Textbook of Periodontology and Oral Implantology, 2nd Ed. 9788131237410, 9788131238653, 8131237419

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Textbook of

Periodontology and Oral lmplantology

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Textbook of

Periodontology and Oral lmplantology SECOND EDITION Edited by DILIP

G N AYAK

MDS

Dean and Professor Department of Periodontology Manipal College of Dental Sciences Mangalore, India ASHITA UPPOOR MDS

Associate Dean and Professor Department of Periodontology Manipal College of Dental Sciences Mangalore, India MAHESH

CP

MDS

Professor and Head Department of Periodontology NIMS Dental College Jaipur, India

ELSEVIER

ELSEVIER Reed Elsevier India Pvt. Ltd. Registered Office: 818, 8th Floor, Indraprakash Building, 21, Barakhamba Road, New Delhi 110001 Corporate Office: 14th Floor, Building No. lOB, DLF Cyber City, Phase II, Gurgaon-122 002, Haryana, India Textbook of Periodontology and Oral Implantology: 2e, Nayak DG, Uppoor A, CP Mahesh Copyright© 2015, by Reed Elsevier India Pvt. Ltd. All rights reserved. ISBN: 978-81-312-3741-0 e-Book ISBN: 978-81-312-3865-3 No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher's permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www. elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/ or damage to persons or property as a matter of product liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Although all advertising material is expected to conform to ethical (medical) standards, inclusion in this publication does not constitute a guarantee or endorsement of the quality or value of such product or of the claims made of it by its manufacturer. Please consult full prescribing information before issuing prescription for any product mentioned in this publication.

Sr Project Manager-Education Solutions: Shabina Nasim Content Strategist: Nimisha Goswami Managing Editor: Anand K Jha Project Manager: Nayagi Athmanathan Project Coordinator: Isha Bali Sr Operations Manager: Sunil Kumar Sr Production Executive: Ravinder Sharma Sr Cover Designer: Milind Majgaonkar Laser typeset by Thomson Digital Printed in India by

Foreword

The second edition Textbook of Periodontology and Oral Implantology brought out by Dr Dilip Nayak, Dr Ashita

The spread of dental education worldwide has created a scenario where dental knowledge can be sourced from unexplored quarters. Unlike before, when quality sources of dental information were exclusively textbooks from the West, we are now seeing a growing acceptance of textbooks written by authors from developing countries, especially from India. The increase in the number of Indian textbooks is a welcome sign. However, one should be selective in the choice of books to refer because this will have a bearing on our clinical decision making. Indian authors must focus on providing books of international standard with quality content, illustrations, and references.

Uppoor, and Dr Mahesh CP is a step in this direction. The authors are committed academicians and experienced teachers of the subject of periodontology. They have various scientific publications and clinical trials to their credit. A brief overview of the book reveals the amount of effort put in by the authors and the contributors to update the latest advances in the field of periodontology. I wish them all the best in their endeavor to spread knowledge in periodontology and implantology. I wholeheartedly recommend this book to all those who seek the same.

Dr V Surendra Shetty, MDS Pro Vice Chancellor Manipal University, Manipal Karnataka, India

V

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List of Contributors

Abhay Kolte MOS Professor and Head Department of Periodontology VSPM Dental College and Research Center Nagpur, Maharashtra, India

Ashish Nichani MOS Professor AECS Maaruti Dental College and Research Centre Bangalore, Karnataka, India Ashwini Rao MOS Professor and Head Department of Public Health Dentistry Manipal College of Dental Sciences Mangalore, Karnataka, India

Ambalavanan N MOS Professor and Head Department of Periodontology Meenakshi Ammal Dental College Maduravoyal, Chennai, Tamil Nadu, India

Ananthakrishna NC (Late) MD, Formerly Professor Emeritus Department of Microbiology KS Hegde Medical Academy Mangalore, Karnataka, India

Betsy Thomas MOS Professor and Head Department of Period ontology Faculty of Dentistry, MAHSA University Jalan Elmu, Off Jalan University Kuala Lumpur, Malaysia

FCCP

Bhat KM MOS Professor Department of Period ontology Manipal College of Dental Sciences Manipal, Karnataka, India

Arvind Shetty MOS Professor and Head Department of Periodontology DY Patil University School of Dentistry Nerul Navi Mumbai, Maharashtra, India

Bhongade ML MOS Professor and Head Department of Period ontology Sharad Pawar Dental College Wardha, Maharashtra, India

Ashita Uppoor MOS Associate Dean and Professor Department of Periodontology Manipal College of Dental Sciences Mangalore, Karnataka, India Arun Kumar MS, MOS Professor, Department of Periodontology Yenepoya Dental College Deralakatte, Mangalore, Karnataka, India

Biju Thomas MOS Professor and Head Department of Period ontology AB Shetty Memeorial Institute of Dental Sciences Deralakatte, Mangalore, Karnataka, India

Aravind Shenoy MOS Professor Department of Conservative Dentistry Bapuji Dental College Davangere, Karnataka, India

David Kadakampally MOS Associate Professor Department of Period ontology Manipal College of Dental Sciences Mangalore, Karnataka, India

Asavari Desai MOS Assisitant Professor Department of Orthodontics Manipal College of Dental Sciences Mangalore, Karnataka, India

Deepa G Karnath MOS Professor and Head Department of Period ontology Manipal College of Dental Sciences Mangalore, Karnataka, India

vii

viii

LIST OF CONTRIBUTORS

Dilip G Nayak MOS Dean and Professor Department of Periodontology Manipal College of Dental Sciences Mangalore, Karnataka, India

Nancy Srivastava MOS Senior Lecturer Department of Periodontology NIMS Dental College and Hospital Shobhanagar, Jaipur, Rajasthan, India

Dipen Shah MOS Former Senior Lecturer AMC Dental College, Khokra Ahmedabad, Gujarat, India

Nandini Manjunath MOS Professor and Head Department of Periodontology AJ Institute of Dental Sciences Mangalore, Karnataka. India

Dwarakanath CD MOS Professor and Head Vishnu Dental College Bhimavaram, Andhra Pradesh, India Faizuddin M MOS Formerly Professor and Head Department of Periodontology MR Ambedkar Dental College Bangalore, Karnataka, India Mahesh CP MOS Professor and Head Department of Periodontology NIMS Dental College Jaipur, Rajasthan, India Mehta DS MOS Vice Principal Professor and Head Department of Periodontology Bapuji Dental College and Hospital Davangere, Karnataka, India

Neena Shenoy MOS Professor Department of Periodontology AB Shetty Memorial Instiute of Dental Sciences Mangalore, Karnataka, India Neetha J Shetty MOS Associate Professor Department of Periodontology Manipal College of Dental Sciences Mangalore, Karnataka, India Neha Gupta MOS Reader Department of Periodontology Shree Bankey Bihari Dental College Ghaziabad, Uttar Pradesh, India Prathibha PK MOS Professor and Head Department of Periodontology Manipal College of Dental Sciences Manipal, Karnataka. India

Mohan Alexander MOS Professor and Head Department of Oral and Maxillifacial Surgery Faculty of Dentistry MAHSA University, Jalan Elmu, Off Jalan University Kuala Lumpur, Malaysia

Rajesh H MOS Professor Department of Periodontology Yenepoya Dental College, Deralakatte Mangalore, Karnataka, India

Nagarathna DV MOS Professor Department of Periodontology AJ Institute of Dental Sciences Mangalore, Karnataka, India

Rajesh Kashyap MOS Professor Department of Periodontology Yenepoya Dental College Deralakatte, Mangalore, Karnataka, India

Nandakumar K MOS Professor and Head Department of Periodontology Azeezia College of Dental Sciences & Research Kollam, Kerala, India

Rahul Nair MPH, MS Assistant Professor ARCPOH School of Dentistry University of Adelaide SA, Australia-SOOS

LIST OF CONTRIBUTORS

Ravikiran Ongole MOS Professor Department of Oral Medicine and Radiology Manipal College of Dental Sciences Mangalore, Karnataka, India

Suresh RMOS Professor and Head Department of Periodontology Sri Ramachandra Dental College Chennai, Tamil Nadu, India

Ruchika Goel MOS Formerly Assistant Professor Department of Periodontology Manipal College of Dental Sciences Mangalore, Karnataka, India

Suruchi Jain MOS Formerly Assistant Professor Department of Orthodontics Manipal College of Dental Sciences Mangalore, Karnataka, India

Sachin Goyal MOS Reader Department of Periodontology Bhojia Dental College and Hospital Bhud, Baddi, Himachal Pradesh, India

Sangeeta U Nayak MOS Assistant Professor Department of Periodontology Manipal College of Dental Sciences Mangalore, Karnataka, India

Siddarth Shetty MOS Professor and Head Department of Orthodontics Manipal College of Dental Sciences Mangalore, Karnataka, India

Subraya Bhat MOS Associate Professor College of Dentistry University of Dammam Dammam, Saudi Arabia

Sumita Singh MOS Senior Lecturer Department of Periodontology Sardar Patel Post Graduate Institute of Dental & Medical Sciences Raibareli Road Lucknow, Uttar Pradesh, India

Swati MOS Reader Department of Periodontology Manipal College of Dental Sciences Mangalore, Karnataka, India Vandana KL MOS Senior Professor Department of Periodontology College of Dental Sciences Davangere, Karnataka, India Vidya Shenoy MOS Professor Department of Periodontology AJ Institute of Dental Sciences Mangalore, Karnataka, India Vijendra Singh Gangwar MOS Former Senior Lecturer Department of Periodontology Sardar Patel Postgraduate Institute of Dental and Medical Sciences Raebareli Road Lucknow, Uttar Pradesh, India Yeltiwar RK MOS Professor and Head Department of Periodontology Rungta College of Dental Sciences & Research Bhilai, Chhattisgarh, India

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Preface

I believe life is constantly testing us for our level of commitment, and life's greatest rewards are reserved for those who demonstrate a never-ending commitment to act until they achieve. This level of resolve can move mountains, but it must be constant and consistent. As simplistic as this may sound, it is still the common denominator separating those who live their dreams from those who live in regret. - Anthony Robbins

also attempted to envisage upon the task of including topics such as, genetics, the biological, diagnostic, and prosthodontic aspects of dental implants. Besides, the recent advances in periodontal surgery and the management of peri-implant diseases have been elaborated painstakingly by the authors. In the course of writing the second edition of this textbook, careful attention has been devoted to include the procedures and concepts, as they were outlined originally, as well as recent concepts and developments in the field of clinical periodontology. Any oversights in the previous edition were unintentional and the editors have taken utmost care to set right the same if any in this edition as compared to the previous edition. The editors would like to acknowledge the support and help provided by every individual who has been directly or indirectly associated with the making of this edition. We sincerely believe that we have succeeded in encompassing the rapid and constant change related to the field of periodontology in a structured and simplified manner in this edition.

The Textbook of Periodontology and Oral Implantology was conceived with two primary goals in mind: to create a book that would focus on the needs of undergraduates during their training program in periodontology and to facilitate the understanding of the complexities of the subject of periodontology, as it relates to dental practice, without omitting salient concepts and diluting the content of information provided. The second edition, in keeping with the ethos of selecting contributors on the basis of their respectable stature as leading researchers, clinicians, or teachers in periodontology, implant dentistry, and associated domains, has

Dilip G Nayak Ashita Uppoor Mahesh CP

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Acknowledgments

Pathology; and Dr Evelyn Wagiyu, Dean, Faculty of Dental Sciences, University Dental Hospital, Nairobi, Kenya for providing us the photographs for various chapters. We would also like to acknowledge the able and dedicated assistance provided in the compilation of specific chapters by Dr Cham Shrestha, Dr Sunita Sharma, Dr Priti Shrestha, Dr Bhageshwar Dhami, Dr Pragyan Das, Dr Sridevi Shetty, Dr Clany D'souza, and Dr Sulagna Chakrabarty. We would like to thank our publisher Elsevier (India) for its constructive suggestions and unstinted support in publishing this book. We hope this book will be helpful to all students of periodontology in understanding the contemporary scenario in the field of etiopathogenesis, diagnosis and therapeutic aspects of periodontal diseases, and the intricacies associated with the field of oral implantology.

The editors would like to express their deep gratitude to all the individuals who have extended their dedicated and selfless efforts in the completion of this edition of the

Textbook of Periodontology and Oral Implantology. We sincerely acknowledge the encouragement and guidance provided to us by Dr V. Surendra Shetty, Pro Vice Chancellor, Manipal University, Karnataka, India. We are thankful for all the furtherance and support rendered by him. We offer our gratitude to all the contributors who have shared their valuable knowledge and ideas for the compilation of this book. We appreciate the willing help and support offered by our colleagues, especially Dr Karen Boaz, Professor and Head, Department of Oral Pathology; Dr Arati Rao, Professor and head, Department of Pedodontology; Dr Nandita KP, Associate Professor, Department of Oral

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Brief Contents

I TISSUES OF THE PERIODONTIUM 1. 2. 3. 4. 5.

Gingiva Periodontal Ligament Cementum Alveolar Bone Age-related Changes in the Periodontium

3 12 17 23 29

II CLASSIFICATION AND EPIDEMIOLOGY OF PERIODONTAL DISEASES 6. Classification of Periodontal Diseases 7. Epidemiology of Periodontal Diseases

35 41

Ill ETIOLOGY OF PERIODONTAL DISEASES 8. Dental Plaque and Microorganisms Associated with Periodontal Health and Disease 9. Host Response - Basic Concepts 10. Host Microbial Interaction in Periodontal Disease 11. Dental Calculus 12. Smoking and the Periodontium 13. Trauma from Occlusion 14. Role oflatrogenic and Other Local Factors in Periodontal Disease 15. Systemic Diseases and Periodontium 16. Periodontal Medicine 17. Role of Genetics in Periodontal Therapy

55 64 76 83 88 93 108 120 131 140

IV PERIODONTAL PATHOLOGY 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31.

Defense Mechanisms of the Gingiva Gingival Inflammation Clinical Features of Gingivitis Gingival Enlargement Acute Gingival Infections Desquamative Gingivitis Periodontal Diseases in Childhood and Adolescents Periodontal Pocket Bone Loss in Periodontal Disease Periodontitis: Chronic, Refractory, and Necrotizing Ulcerative Aggressive Periodontitis Periodontal Abscess AIDS and Periodontium Halitosis

xv

153 161 166 172 181 190 198 204 211 218 225 234 238 24 7

xvi

BRIEF CONTENTS

V 32. 33. 34. 35. 36. 3 7. 38.

DIAGNOSIS, PROGNOSIS, AND TREATMENT PLANNING

Clinical Diagnosis Role of Radiology in the Diagnosis of Periodontal Diseases Advanced Diagnostic Methods Determination of Prognosis Periodontal Treatment Plan Treatment of Periodontal Diseases in Medically Compromised Patients Risk Assessment

VI 39. 40. 41. 4 2. 4 3. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53. 54. 55. 56. 57. 58. 59. 60. 61. 62. 63. 64.

PERIODONTAL THERAPY

Periodontal Instrumentation Sonic and Ultrasonic Instrumentation Plaque Control Scaling and Root Planing Chemotherapeutic Agents Host Modulation Periodontal Splints General Principles of Periodontal Surgery Gingival Surgical Procedures Flap Surgery Resective Osseous Surgery Regenerative Osseous Surgery Furcation Involvement and Its Management Endodontic Periodontal Lesions and Their Management Periodontal Plastic Surgery Recent Advances in Periodontal Surgical Techniques Periodontal Considerations in Restorative Dentistry Ortho-Perio Interrelationships Infection Control Supportive Periodontal Treatment Biological Aspects of Dental Implants Diagnosis and Treatment Planning in Implantology Prosthodontic Considerations in Implant Restorations Advanced Surgical Procedures for Dental Implants Peri-Implant Diseases and Management Evidence-Based Periodontics

Index

253 267 279 290 297 300 313

321 346 353 3 75 3 79 393 397 401 412 419 4 31 440 450 458 468 486 499 505 514 523 527 530 54 7 560 571 576

585

Contents

Foreword List of Contributors Preface Acknowledgments Brief Contents

25 26 26 27 28 28

Composition of Alveolar Bone Osseous Topography Fenestration and Dehiscence Remodeling of Alveolar Bone Questions Suggested Readings

V

vii xi xiii xv

5. Age-related Changes in the Periodontium

I

Dilip G Na yak

1. Gingiva Gingiva Gingival Connective Tissue Questions Suggested Readings

2. Periodontal Ligament Origin and Development of the Periodontal Ligament Features of Periodontal Ligament Functions of Periodontal Ligament Clinical Considerations Questions Suggested Readings

3. Cementum Physical Characteristics Composition Functions of Cementum Classification Cementoenamel Junction Cementodentinal Junction Developmental and Acquired Anomalies of Cementum Cementum Resorption and Repair Cementa! Tears Questions Suggested Readings

4. Alveolar Bone Parts of Alveolar Process Hisrology of Alveolar Bone lnterdental Septum Bone Marrow

29 29 30 30 30 30 31 31 31 31

Vasculature Tooth-periodontium Relationship Gingival Epithelium Gingival Connective Tissue Periodontal Ligament Cementum Alveolar Bone Bacterial Plaque Immune Responses Summary Questions Suggested Readings

TISSUES OF THE PERIODONTIUM Neha Gupta 3 8 11 11

Neetha] Shetty

32 32

II

12 12 15 16 16 16

CLASSIFICATION AND EPIDEMIOLOGY OF PERIODONTAL DISEASES 6. Classification of Periodontal Diseases

Ashita Uppoor

Ashita Uppoor

17 17 18 18 19 20 20 21 21

22 22

Definition Requirement Need for Classification Uses of Classification Hisrorical Development of the Classification System Changes Made in the Classification Future Challenges in Classifying Periodontal Diseases Conclusion Questions Suggested Readings

35 35 35 35 35 39 39 39

40 40

Neetha] Shetty 23 23 24 25

7. Epidemiology of Periodontal Diseases Ashwini Rao Basic Considerations Classification of Indices Public Health Significance of Periodontal Disease

xvii

41 42 42

xviii

CONTENTS

42

Indices Used in Periodontics Questions Suggested Readings

51 51

III ETIOLOGY OF PERIODONTAL DISEASES 8. Dental Plaque and Microorganisms Associated with Periodontal Health Ambalavanan N and Disease Oral Flora 55 Dental Plaque 56 Specific Plaque Hypothesis 58 Virulence Mechanisms of Periodontal Pathogens 59 Microorganisms Associated with Periodontal Health and Disease 59 Description of Important Periodontal Pathogens 60 Questions 63 Suggested Readings 63

9. Host Response - Basic Concepts

Ananthakrishna NC (Late) Cells of the Immune System Role of Antibodies in Inflammatory Diseases Immune Reactions Mediators of Immune Response and Inflammation Influence of Host Response on Periodontal Disease Periodontal Disease Activity Models of Periodontal Disease Activity (Socransky) Clinical Indications of Disease Activity Prerequisites for Periodontal Disease Initiation and Progression Conclusion Questions Suggested Readings

