniques –– AMSA injection  119 –– nasopalatine nerve block  119, 120 –– P-ASA 120 –– systemic complications  126 –– topical anesthesia  115, 117 –– topical anesthetics  112 –– vasoconstrictor 113 Local infiltration anesthesia  116–119 Localized aggressive periodontitis  353 Localized anterior crossbite  208, 210, 217 Localized gingivitis  349 Localized juvenile spongiotic gingival hyperplasia (LJSGH)  350, 351 Localized periodontitis  356 Luxation injuries  372–375 Lymphangiomas 491 Lymphomas 505

M Malocclusion  479, 546 Mandibular anterior teeth  284 Mandibular primary molars  317 Mandibular torus  488 Marginal fractures  305 Masticatory system  478 Maxillary impacted permanent canine  240 Maxillary incisors  297 Maxillary lateral incisor agenesis  238 Maxillary primary canine  319 Maxillary primary left central incisor  373 Maxillary primary right central incisor  291, 372 Maxillofacial disorders  548 McNamara-type RME  212 Measles  498, 499 Medical history  80–82 Medicines, dental erosion  469 Medium ankyloglossia  360 Melanocorin-1 receptor gene (MC1R)  44 Mesio-buccal root  333 Mesiodens 238 Methacryloyl-oxy-dodeca-pyridinium bromide (MDPB)  311 Microflora transmission  250 Midparental height (MPH)  27 Milk fluoridation  263 Mineral trioxide aggregate paste (ΜΤΑ)  326, 329–330 Mixed dentition analysis  233 Molar-incisor hypomineralization (MIH)  296, 378, 436–442

Molar incisor malformation (MIM)  441, 442 Monofluorophosphate fluoride (MFP)  264 Mouth breathing  243 Mouth-guards 407–409 Moyers' analysis  233 Moyers' mixed dentition analysis  233 Mucoceles 510 Mucocutaneous disease  503 –– allergic reactions  504, 505 –– erythema multiforme  503, 504 –– GvHD  504, 505 Mucositis 517 Multifactorial disease  248 Multifocal epithelial hyperplasia (MEH)  500 Mumps 499 Muscular dystrophy  543, 544

N Nail biting  243 Nance button anchorage  211 Necrotic immature (open apex) teeth  402 Necrotic mature (closed apex) teeth  402 Needle-phobia  74, 75 Neoplasms –– acute lymphoblastic leukemia  516 –– clinical finding and treatment  517–519 –– dental care protocol  518 –– osteosarcomas 516 Neurofibromatosis type I (NF1)  352, 547, 549 Neuropsychiatric/psychological disorders –– ADHD 535–537 –– ASD 534–536 –– epilepsy 537 –– nutrition and weight  537–539 Neurotoxicity 518 Neutropenia  507, 508 Nitrous oxide (N2O) –– adverse effects  142 –– breathing practice  140 –– contraindications  141, 142 –– in COVID-19 era  142 –– informed consent  140 –– inhalation sedation  137–140 –– monitoring 141 –– personnel safety  142 –– rapid induction technique  141 –– rubber dam  141 –– standard titration technique  141 Non-complicated crown fracture  392 Non-Hodgkin’s lymphoma (NHL)  500, 506 Noonan syndrome  547, 548 NuSmile 307 NuSmile zirconium crown  308 Nutrition 537–539 Nyvad’ visual-tactile classification system  254

O Obesity 539 Odontoma-type dysplasia  379 Omni-matrix ™  302 One-phase treatment  212 OptiView™ (Kerr)  301 Oral dryness  511, 512 Oral hairy leukoplakia (OHL)  500