10. Host Microbial Interaction in Periodontal Disease

64 68 71 72 73 73 73 74 74 74 74 75

Mahesh CP

Identifying Putative Pathogens Key Organisms Secondary Organisms Host Bacterial Interaction Microbiologic Aspects of Microbial-host Interactions Microbial Mechanism of Host Tissue Damage Immunologic Aspects of Microbial-host Interaction Host Response of Gingiva and Periodontium in Different Stages of Gingivitis Inflammatory Cells, Molecules, and Processes Adaptive Host Response Humoral Immune Response Cell-mediated Immunity Microbiology and Immunology in Periodontal Diseases Conclusion Questions Suggested Readings

76 76 76 76 77

78 78 79 79

80 80 80 80 81 82 82

Ashita Uppoor

11. Dental Calculus

83 83 83

Definition Classification Composition Structure of Dental Calculus Attachment of Calculus on Tooth Surface Rate of Calculus Formation Detection of Calculus Formation of Calculus Theories Regarding Mineralization of Calculus Role of Microorganisms in Calculus Mineralization Role of Calculus in Periodontal Disease (Clinical Implications) Questions Suggested Readings

84 84 85 85 85 86

87 87 87 87

12. Smoking and the Periodontium

Vijendra Singh Gangwar Effect of Smoking on Periodontal Disease Clinical Features of Oral Tissues Associated with Smoking Pathogenesis of Periodontal Disease in Smokers Response to Periodontal Therapy in Smokers Recurrent Periodontal Disease Tobacco Use Cessation Questions Suggested Readings

13. Trauma from Occlusion History Definition and Terminology Physiologic Adaptive Capacity of Periodontium to Occlusal Forces Types of Occlusal Forces Occlusal Forces and Jaw Movement Classification of Trauma from Occlusion Etiology of Trauma from Occlusion Trauma from Occlusion and Plaque Associated Periodontal Disease Glickman's Concept Animal Studies Human Trials Tissue Response to Increased Occlusal Forces Clinical Epidemiologic Studies Examination and Diagnosis of Trauma from Occlusion Signs ofTFO Symptoms ofTFO Reversibility of Traumatic Lesion TFO and Implants Latest Advances in Evaluation of Occlusal Stresses in the Periodontal Tissues Treatment Practical Clinical Conclusions and Guidelines Pathologic Migration Conclusion Questions Suggested Readings

88 89 89 91 91 91

92 92

Vandana KL 93 93 94 94 94 94 95 96 96 97 98 98 99 99 100 101 102 102 102 102 102 103 106 107 107

xix

CO N T EN T S

14. Role of Iatrogenic and Other Local Factors in Periodontal Disease

Prathibha PK

Iatrogenic Factors Local Contributing Factors Conclusion Questions Suggested Readings

108 115 118 118 118

15. Systemic Diseases and Periodontium

Deepa G Karnath Metabolic and Endocrine Disorders Hormonal Changes Psychosomatic Disorders Hematological and Immune Disorders Influence of Nutrition Other Systemic Conditions Questions Suggested Readings

16. Periodontal Medicine

120 123 126 127 128 129 130 130

Suresh R

Periodontitis as a Risk Factor for Systemic Disease Periodontitis and Coronary Heart Disease Periodontitis as a Risk Factor for Preterm Low-birth-weight Babies Periodontal Disease and Diabetes Mellitus Periodontal Disease and Chronic Obstructive Pulmonary Disease Questions Suggested Readings

131 131 133 135 137 139 139

1 7. Role of Genetics in Periodontal Therapy Mahesh CP and Nancy Srivastava Terminologies Genetics Types of Genetic Disorders Mutation Versus Polymorphism Human Gene Polymorphism Polymorphisms and Their Relationship to Periodontal Disease Methods of Genetic Analysis Role of Genetics in Aggressive Periodontitis Association of Aggressive Periodontitis with Genetic and Inherited Conditions Role of Genetics in Chronic Periodontitis Epigenetics Conclusion Questions Suggested Readings

140 140 14 2 143 143 143 144 145 14 7 14 7 149 149 150 150

IV PERIODONTAL PATHOLOGY 18. Defense Mechanisms of the Gingiva Epithelial Barrier Gingival Crevicular Fluid

Orogranulocytes Saliva Questions Suggested Readings

157 158 160 160

Neha Gupta

19. Gingival Inflammation Definition Stages in the Pathogenesis of Gingivitis Questions Suggested Readings

161 161 165 165

Neha Gupta

20. Clinical Features of Gingivitis Correlation of Clinical and Microscopic Features in Health and Gingivitis Questions Suggested Readings

166 171 1 71

Faizuddin M

21. Gingival Enlargement Classification Inflammatory Gingival Enlargement Fibrotic Gingival Enlargement Combined Enlargement Pregnancy-associated Gingival Enlargement Vitamin C Deficiency Pyogenic Granuloma Leukemia Wegener Granulomatosis Sarcoidosis Benign Lesions of Gingiva Malignant Lesions of Gingiva False Gingival Enlargement Questions Suggested Readings

22. Acute Gingival Infections

1 72 173 174 176 1 77 1 77 177 178 178 178 178 1 79 180 180 180

Deepa G Karnath

Necrotizing Ulcerative Gingivitis Primary Herpetic Gingivostomatitis Pericoronitis Questions Suggested Readings

181 186 188 189 189

23. Desquamative Gingivitis

Nagarathna DV

Classification of Diseases that Clinically Present as Desquamative Gingivitis Dermatologic Lesions Allergic Reactions Miscellaneous Conditions: Mimicking Desquamative Gingivitis Questions Suggested Readings

190 191 195 196 197 197

24. Periodontal Diseases in Childhood and Adolescents Deepa G Karnath

Mahesh CP 153 155

Periodontium of Deciduous Dentition Gingivitis Types of Gingival Diseases in Childhood

198 200 200

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CONTENTS

Types of Periodontal Diseases Aggressive Periodontitis Questions Suggested Readings

202 202 203 203

25. Periodontal Pocket

Neha Gupta

Differential Diagnosis Treatment Periodontal Cyst Questions Suggested Readings

236 236 237 237 237

Biju Thomas

30. AIDS and Periodontium Classification Clinical Features Pathogenesis Histopathology Microtopography of the Gingival Wall of the Pocket Morphology of the Tooth Wall Questions Suggested Readings

26. Bone Loss in Periodontal Disease Etiology of Bone Destruction Histopathology Mechanism of Bone Destruction Topography of the Alveolar Bone Factors Determining Bone Morphology in Periodontal Disease Bone Loss Patterns in Periodontal Disease Diagnosis Questions Suggested Readings

204 204 206 206 207 208 210 210

Sumita Singh 211 211 212 213 213 214 215 217 217

2 7. Periodontitis: Chronic, Refractory, and Necrotizing Ulcerative Deepa G Karnath Chronic Periodontitis Refractory Periodontitis Systemic Antibiotic Therapy in the Management of Refractory Periodontitis Necrotizing Ulcerative Periodontitis Necrotizing Ulcerative Periodontitis in HIV/AIDS Patients Questions Suggested Readings

28. Aggressive Periodontitis Classification Historical Background Epidemiology Prevalence Localized Aggressive Periodontitis Generalized Aggressive Periodontitis (GAP) Treatment Questions Suggested Readings

29. Periodontal Abscess Classification Etiology Pathogenesis and Histopathologv Diagnosis

218 221

238 238 240 240 240

Definition of AIDS Human Immunodeficiency Virus Classification and Staging Oral and Periodontal Manifestations of AIDS General Clinical Signs in AIDS Patient Classification of Oral Lesions Associated with HIV Infection Investigations Management of HIV/ AIDS Antiretroviral Treatment Infection Control Measures with a Focus on the Dental Setting Precautions for Dentists Sterilization and Disinfection Questions Suggested Readings

240 243 244 244 245 245 246 246

David Kadakampally

31. Halitosis Incidence Etiology Intraoral Causes Extraoral Causes Diagnosis Treatment Aspects of Oral Malodor Questions Suggested Readings

24 7 247 24 7 248 248 249 250 250

222 222

V

222 224 224

Mehta DS 225 225 225 226 226 230 231 233 233

Sachin Goyal 234 234 235 235

DIAGNOSIS, PROGNOSIS, AND TREATMENT PLANNING 32. Clinical Diagnosis

Subraya Bhat

Importance of Diagnosing the Periodontal Condition Components of Periodontal Examination Mucogingival Problems or Problems Related to Plastic Periodontal Surgery Teeth in Occlusion Questions Suggested Readings

253 253 262 264 265 265

33. Role of Radiology in the Diagnosis of Periodontal Diseases Ravikiran Ongole Radiographic Application in the Diagnosis and Treatment Planning of Periodontal Disease Limitations of Radiographs

267 267

xxi

CO N T EN T S

Radiographs Useful for Diagnosing Periodontal Disease Imaging Considerations for Periodontal Disease Characteristic Radiographic Features of Periodontal Diseases Systemic Conditions Influencing Periodontitis Systemic Conditions Mimicking Periodontitis Radiographically Questions Suggested Readings

268 269 274 277

Clinical Risk Assessment in Periodontal Disease Questions Suggested Readings

277 278 278

315 316 316

VI PERIODONTAL THERAPY

34. Advanced Diagnostic Methods

Rajesh Kashyap and Rajesh H Uses Conventional Diagnosis True Disease Status AIDS in Clinical Diagnosis AIDS in Radiographic Diagnosis AIDS in Microbiological Diagnosis AIDS Used in Immunological and Biochemical Diagnosis Questions Suggested Readings

35. Determination of Prognosis Definition Overall Versus Individual Prognosis Determination of a Prognosis Reevaluation of Prognosis After Phase 1 Therapy Questions Suggested Readings

279 279 280 281 283 284 284 288 289

Dilip G Nayak 290 290 290 295 296 296

36. Periodontal Treatment Plan

Ashish Nichani

Rationale for Treatment Plan Preferred Sequence of Treatment Phases Questions Suggested Readings

297 297 299 299

3 7. Treatment of Periodontal Diseases in Medically Compromised Patients Nandini Manjunath Cardiovascular Diseases Endocrine Disorders Renal Diseases Liver Diseases Pulmonary Diseases Immunosuppression and Chemotherapy Radiation Therapy Pregnancy Leukemia Coagulation Disorders Infectious Diseases Questions Suggested Readings

38. Risk Assessment So What Is "Risk?" Risk Factors for Periodontal Disease Risk Indicators Risk Markers/Predictors

300 304 306 307 307 308 308 308 309 309 311 312 312

Suresh R 313 314 315 315

39. Periodontal Instrumentation

Mahesh CP

Classification of Periodontal Instruments Types of Strokes Questions Suggested Readings

321 339 345 345

40. Sonic and Ultrasonic Instrumentation

Neha Gupta Sonic Scalers Ultrasonic Scalers Dental Contraindications Recommendations for Use Technique Clinical Comparisons Questions Suggested Readings

41. Plaque Control Definition of Dental Plaque Fate of Dental Plaque Time and Rate of Plaque Formation Disclosing Agents Plaque Control - Instruction Procedures Toothbrushes Classification of Gingival Embrasures Gingival Physiotherapy Tongue Scraping Chemical Plaque Control Mouthrinses Classification of Chemical Plaque Control Agents Anticalculus Agents Dentifrices Questions Suggested Readings

42. Scaling and Root Planing Objective of Root Planing Rationale for Root Planing Indications of Root Planing as a Specific Periodontal Treatment in Periodontitis Instrumentation Procedure Use of Lasers in Root Planing Questions Suggested Readings

346 346 350 350 350 351 352 352

Mahesh CP 353 353 353 354 356 356 363 366 366 366 366 367 371 372 374 374

Bhat KM 375 375 376 376 376 377 378 378

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CONTENTS

Dipen Shah

43. Chemotherapeutic Agents

3 79

Rationale of Antibiotic Therapy Importance of Combined Therapy Treatment Goals Routes of Drug Administration Antimicrobial Agents in Periodontal Therapy Ocher Antibiotics Guidelines for the Use of Antibiotic in Periodontal Disease Local Delivery of Antibiotics in Periodontal Disease Local Delivery of Antiseptics in Periodontal Pocket Local Versus Systemic Delivery of Antibiotics Analgesics in Periodontal Therapy Questions Suggested Readings

44. Host Modulation

380 380 380 381 383 384 385 386 387 387 392 392

Subraya Bhat

Host Immunoinflammatory Response Related to Periodontal Destruction Antioxidants Questions Suggested Readings

393 396 396 396

Neetha] Shetty

48. Flap Surgery Definition Objectives of Periodontal Flap Surgery Classification of Flaps Incisions in Periodontal Flaps Healing after Flap Surgery Suturing Questions Suggested Readings

419 419 419 420 426 427 430 430

49. Resective Osseous Surgery

Bhongade ML

Historical Background Classification of Osseous Defects Definitions Surgical Procedure Osteoplascy Factors Affecting Outcome of Resective Osseous Surgery Anatomic Limitations and Considerations Current Status of Osseous Resective Surgery Questions Suggested Readings

50. Regenerative Osseous Surgery 45. Periodontal Splints

Ashita Uppoor

Definition Rationale of Splinting Characteristics of an Ideal Splint Indications Contraindications Basic Principles of Splinting Disadvantages of Splinting Classification Questions Suggested Readings

397 397 397 397 398 398 398 398 400 400

437 437 438 438 438

N andakumar K

Principles of Osseous Regeneration Periodontal Regeneration Grafe Materials for Regeneration Types of Ceramic and Their Characteristic Tissue Interaction Behavior Regenerative Surgical Procedures Future Bone Regeneration Approaches Questions Suggested Readings

440 442 442 444 445 448 449 449

51. Furcation Involvement and Its Management

Abhay Kolte and Yeltiwar RK

46. General Principles of Periodontal Surgery

Mahesh CP Objectives of Surgical Treatment Indications for Surgical Treatment Contraindications for Periodontal Surgery Outpatient Surgery Questions Suggested Readings

401 401 402 403 411 411

4 7. Gingival Surgical Procedures

Neetha J Shetty

Inadvertent Gingival Curettage Surgical Gingivectomy Gingivoplasty Healing after Surgical Gingivectomy Gingivectomy by Electrosurgery Laser Gingivectomy Chemical Gingivectomy Questions Suggested Readings

431 431 432 433 437

412 414 414 414 414 417 418 418 418

Furcation Furcation Involvement Therapeutic Modalities in Furcation Involvement Questions Suggested Readings

450 450 454 456 456

52. Endodontic Periodontal Lesions and Their Aravind Shenoy and Neena Shenoy Management Relationship of Pulpal and Periodontal Disease Pathways of Communication Between Pulp and Periodontium Periodontal Disease Pulpal Disease Classification of Endodontic Periodontal Lesions Diagnosis of Endodontic Periodontal Lesions Tests Treatment Protocol

458 459 459 459 459 462 464 465

xxiii

CO N T EN T S

Conclusion Questions Suggested Readings

53. Periodontal Plastic Surgery

466 466 466

Dwarakanath CD

Common Mucogingival and Aesthetic Problems Significance of Attached Gingiva, Vestibular Depth, and Frenum General Factors Affecting the Outcome of PPS Procedures Augmentation of Attached Gingiva Management of Aberrant Frenum Vestibular Deepening Gingival Depigmentation Crown Lengthening Reconstruction of Interdental Papilla Ten Commandments of PPS Acknowledgment Questions Suggested Readings

468 468 470 471 475 478 480 480 483 485 485 485 485

54. Recent Advances in Periodontal Surgical Techniques Swati and Ruchika Goel Laser in Periodontics Components of a Laser Unit Laser-tissue Interactions Laser Application in Periodontal Therapy Photodynamic Therapy Photodynamic Antimicrobial Therapy Clinical Cases Done Using 810 nm Diode Laser (Picasso, AMO Lasers®) in Department of Periodontology, MCODS, Mangalore, Manipal University Microsurgery Conclusion Questions Suggested Readings

55. Periodontal Considerations in Restorative Dentistry Restoration Margins Restoration Contours Occlusal Considerations Restorative Materials Provisional Restorations Pontic Design Conclusion Questions Suggested Readings

486 486 488 490 492 492

494 494 498 498 498

5 7. Infection Control

Arun Kumar 499 501 502 502 502 502 503 504 504

Siddarth Shetty, Suruchi Jain and Asavari Desai 505 505 505 506

509 511 512 513

Sangeeta U Na yak

Exposure Prevention Strategies Protective Measures Personal Protective Equipment or Barrier Precautions Transport and Processing of Contaminated Instruments Environmental Infection Control Questions Suggested Readings

514 515 516 51 7 521 522 522

58. Supportive Periodontal Treatment

Deepa G Karnath Rationale for Supportive Periodontal Treatment Parts of Maintenance Phase Recurrence of Periodontal Disease Recall Intervals for Various Classes of Recall Patients Referral of Patients to the Periodontist Maintenance for Implant Patients Conclusion Questions Suggested Readings

523 524 524 524 524 526 526 526 526

59. Biological Aspects of Dental Implants

Arvind Shetty Osseo integration Bone Characteristics Implant Soft Tissue Interface Conclusion Questions Suggested Readings

60. Diagnosis and Treatment Planning in lmplantology

56. Ortho-Perio Interrelationships Orthodontic Treatment Considerations Biomechanical Considerations Timing and Sequence of Treatment Adjunctive Orthodontics

Orthodontic Stability Considerations in Periodontally Compromised Patients Periodontally Accelerated Osteogenic Orthodontics Questions Suggested Readings

Indications Contraindications Patient Evaluation Clinical Examination and Evaluation Surgical Aspects of Implant Placement Implant Surgery Complications Immediate Implant Treatment Modality Surgical Protocol Conclusion Questions Suggested Readings

61. Prosthodontic Considerations in Implant Restorations Impression Techniques Abutments in Implants

527 527 528 529 529 529

Betsy Thomas 530 530 531 532 537 537 539 542 543 545 546 546

Vidya Shenoy 547 552

xxiv

CONTENTS

Provisional Restorations Occlusal Considerations in Implant-Supported Prosthesis Cementation of the Implant Crowns Types of Implant-Supported Restorations Conclusion Questions Suggested Reading

555 555 556 557 558 559 559

62. Advanced Surgical Procedures for Dental Implants Maxillary Sinus Lift Surgery Bone Augmentation Ridge Splitting Guided Bone Regeneration Distraction Osteogenesis Bone Grafts Inferior Alveolar Nerve Repositioning Conclusion Questions Suggested Readings

Mohan Alexander 560 564 566 566 566 566 569 570 570 570

63. Peri-Implant Diseases and Management Betsy Thomas Etiology Risk Factors Ailing, Failing, and Failed Implants Diagnosis of Peri-Implant Tissue Breakdown Peri- Implantitis: Treatment Options Conclusion Questions Suggested Reading

64. Evidence-Based Periodontics Basic Concepts Clinical Practice and Evidence Conclusion Questions Suggested Readings

Index

571 571 572 573 573 575 575 575

RahulNair 576 578 582 583 583

585

SECTION

I

TISSUES OF THE PERIODONTIUM

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CHAPTER

1 Gingiva

Periodontium consists of the tissues that surround and support the teeth. The word comes from the Greek terms peri- meaning "around" and-odons meaning "tooth." Literally taken, it means that which is "around the tooth." The

tissues of periodontium are (i) gingiva, (ii) periodontal ligament, (iii) cementum, and (iv) alveolar process. Gingiva is considered as an investing tissue and periodontal ligament, cementum, and alveolar process are the supporting tissues.

GINGIVA

epithelial keratinization, and pigmentation. Gingiva is demarcated clinically into:

The oral mucosa can be divided into three categories on the basis of its function:

1. Marginal gingiva (free or unattached) 2. Attached gingiva 3. Interdental gingiva (papillary)

Marginal Gingiva (Free or Unattached) Oral mucosa

Masticatory mucosa

Specialized mucosa

(gingiva, hard palate)

(dorsum of the tongue)

Marginal gingiva is the portion of the gingiva surrounding the neck of the tooth that forms the soft tissue wall of the gingival sulcus. After complete tooth eruption, the free gingival margin is located on the enamel surface approximately 1.5-2 mm coronal to the cementoenamel junction (CEJ). It is demarcated from the attached gingiva by a shallow depression called the free gingival groove.

Lining mucosa (lips, cheeks, floor of the mouth, soft palate, ventral aspect of the tongue)

A. FREE GINGIVAL GROOVE

The free gingival groove is delineated from the attached gingival by the free gingival groove. It corresponds with the coronal margin of the junctional epithelium, i.e., the bottom of the sulcus. It was observed that a free gingival groove is only present in about 30-50% of the total population.

Gingiva is defined as that part of the oral mucosa which covers the alveolar process of the jaws and surrounds the necks of the teeth. The gingiva extends from the gingival margin to the mucogingival junction except on the palatal surfaces of maxillary molars where it merges with the palatal mucosa.

B. GINGIVAL SULCUS

The gingival sulcus is a shallow crevice between the marginal gingiva and the tooth. It is bordered by the sulcular epithelium on one side, the tooth on the opposite side, and the coronal end of junctional epithelium at its most apical end. In germ-free animals or after intense plaque control, the depth is 0 mm.

Macroscopic Features of the Gingiva The normal color of gingiva is "coral pink," and it is pigmented by melanin which makes the gingiva appear darker. This melanin pigmentation varies in different races. The color varies according to degree of vascularity, 3

4

SECTION I TISSUES OF THE PERIODONTIUM

Functions of the attached gingiva are as follows: • It braces the marginal gingiva and it lies in between two epithelium that are movable, i.e., free gingiva and alveolar mucosa. • It allows for proper deflection of food. • It provides room for proper placement of the toothbrush. • It has an esthetic value. • It is critical for overall maintenance of gingival health. • It prevents the apical spread of inflammation from marginal gingiva to the deeper periodontium. FIGURE 1.1

Normal clinical sulcus depth.

A probing depth of 1-3 mm is usually considered compatible with gingival health (Fig. 1.1). Attached Gingiva • It is continuous with marginal gingiva and extends to the mucogingival junction on the facial and lingual aspects of the mandible and the facial aspect of the maxilla. In the palate, there is no demarcation between the attached gingiva and the masticatory mucosa. • It is firm, resilient, and tightly bound to periosteum of alveolar bone. • In 40% of adults the surface texture of attached gingiva shows stippling (orange peel appearance) (Fig. 1.2). When present, it is more prominent on maxillary than mandibular arch; anterior maxilla than on the posterior and facial surfaces than on lingual surfaces. It is absent in infancy, appears at 5 years, increases until adulthood, and frequently disappears in old age. Width of the attached gingiva: Usually, the facial attached gingiva is widest in the area of upper and lower incisors (3.5-4.5 mm in the maxilla and 3.3-3.9 mm in the mandible), and narrowest in the posterior segments (1.9 mm in maxillary and 1.8 mm in mandibular first premolars). On the lingual aspect of the mandible, it is narrow in the incisor region and wide in the molar region. The width of attached gingiva increases with age and supraeruption of teeth.

The mucogingival junction is the line between the alveolar mucosa and the attached gingiva. The position of this junction is fixed. Interdental Gingiva (Papillary) The interdental gingiva occupies the gingival embrasures apical to the contact areas. The shape of the interdental gingiva is determined by the distance between the contact point and the crest of alveolar bone, amount of embrasure space, root angulation, periodontal biotype, and the course of the CEJ. Since the interdental papilla has a shape in conformity with the outline of the interdental contact surfaces, a concavity - a col - is established in the premolar and molar regions. • It is a valley-like depression that connects the facial and lingual papillae. • It conforms to the shape of interproximal contact. • The epithelium of the col is nonkeratinized due to which it is prone to inflammation. In the presence of diastema, the interdental papilla is absent. It is pyramidal-shaped interdental papilla in the incisor region. Due to the presence of interdental papillae, the free gingival margin follows a more or less accentuated, scalloped course through the dentition (Fig. 1.3).

Microscopic Features The gingival epithelium comprises the epithelial tissue that covers the external surface of the gingiva called as outer epithelium, epithelium lining, the gingival sulcus

~:

. , ·•

Alveolar mucosa MGJ Attached gingiva Marginal glngiva I> lnterdental papilla

FIGURE 1.2 Stippling seen in the core of the interdental papilla and attached gingiva.

FIGURE 1.3

Anatomical features of normal gingiva.

C H A PTER I G IN G IVA

5

The gingival epithelium is subdivided into three sections: (i) the oral epithelium; (ii) the sulcular epithelium; and (iii) the junctional epithelium. The histologic characteristics and functions of these types of epithelium are different.

FIGURE 1.4 Generalized melanin pigmentation.

known as sulcular epithelium, and the junctional epithelium that forms the base of the gingival sulcus. The principal cell type of the gingival epithelium is the keratinocyte. In addition to the keratin-producing cells, which comprise about 90% of the total cell population, the epithelium contains the nonkeratinocytes, which are as follows: 1. 2. 3. 4.

Melanocytes Langerhans cells Merkel cells Inflammatory cells

They are also called "clear cells" since in histologic sections, the zone around their nuclei appears lighter than that in the surrounding keratin-producing cells. Melanocytes Melanocytes are specialized cells that synthesize melanin pigment. They are responsible for the melanin pigmentation occasionally seen on the gingiva (Fig. 1.4). Melanocytes are derived from neural crest cells that eventually migrate into the basal and the spinous layer of the epithelium. In both light- and dark-pigmented individuals, melanocytes are present in the epithelium. In darkskinned individuals, the gingiva may contain melanin pigment to a greater extent than the adjacent alveolar mucosa. The melanin is produced in granules called as the melanosomes, stored within the cytoplasm of the melanocytes, and the adjacent keratinocytes. Langerhans Cells Langerhans cells are dendritic cells located among keratinocytes at suprabasal levels containing large granules called Birbeck granules. They are derived from the cellular differentiation of monocytes. The Langerhans cells are believed to play a role in the defense mechanism of the oral mucosa. In the presence of an infection, Langerhans cells will take up and process microbial antigen to become fully functional antigen-presenting cells, thereby inhibiting or preventing further antigen penetration of the tissue. Merkel Cells Merkel cells have been suggested to have a sensory function.

Oral Epithelium Oral epithelium (OE) is a stratified, squamous keratinizing epithelium that lines the vestibular and oral surfaces of the gingiva. It extends from the mucogingival junction to the crest of gingival margin. However, in the palatal surface it blends with the palatal epithelium. Oral epithelium can be divided into the following cell layers: 1. 2. 3. 4.

Basal cell layer (stratum basale or stratum germinativum) Prickle cell layer (stratum spinosum) Granular cell layer (stratum granulosum) Keratinized cell layer (stratum corneum)

1. Basal cell layer (stratum basale). The basal cell layer

represents the germinative layer. Basal layer cells are mainly cylindrical or cuboidal in appearance in contact with the basal lamina. Some cells of this layer migrate through the entire epithelial thickness and eventually keratinize; these are known as keratinocytes. Cells in other layers cannot divide. Hence, the basal cells are responsible for the important function of protecting the underlying structure and producing new epithelial cells. In addition, these cells synthesize and secrete the macromolecules that constitute the basal lamina. The basal lamina (basement membrane) under the electron microscope reveals an electron-dense layer, the lamina densa (LD) in contact with the connective tissue compartment, and an electron-lucent layer, the lamina lucida (LL) in contact with the epithelial cells. The cell membrane of the epithelial cells facing the lamina lucida harbors a number of electrondense, thicker zones appearing at various intervals along the cell membrane. These structures are called hemidesmosomes (HDs). The hemidesmosomes are involved in the attachment of the epithelium to the underlying basement membrane. The lamina lucida is composed of laminin and other glycoproteins. The lamina densa is composed of an afibrillar type of collagen, type IV collagen. The so-called anchoring fibers (AF) composed of type VII collagen extend from the undersurface of the lamina densa into the lamina propria where they appear to form loops around collagen fibers. 2. Prickle cell layer (stratum spinosum). The cells are polyhedral shaped characterized at the light microscopic level by apparent intercellular bridges. These cells possess decreased number of mitochondria equipped with short cytoplasmic processes resembling

6

SECTION I TISSUES OF THE PERIODONTIUM

spines. The cytoplasmic processes occur at regular intervals and give the cells a prickly appearance. Together with intercellular protein-carbohydrate complexes, cohesion between the cells is provided by numerous desmosomes" (pairs of hemidesmosomes) which are located between the cytoplasmic processes of adjacent cells. 3. Granular cell layer (stratum granulosum). The layer between the stratum spinosum and the stratum comeum consists of cells which are flatter and have granules called as keratohyalin granules. They contain the keratolinin and involucrin precursors of envelope which lies below the cell membrane and fillagrin. Epithelial cells become flattened. Tonofibrils take up an increasing volume of the cytoplasmic contents. Keratohyalin granules contain Odland bodies. Odland bodies or keratinosomes, which are modified lysosomes, are present in the uppermost layers of the stratum spinosum and between the stratum spinosum and stratum granulosum. 4. Keratinized cell layer (stratum corneum). This is the outermost layer of keratinized oral mucosa. It has cells that are flat and tightly packed. The epithelial cell here is the most differentiated and its matrix is formed of fillagrin which has bundles of keratin tonofilaments. There is no nuclei present. This form of keratinization is referred to as orthokeratinization, i.e., complete keratinization of the epithelial cells. II

Schroder and Page have summarized the events of continued differentiation that occurs as a new basal

cell derives from a mitotic activity in the stratum basale and makes its way toward the intraoral epithelial surface: • There is no cell division. • The cells are abundant in keratohyalin granules, keratin filaments, and macromolecules for the matrixlike fillagrin. • The organelles required for protein synthesis and energy production are lost. • The cells are finally completely keratinized but still interconnected by intercellular junctions. • The cells are finally sloughed away from the epithelial surface and into the oral cavity as the cell-cell attachment (hemidesmosomes and gap junctions ultimately disintegrate).

Sulcular Epithelium The sulcular epithelium is a stratified, squamous, nonkeratinized epithelium. It lies between the junctional epithelium and the crest of the free marginal gingiva coronally. It is epithelium that is continuous with the oral epithelium and lines the lateral surface of the sulcus. Apically, it overlaps the coronal border of the junctional epithelium, a structural design that minimizes ulceration of the epithelial lining in this region (Fig. 1.5). This epithelium shares many of the characteristics of the oral epithelium, including good resistance to mechanical forces and relative impermeability to fluid and cells. It has the potential to keratinize if:

Lipid droplet

9• 1l ~

Keratohyaline Lamellated granules

i'Ci=

,

Golgi complex

~

Mltochood,ia

½, •

lntercellular """"

A,~~

Granular endoplasmic reticulum -----------Desmosome

FIGURE 1.5

Stratified squamous epithelium: different layers.

7

C H A PTER I G IN G IVA

• It is reflected and exposed to the oral cavity. • Bacterial flora of the sulcus is totally eliminated. • Conversely, the outer epithelium loses its keratinization when it is placed in contact with the tooth. These findings suggest that the local irritation of the sulcus prevents sulcular keratinization. The overall structure of the sulcular epithelium resembles that of the oral epithelium, except for the surface layer that is nonkeratinized than its counterpart in the oral epithelium. The tightly sealed intercellular spaces (ICS) contribute to the low permeability of sulcular epithelium unlike the junctional epithelium, which is heavily infiltrated by PMNs.

Junctional Epithelium Junctional epithelium is a collar-like band of epithelium that surrounds the tooth. It is a stratified squamous nonkeratinizing epithelium. One aspect of this epithelium faces the gingival connective tissue (i.e., the lamina propria of the gingiva) and the other aspect the tooth surface. The junctional epithelium consists of 15-30 cell layers coronally, and only 1-3 cell layers at its apical termination giving it a wedge shape. The length of the junctional epithelium ranges from 0.25 to 1.35 mm. The suprabasal layer and the basal layer are the two strata seen in the junctional epithelium. The basal layer is the layer where mitotic division takes place rapidly. New cells travel continuously coronally and are shed in the gingival sulcus. Few cells of the suprabasal layer help in the formation of epithelium attachment which consists of internal basal lamina, hemidesmosomes, and suprabasal cells facing the tooth structure. Compared with other epithelia, junctional epithelial cells are interconnected by a few desmosomes only and occasionally by gap junctions. A variety of mononuclear leukocytes occupy these interstitial spaces. Antigen-presenting cells and Langerhans and other dendritic cells are present as well. The junctional epithelium, particularly its basal cell layers, is well innervated by sensory nerve fibers. The junctional epithelium has two basal laminae, the internal basal lamina and the external basal lamina (Fig. 1.6).They are continuous apically. The external basement lamina of the junctional epithelium faces the lamina propria and is similar to, in its structure and composition, with other basement membranes that are present between an epithelium and a connective tissue. The internal basal lamina is unique. It forms the epithelial attachment, i.e., the adhesion of gingiva to the tooth. The structure of this lamina lacks collagen types IV, VII, and laminin, which is present in the external basal lamina that faces the connective tissue. It comprises two zones: the electron-lucent zone, the lamina lucida and the electron-dense zone, the lamina densa. The lamina densa is near the enamel and the organic projections from the enamel extend into this zone. Hemidesmosomes attach to the lamina lucida which

1-Normal gingival sulcus 2-lntemal basal lamina (epithelial attachment) 3-Apical extent of JE

FIGURE 1.6 Structure of junctional epithelium.

play a key role in attachment of junctional epithelium cells to the internal basal lamina. The internal basal lamina and the hemidesmosomes form the epithelial attachment. This term is not synonymous with junctional epithelium, which refers to the entire epithelium. The junctional epithelium is divided into three zones: coronal, middle, and apical. The junctional epithelium cells divide continuously and this mitotic activity happens in all the cell layers. After the division the cells move coronally toward and along the tooth surface providing attachment and then desquamate at the base of the gingival sulcus. This mechanism gives a self-renewing and a protective capacity to the JE. The junctional epithelium is more permeable than the oral or sulcular epithelium due to wide intercellular spaces. Bacterial substances can enter and gingival crevicular fluid, host immune products, and inflammatory mediators can reach the gingival sulcus through it. While cell mitosis occurs in basal layer and possibly also in some areas adjacent to it, the zone becomes infiltrated with chronic inflammatory cells, primariy lymphocytes and plasma cells. Since there are fewer intercellular junctions between the junctional epithelium cells and wider spaces intercellularly the leukocytes can migrate from the vessels in the lamina propria into the gingival sulcus. In an healthy individual approximately 30,000 PMNs migrate per minute through the junctional epithelia of all human teeth into the oral cavity. These PMNs together with the host

8

SECTION I TISSUES OF THE PERIODONTIUM

immune products play a vital role in defense mechanism of gingiva.

GINGIVAL CONNECTIVE TISSUE The gingival connective tissue is called as lamina propria. It has two layers, i.e., papillary layer which are present between the finger-like projections of epithelium called as rete ridges and the reticular layer present below the rete ridges. It is continuous with the periosteum of the alveolar bone. At its junction with the lining mucosa, is the mucogingival junction. The lamina propria encloses the cells, fibers, and the neurovascular elements. The gingival connective tissue is occupied by: • collagen fiber bundles 60-65%; • cellular elements (fibroblasts 5%, various leukocytes, mast cells, tissue macrophages, etc. 3%); • vascular elements (blood and lymph vessels), nerves, and ground substance about 35%. The ground substance occupies the space between cells, fibers, and neurovascular elements. It has high water content, glycoproteins, e.g., fibronectin, and proteoglycans such as hyaluronic acid and chondroitin sulfate. The ground substance permits the diffusion of biological substances between various structural elements.

A. GINGIVAL FIBERS (FIG. 1.7)

These are made of bundles of type I collage mainly. There are few elastic and oxytalan fibers present in perivascular areas in the lamina propria. These gingival fibers are also called supragingival fiber apparatus. This provides a resiliency to the attached gingiva and helps to maintain the position of teeth within the dental arch. They consists of the microfibrillar component only, thereby resembling very immature elastic fibers. Elastic fibers are rather scarce in the lamina propria. They are a more common constituent of the lining submucosa. The collagen fibers are irregularly or randomly distributed but most tend to be arranged in groups of bundles with a distinct orientation. According to their insertion and course in the tissue, they have been divided into the following (Table 1.1): a. Principal fibers - Dentogingival - Alveologingival - Dentoperiosteal - Circular - Transseptal b. Secondary fibers - Periosteogingival - Interpapillary - Transgingival - Intercircular - Intergingival - Semicircular

1. Dentogingival - Coronal - Horizontal -Apical 2. Alveologingival 3. lnterpapillary 4. Transgingival 5. Circular 6. Dentoperiosteal 7. Transseptal 8. Periosteogingival 9. lntercircular 10. lntergingival

FIGURE 1. 7 Gingival fiber groups.

10

5

4

7

9

3

9

C H A PTER I G IN G IVA

TABLE 1.1

Classification of Collagen Fibers

Name of fiber group

Origin and orientation

PRINCIPAL GROUPS Dentogingival group

Originates from cementum and spreads laterally into the lamina propria

Alveologingival group

Originates from the periosteum of the alveolar and spreads coronally into the lamina propria bone

Dentoperiosteal group

Originates from cementum near the cementoenamel junction into the periosteum of the alveolar crest

Circular group

Originates from within the free marginal and attached gingival coronal to the alveolar crest and encircles each tooth

Transseptal group

Originates from interproximal cementum coronal to the alveolar crest and courses mesially and distally in the interdental area into the cementum of adjacent teeth

SECONDARY GROUPS Periosteogingival group

Originates from the periosteum of the lateral aspect of the alveolar process and spreads into the attached gingiva

Interpapillary group

Originates from within the interdental gingiva and follows an orofacial course

Transgingival group

Originates within the attached gingiva intertwining along the dental arch between and around the teeth

Intercircular group

Originates from cementum on the distal surface of a tooth spreading buccally and lingually around adjacent tooth and inserting on the mesial cementum of the next tooth

Intergingival group

Originates within attached gingiva immediately subjacent to epithelial basement membrane and courses mesiodistally

Semicircular group

Originates from cementum of the mesial surface of a tooth and courses distally and inserts on the cementum of the distal surface of the same tooth

These collagen fiber groups provide support to gingiva, attach gingiva to bone, anchor tooth to bone, protect periodontal ligament, maintain contour and position of free marginal gingiva, maintain relationships of adjacent teeth, protect interproximal bone, secure alignment of the teeth in the arch, and stabilize teeth in the arch.