G–O

572

Index

Oral health-related quality of life (OHRQoL)  554, 555 Oral hygiene  106 Oral hygiene instructions  350 Oral lesions –– bacterial infections –– acute necrotizing ulcerative gingivitis  502 –– impetigo  500, 501 –– scarlet fever  501 –– tuberculosis  501, 502 –– fungal infections  502, 503 –– hematological disease –– anemia 506 –– bleeding disorders  508, 509 –– Hodgkin’s disease  505 –– langerhans cell histiocytosis  506 –– leukemias 506 –– lymphomas 505 –– neutropenia  507, 508 –– NHL 506 –– sickle cell diseases  507 –– thalassemias 507 –– lymphangiomas 491 –– mucocutaneous disease  503 –– allergic reactions  504, 505 –– erythema multiforme  503, 504 –– GvHD  504, 505 –– oral mucosal and boney abnormalities –– cysts 488 –– erythema migrans  487, 488 –– mandibular torus  488 –– palatal torus  488 –– reactive overgrowths –– congenital granular cell tumor  490 –– fibroepithelial polyp  489 –– peripheral giant cell lesion  489, 490 –– peripheral ossifying fibroma  489 –– pyogenic granulomas  488, 489 –– swellings 490 –– salivary gland disease –– acute suppurative sialadenitis  511 –– drooling 512 –– mucoceles 510 –– ranula 510 –– recurrent parotitis  511 –– sialolithiasis  510, 511 –– xerostomia  511, 512 –– ulceration (See Oral ulceration) –– vascular malformations  490, 491 –– viral infections –– hand foot and mouth disease  498 –– herpangina 498 –– herpes simplex  495, 496 –– herpes zoster  496, 497 –– HIV 500 –– HPV 499 –– infectious mononucleosis  497, 498 –– measles  498, 499 –– MEH 500 –– mumps 499 –– warts 499 Oral ulceration –– aphthous ulceration  492–494 –– Crohn’s disease  494, 495 –– gastrointestinal disease  494 –– GSE 495 –– traumatic oral ulceration  491–493 Orange plaque (biofilm)  262

Orofacial system (OFS) –– anamnestic records  480 –– centric relation/centric occlusion  476, 477 –– clinical examination  480, 481 –– components 476 –– diagnosis  480, 481 –– eccentric mandibular movements  477 –– eccentric positions  477 –– epidemiology 478 –– etiology 478–480 –– functions 476 –– imaging 480 –– maxillomandibular relationships  476 –– maximum intercuspation  476 –– rest position  477 –– treatment strategies  482 –– vertical dimension  477, 478 Orofacial-myofunctional therapy  243 Orthodontic brackets  239, 251 Orthodontic management –– harmful oral habits –– lip sucking  243–244 –– mouth breathing  243 –– nail biting  243 –– pacifier overuse  240–242 –– position of tongue at swallowing  242–243 –– thumb sucking  240–242 –– intervention in mixed dentition –– arch space anomalies  229–233 –– dental spacing  233–234 –– Moyers' mixed dentition analysis  233 –– occlusal anomalies  234–237 –– partial archwire and springs  232 –– Staley and Kerber analysis  233 –– Tanaka and Johnston analysis  233 –– tooth number and eruption related anomalies  237–240 –– intervention in primary dentition –– arch space anomalies  218–223 –– occlusal anomalies  223–229 –– profile evaluation –– convex profile  212–218 –– orthodontic vs. orthopedic treatment  208 –– straight profile  208–210 Orthodontic treatment  2 Orthodontics  479, 480 Orthopantomographic (OPG) radiograph  27, 30 Osler-Weber-Rendu syndrome  508 Osteogenesis imperfecta (OI) –– bisphosphonates  545, 546 –– classification 545 –– malocclusion 546 –– prevalence  545, 546 Osteopetrosis 453 Osteosarcomas 516 Over-the-counter fluoridated toothpaste  264

P Palatal anterior superior alveolar block (P-ASA)  120 Palatal torus  488 Panoramic radiography  101, 102 Partial pulpotomy  337, 338, 341, 384, 385 Passive immobilization  72–74 Patient-reported experience measures (PREMs)  557 Patient-reported outcome measures (PROMs)  557 Perikymata 258 Perimylolysis 470