1. Periodontal ligament 2. Alveolar process 3. Supraperiosteal blood vessel

B. CELLULAR ELEMENTS

The major cellular elements in the gingival connective tissue include fibroblasts, macrophages, mast cells, polymorphonuclear leukocytes and plasma cells, and cells that make up vascular channels and nerves. Adipose cells and eosinophils, although scarce, are also present. During inflammation the fibrous component of gingiva is replaced by the inflammatory cells such as neutrophils, lymphocytes, and plasma cells. The predominant cell of the gingival connective tissue is fibroblasts. They are mesenchymal in origin and are responsible for the development, remodeling, and repair of gingiva. These cells synthesize collagen and elastic fibers and the ground substance in which they are embedded. They phagocytose collagen and also release the collagenase enzyme to regulate collagen degradation.

2 3

C. VASCULAR ELEMENTS a. Blood supply. The gingiva is supplied by blood vessels

in the periodontal ligament, the crest of the alveolar process, and supraperiosteal blood vessels (Fig. 1.8).

FIGURE 1.8

Blood supply of gingiva.

10

SECTION I TISSUES OF THE PERIODONTIUM

b. Lymphatics. The gingival tissues are supplied with lymphatic vessels that drain principally to submaxillary lymph nodes. c. Nerves. Branches of the trigeminal nerve provide sensory and proprioceptive functions. In addition, autonomic nerve endings are associated with the vasculature. CONNECTIVE TISSUE-EPITHELIAL INTERACTIONS

The interaction of connective tissues and adjacent epithelia has a significant effect on epithelial tissue differentiation. The stratified squamous epithelium of masticatory mucosa is maintained by the dense lamina

propria found under it. Similarly, the loose connective tissue that supports the nonkeratinizing lining epithelium is largely responsible for the absence of keratinization in this epithelium. If a connective tissue graft is taken from the masticatory mucosa of the hard palate and is transplanted to a region which lacks an adequate covering of keratinizing mucosa, it will induce the overlying growing epithelium to keratinize, even if the epithelium originates from an adjacent, nonkeratinized mucosal surface. This interaction helps clinically in surgical procedures which are used to create a band of keratinized tissue where it is inadequate.

KEY POINTS • The tissues that surround and support the teeth are as follows: 1. Gingiva 2. Periodontal ligament 3. Cementum 4. Alveolar process • The color of gingiva is "coral pink"; normal racial pigmentation makes the gingiva appear darker. • It varies according to the degree of vascularity, epithelial keratinization, and pigmentation. • Gingiva is demarcated clinically into the following: 1. Marginal gingiva (free or unattached) 2. Attached gingiva 3. Interdental gingiva (papillary) • The gingival groove is an indentation that parallels the oral or vestibular surface of the gingival margin at a level corresponding to the level of the CEJ. • In 40% of adults, the surface texture of attached gingiva shows stippling (orange peel appearance). • Usually, the facial attached gingiva is widest in the area of upper and lower incisors (3.5-4.5 mm in the maxilla and 3.3-3.9 mm in the mandible), and narrowest in the posterior segments (1.9 mm in maxillary and 1.8 mm in mandibular first molars). On the lingual aspect of the mandible, it is narrow in the incisor region and wide in the molar region. • Functions of the attached gingiva are as follows: 1. It braces the marginal gingiva. 2. It allows for proper deflection of food. 3. It provides room for proper placement of the toothbrush. 4. It has esthetic value. 5. It is critical for overall maintenance of gingival health.

• Nonkeratinocytes include the following: 1. Melanocytes 2. Langerhans cells 3. Merkel cells 4. Inflammatory cells • Melanocytes are pigment-synthesizing cells and are responsible for the melanin pigmentation occasionally seen on the gingiva. • Langerhans cells are dendritic cells located among keratinocytes at suprabasal levels containing large granules called Birbeck granules. • The gingival epithelium is subdivided into three sections: 1. The oral epithelium (OE) 2. The sulcular epithelium (SE) 3. The junctional epithelium (JE) • Oral epithelium is divided into the following layers: l. Basal cell layer (stratum basale or stratum germinativum) 2. Prickle cell layer (stratum spinosum) 3. Granular cell layer (stratum granulosum) 4. Keratinized cell layer (stratum corneum) • The basal cell layer represents the germinative layer. • The basal lamina (basement membrane) under the electron microscope reveals an electron-dense layer, the lamina densa (LD) (in contact with the connective tissue compartment), and an electron-lucent layer, the lamina lucida (LL) (in contact with the epithelial cells). • The sulcular epithelium is the stratified, squamous, nonkeratinized epithelim which lines the gingival sulcus. • Junctional epithelium is a stratified squamous nonkeratinizing epithelium that surrounds the tooth like a collar with a cross-section resembling a thin wedge.

C H A PTER I G IN G IVA

KEY POINTS • The junctional epithelium tapers off in the apical direction, and it consists of 15-30 cell layers coronally and only 1-3 cell layers at its apical termination. The length of the junctional epithelium ranges from 0.25 to 1.35 mm. • The junctional epithelium has two basal laminas, one that faces the tooth (internal basal lamina) and one that faces the connective tissue (external basal lamina). • The term "epithelial attachment" refers to the attachment apparatus, i.e., the internal basal lamina and hemidesmosomes, that connects the junctional epithelium to the tooth surface. • The junctional epithelium is more permeable than the oral or sulcular epithelium due to wide intercellular spaces. • In the absence of clinical signs of inflammation, approximately 30,000 PMNs migrate per minute through the junctional epithelia of all human teeth into the oral cavity.

QUESTIONS Describe the ultrastructure of junctional epithelium. Enumerate the blood supply of gingiva. Write a short note on gingival fibers. Describe the age-related changes in gingiva. Write a short note on "col." Enumerate the functions of gingival fibers. Enumerate the differences between attached gingiva and alveolar mucosa. 8. Write a short note on the development of gingival sulcus.

1. 2. 3. 4. 5. 6. 7.

11

(cont'd) 1. Principal fibers - Dentogingival - Alveologingival - Dentoperiosteal - Circular - Transseptal 2. Secondary fibers - Periosteogingival - Interpapillary - Transgingival - Intercircular - Intergingival - Semicircular

• The gingival blood supply originates from blood vessels in the periodontal ligament, the marrow spaces of the alveolar process, and supraperiosteal blood vessels.

Suggested readings 1. Hassel T. Tissues and cells of the periodontium. Periodontology 2000 1993;3:9-23. 2. Lindhe J, Lang N, Karring T. Clinical Periodontology and Implant Dentistry. 5th ed. Copenhagen: Blackwell Munksgaard; 2008. 3. Newman MG, Takei H, Klokkevold PR, Carranza FA. Clinical Periodontology. 10th ed. Philadelphia: Saunders; 2006. 4. Page RC, Schroder HE. Periodontal Diseases. 2nd ed. New York: Lea & Febiger; 1990. 5. Schroder HE, Listgarten MA. The gingival tissues: the architecture of periodontal protection. Periodontology 2000 1997;13:91-120.

CHAPTER

2 Periodontal Ligament

The periodontal ligament occupies the space between the cementum and the alveolar bone, thereby providing a functional and dynamic link between the two structures. It

maintains a constant soft tissue space between the mineralized fronts of the root cementum and the alveolar bone that is referred to as the periodontal ligament space.

ORIGIN AND DEVELOPMENT OF THE PERIODONTAL LIGAMENT

for physiologic movement of tooth is in the middle of the root. So, when the tooth moves during a function, the space available for development of periodontal ligament space is less in the middle third, and so it is very thin. In multirooted teeth, the axis of rotation is located in the bone between the roots. In compliance with the mesial teeth migration, the periodontal ligament is thinner on the mesial root surface than on the distal surface.

Embryologically, periodontal ligament is derived from the dental follicle. From the cervical loop of the dental organ the internal and external enamel epithelia proliferate to form Hertwig epithelial root sheath. As the growth changes take place, the root sheath stretches and fragments to form the epithelial cell rests of Malassez. During eruption of teeth, the cells and the fibers of the dental follicle, which will form the future periodontal ligament, orient themselves initially, parallel to the long axis of the root.

Formative Cells The various formative cells are given in Table 2.1. • Fibroblasts • Fibroblasts are the most abundant and active cells. • They are stellate in shape with numerous cytoplasmic projections. Cell-to-cell communication is through gap junctions. • Functions - Fibroblasts help in the production of collagen, elastin, and ground substance. - They help in homeostasis and phagocytosis of old collagen fibers and degrade them. - Myofibroblasts help in tooth eruption. • Cementoblasts • Single layer along the cemental surface of periodontal ligament • Separated from cementum by cementoid tissue • Cuboidal in shape • Usually closely packed, but due to gaps in certain areas, the principal fibers pass through them and get embedded into the cementum as Sharpey fibers (Fig. 2.1)

FEATURES OF PERIODONTAL LIGAMENT 1. Periodontal ligament occupies the periodontal space, which is between the cementum and alveolar bone proper. This extends coronally to the most apical part of connective tissue of gingiva. 2. Periodontal ligament space can be seen in the radiograph as a radiolucent area or line between the lamina dura and the root surface. 3. Width of periodontal ligament: Width varies in different individuals, at different age in the same individual, and with different locations of the same tooth, location on the root, functions, and age. It ranges from 0.15 to 0.38 mm, the average being 0.21 mm. 4. Shape of periodontal ligament: Periodontal ligament is hourglass in shape, being wider at both ends and narrower in the middle. Reason for this is that fulcrum

12

C H A PT ER 2 PER IO D O N TA L LIG A M EN T

TABLE 2.1

Structural Components of Periodontal Ligament

Cellular components Synthesizing cells Fibroblasts Cementoblasts Osteoblasts Resorptive cells Fibroblasts Cementoclasts Osteoclasts Epithelial cells Cell rests of Malassez Progenitor cells Undifferentiated mesenchymal cells Defense cells Mast cells Macrophages

Extracellular components

Connective tissue components

Fibers Collagen Principal group Secondary group Elastic Oxytalan Elaunin Ground substance Protein Polysaccharides Glycosaminoglycans Proteoglycans Glycoproteins, especially fibronectin

Blood vessels Nerves Lymphatics

• Osteoblasts • Present on the alveolar bone side of periodontal ligament • Help in formation of bone • Cuboidal in shape • Separated from mineralized bone by osteoid tissue • Provide gap for principal fibers.

Resorptive Cells • Fibroblasts: Also act as resorptive cells, showing a dual role. • Osteoclasts • Osteoclasts are bone-resorption cells. • They are larger than osteoblasts with multiple nuclei.

13

• Under light microscope, the surface of alveolar bone shows resorption concavities called Howship lacunae in which lie the osteoclasts. • Osteoclasts lying adjacent to the bone have a striated appearance called brush border or ruffled border. • Underlying cytoplasm is devoid of organelles and is called clear zone or annular zone. • Cementoclasts • Cementoclasts are cementum-resorbing cells. • They undergo resorption only during pathology unlike bone and fibers. • During resorption, these are multinucleated giant cells.

Epithelial Cells • These are found close to cementum throughout the periodontal ligament mostly seen in the apical and cervical regions. They diminish in number with age by degenerating and disappearing or by undergoing calcification to become cementicles. • As soon as root dentinogenesis begins, the Hertwig epithelial root sheath loses its continuity and breaks into small islands or epithelial cell rests. • These islands persist in periodontal ligament and are called epithelial cell rests of Malassez. • Epithelial cells are cuboidal in shape and are arranged in clusters called rests. • They do not have any function, but during inflammation, undergo mitosis to give rise to cysts, especially periapical cysts.

Progenitor Cells These are cellular entities of mesenchymal origin, which are capable of differentiating into formative cells (viz., cementoblasts, osteoblasts, and fibroblasts) and resorptive cells (viz., osteoclasts). The presence of these progenitor cells in the periodontal ligament gives it the potential to provide cells during the regenerative and reparative phases of healing following periodontal disease. However, due to their slower migratory potential, these cells take a longer time to repopulate the root surfaces to form new cementum and fibers.

Other Connective Tissue Cells

FIGURE 2.1

Sharpey fibers.

• Mast cells • Mast cells are oval/round in shape. • They contain cytoplasmic granules.

14

SECTION I TISSUES OF THE PERIODONTIUM

• Granules contain - Mediators of inflammation such as histamine and serotonin - Anticoagulants such as heparin • When stimulated, they degranulate, disseminating their granular contents into the surrounding connective tissue. • Macrophages • Situated near blood vessels • Phagocytic cells • Derived from blood monocytes • Synthesize and release - Interferon (antiviral) - Prostaglandins (chemical mediator) - Growth factors of fibroblasts • Functions - Phagocytosis of dead cells in periodontal ligament and microbes - Secretion of growth factor for fibroblasts. The periodontal ligament fibers are mainly composed of collagen fibers. Collagen is secreted by fibroblasts, chondroblasts, osteoblasts, and odontoblasts. The fibers are made up of collagen macromolecules called tropocollagen. Type I collagen is predominant and type III is found to some extent. The collagen fibers are arranged as principal fiber bundle and secondary fibers. The other fibers present are the elastic fibers.

Transseptal Fibers These fibers are present between the cementum of adjacent teeth just apical to the area where the gingiva attaches to the tooth. FUNCTIONS

They maintain the teeth in the arch. Alveolar Crest Fibers Alveolar crest fibers extend obliquely beneath the junctional epithelium from the cementum to the alveolar crest. FUNCTIONS

They secure teeth in the socket. They resist lateral forces applied to the tooth. Horizontal Fibers Horizontal fibers extend from cementum to the alveolar bone at right angles to the long axis of the tooth. FUNCTIONS

They prevent lateral tooth movement. Oblique Fibers Oblique fibers are the most numerous fibers in the periodontal ligament. They extend from cementum obliquely to the bone in a coronal direction. As these fibers are found in abundance, they are believed to be responsible for absorbing the chewing forces.

Principal Fibers The periodontal ligament fibers are categorized according to their orientation to the tooth as transseptal fibers, alveolar crest fibers, horizontal fibers, oblique fibers, apical fibers, and interradicular fibers (Fig. 2.2).

FUNCTIONS

They resist apically directed masticatory forces. Apical Fibers Apical fibers radiate from cementum in a rather irregular manner to the bone at the apical region of the socket. FUNCTIONS

They prevent tooth tipping, resist forces of luxation, and protect blood, lymph, and nerve supply. Interradicular Fibers Interradicular fibers fan out in the furcation areas of multirooted teeth from the cementum. Horizontal group / lnterradicular group Oblique group

I •

~

I ~ r

"

a ~~

FUNCTIONS

They resist tipping of tooth, and forces of luxation and rotation.

Elastic Fibers

FIGURE 2.2 Principal fibers of the periodontal ligament.

Mature elastic fibers are not found in the periodontal ligament. Two immature forms of this tissue, the oxytalan and the elaunin fibers, are present. They form a meshwork

C H A PT ER 2 PER IO D O N TA L LIG A M EN T

15

extending from cementum to bone and sheathing the collagen fiber bundles.

• Resistance to impact of occlusal forces (shock absorption).

Secondary Fibers

To explain shock absorption, three theories have been put forward:

They are located between and among the principal fibers. These are nondirectional and randomly oriented collagen bundles of unknown function. They traverse the periodontal ligament space coronoapically.

Ground Substance The ground substance comprises glycoproteins such as fibronectin and laminin, and glycosaminoglycans such as hyaluronic acid. Both groups are composed of proteins and polysaccharides, but of different type and arrangement. The ground substance also contains high water content.

Blood Supply Main blood supply is from superior and inferior alveolar arteries. The blood supply of periodontal ligament can be divided into three groups. • Apical group of arteries: from vessels supplying the pulp • Alveolar group of arteries: also called perforating arteries • Gingival group of arteries: from gingival blood supply.

1. The tensional theory: This theory describes principal

fibers as the major factor responsible for supporting tooth and transmitting forces to the underlying bone. When force is applied to the crown, the principal fibers unfold and straighten and transmit force to the underling bone. The bone undergoes elastic deformity till the limit is reached and then the load is transmitted to the basal bone. 2. The viscoelastic theory: Tooth displacement is controlled by fluid movement and fibers play a secondary role. When forces are applied on a tooth, there is movement of the extracellular fluid from the periodontal ligament into the marrow spaces of the bone through the cribriform plate. Once the tissue fluids are depleted, the fiber bundles absorb the slack and tighten leading to stenosis of the blood vessels. There is ballooning of the vessels due to arterial back pressure causing passage of blood ultrafiltrates into tissues, replenishing them. 3. The thixotropic theory: This theory suggests that periodontal ligament has the rheologic behavior of a thixotropic gel (the property of becoming fluid when shaken or stirred and then becoming semisolid again). The shock absorption concept can also be explained by this theory.

Transmission of Occlusal Forces to Bone Nerve Supply The superior and inferior alveolar nerves supply the periodontal ligament.

Lymphatic Drainage Networks of lymphatic vessels run parallel to the blood vessels providing lymph drainage and drain into the regional lymph nodes, particularly the submaxillary group.

FUNCTIONS OF PERIODONTAL LIGAMENT Physical Functions • Protection of the underlying vessels and nerves from injury by mechanical forces by providing a soft tissue casing • Transmission of occlusal forces to the bone • Attachment of teeth to the bone • Maintenance of gingival tissues in their proper relationship to the teeth

Periodontal ligament transmits occlusal forces to the bone differently for different types of forces. When axial force is applied to a tooth, the root has a tendency to displace into the alveolus. When a horizontal force is applied, tooth movement occurs in two phases: the first is within the confines of the periodontal ligament and the second produces a displacement of the facial and lingual bony plates. The apical portion of the tooth moves in a direction opposite to the coronal portion. In sites of tension, the principal fiber bundles become taut rather than wavy. In sites of pressure, they become compressed, displacing the tooth, and, correspondingly, distorting the bone that exists in the direction of root movement. In single-rooted teeth, the axis of rotation is located between the apical and middle third of the root. In multirooted teeth, the axis of rotation is located in the bone between the roots.

Formative and Remodeling Cells of the periodontal ligament take part in the formation and resorption of cementum and bone.

16

SECTION I TISSUES OF THE PERIODONTIUM

The periodontal ligament cells constantly undergo remodeling. Fibroblasts form the collagen fibers and the mesenchymal cells differentiate into osteoblasts and cementoblasts.

Nutritive and Sensory The periodontal ligament supplies nutrients to the bone and gingiva by way of blood vessels. It is also supplied with abundant nerve fibers capable of transmitting tactile, pain, and pressure sensations. Nerve bundles pass into the periodontal ligament from the periapical area and through channels from the alveolar bone. The bundles divide into single myelinated fibers and end in one of the four types of neural termination: 1. 2. 3. 4.

Free endings - carry pain sensation Ruffini-like mechanoreceptors Coiled Meissner corpuscles - mechanoreceptors Spindle-like endings - pressure and vibration.

CLINICAL CONSIDERATIONS Response of Periodontal Ligament to Trauma Periodontal tissue responds in various stages: (i) injury, (ii) repair, and (iii) adaptive remodeling. In cases of acute trauma to the tooth, e.g., accidentally biting hard substances or accidental blow, periodontal tissue injury occurs. Nature attempts to repair the injury and restore the periodontium. This can occur if the trauma is removed or if the tooth drifts away from them. In case of chronic trauma, the periodontal ligament is remodeled. The ligament is widened at the expense of the bone, angular bone defects occur without pockets, and tooth becomes loose. Orthodontic tooth movement occurs when there is resorption and formation of both alveolar bone and periodontal ligament. When the orthodontic forces are applied, the compression of the periodontal ligament on the pressure side results in bone resorption and on the tension side bone formation occurs.

KEY POINTS • The periodontal ligament is a specialized connective tissue that attaches a tooth to the jawbone. • It is defined as a soft, specialized connective tissue situated between the cementum covering the root of the teeth and the bone forming the socket wall. • Thickness ranges from 0.15 to 0.38 mm, the average being 0.21 mm. • Periodontal ligament is hourglass in shape, being wider at both ends and narrower in the middle. • Fibroblasts are the most abundant and active cells. • Principal fibers get embedded into the cementum as Sharpey fibers.

QUESTIONS 1. Enumerate various cells of the periodontal ligament. 2. Enumerate periodontal ligament fibers. 3. State the functions of periodontal ligament. 4. Write a note on oxytalan fibers. 5. Enumerate blood supply of periodontal ligament.

Suggested readings 1. Beertsen W, Mcculloch Christopher AG, Sodek J. The periodontal ligament: a unique, multifunctional connective tissue. Periodontal 20001997;13:20-40.

• The periodontal ligament fibers are mainly composed of collagen fibers. • Type I collagen is predominant and type III is found to some extent. • Oblique fibers are the most numerous fibers in the periodontal ligament. • Main blood supply is from superior and inferior alveolar arteries. • The periodontal ligament supplies nutrients to the bone and gingiva by way of blood vessels.

2. Bhaskar SN. Orban's Oral Histology and Embryology. 11th ed. St. Louis: Mosby; 2005. 3. Lindhe J. Clinical Periodontology and Implant Dentistry. V ed. Oxford: Blackwell Munksgaard Publications; 2008. 4. Newman MG, Takei H, Carranza FA. Clinical Periodontology. 10th ed. Philadelphia: Saunders; 2006. 5. Ten Cate AR. Oral Histology, Development, Structure and Function. V ed. St. Louis: Mosby; 1998.

CHAPTER

3 Cementum

Cementum is a mineralized avascular noninnervated dental tissue that covers the anatomic root of human teeth. It forms the interface between root dentine and periodon-

tal ligament. It is derived from Latin word "caementum" which means "quarried stone."

COMPOSITION

Cementum was first demonstrated in 1835 by two pupils of Purkinje. It resembles bone structurally but differs in several important functional aspects. It has no innervation, no direct blood supply, and no lymph drainage.

Cementum comprises 45-50% inorganic salts which are present in the form of hydroxyapatite crystals; the remaining matrix is made of collagen fibers and noncollagenous matrix protein. Type I collagen is the predominant form and constitutes 90% of its organic components. It is known to promote cell attachment, and also is a critical molecule for maintaining the integrity of both soft and hard connective tissues, during development as well as in repair.

PHYSICAL CHARACTERISTICS • Hardness: Hardness of cementum is less than dentin but greater than bone. • Color: Cementum is light yellow in color, distinguished from enamel due to its darker hue and luster. • Cementum is relatively brittle. • Permeability: Cementum is softer and more permeable than dentin.

• The noncollagenous components of the interfibrillar ground substance are proteoglycans, glycoproteins, and phosphoproteins. • The following are the two apparently unique cementum molecules: • Cementum-derived attachment protein: An adhesion molecule that mediates the attachment of connective tissue cells • Cementum-derived growth factor: Insulin-like growth factor.

Permeability decreases with age. In cellular cementum, the canaliculi of cementocytes in lacunae are continuous with dentinal tubules in some areas. • Thickness: Cementum deposition is a continuous process that proceeds at varying rates throughout life. • At CEJ, its thickness is 20-50 µm; it increases at apex and inter-radicular area to about 150-200 µm.

The inorganic content of cementum is less than that of bone (65%), enamel (97%), and dentine (70%). Cementum has the highest fluoride content.

Thickness of cementum is more on the distal side than on the mesial side; this contributes to the physiologic mesial drift.

Cementoblasts

Cellular Elements of Cementum They are present along the forming cementa! surface. The earlier cementoblasts originate from ectomesenchymal

17

18

SECTION I TISSUES OF THE PERIODONTIUM

cells of dental follicle and the later ones from undifferentiated mesenchymal cells of periodontal ligament. They are responsible for producing the network of collagen fibrils and a proteoglycan ground substance, and also participate in mineralization of cementum.

Cementocytes When cellular cementum is being formed, the cementoblasts become trapped in lacunae within their matrix and are known as cementocytes. Unlike cementoblasts their metabolic activity is low. They have numerous cytoplasmic processes coursing into canaliculi; hence, they are referred to as spider-like cementocytes.

Cementoclasts They are multinucleated giant cells which are indistinguishable from osteoclasts. They are responsible for the extensive root resorption that leads to primary tooth exfoliation and localized cemental resorption in adult dentitions.

FIGURE 3.1 Acellular cementum showing incremental lines running parallel to the long axis of the tooth.

FUNCTIONS OF CEMENTUM It furnishes a medium for attachment of collagen fibers, which binds the tooth to the alveolar bone. Its continuous deposition also helps in achieving the crown length lost due to attrition; thus, it is crucial for maintaining occlusal relationship. It also serves as a major reparative tissue for root surfaces, thereby maintaining integrity of the root surface.

CLASSIFICATION Cementum can be classified as follows: I

1. Depending on location a. Radicular cementum: It refers to cementum that covers the root; in humans, radicular cementum accounts for the bulk of cementum. b. Coronal cementum: It refers to cementum found on enamel; in humans, it is thin and poorly developed. 2. Depending on cellularity a. Acellular/primary cementum (Fig. 3.1) b. Cellular/ secondary cementum (Fig. 3.2). Both acellular and cellular cementum consist of a calcified interfibrillar matrix and collagen fibers. The two sources of collagen fibers are as follows: - Sharpey ( extrinsic) fibers are formed by the fibroblasts and are embedded in cementum. - Intrinsic fibers are produced by cementoblasts and belong to the cementum matrix.

FIGURE 3.2

__,.

Cellular cementum showing cementocytes lying within

lacunae.

Their differences are depicted in Table 3.1. 3. Depending on the presence or absence of fibrils a. Fibrillar cementum: It is the most common form and contains well-defined, densely packed collagen fibrils in its matrix. b. Afibrillar cementum: It lacks the dense array of collagen fibrils in its organic matrix. A separate classification of cementum has been summarized by Schroeder and Page:

19

C H A PT ER 3 C EM EN T U M

TABLE 3.1

Summary of Differences Between Acellular and Cellular Cementum

Acellular cementum

Cellular cementum

No cellular elements

Lacunae and canaliculi containing cementocytes and their processes

Rate of development is relatively slow

Rate of development is relatively fast

Forms during root formation

Forms after root formation and in response to functional demands

Collagen fibers are more organized

Collagen fibers are irregularly organized

1. Acellular afibrillar cementum: This is found exclusively on the enamel near the cementoenamel junction (CEJ). It consists of a mineralized matrix but contains neither collagen fibrils nor cells. The lack of collagen fibrils indicates that it has no function in tooth attachment. It is formed when cementoblasts comes in contact with enamel in the developmental phase. 2. Acellular extrinsic fiber cementum: This is confined to the coronal half of the root. It is composed of extrinsic fiber system consisting of Sharpey fibers but does not harbor cementocytes within lacunae. The formation commences shortly after crown formation is completed. The matrix consists of short type I collagen fibers that are oriented perpendicular to the root surface. The fibers remain short till the tooth is about to reach the occlusal plane, and then they elongate and become continuous with periodontal fibers. The cementoblasts produce loosely packed collagen fibrils that form a meshwork surrounding the principal fiber of the ligament in a plane parallel to cemental surface. These "indifferent" cemental fibrils as well as the principal fibers are surrounded by a proteoglycan ground substance also synthesized by cementoblasts. 3. Cellular intrinsic fiber cementum: This does not encase any Sharpey fiber; instead, its organic matrix consists of intrinsic fibers which are synthesized by cementoblasts and not POL fibroblasts. This cementum exhibits lacunae with cementocytes. Also, it grows at a faster rate than any other type and hence can repair a resorptive defect in reasonable time. 4. Cellular mixed stratified cementum: The intrinsic fibers predominate over Sharpey fibers. Cellular mixed stratified cementum appears primarily in the apical third of the roots, the apices, and furcation areas. It harbors both intrinsic and extrinsic fibers within calcified matrix that also houses viable cementocytes. It increases in thickness throughout life. 5. Intermediate cementum (or) the hyaline layer of Hopewell Smith: It is an ill-defined zone (10 µm)

extending from pre-CEJ to the apical third of the root. It appears to contain cellular remnants of Hertwig epithelial root sheath. The clinical significance of the layer is that it contains enamel-like protein (amelogenin) which helps in attachment of cementum to dentine.

CEMENTOENAMEL JUNCTION The cementoenamel junction follows the overlappingmeeting-gap rule (OMG) . The clinical importance of cementoenamel junction lies in root scaling procedures. • The relation between cementum and enamel at cervical region of teeth is variable. There are three types of CEJ (Figs 3.3-3.5) as per Hopewell Smith (1918). In about 60% of teeth, cementum overlaps cervical end of enamel for a short distance. This occurs when the enamel epithelium degenerates at its cervical termination, permitting connective tissue to come in direct contact with the enamel surface (Fig. 3.3). • In approximately 30% of all teeth, the cementum and enamel meet as a butt joint forming a distinct delineation at the cervical margin (Fig. 3.4) and 10% have a gap between the cementum and enamel, exposing root which can lead to sensitivity at the site. This occurs when enamel epithelium in the cervical portion of the root is delayed in its separation from dentine (Fig. 3.5). It has a clinical importance in gingival recession since it is associated with increased sensitivity because of the exposed dentin.

FIGURE 3.3

Cementum overlapping the enamel.

20

SECTION I TISSUES OF THE PERIODONTIUM

• According to scanning electron microscopy, its width is 2-3 µm. • With age, it has no effect as its width remains stable. • CDJ is relatively smooth in permanent teeth while scalloped in deciduous teeth. • In decalcified and stained histologic sections cementum stains more intensely than dentin. • Dentin can be separated from cementum by a zone known as intermediate cementum, which does not show features of either cementum or dentin. • CDJ represents areas where cells of Hertwig epithelial root sheath become trapped in rapidly deposited cementum or dentin.

Sharpey Fibers

FIGURE 3.4 End-to-end relationship of enamel and cementum.

• Sharpey fibers are the portions of principal fibers of the PDL which are embedded in the root cementum and in alveolar bone proper. • These constitute extrinsic fiber system of cementum and are produced by fibroblasts in the PDL. • Sharpey fibers in the primary acellular cementum are mineralized fully; however, those in cellular cementum and bone are mineralized only partially at their periphery.

DEVELOPMENTAL AND ACQUIRED ANOMALIES OF CEMENTUM The following anomalies in cementogenesis may have an impact on the susceptibility of teeth to periodontal disease and affect the treatment:

FIGURE 3.5

Space between enamel and cementum with dentine

exposed.

CEMENTODENTINAL JUNCTION Cementodentinal junction (CDJ) is defined as terminal apical area of cementum where it joins the internal root canal dentin. • It is important clinically as during root canal treatment obturating material should end at CDJ.

• Enamel projections: They are seen in localized areas in the furcation of mandibular molars during development. If amelogenesis does not stop before the root formation, enamel projection may form over portion of a root which is normally covered by Hertwig epithelial root sheath. • Enamel pearls: Globules of enamel on the root surface in the cervical region are referred to as enamel pearls. They appear as a result of localized failure of Hertwig epithelial root sheath to separate from dentine surface, thereby allowing cementogenesis to proceed. Large pearls may contain pulpal extensions. • Hypercementosis (cementa! hyperplasia) (Fig. 3.6): It indicates a prominent thickening of cementum. It may be localized or generalized. It is not possible to distinguish between physiologic thickening of cementum that occurs with age and hypercementosis. It occurs as a generalized thickening of root cementum with a nodular enlargement at the apical one-third or as spike-like excrescences due to fusion of cementicles

21

C H A PT ER 3 C EM EN T U M

FIGURE 3.6

Hypercementosis.

to the roots or due to calcification of periodontal ligament fibers which are inserted into cementum. Their etiology is attributed to excessive orthodontic or occlusal forces. Localized hypercementosis is seen in teeth without antagonists to keep pace with active eruption or due to low-grade periapical irritation as a result of pulpal disease. It is believed to be a compensatory mechanism to counteract the destruction of fibrous attachment of the tooth. Generalized hypercementosis may be hereditary or observed in patients with Paget disease. • Cementicles: These are globular masses of cementum arranged in concentric lamella that may be found either lying free in PDL or adhering to the root surface. They may develop from • Calcified epithelial cell rests of Malassez • Small spicules of cementum or alveolar bone that are traumatically displaced into PDL • Calcified Sharpey fibers • Calcified thrombosed vessels in PDL.

CEMENTUM RESORPTION AND REPAIR Cementum of erupted as well as of unerupted teeth is subject to resorption. It may be of microscopic proportion or extensive to be observed in a radiograph. Cementum resorption appears microscopically as baylike concavities in the root surface, which are lined by multinucleated giant cells and large mononuclear macrophages. Cementa! resorption may be due to local or systemic causes. Among the local causes are trauma from occlusion, active orthodontic movement, pressure from malaligned erupting teeth, cysts and tumors, teeth without functional

antagonists, embedded, replanted, and transplanted teeth, and periapical or periodontal disease. Systemic cases may be due to deficiency of calcium, vitamin D, and vitamin A, hypothyroidism, fibrous osteodystrophy, and Paget disease. Cementum resorption is not continuous and may alternate with periods of repair and deposition of new cementum. The newly formed cementum is demarcated from the root by a deep-staining irregular line known as reversal line. During repair there could be formation of acellular or cellular cementum or alternate formation of both. Cementum repair requires the presence of viable connective tissue. If epithelium proliferates into an area of resorption, repair will not take place. If during repair the former outline of the root surface is reestablished, it is called anatomic repair. If only thin layer of cementum is deposited on the surface of deep resorption, it is called functional repair.

CEMENTAL TEARS It could be defined as the detachment of a fragment of cementum from root surface, owing to an acute injury or from intermittent episodes of sustained pressure. • It follows one of the incremental lines. • Tears have been observed within unexposed cementum and exposed cementum within the pocket. • The cementa! tears can remain partially attached or completely detached from the root surface.

Ankylosis Fusion of cementum and alveolar bone with obliteration of periodontal ligament is known as ankylosis. It occurs in teeth with cementa! resorption which may represent a form of abnormal repair. Ankylosis may also develop following chronic periapical inflammation, tooth replantation, and occlusal trauma around embedded teeth.

Clinical Significance • Ankylosed teeth are difficult to extract. • Ankylosed teeth lack physiologic mobility, which is a diagnostic sign of ankylotic resorption. • Ankylosed teeth show special metallic percussion sound. • Affected tooth is in infraocclusion. • Affected tooth exhibit loss of proprioception due to deletion of receptors in PDL. • Due to ankylosis, physiologic drifting and eruption cannot take place. • Radiographically ankylosed teeth exhibit resorption lacunae filled with bone and PDL space missing.

22

SECTION I TISSUES OF THE PERIODONTIUM

KEY POINTS • Cementum is a mineralized avascular dental tissue that covers the anatomic root of teeth. • It comprises 45-50% inorganic salts which are present in the form of hydroxyapatite crystals and the remaining matrix is made of collagen fibers and noncollagenous matrix protein. • Cementum has the highest fluoride content. • Sharpey (extrinsic) fibers are formed by the fibroblasts and are embedded in cementum. • A separate classification of cementum has been summarized by Schroeder and Page:

QUESTIONS 1. Describe the structure of cementum and clinical

significance of cementoenamel junction (CEJ). 2. Enumerate the functions of cementum. 3. Enumerate various types of cementoenamel junction 4. 5. 6. 7.

(CEJ). Enumerate the causes of hypercementosis. State the cemental changes during periodontal diseases. Classify cementum. Define ankylosis.

1. Acellular afibrillar cementum 2. Acellular extrinsic fiber cementum 3. Cellular intrinsic fiber cementum 4. Cellular mixed stratified cementum. • In about 60% of teeth, cementum overlaps cervical end of enamel for a short distance. • Fusion of cementum and alveolar bone with obliteration of periodontal ligament is known as ankylosis. • Acellular cementum forms during root formation.

Suggested readings 1. Bhaskar SN. Orban's Oral Histology and Embryology. 11th ed. St. Louis: Mosby;2005. 2. Bosshardt DD, Selvig KA. Dental cementum: the dynamic tissue covering of the root. Periodontal 2000 1997;13:41-75. 3. Hassel T. Tissues and cells of the periodontium. Periodontal 2000 1993;3:9-23. 4. Newman T, Carranza FA. Clinical Periodontology. 10th ed. Saunders: St. Louis; 2006. 5. Ten Cate AR. Oral Histologi;, Development, Structure and Function. 3rd ed. Mosby: St. Louis; 1989.

CHAPTER

4 Alveolar Bone

The portion of the maxilla and the mandible that forms and supports the tooth socket is called the alveolar process. Alveolar bone in conjunction with the cementum and periodontal ligament constitutes the tooth attachment

apparatus which helps in distributing the forces such as masticatory forces (Fig. 4.1). It forms with the development and eruption of the teeth and it gradually regresses once the tooth is lost.

PARTS OF ALVEOLAR PROCESS

• The spongy bone fills the space between the facial and the lingual cortical plates and mesially and distally between the alveolar bone proper. The facial and the lingual cortical plates meet at the alveolar crest 1.5-2 mm apical to the cementoenamel junction.

The alveolar process, depending on the functional adaptation, consists of the parts mentioned in the following subsections.

Alveolar Bone Proper Alveolar bone proper is a thin layer of bone lining the roots of the teeth and provides attachment to periodontal ligament fibers. It is also referred to as the bundle bone because the bundles of the periodontal ligament fibers continue into the bone as Sharpey fibers (Fig. 4.2). Radiographically, this bundle bone appears as a thin radiopaque line surrounding the roots of teeth, called the lamina dura. The alveolar bone is perforated with numerous openings by branches of intra-alveolar nerves and blood vessels and is therefore called the cribriform plate. It is also known as lamellated bone, as lamellae structure with haversian canal system is present. The most coronal aspect of the alveolar bone is the alveolar crest which is parallel to the cementoenamel junction (CEJ) and is situated about 1-2 mm apical to it.

HISTOLOGY OF ALVEOLAR BONE Mature bones, whether compact (Fig. 4.3) or cancellous (Fig. 4.4), consist of layers or lamellae. Three different types of lamellae are present: 1. Circumferential lamellae: These form the outer casing

of the adult bone. 2. Concentric lamellae: These form the basic unit of bone, the osteon, and also make up the bulk of the compact bone. The osteons are arranged parallel to the long axis of the bone with the haversian canal as its center. Adjacent haversian canals are interconnected by the horizontal Volkmann canals. 3. Interstitial lamellae: These lamellae are present between two adjacent concentric lamellae.

Supporting Alveolar Bone

Periosteum

Supporting alveolar bone supports the alveolar bone proper. It consists of two parts:

Surrounding each compact bone is the periosteum, a connective tissue membrane. The periosteum consists of two layers: an inner layer and an outer layer. The inner layer, called the cambium, is next to the bone

• The cortical plates form the outer and inner plates of the alveolar process, made up of compact bone.