573 Index

Periodontal diseases –– frenum pull  358–359 –– gingival hyperplasia  351, 352 –– gingival recession  358 –– gingivitis 348–350 –– LISGH  350, 351 –– periodontitis –– acute ulcerative gingivitis  357–358 –– chronic periodontitis  353–356 –– diabetes mellitus and  357 –– localized aggressive periodontitis  353 –– with systemic disease  356 Peripheral giant cell lesion  489, 490 Peripheral ossifying fibroma  489 Permanent teeth –– endodontic evaluation and management of   401–405 –– follow-ups of   390, 398, 401 –– fractures of –– complete enamel fracture  380–381 –– complicated crown fracture  383–386 –– crown-root fractures  386, 387 –– enamel infraction  380 –– root fracture  387–389 –– uncomplicated crown fracture  381–383 –– luxation injuries to –– avulsion 394–396 –– concussion 389–390 –– extrusive luxation  393, 394 –– intrusive luxation  391, 393 –– lateral luxation  390–391 –– subluxation (loosening)  390 –– post-traumatic complications of   396–401 Pervasive developmental disorder (PDD)  534 Pharmacologic behavioral management –– general anesthesia (See General anesthesia (GA)) –– sedation –– acceptance and preferences  133, 134 –– anatomical airway  134, 135 –– anxiolysis (See Anxiolysis) –– BLS training  135 –– child and parent preparation  135 –– deep sedation  133 –– definition 132 –– documentation  136, 137 –– general anesthesia  133 –– guidelines 132 –– health status and cooperation assessment  134, 135 –– informed consent  135 –– minimal sedation  132 –– moderate sedation  133 –– monitoring and resuscitation equipment  136, 137 –– parental expectations  132 –– physical status  134 –– pre-operative assessment and consultation  134 –– respiratory airway  134 –– safety 151 Phenoxymethylpenicillin 323 Physical disability  530–532 Plaque index (PI)  83 Plasma cell gingivitis (PCG)  351 Polyacid modified composites  306 Posterior cross bite  228 Postgraduate education  8 Post-traumatic root resorptions  377 Prader-Willi syndrome  549 Predominant type  540 Preformed metal crowns (PMCs)  145, 287–289, 307

Preventive resin restoration (PRR)  292–293 Prevotella sp.  348 Primary failure of eruption (PFE)  183 Primary molar hypomineralization  254 Primary molar pulpotomy  328–331 Primary molar restorations  286–287 Probably toxic dose (PTD)  266 Pseudomembraneous candidiasis  500 Psychotropic analgesic nitrous oxide (PAN)  139 Puberty –– delayed puberty  35 –– development 34 –– environmental, metabolic and genetic factors  34 –– precocious puberty  34, 35 Public health systems  85 Pulp canal obliteration  399 Pulp necrosis  398 Pulp sensibility testing  398 Pulp therapy –– cariously necrotic primary teeth  316 –– diagnostic procedure –– clinical examination  318–320 –– dental surgery  316–318 –– medical history  316 –– radiographic examination  320–321 –– symptoms and signs in  323 –– management of emergency  321–324 –– treatment of –– direct pulp capping  325–327 –– indirect pulp capping  323, 325 –– primary molar pulpotomy  328–331 –– pulpectomy/root canal treatment  331–334 –– young carious permanent teeth –– cervical pulpotomy  337 –– direct pulp capping  336–337 –– immature carious teeth immature carious teeth  337–341 –– indirect pulp capping  335–336 –– partial pulpotomy  337 –– restoring color of discolored teeth  341–342 Pulpitis 376 Pyogenic granulomas  488, 489

Q 22q11 deletion syndrome  549 Qualitative methods  559 Quantitative light-induced fluorescence (QLF)  257 Quantitative methods  558

R Rampant caries  518 Ranula 510 Rapid induction technique  141 Rearmost, upmost, and midmost (RUM)  476 Recurrent aphthous stomatitis (RAS)  492 Recurrent parotitis  511 Regenerative’ endodontic approach  339, 403 Regional odontodysplasia (ROD)  451, 452 Relative analgesia (RA)  139, 140 Replacement resorption (ankylosis)  387, 399 Resin based composites  305–307 Resin-modified glass ionomer cement (RMGIC)  304, 440 Revised Iowa Dental Control Index (R-IDCI)  19 Rickets 452 Riga-Fede disease  492, 493

O–R

574

Index

Riga-Fede granuloma  492, 493 Root canal obliteration  320, 396 Root canals  332 Root duplication  379 Root fractures  372, 387–389 Rubber dam isolation  383

S Safeguarding  556, 557 Sagittal maxilla-mandible discrepancy  212 Salivary gland disease –– acute suppurative sialadenitis  511 –– drooling 512 –– mucoceles 510 –– ranula 510 –– recurrent parotitis  511 –– sialolithiasis  510, 511 –– xerostomia  511, 512 Save-Tooth® 395 Scarlet fever  501 Second primary molar  325 Sedation –– acceptance and preferences  133, 134 –– anatomical airway  134, 135 –– BLS training  135 –– child and parent preparation  135 –– deep sedation  133 –– definition 132 –– documentation  136, 137 –– general anesthesia  133 –– guidelines 132 –– health status and cooperation assessment  134, 135 –– informed consent  135 –– minimal sedation  132 –– moderate sedation  133 –– monitoring and resuscitation equipment  136, 137 –– parental expectations  132 –– physical status  134 –– pre-operative assessment and consultation  134 –– respiratory airway  134 Selenomonas sp.  348 Sensory disabilities –– hearing problems (deafness)  533, 534 –– visual impairment blindness  533 Service evaluation  557 Severe early childhood caries (S-ECC)  283 Severe infra-occlusion  242 Severe periodontal lesions  354 Shingles 497 Short stature  30–34 Sialolithiasis  510, 511 Sickle cell diseases  507 Silver diamine fluoride (SDF)  265 Skeletal discrepancy  210 Skeletal open bite  234 Sleep bruxism  467, 479 Small for gestational age (SGA)  30 Social learning theory  42, 43 Sodium fluoride (NaF)  264 Soft tissue swellings  490 Sound analgesia  69 Space regaining  232 Space-maintainer obsolete  231 Special care dentistry  528 Squamous papilloma  499