23

24

SECTION I TISSUES OF THE PERIODONTIUM

Gingiva Cementum

,

,?;."j

FIGURE 4.1

Normal periodontium.

FIGURE 4.2

Sharpey fibers.

FIGURE 4.3

Histologic section showing compact bone.

FIGURE 4.4

Cancellous bone with marrow spaces.

INTERDENTAL SEPTUM surface and consists of bone cells, their precursors that have the potential to differentiate into osteoblasts. The outer layer contains collagen fibers, fibroblasts, and rich blood supply.

Endosteum The inner surface of both compact and cancellous bones is called the endosteum and is made up of single bone cell layer that separates the bone surface from the bone marrow within. The inner layer is osteogenic and the outer layer is fibrous in nature.

The interdental septum consists of cancellous bone bordered by the socket wall made up of cribriform plate approximating facial and lingual cortical plates (Fig. 4.5). In case of narrow interdental space, the septum consists of only cribriform plate. Radiographically, the position of the interdental septum helps in determining the root proximity. The mesiodistal angulation of the crest of the interdental septum (Fig. 4.6) usually parallels a line drawn between the CEJ of the adjacent teeth. The distance between the crest of the alveolar bone and the CEJ in young adults varies between 0.75 and 1.49 mm. This distance increases with age to an average of 2.81 mm. The shape and dimensions of the interdental septum are

25

CH A PT ER 4 A LV EO LA R BO N E

FIGURE 4. 7

FIGURE 4.5

Interradicular septum.

Histologic section showing marrow spaces.

inactive type of marrow. In adults, the yellow marrow is found in the jaws, and the red marrow is found in the ribs, sternum, vertebrae, skull, and humerus. Common sites of yellow marrow in the jaws are the maxillary tuberosity, maxillary and mandibular molar and premolar areas, the mandibular symphysis, and the ramus area.

COMPOSITION OF ALVEOLAR BONE Bone consists of 65% inorganic and 35% organic substances (Fig. 4.8).

Cells of the Alveolar Bone Three types of cells are found in the alveolar bone. All cell names start with "osteo" meaning "bone" in Greek.

The bone-forming cells are called the osteoblasts. They are derived from the bone marrow and are FIGURE 4.6

Alveolar crest.

governed by the size and convexity of the crowns of the two approximating teeth, as well as by the position of the teeth in the jaw and their degree of eruption.

BONE MARROW In embryos and newborns, all the bones are occupied by red hematopoietic marrow (Fig. 4.7). It gradually undergoes physiologic changes and is replaced by yellow

ORGANIC INORGANIC

(hydroxy apatite) Calcium and phosphate along with carboxyl, citrate, and traces of sodium, magnesium, fluorine

FIGURE 4.8

Type I collagen - 90%, noncollagenous osteocalcin, osteonectin, bone morphogenetic proteins, and proteoglycans. Osteopontin and bone sialoprotein are cell adhesion proteins

Composition of alveolar bone.

26

SECTION I TISSUES OF THE PERIODONTIUM

mononucleated. They lay down a matrix called osteoid that consists of bone collagen and other proteins. Their function is to regulate calcium and mineral deposition. They are present on the new bone surface.

Once the osteoblasts have completed filling the bone cavity, they become flat and reach the bone surface and are called the lining cells. Their function is then to regulate the passage of calcium in and out of the bone and to stimulate the production of osteoclasts in the presence of certain hormones.

FIGURE

4.9

Osteoclast in histologic section.

in lingual version, the margins are more coronally placed, with the margins being blunt, rounded, and horizontal. The cells within the bone matrix are called the osteocytes. These are derived from the osteoblasts. As the osteoblasts are secreting bone matrix, a few of them get entrapped in the matrix and become osteocytes. The space in the matrix occupied by the osteocyte is called the osteocytic lacuna. Once the cells become osteocytes, they gradually lose their matrix-synthesizing property and get reduced in size. The radiating osteocytic processes are housed by enclosed canaliculi of the lacunae, thus maintaining contact with adjacent osteocytes and the osteoblasts or the lining cells.

Osteoclasts (Fig. 4.9) are large cells that dissolve the bone. They originate from the bone marrow. They are formed from two or more cells that fuse together, so the osteoclasts usually have more than one nucleus. They are found on the surface of the bone mineral next to the dissolving bone. They occupy shallow, hollowed-out depressions on the bone surface created by themselves called the Howship lacunae.

FENESTRATION AND DEHISCENCE Isolated areas where the root is devoid of the overlying bone and is covered only by the soft tissue are called fenestration. Here, the marginal bone will be intact (Fig. 4.10). When the denuded area of the root involves the marginal bone also, it is called dehiscence. Approximately 20% of the teeth are seen to have these defects occurring commonly bilaterally, on the facial aspect of anterior teeth. These defects occur on approximately 20% of the teeth; they are more commonly seen on facial bone and anterior teeth, and are frequently bilateral. The causes of these defects are still not clear. The reasons could be prominent root contours, tooth malposition, and labial protrusion of the root combined with a thin bony plate.

OSSEOUS TOPOGRAPHY The bony contour conforms to the root prominence. On teeth in labial version, the margins of the alveolar bone are located apically when compared with teeth with normal alignment. The bone margins are knife edged. On teeth

FIGURE 4.10

Fenestration and dehiscence.

27

CH A PT ER 4 A LV EO LA R BO N E

REMODELING OF ALVEOLAR BONE Remodeling of bone takes place due to continuous bone formation and resorption that helps the bone to adapt itself to mechanical loads. Homeostasis is brought about by the balance in resorption and formation due to which old bone is replaced by new bone. Because of this, there is no change in the morphology of the bone and also the mechanical integrity of the bone is maintained. This process is called remodeling. The appearance of the osteoclasts on the quiescent bone marks the beginning of the remodeling process. • They attach to the bone tissue matrix and form a ruffled border at the bone/ osteoclast interface that is completely surrounded by a "sealing zone." Thus, the osteoclast creates an isolated microenvironment. • Subsequently the osteoclast acidifies the microenvironment and dissolves the organic and inorganic matrices of the bone. • Once the resorption stops, osteoblasts that are derived from bone marrow, periosteum, and soft tissues appear on the surface to deposit osteoid that undergoes mineralization to form new bone. • Some of the osteoblasts are encapsulated in the osteoid matrix and differentiate to osteocytes. Remaining osteoblasts continue to synthesize bone until they eventually stop and transform to quiescent lining cells that completely cover the newly formed bone surface. A few osteoblasts get encapsulated in the bone matrix and differentiate to form osteocytes. A few others continue synthesizing bone and, once their function is over, are transformed into lining cells that cover the newly formed

+

Blood calcium

~homeostasis

l

timulanon or~

timulnnon of osteoblasts

Bone formation

FIGURE 4.11

i

"'°"'''"

~ of IL-6 -+ Stimulation of osteoclast

-

Mechanism of bone resorption and formation.

bone. Bone remodeling is regulated by certain hormones and local factors. Bone contains 99% of body's calcium, forming the major source of calcium when blood calcium levels decrease. Parathyroid hormone (PTH) is essentially the major hormone that mediates and regulates calcium homeostasis. It brings about homeostasis by stimulating the release of calcium from the skeleton. The PTH stimulates bone resorption by stimulating the ostoblastic cells to secrete paracrine substances such as interleukin-1 which brings about osteoclastogenesis. Recently, it has been demonstrated that the cytokine interleukin-6 (IL-6), which potently induces osteoclastogenesis, is produced by osteoblastic cells in response to PTH. Thus, IL-6 may play a permissive role in PTH-induced bone resorption and plays a role in coupling PTH-induced bone resorption and formation (Fig. 4.11).

KEY POINTS • The alveolar process is the thickened ridge of bone that contains the tooth sockets on bones that bear teeth. • Alveolar bone proper is a thin layer of bone lining the roots of the teeth and provides attachment to principal fibers of periodontal ligament. • Radiographically, this bundle bone appears as a thin radiopaque line surrounding the roots of teeth, then called the lamina dura. • The alveolar bone is perforated with numerous openings by branches of intra-alveolar nerves and blood vessels and is therefore called the cribriform plate. • Mature bones, whether compact or cancellous, consist of layers or lamellae. Three different types of lamellae are present.

• The inner surface of both compact and cancellous bones is covered by endosteum, a single layer of bone cells that separates the bone surface from the bone marrow within. • The distance between the crest of the alveolar bone and the cementoenamel junction in young adults varies between 0.75 and 1.49 mm. • Bone consists of 65% inorganic and 35% organic substances. • Osteoclasts occupy shallow, hollowed-out depressions on the bone surface created by themselves called the Howship lacunae. • Isolated areas in which the root is denuded of bone and is covered only by the periosteum and overlying gingiva are called fenestration.

28

SECTION I TISSUES OF THE PERIODONTIUM

KEY POINTS • When the denuded area includes the marginal bone, the defect is called dehiscence. • Parathyroid hormone (PTH) functions as a major mediator of bone remodeling and as an essential regulator

QUESTIONS 1. Describe the structure and composition of alveolar bone. 2. Define lamina dura. 3. Define fenestration and dehiscence.

4. Define bundle bone. 5. Define remodeling of alveolar bone. 6. Define periosteum and endosteum.

Suggested readings 1. Grant DA, Sternn IB, Listgarten MA. Periodontics. 6th ed. St. Louis: Mosby; 1998.

(cont'd) of calcium homeostasis, producing several distinct and independent effects on the bone-remodeling process, resulting in both bone formation (anabolic activity) and bone resorption (catabolic activity).

2. Lindhe J. Clinical Periodontology and Implant Dentistry. V ed. Oxford: Blackwell Munksgaard Publications; 2008. 3. Newman MG, Takei H, Carranza FA. Clinical Periodontology. 10th ed. Philadelphia: Saunders; 2006. 4. Saffar JL, Lasfargues JJ, Cherruau M. Alveolar bone and the alveolar process: the socket that is never stable. Periodontal 2000 1997;13:76-90. 5. Ten Cate AR. Oral Histology, Development, Structure and Function. 5th ed. St. Louis: Mosby; 1998.

CHAPTER

5 Age--related Changes in the Periodontium

Aging is slowing of natural function, a disintegration of the balanced control and organization that characterize the young adult. It is important to recognize age-related changes in periodontium, since these may affect function. While the option has been stated that age-related

changes may prepare the way for a pathologic state, this later hypothesis cannot be correlated with epidemiologic data and the evidence is equivocal. Age-related changes affect the periodontal tissues mentioned in the following sections.

VASCULATURE

capable of regeneration. The rate of collagen synthesis decreases with age in rats as measured by in vitro labeling technique. Also, it has been shown that the cells of the periodontal ligament of aged mice do not renew as rapidly as those of young animals.

Arteriosclerosis is a frequent finding in aging humans, and may be seen in large vessels with muscular elements in the vessel wall, vessel in the alveolar bone, and vessels in the periodontal ligament. The relationship of this vascular pathologic condition to other changes in the periodontium is inconclusive. The relative ischemia that arteriosclerosis may produce in periodontal tissues because of the reduction in blood flow has been hypothesized as predisposing these tissues to disease or provoking other changes such as fibrosis, loss of cellularity, and focal calcification. It may also reduce bone metabolism and may be correlated with slower or altered wound healing. The reduced arterial flow may be related to changes that have been observed elsewhere in the body and in experimental animals. For instance, the loss of ground substance may be a result of the reduced supply of oxygen associated with diminished arterial flow. Also, basement membranes have been reported to be thicker in aged persons and markedly distinct from the surrounding ground substance. Several other changes are noted in periodontal tissues. There is a decrease in connective tissue cellularity and an increase in number and coarseness of collagenous fibers. The number of synthesizing cells is significantly greater in younger animals and a greater number of cells are

TOOTH-PERIODONTIUM RELATIONSHIP • There is loss of tooth substance due to attrition. • There is reduction in cuspal height and inclination due to wear. • Bone loss results in an increase in crown/ root ratio. • Tooth wear tends to modify increase in crown/root ratio. • Wear on proximal surfaces results in physiologic mesial drifting. Attrition of tooth substance on occlusal and incisor surfaces and at the contact points is a well-recognized characteristic of aging. Vertical dimension and arch continuity are usually maintained in old age, since wear is compensated for bone apposition on distal surfaces and at the fundus of the sockets. Continuous apposition of the cementum at the apex also helps to compensate for such wear.

29

30

SECTION I TISSUES OF THE PERIODONTIUM

GINGIVAL EPITHELIUM Thinning and decreased keratinization of the gingival epithelium have been reported with age. The significance of these findings could mean an increase in epithelial permeability to bacterial antigens, a decreased resistance to functional trauma, or both, which might influence longterm periodontal outcomes. Some reports show migration of the junctional epithelium from its position in healthy individuals (i.e., on enamel) to a more apical position on the root surface with accompanying gingival recession. With increasing age, there is an increase in the width of the attached gingiva, a change that is attributed to the eruptive movement of the teeth rather than to the intrinsic aging phenomenon. The migration of the junctional epithelium to the root surface could be caused by the tooth erupting through the gingiva in an attempt to maintain occlusal contact with its opposing tooth (passive eruption) as a result of tooth surface loss from attrition. Aging also brings an increased prevalence of gingival recession. This finding appears to be largely due to cumulative environmental effect of vigorous tooth brushing rather than due to inflammatory periodontal disease or aging.

GINGIVAL CONNECTIVE TISSUE The fibroblasts that make up the gingival connective tissue are heterogeneous with respect to their biochemical traits. It may be that with increasing age, selective pressures favor predominance of fibroblast subpopulations with the phenotypic expression. Tissue culture studies of gingival fibroblasts obtained from older individuals have revealed a reduction in the rate of proliferation, a decrease in the quantity and quality of proteoglycans, and diminished protein and collagen production. Increasing age results in coarser and more dense gingival connective tissues. Qualitative and quantitative changes to collagen have been reported. These include an increased rate of conversion of soluble to insoluble collagen, increased mechanical strength, and increased denaturing temperature. These results indicate increased collagen stabilization caused by changes in the macromolecular conformation. Not surprisingly, a greater collagen content has been found in the gingiva of older animals despite a lower rate of collagen synthesis decreasing with age.

PERIODONTAL LIGAMENT The principal fibers of the periodontal ligament are thicker in aging humans than in younger individuals. The well-organized bundles are broad and wavy. The

interfibrillar areas are reduced in size. There is a decrease in the ratio of ground substance to collagen. The periodontal ligament shows degenerative hyaline changes and also chondroid degeneration. Both the hyalinization and chondroid degeneration may be • Casually related to or an accompaniment of a reduced vascular supply • A response to injury • An undetermined effect of aging. Calcified bodies are common in the periodontal ligament of elderly humans. Two types of rounded calcospheroid-like bodies are demonstrable: small rounded calcospherites and larger, irregularly shaped calcifications. The calcospherites appear to be formed in relation to fiber bundles. They coalesce to form the larger rounded or irregularly shaped bodies. Occasionally, they increase in number and appear to calcify a complete fiber bundle, leading to ankylosis. Epithelial rests in the periodontal ligament show altered forms of aggregation. Rest aggregates tend to contain more cells with both proliferative and degenerative morphology. The aggregates are frequently encircled by a thickened basement membrane. Rather than being situated near the root surface (as in young persons), these epithelial rests are found irregularly located in the periodontal ligament, near the tooth, midway between the tooth and bone, and near the bone. While some rests may degenerate, others may become calcified. Also, changes include decreased numbers of fibroblasts and a more irregular structure, paralleling the changes in the gingival connective tissues. Other findings include decreased organic matrix production and epithelial cell rests and increased amounts of elastic fiber. Conflicting results have been reported for changes in the width of periodontal ligament in human and animal models. Although true variation might exist, this finding probably reflects the functional status of the teeth in the studies because the width of the space will decrease if the tooth is unopposed (hypofunction) or will increase with excessive occlusal loading.

CEMENTUM An increase in cemental width is a common finding; this increase may be 5-10 times with increasing age. The increase in width is greater apically and lingually. This may be attributable to occlusal wear and eruption of teeth, although it has also been noted in impacted teeth. This finding is not surprising because deposition continues after tooth eruption. Although cementum has limited capacity for remodeling, an accumulation

CH A PT ER 5 A G E-R ELATED CH A N G ES IN TH E PERIO DO N T IU M

of resorption bays explains the finding of increasing surface irregularity. Indications exist that cemental deposition slows in old age. In addition, the attachment of cementum to dentin may be weakened. The frequent cemental tears seen in specimens of aging humans may be related to age-related changes in the ground substance of cementum, to reduced vascular supply, or to thickened and less extensible ligament fibers embedded in the cementum. Spurring of cementum is sometimes the result of the fusion of calcospheroid bodies near cementum or due to the calcification of epithelial rest aggregates.

ALVEOLAR BONE Little evidence of continued bone apposition is present in senescence. In view of this, physiologic tooth migration may be slowed or even halted in old age. Specific to the periodontium are findings of a more irregular periodontal surface of bone and less regular insertion of collagen fibers. Although age is a risk factor for the bone mass reductions in osteoporosis, it is not causative and therefore should be distinguished from physiologic aging processes. The healing rate of bone in extraction sockets appears to be unaffected by increasing age. The success of osseointegrated dental implants, which relies on intact bone healing responses, does not appear to be age related. However, balancing this view is the recent observation that bone graft preparations (decalcified freeze-dried bone) from donors more than 50 years old possessed significantly less osteogenic potential than graft material from younger donors. The possible significance of this phenomenon on normal healing responses needs to be investigated. Osteoporosis has been reported in aging, particularly in alveolar bone of postmenopausal women, since the decrease in the trabeculation of alveolar bone sometimes seen radiographically is more often related to the loss of function.

BACTERIAL PLAQUE Dentogingival plaque accumulation has been suggested to increase with age. This might be explained by the increase in hard tissue surface area as a result of gingival recession and the surface characteristics of the exposed root surface as a substrate for plaque formation compared with enamel. Other studies have shown no difference in plaque quantity with age. This contradiction might reflect the different age ranges of experimental groups as variable degrees of gingival recession and root surface exposure.

31

For supragingival plaque, no real qualitative differences have been shown for plaque composition. For subgingival plaque, one study has shown subgingival flora similar to a normal flora, whereas another study reported increased numbers of enteric rods and pseudomonads in older adults. Mombelli suggests caution in the interpretation of this finding because of increased oral carriage of these species among older adults. It has been speculated that a shift occurs in the importance of certain periodontal pathogens with age, specifically including an increased role for Porphyromonas gingivalis and a decreased role for Actinobacillus actinomycetemcomitans. However, differentiating true age effects from the changes in ecological determinants for periodontal bacteria will be difficult.

IMMUNE RESPONSES Age has been recognized as having much less effect in altering the host response than previously thought. Differences between young and older individuals can be demonstrated for T and B cells, cytokines, and natural killer cells but not for polymorphonuclear cells and macrophage activity. McArthur concludes, "Measurement of indicators of immune and inflammatory competency suggested that, within the parameters tested, there was no evidence for age-related changes in host defenses correlating with periodontitis in an elderly (65 to 75 years) group of individuals, with and without disease."

SUMMARY Periodontal disease increases in prevalence and severity with increasing age. The increase may be caused by the cumulative effect of the number of bursts of periodontal destruction, deterioration in plaque removal efficiency, or an increase in the number of teeth retained in old age and therefore affected by plaque-induced disease. Attention should be directed toward the decline in immune function with age. Clinical studies have led the investigators to conclude that chronological aging, per se, does not inevitably lead to attachment loss or decrease in alveolar bone support. Although many contradictions exist, a survey of the literature demonstrates that some age-related changes are evident in the periodontium and host response.

32

SECTION I TISSUES OF THE PERIODONTIUM

KEY POINTS • The relative ischemia that arteriosclerosis may produce in periodontal tissues with age causing a reduction in blood flow has been hypothesized as predisposing these tissues to disease or provoking other changes such as fibrosis, loss of cellularity, and focal calcification. • There is a decrease in connective tissue cellularity and an increase in number and coarseness of collagenous fibers. • Thinning and decreased keratinization of the gingival epithelium have been reported with age. • With increasing age, there is an increase in the width of the attached gingiva. • Tissue culture studies of gingival fibroblasts obtained from older individuals have revealed a reduction in the rate of proliferation.

QUESTIONS 1. What is the effect of aging on the supporting tissues of

the periodontium? 2. What is the effect of aging on composition of bacterial plaque? 3. What are the effects of aging on immune response?

• Qualitative and quantitative changes to collagen include an increased rate of conversion of soluble to insoluble collagen, increased mechanical strength, and increased denaturing temperature. • The periodontal ligament shows degenerative hyaline changes and also chondroid degeneration. • An increase in cemental width is a common finding; this increase may be 5-10 times with increasing age. • Dentogingival plaque accumulation has been suggested to increase with age. • It has been speculated that a shift occurs in certain periodontal pathogens with age, specifically including an increased role for Porphyromonas gingivalis and a decreased role for Actinobacillus actinomycetemcomitans.

Suggested readings 1. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Clinical Periodontology. 10th ed. Philadelphia: Saunders; 2006. 2. Wilson Jr TG, Kornman KS. Fundamentals of Periodontics. New York: Quintessence Publishers; 1996.

SECTION

II

CLASSIFICATION AND EPIDEMIOLOGY OF PERIODONTAL DISEASES

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CHAPTER

6 Classification of Periodontal Diseases CHAPTER OVERVIEW Classification of diseases is required to scientifically study the etiology, pathogenesis, and treatment of a disease. There have been numerous classification systems of periodontal diseases over the years. Unfortunately,

all of them have shortcomings. To overcome them, in 1999, the International Workshop for Classification of Periodontal Diseases of Conditions came up with a new classification.

DEFINITION

USES OF CLASSIFICATION

Classification is the systematic collection of data or knowledge and its arrangement in sequential manner in order to facilitate its understanding or knowledge. Classification systems can be classified based on

• Identification of the etiology and understanding of the pathology • Diagnosis, prognosis, and treatment planning • Facilitation of communication among the clinicians, researchers, educators, students, epidemiologists, and public health workers.

1. Topography 2. Morphology 3. Etiology.

HISTORICAL DEVELOPMENT OF THE CLASSIFICATION SYSTEM

REQUIREMENT

Development of classification systems was largely influenced by paradigms that reflect the understanding of periodontal diseases during a given historical period. Classification systems are placed into three paradigms primarily based on the following:

1. Classification should not be rigid, should be adaptable,

and should respond to changing knowledge. 2. It should be consistent.

NEED FOR CLASSIFICATION

• Clinical characteristic paradigm (1870-1920) • Classical pathology paradigm (1920-1970) • Infection/host response paradigm (1970 to present).

It allows for logical and systematic separation and organization of knowledge about the disease so that one may reason • from the signs and symptoms seen in the patient to a presumed etiologic history; • from the presumed etiologic history to identification of the condition; and • from there to the prescribed course of treatment.

C.G. Davis Classification - 1879 1. Gingival recession with minimal or no inflammation 2. Periodontal destruction secondary to lime deposits 3. "Riggs disease" - loss of alveolus without loss of gums.

35

36

SECTION II CLASSIFICATION AND EPIDEMIOLOGY OF PERIODONTAL DISEASES

G.V. Black Classification - 1886 1. Constitutional gingivitis: Mercurial gingivitis; scurvy 2. A painful form of gingivitis: Similar to necrotizing

ulcerative gingivitis (NUG) 3. Simple gingivitis: Associated with accumulation of debris that eventually led to calcic inflammation of periodontal membrane 4. Calcic inflammation of periodontal membrane: Associated with salivary calculus 5. Phagedenic pericementitis.

Orban Classification - 1942 He postulated, "Periodontal diseases followed the same course as the diseases of the other organs. Minor changes may be present but the basic pathologic changes however are the same as those of other organs." According to the principles of general pathology, there are three major tissue reactions: • Inflammatory • Dystrophic • Neoplastic. Note: Neoplastic changes are not in the therapeutic realm of periodontics. Environmental factors, however, dictate the inclusion of a third category in the periodontology - "pathologic reaction produced by occlusal trauma." • Inflammation: • Gingivitis - Local (calculus, food impaction irritating restoration, drug actions) o Systemic (pregnancy, endocrine disorders, TB, syphilis, nutritional disturbances, drug action, allergy, etc.) • Periodontitis - Simplex (secondary to gingivitis) - bone loss, pockets, abscess, calculus - Complex (secondary to periodontosis) - etiologic factors similar to periodontitis; have little, if any, calculus • Degenerative • Periodontosis (attacks young girls and older men, often caries immunity) - Systemic (pregnancy, endocrine disorders, TB, syphilis, nutritional disturbances, drug action, allergy, etc.) • Atrophy • Periodontal atrophy (recession, no inflammation, no pockets, osteoporosis) due to local trauma, senile, disuse, following inflammation, idiopathic • Hypertrophy • Gingival hypertrophy

• Chronic irritation, drug action, idiopathic (gingivoma, elephantiasis, fibromatosis) • Traumatism • Periodontal traumatism - occlusal trauma.

Demerits • Conclusion that some forms of periodontal diseases were caused by noninflammatory or degenerative process was primarily based on overinterpretation of histopathologic studies. • There is no scientific basis for retaining the concept that there were noninflammatory or degenerative forms of destructive periodontal diseases.

American Academy of Periodontology - 1986 1. Gingival diseases and conditions a. Gingivitis

- Marginal gingivitis - Acute necrotizing ulcerative gingivitis (ANUG) b. Gingivitis and other gingival changes with systemic involvement - Gingival changes associated with sex hormones - Gingival changes associated with diseases of the skin and mucous membrane - Gingivitis in generalized systemic diseases - Infective gingivostomatitis - Drug-associated gingival changes o Systemic medications o Compounds with local effects (caustic compounds, heavy metals) - Miscellaneous gingival conditions o Gingival cysts, fistula, neoplasms, gingival clefts, recession, aberrant frena, epulis, and abscess 2. Periodontal diseases and conditions a. Periodontitis in adults with no systemic involvement b. Periodontitis in juveniles - Localized/ generalized c. Periodontitis with systemic involvement - Periodontitis in primary neutrophil disorders - Periodontitis in systemic diseases with secondary or associated neutrophil impairments - Other systemic diseases associated with changes in the structure of periodontal attachment - Miscellaneous 3. Periodontal changes associated with occlusal trauma a. Primary - bruxism, other parafunctional habits b. Secondary - periodontal diseases. This classification is intended to provide a current basis of terminology that is useful for communication among practitioners, patients, and third parties involved in practice.

CHAPTER 6 CLASSIFICATION OF PERIODONTAL DISEASES

Merits 1. Clearly differentiates gingivitis, gingival enlargement,

NUG, periodontitis, and so on 2. Useful in teaching.

Demerits 1. Age-dependent criteria 2. Rate of bone destruction.

World Workshop in Clinical Periodontology - 1989 The workshop classified periodontal diseases into the following categories: 1. Adult periodontitis 2. Early onset periodontitis a. Prepubertal periodontitis - localized/ generalized

b. Juvenile periodontitis - localized/ generalized c. Rapidly progressing periodontitis 3. Periodontitis associated with systemic diseases a. Down syndrome b. Diabetes, Papillon-Lefevre syndrome c. AIDS, etc. 4. Necrotizing ulcerative periodontitis (NUP) 5. Refractory periodontitis. Classification depended on the following factors: 1. Age criteria 2. Rate of progression

3. Host response of the affected patient 4. Other forms not responding to conventional therapy,

i.e., refractory periodontitis. Merits 1. Ease with which patients could be placed into age-

37

• Periodontal diseases that progress from marginal gingiva are infectious diseases caused by bacteria. • Inflammatory conditions restricted to the gingiva itself fit into the defining term gingivitis, whereas inflammation extending deeper to involve periodontal ligament, cementum, and alveolar bone fits within the term periodontitis. • Although both gingivitis and periodontitis are of local origin, they can be influenced in their expression by systemic conditions; same gingival abnormalities may be caused primarily by systemic conditions as well. No periodontitis has been documented to be of purely systemic origin. This classification accepts occlusal trauma as a physiologic adaptation rather than a disease. 1. Gingivitis a. Gingivitis, plaque induced

- Nonaggravated - Aggravated by sex hormones, drugs, and systemic diseases b.NUP - Systemic determinants unknown - Related to HIV c. Gingivitis, non plaque induced - Associated with skin diseases - Allergic infections 2. Periodontitis a. Adult periodontitis: nonaggravated/ systemically aggravated b. Early onset periodontitis: localized/ generalized c. Related to systemic diseases 3. NUP: systemic determinants unknown - related to HIV a. Related to nutrition 4. Periodontal abscess.

based categories Demerits 1. It did not include gingivitis or gingival disease category. 2. Periodontitis categories had nonvalidated agedependent criteria. 3. There was extreme crossover in rates of progression of the different categories of periodontitis. 4. There was extensive overlap in the clinical characteristics of different categories of periodontitis. 5. Refractory periodontitis and prepubertal periodontitis were heterogeneous categories.

Ranney Classification - 1993 Classification is based on principles including the following:

Merits This system includes not only forms of gingivitis and periodontitis other than those caused by plaque but also modifying factors, e.g., systemic aggravating factors, general diseases status, and viral infections. Compared with the World Workshop in Clinical Periodontology, 1989, this classification system • Eliminated the "refractory periodontitis" category, since it was a heterogeneous group and it was impossible to standardize the treatment that necessarily would have to be given prior to making diagnosis • Eliminated the "periodontitis associated with systemic disease" category, since the expression of all forms of periodontitis can be modified by some systemic disease or abnormality.

38

SECTION II CLASSIFICATION AND EPIDEMIOLOGY OF PERIODONTAL DISEASES

European Workshop on Periodontics - 1993 1. Adult periodontitis a. Onset fourth decade b. Slow rate of progression c. No host response defect 2. Early onset periodontitis a. Onset prior to fourth decade b. Rapid rate of progression c. Defect in host response 3. Necrotizing periodontitis a. Tissue necrosis with attachment and bone loss.

2.

Demerits • Lacked adequate categorization of the broad spectrum of periodontal diseases encountered in clinical practice • Gingival diseases not included.

International Workshop for Classification of Periodontal Diseases and Conditions - 1999 Goal "Course correction" or "fine-tuning" of 1989 classification 1. Gingival diseases a. Dental plaque induced - Associated with dental plaque only with/ without other local contributing factors - Gingival diseases modified by systemic factors o Associated with the endocrine system: puberty-associated gingivitis, menstrual cycleassociated gingivitis, pregnancy-associated gingivitis, pyogenic granuloma, and diabetes mellitus-associated gingivitis o Associated with blood dyscrasias: leukemiaassociated gingivitis and others - Gingival diseases modified by medications o Drug-induced gingival enlargements o Drug-influenced gingivitis, for example, oral contraceptives - Gingival diseases modified by malnutrition, for example, vitamin C, and others b. Non plaque-induced gingival lesions - Specific bacterial origin: Neisseria gonorrhoeae, Treponema pallidum, Streptococcal species, and others - Viral origin: herpes virus infections and others - Fungal origin: Candida species infections, linear gingival erythema, histoplasmosis, and others - Genetic origin: hereditary gingival fibromatosis, and others - Manifestations of systemic conditions o Mucocutaneous disorders: lichen planus, pemphigus, pemphigoid, etc.

3.

4.

5. 6.

7. 8.

o Allergic reactions ,,, Dental restorative materials - mercury, acrylic, etc. ,,, Reactions attributed to toothpastes/ dentifrices, mouth rinses/washes, chewing gum additives, food, and additives ,,, Others - Traumatic lesions - chemical, physical, thermal, factitious, iatrogenic, accidental - Foreign body reactions - Not otherwise specified Chronic periodontitis (based on clinical, radiographic, historical, and laboratory characteristics) a. Localized ( 30% of sites involved) Both groups can be categorized as - slight: 1-2 mm CAL; moderate: 3-4 mm CAL; severe: ?.5 mm CAL. It is prevalent in adults but can occur in children; amount of destruction consistent with local factors; variable microbial pattern; subgingival calculus present; slow to moderate rate of progression; possibly modified by systemic diseases, local factors, and environmental factors. Aggressive periodontitis (otherwise clinically healthy individuals, rapid attachment and bone loss, not consistent with local deposits, familial aggregation) a. Localized (circumpubertal onset; first molar or incisor has proximal attachment loss; robust serum antibody response to infective agents) b. Generalized (affects under 30 years of age; generalized proximal attachment loss; poor serum antibody response to infective agents; episodic nature of periodontal disease) Periodontitis as a manifestation of systemic diseases a. Associated with hematologic disorders - Acquired neutropenia, leukemia, and others b. Associated with genetic disorders - LAD deficiency syndromes, and others Necrotizing periodontal diseases - NUG, NUP Abscesses of the periodontium a. Gingival, periodontal, pericoronal Periodontitis associated with endodontic lesions combined periodontal-endodontic lesions Developmental or acquired deformities and conditions a. Localized tooth-related factors that modify or predispose to plaque-induced gingival diseases/ periodontitis - Tooth anatomic factors - Dental restorations/ appliances - Root fractures - Cervical root resorption and cemental tears

CHAPTER 6 CLASSIFICATION OF PERIODONTAL DISEASES

b. Mucogingival deformities and conditions around teeth - Gingival/ soft tissues recession on facial/lingual/ interproximal/ papillary - Lack of keratinized gingiva - Decreased vestibular depth - Aberrant frenum/ muscle position c. Gingival excess Pseudopockets, inconsistent gingival margin, excessive gingival display, gingival enlargement, abnormal color d. Mucogingival deformities and conditions on edentulous ridges - Vertical and/ or horizontal ridges deficiency - Lack of gingival/keratinized tissue - Gingival/ soft tissue enlargement - Aberrant frenum/ muscle position - Decreased vestibular depth - Abnormal color - Occlusal trauma o Primary occlusal trauma o Secondary occlusal trauma

Classification of Periodontal Diseases and Conditions 1. Gingival diseases a. Plaque-induced gingival diseases b. Non plaque-induced gingival diseases 2. Chronic periodontitis a. Localized b. Generalized 3. Aggressive periodontitis a. Localized b. Generalized 4. Periodontitis as a manifestation of systemic diseases 5. Necrotizing periodontal diseases a. Necrotizing ulcerative gingivitis b. Necrotizing ulcerative periodontitis 6. Abscesses of the periodontium a. Gingival abscess b. Periodontal abscess c. Pericoronal abscess 7. Periodontitis associated with endodontic lesions a. Endodontic-periodontal lesion b. Periodontal-endodontic lesion c. Combined lesion 8. Developmental or acquired deformities and conditions a. Localized tooth-related factors that predispose to plaque-induced gingival diseases or periodontitis b. Mucogingival deformities and conditions around teeth c. Mucogingival deformities and conditions on edentulous ridges d. Occlusal trauma.

39

CHANGES MADE IN THE CLASSIFICATION 1. Addition of a section on gingival diseases 2. Replacement of "adult periodontitis" with "chronic periodontitis" 3. Replacement of "early onset periodontitis" with "aggressive periodontitis" 4. Elimination of separate disease category for refractory periodontitis 5. Clarification of the designation "periodontitis as a manifestation of systemic diseases" 6. Replacement of "necrotizing ulcerative periodontitis" with "necrotizing periodontal diseases" 7. Addition of a category on "periodontal abscess" 8. Addition of a category on "periodontal-endodontic lesions" 9. Addition of a category on "developmental or acquired deformities and conditions."

FUTURE CHALLENGES IN CLASSIFYING PERIODONTAL DISEASES As we enter the postgenomic era with our increased understanding of the bacteria associated with periodontal infections and the genetic factors controlling host responses to these infections, it would seem that a more mechanistic or etiologic classification could be devised. One of the problems associated with any attempt at subclassifying chronic periodontitis or other forms of period on ti tis is that these infections are polymicrobial and polygenic. The clinical expression of these diseases is altered by important environmental and host-modifying conditions. It may eventually be possible to subclassify the multiple forms of chronic periodontitis into discrete microorganism/host genetic polymorphism groups such as Group A - set no. 1 of microorganisms + set no. 1 of genetic polymorphisms Group B - set no. 2 of microorganisms + set no. 2 of genetic polymorphisms Group C - set no. 3 of microorganisms + set no. 3 of genetic polymorphisms Group D - set no. 4 of microorganisms + set no. 4 of genetic polymorphisms.

CONCLUSION All classification systems have inconsistencies or inaccuracies. The present effort is no exception. With our increased understanding of the bacterial association with

40

SECTION II CLASSIFICATION AND EPIDEMIOLOGY OF PERIODONTAL DISEASES

periodontal infection and genetic factors controlling these infections, it would seem that a new mechanistic or etiologic classification could be devised. Thus, it is anticipated

that as we learn more about the etiology and pathogenesis of periodontal diseases, future revisions to the classification will be needed.

KEY POINTS • Classification is the systematic collection of data or knowledge and its arrangement in sequential manner in order to facilitate its understanding or knowledge. 1. Uses of classification are identification of the etiology and understanding of the pathology, diagnosis, prognosis, treatment planning, and facilitation of communication among the clinicians, researchers,

QUESTIONS 1. Classify periodontitis. Add a note on refractory

periodontitis. 2. Explain the 1999 classification of gingival diseases.

Suggested readings 1. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999;4 (1):1-6.

educators, students, epidemiologists, and public health workers. 2. Classification systems are placed into three paradigms: a. Clinical characteristic paradigm (1870-1920) b. Classical pathology paradigm (1920-1970) c. Infection/host response paradigm (1970 to present).

2. Armitage GC. Classifying periodontal diseases - a long standing dilemma. Periodontal 2000 2002;30:9-23. 3. Genco RJ. Classification and clinical and radiographic features of periodontal disease. In: Contemporary Periodontics. St. Louis: Mosby; 1990. p. 63-81. 4. Grant DA, Sternn IB, Listgarten MA. Periodontics. VI ed. St. Louis: Mosby; 1988. 5. Newman MG, Takei H, Klokkevold PR, Carranza FA. Clinical Periodontology. 9th ed. Philadelphia: Saunders; 2006.

CHAPTER

7 Epidemiology of Periodontal Diseases CHAPTER OVERVIEW Dental index or indices are devices to find out the incidence, prevalence, and severity of the disease, based on which preventive programs can be adopted. An index is an expression of the clinical observation as a numerical value.