Standard titration technique  141 Stannous fluoride (SnF2) 264 Stephan curves  274 Steven’s Johnson syndrome (SJS)  504 Streptococcus mutans  248, 249 Subluxation (loosening)  373 Supernumerary teeth  238 Systemic auto-inflammatory disorder (SAID)  494

T Tall stature  32, 34 Target height  27 Telescopic occlusion  229 Tell-show-do technique  533 Temperament  44, 45 Temporomandibular disorders (TMD), see Orofacial system (OFS) Temporomandibular joint (TMJ)  81 Thalassemias 507 Thrombocytopenia  508, 509 Tongue thrusting  242 Tooth brushing  268, 269 Tooth brushing method  470 Tooth decay (DMFT)  4 Tooth eruption –– ankylosis 190–193 –– delayed eruption –– generalized delay  183, 184 –– localized delay  184–188 –– ectopic eruption  188–191 –– eruption cysts  191, 194 –– eruption mechanism  179, 180 –– eruption sequence  178, 179 –– eruptive phase  178 –– functional phase  178 –– inflammation  192, 194, 195 –– neonatal teeth  182, 183 –– pre-eruptive phase  178 –– primary teeth –– extraction 196–200 –– shedding  196, 197 –– teething symptoms –– cross-sectional survey  180 –– dental follicle  180 –– local treatment  181 –– systemic treatment  181, 182 –– transplantation –– extraction and re-implantation  200–202 –– intentional re-implantation  203, 204 –– teeth anterior  202, 203 Tooth revascularization treatment  340 Tooth wear –– attrition and abrasion  466, 467 –– bruxism 467–469 –– erosion –– abfraction 467 –– clinical examination and diagnosis  470, 471 –– definition 466 –– extrinsic factors  469, 470 –– intrinsic factors  470 –– prevalence and severity  467–469 –– prevention 471 –– restoration  471, 472 Topical anesthesia  115, 117 Topical anesthetics  112 Total care treatment plan  103

575 Index

–– factors 105–108 –– presentation to parents  105 –– specialist pediatric dentist, referral to  109 Tourette syndrome  546 Toxic epidermal necrolysis syndrome (TENS)  504 Transmission electron microscope  250 Transpalatal arch  231 Transverse discrepancy  208, 210 Traumatic dental injuries (TDI)  367 Traumatic oral ulceration –– causes 491 –– chronic mucosal biting  492, 493 –– diagnosis 491 –– Riga-Fede disease and granuloma  492, 493 Treacher Collins syndrome  546, 547 Tricho-dento-osseous syndrome  549 Tuberculosis (TB)  501, 502 Tuberous sclerosis  453 Tunnel restorations  297 Turner syndrome  547 Two-phase treatment  212

U Unilateral posterior crossbite (UPCB)  479 Upper left canine  219 Upper lip edema  365 US dental schools  2

V Varicella zoster  496, 497 Verruca vulgaris  499 Viral infections –– hand foot and mouth disease  498

–– herpangina 498 –– herpes simplex  495, 496 –– herpes zoster  496, 497 –– HIV 500 –– HPV 499 –– infectious mononucleosis  497, 498 –– measles  498, 499 –– MEH 500 –– mumps 499 –– warts 499 VistaProof (Durr Dental) systems  256 Visual impairment blindness  533 Vomiting 470 von Recklinghausen disease  352, 547, 549 von Willebrand’s disease (vWD)  509

W Warts 499 Water fluoridation  263 Weight loss  538 White or yellow-brown spots  378 White ΜΤΑ 329

X Xerostomia  511, 512 X-linked recessive trait (Xq13.1 gene)  542 Xylitol 267

Z Zone of proximal development (ZPD)  15 Z-shaped spring  236

R–Z