It helps to describe the status of the individual or group with respect to a condition being measured. An index score can be more consistent and less subjective than a word description of that condition.

BASIC CONSIDERATIONS

• Point prevalence • Period prevalence

Index

Point prevalence of a disease is defined as the number of all current cases (old and new) of a disease at one point in time in relation to a defined population. It is calculated as follows:

An index has been defined as a numerical value describing the relative status of a population on a graduated scale with definite upper and lower limits, which is designed to permit and facilitate comparison with other populations classified by the same criteria and methods (A.L. Russel). Epidemiologic indices are attempts to quantitate clinical conditions on a graduated scale, thereby facilitating comparison among populations examined by the same criteria and methods (Irving Glickman).

number of all current cases ( old and new) of a specified disease existing at a given . point in time Point prevalence=-----=--------- x 100 estimated population at the same point in time Period prevalence measures the frequency of all current cases (old and new) existing during a defined period of time expressed in relation to a defined population. It is calculated as follows:

Incidence Incidence rate is defined as "the number of new cases occurring in a defined population during a specified period of time." It is calculated as follows:

number of all existing cases ( old and new) of a specified disease existing at a given . d period of time interval P eno preva 1 ence = x 100 estimated midinterval population at risk

number of new cases of specific .d disease during a given time period InCI ence = --------='---=-----=----x 1 00 population at risk during that period

Prevalence Disease prevalence refers specifically to all current cases (old and new) existing at a given point in time, or over a period of time, in a given population. Prevalence is of two types:

Epidemiology It is the study of the distribution and determinants of health-related states or events in specified populations

41

42

SECTION II CLASSIFICATION AND EPIDEMIOLOGY OF PERIODONTAL DISEASES

and the application of this study to the control of health problems (John M. Last, 1988).

Epidemic It is the unusual occurrence in a community or region of a disease, specific health-related behavior, or other healthrelated events clearly in excess of expected occurrence.

Endemic It is the constant presence of a disease or infectious agent within a given geographic area or population group, without importation from outside, e.g., common cold.

The "D" (decayed) portion of DMFT index best exemplifies a disease index. The indices measuring gingival/ sulcular bleeding are essentially symptom indices. The "F" (filled) portion of DMFT index best exemplifies treatment index. 4. Dental indices can also be classified under special categories as simple or cumulative: a. Simple index It is the index that measures the presence or absence of the condition, e.g., an index that would measure the presence or absence of dental plaque. b. Cumulative index It is the index that measures all the evidences of a condition, past and present, e.g., DMF index for dental caries.

Pandemic It is an epidemic usually affecting a large proportion of the population, occurring over a wide geographic area such as section of a nation, the entire nation, a continent, or the world.

CLASSIFICATION OF INDICES 1. Based on the direction in which their scores can

fluctuate, indices are classified as either reversible or irreversible. a. Reversible index It is the index that measures conditions that can be changed. Reversible index scores can increase or decrease on subsequent examination, e.g., indices that measure plaque or gingivitis. b. Irreversible index It is the index that measures conditions that will not regress. Irreversible index scores, once established, cannot decrease in value on subsequent examination, e.g., indices that measure dental caries. 2. Depending on the extent to which areas of oral cavity are measured, indices are classified into full mouth or simplified. a. Full mouth index These indices measure the patient's entire periodontium or dentition, e.g., Russell Periodontal Index. b. Simplified index These indices measure only a representative sample of the dental apparatus, e.g., Oral Hygiene Index Simplified. 3. Indices may be classified under certain general categories according to the entity which they measure, such as a. Disease index b. Symptom index c. Treatment index

PUBLIC HEALTH SIGNIFICANCE OF PERIODONTAL DISEASE Although many oral diseases are not always lifethreatening, they are important public health problems because of their high prevalence, public demand, and their impact on individuals and society in terms of pain, discomfort, social and functional limitations and handicap, and the effect on the quality of life. In addition, the financial impact on the individual and community is very high. Periodontal disease affects people physically and psychologically and influences how they enjoy life, look, speak, chew, taste food, and socialize as well as their feelings of social well-being. They experience pain, discomfort, disfigurement, acute and chronic infections, and eating and sleep disruption as well as higher risk of hospitalization and high treatment costs. The impact of oral diseases in pain, suffering, impaired function, and reduced quality of life is both extensive and expensive. Treatment is estimated to account for a considerable proportion of health costs in industrialized countries, and is beyond the resources of many developing countries. The fact that the cost of treating the disease is high because of the organization of dental care qualifies it as a dental public health problem.

INDICES USED IN PERIODONTICS Plaque Index (PU) (Silness and Loe, 1964) Purpose Its purpose is to assess the thickness of plaque only at the gingival surface of the tooth.

43

CHAPTER 7 EPIDEMIOLOGY OF PERIODONTAL DISEASES

TABLE 7.1

Scoring Criteria (Silness and Loe)

Recording Format for Plaque Index

Score

Criteria

0

No plaque in the gingival area

1

A film of plaque adhering to the free gingival margin and adjacent area of tooth. The plaque may be recognized only after application of disclosing agent or by running a probe across the tooth surface

D 1\-1

Moderate accumulation of soft deposits within the gingival pocket, on the gingival margin, and/ or on adjacent tooth surface, which can be seen by the naked eye

2

3

; 111

IIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIII

17

16

47 46

: 1111

15

I4

IJ

12

11

45 44 4J 42 41

21

JI

22 2J

24

25 26

32 33 J4 35

2

J6 J

I I I I I I I• 1 I •1• I 1 • I 1 •• 1 I •1 I I 111 I I• 1 I I 1• I I

Abundance of soft matter within the gingival pocket and/ or on the gingival margin and adjacent tooth surface

-r"

Exccllcnt/Good/Fair/l'oor

Instruments Instruments used are mouth mirror, dental explorer, and light source. Selection of Teeth Teeth are selected on the following basis (Table 7.1): • Whole mouth basis - entire dentition • Selected mouth basis - 16, 12, 24, 36, 32, 44 Surfaces Examined • Only plaque at the cervical third of the tooth is evaluated with no attention to plaque that has extended to middle or incisal thirds. • Four gingival areas of the tooth: • Distofacial • Facial • Mesiofacial • Lingual Calculation Plaque Index of each tooth = total score of each tooth 4

total of Plaque Index of each tooth Plaque Index for individual= number of teeth examined

Interpretation Excellent: 0 Good: 0.1-0.9 Fair: 1.0-1.9 Poor: 2.0-3.0

Turesky-Gilmore-Glickman Modification of the Quigley-Hein Plaque Index (G. Quigley and J. Hein, 1962) The Quigley-Hein Plaque Index was modified by S. Turesky, N.D. Gilmore, and I. Glickman in 1970. Purpose Quigley and Hein proposed a system for scoring dental plaque. This was modified by Turesky et al. to more explicitly describe mild to moderate plaque deposits. Instruments Instruments used are mouth mirror and disclosing agent. Selection of Teeth Plaque is assessed on the labial, buccal, and lingual surfaces of all of the teeth using a disclosing agent. Procedure Scoring by the Turesky modification (Table 7.2): 1. All teeth are assessed except third molars (maximum

number 28). 2. A staining solution is used to show plaque deposits (Quigley and Turesky used basic fuchsin). 3. Both the facial and lingual surfaces are examined (maximum number 56). 4. A score is assigned to each facial and lingual nonrestored surface. The modification of the Quigley and Hein Plaque Index redefined the scores of the gingival third area, emphasizing the differences in plaque accumulation in the gingival third of the tooth.

44

SECTION II CLASSIFICATION AND EPIDEMIOLOGY OF PERIODONTAL DISEASES

TABLE 7 .2

0

No plaque

1

Separate flecks of plaque at the cervical margin of the tooth

2

A thin continuous band of plaque (up to 1 mm) at the cervical margin of the tooth

The gingival measurement is made with the probe held parallel to the long axis of the tooth and equidistant from the mesial and distal surfaces. The probe should be simultaneously in contact with calculus and the incisal edge of the tooth. The distal measurement is made by holding the probe diagonally so that the tip is in contact with the distal aspect of the tooth and the opposite end (the portion toward the shank of the probe) is bisecting the mesial incisal angle of the tooth. The mesial measurement is made by holding the probe diagonally so that the tip is in contact with the mesial aspect of the tooth and the opposite end (the portion toward the shank of the probe) is bisecting the distal incisal angle of the tooth. The smallest unit to score the presence of calculus is 0.5mm.

3

A band of plaque wider than 1 mm covering less than one-third of the crown of the tooth

Calculation

4

Plaque covering at least one-third but less than two-thirds of the crown of the tooth

The measurement may be calculated and expressed in three different ways:

5

Plaque covering two-thirds or more of the crown of the tooth

• per measurement score; • per tooth score; • per subject score.

Scoring Criteria (Turesky)

Score

Plaque scoring system for Quigley and Hein

0

No plaque

1

Flecks of stain at the gingival margin

2

Definite line of plaque at the gingival margin

3

Gingival third of surface

4

Two-thirds of surface

5

Greater than two-thirds of surface Modified plaque scoring system of Turesky et al.

Calculation total score Pl aque score=-----------number of surfaces examined

The "measurement score" is the total of all of the scores divided by the number of measurements made. The "tooth score" is the total of all of the scores divided by the number of teeth scored. The "subject score" is simply the total of all of the scores (subjects with fewer than six teeth are excluded).

Interpretation • A score of O or 1 is considered low. • A score of 2 or more is considered high.

Probe Method of Calculus Assessment (A.R. Volpe, J .H. Manhold, and S.P. Hazen, 1965)

Papillary Marginal Attachment Index (Maury Massler and I. Schour, 1944) Purpose

Purpose

It is used to quantitatively record the readily observable inflammatory conditions of the gingivae.

It is used to assess the quantity of calculus, especially in longitudinal studies.

Instruments

Instruments

Instruments used are mouth mirror and periodontal probe.

Instruments used are mouth mirror and periodontal probe.

Selection of Scoring Surface

Areas Examined The lingual surfaces of the six mandibular anterior teeth are examined for the presence of calculus.

Procedure A mouth mirror is used to visualize and air is used to dry the teeth prior to examination. Measurements are made in three planes: gingival, distal, and mesial.

A gingival unit was divided into three component parts (Table 7.3): 1. Papillary gingivae (P) - the gingival portion between

the teeth 2. Marginal gingivae (M)- the marginal collar surrounding the teeth 3. Attached gingivae (A) - the gingival portion overlying the bony alveolar process

45

CHAPTER 7 EPIDEMIOLOGY OF PERIODONTAL DISEASES

TABLE 7 .3 Score

Calculation

Scoring Criteria

Plaque scoring system

PMA score= P+M+A

p 0

Normal, no inflammation

Gingival Index (H. Loe and P. Silness, 1963)

1+

Mild papillary engorgement, slight increase in size

Purpose

2+

Obvious increase in size, hemorrhage on pressure

3+

Excessive increase in size, spontaneous hemorrhage

It is used to assess the severity of gingivitis based on color, consistency, and bleeding on probing.

4+

Necrotic papilla

Instruments

5+

Atrophy and loss of papilla due to inflammation

Instruments used are mouth mirror, blunt probe, and light source.

0

Normal, no inflammation

Selection of Teeth

1+

Engorgement, slight increase in size, no bleeding

2+

Obvious engorgement, hemorrhage on pressure

3+

Swollen collar, spontaneous hemorrhage, beginning infiltration into attached gingiva

4+

Necrotic gingivitis

5+

Recession of the free marginal gingiva below the CEJ

0

Normal, pale rose, stippled

1+

Slight engorgement with loss of stippling

2+

Obvious engorgement of attached gingiva with marked increase in redness and pocket formation

3+

Advanced periodontitis, deep pockets evident

M

Teeth are selected on the following basis (Table 7.4): • Whole mouth basis - entire dentition • Selected mouth basis - 16, 12, 24, 36, 32, 44

Surfaces Examined

A

• The tissues surrounding each tooth are divided into four gingival scoring areas of the tooth: • • • •

Calculation

Procedure The presence or absence of inflammation on each gingival unit is recorded. Usually only the facial surfaces of incisors, canines, and premolars are examined.

. . d f . d' .d G mg1va 1 1n ex or m 1v1 ua 1 =

14

13

12

11

21

22

23

24

total of Gingival Index of each tooth number of teeth examined

where

Recording Format 15

Distofacial papilla Facial margin Mesiofacial papilla Lingual margin

. . d f h h total score of each tooth G mg1va 1 1 n ex o eac toot = ---------4

25

p

Interpretation Mild gingivitis: 0.1-1.0 Moderate gingivitis: 1.1-2.0 Severe gingivitis: 2.1-3.0

M

A

TABLE 7.4 p

Score

Criteria

0

Absence of inflammation/normal gingiva

1

Mild inflammation - slight change in color, slight edema; no bleeding on probing

2

Moderate inflammation - glazing, redness, edema, and hypertrophy; bleeding on probing

3

Severe inflammation; marked redness and hypertrophy, ulceration; tendency to spontaneous bleeding

M

A 45

44

43

42

41

31

32

33

34

35

Scoring Criteria (Loe and Silness)

46

SECTION II CLASSIFICATION AND EPIDEMIOLOGY OF PERIODONTAL DISEASES

Recording Format for Gingival Index

Surfaces Examined

D M

: 1111111111111111111111111111111111111111111 17

16

ll

1•

13

12

II

•7

50%

Bone loss

FIGURE 19.5

Advanced gingivitis/periodontitis.

• The advanced lesion represents frank and overt periodontitis. • Continued loss of collagen subjacent to the pocket epithelium with fibrosis at more distant sites can be seen. • The junctional epithelium migrates apically from the cementoenamel junction. • The junctional epithelium is changed and is no longer closely attached to the tooth surface. The pocket epithelium that has now formed has a heavy leukocyte infiltrate, predominantly of polymorphonuclear leukocytes (PMNs), which eventually migrate across the epithelium into the gingival pocket. The pocket epithelium is more permeable to the passage of substances into and out of the underlying connective tissues and is temporarily ulcerated in many places. • Alveolar bone loss occurs. • There are widespread manifestations of inflammatory and immunopathological tissue reactions. • Plasma cells predominate in the lesion, although lymphocytes and macrophages are also present.

CH A PT ER 19 G IN G IV A L IN FLA M M ATIO N

• The lesion is no longer localized; it may extend apically, as well as laterally, to form a variably broad band around the necks and roots of the teeth.

165

• The highly organized fiber bundles of the marginal gingiva lose their characteristic orientation and architecture.

KEY POINTS • Gingivitis or the inflammation of gingiva is the most common form of gingival diseases. • Pristine gingiva, normal gingiva that is free from "significant" accumulation of inflammatory cells, histologically may be described as pristine gingiva or a state of superhealth. • Page and Schroeder in 1976 classified the progression of gingival and periodontal inflammation on the basis of clinical and histopathological evidence. They divided the progressing lesion into (i) Stage I gingivitis or the initial lesion, (ii) Stage II gingivitis or the early lesion, (iii) Stage III gingivitis or the established lesion, and (iv) Stage IV gingivitis or the advanced lesion.

QUESTIONS 1. Enumerate the stages of gingivitis. 2. Discuss the established lesion in gingivitis. 3. Discuss the early lesion in gingivitis.

Suggested readings 1. Lindhe J, Lang NP. Clinical and Implant Dentistry. 5th ed. Copenhagen: Blackwell Munksgaard; 2008.

• The initial response of the gingiva is also called subclinical gingivitis. • In Stage I, the lymphocytes are almost exclusively T cells. • Collagen-fiber content of the affected tissue is reduced by about 70% in Stage II. This alteration, which occurs at an early stage of the disease, especially affects the dentogingival and circular fiber groups that normally support the junctional epithelium. • Stage IV gingivitis, the advanced lesion, is also known as the phase of periodontal breakdown. Here, there is persistence of features described for the established lesion but there is extension of the lesion into the alveolar bone and periodontal ligament.

2. Newman MG, Takei H, Carranza FA. Clinical Periodontology. 10th ed. St. Louis: Saunders; 2006. 3. Page RC, Schroeder HE. Pathogenesis of chronic inflammatory periodontal disease - a summary of current work. Lab Invest 1976;33:235-49. 4. Page RC, Kenneth SK. Pathogenesis of human periodontitis - an introduction. Periodontal 2000 1997;14:9-ll. 5. Rose LF, Mealey BL, Genco R. Periodontal Medicine, Surgery and Implants. 1st ed. St. Louis: Elsevier; 2000.

CH A P T E R

20 Clinical Features of Gingivitis CHAPTER OVERVIEW Inflammatory and immune reactions to microbial plaque are the predominant features of gingivitis and periodontitis. The inflammatory reaction is visible both microscopically and clinically in the affected periodontium and represents the host response to the plaque microbiota and its product. The clinical signs of inflammation in the gingival tissue reflect

Gingivitis is often associated with the following: 1. Presence of dental plaque 2. Signs and symptoms confined to the gingiva

3. Clinical signs of inflammation - enlarged due to edema or fibrosis, color transition to red or bluish red, and bleeding on probing 4. No loss of attachment 5. Reversibility of the lesion by removing the etiology

CORRELATION OF CLINICAL AND MICROSCOPIC FEATURES IN HEALTH AND GINGIVITIS Color The normal color of the gingiva (Fig. 20.1) is described as coral pink or salmon pink. The factors determining the color of gingiva are 1. Vascular supply 2. The thickness and degree of keratinization of the

epithelium 3. Melanin pigmentation Alveolar mucosa is thinner and nonkeratinized, has no rete pegs, and has a high vascularity that gives it a red, smooth, and shiny appearance. It can be clearly distinguished from the coral pink-colored gingiva. Inflamed gingival tissues can exhibit a wide range of color changes (Table 20.1). Most of the changes, how-

the classic signs of inflammation - rubor (redness), tumor (swelling), calor (warmth), and dolor (pain). These signs may be readily apparent to the dentist, but the threshold for discomfort is not commonly reached by patients with plaqueassociated gingivitis, in general, infected sites with one or more of the four common clinical signs of inflammation.

ever, are various hues of red. The best way to detect inflammatory color change is to compare the color of the gingival margin with the color of the adjacent alveolar mucosa. Systemic causes for color changes can be endogenous or exogenous (Table 20.2): 1. Localized pigmentation: Amalgam tattoo, graphite

tattoo, or other tattoos, nevus, melanotic macules, malignant melanoma, and Kaposi sarcoma 2. Multiple or generalized pigmentation (Fig. 20.2): a. Genetics: Idiopathic melanin pigmentation (racial or physiologic pigmentation) and Peutz-Jeghers syndrome b. Drugs: Smoking, betel, antimalarials, antimicrobials, minocycline, amiodarone, chlorpromazine, adrenocorticotropic hormone (ACTH), zidovudine, ketoconazole, methyldopa, busulfan, menthol, contraceptive pills, and heavy metal exposure (gold, bismuth, mercury, silver, lead, copper) c. Endocrine: Addison disease, Albright syndrome, pregnancy, and hyperthyroidism d. Postinflammatory: Periodontal disease and postsurgical gingival repigmentation e. Others: Hemochromatosis, generalized neurofibromatosis, incontinentia pigmenti, Whipple disease, Wilson disease, Gaucher disease, human immunodeficiency virus (HIV) disease, thalassemia, pigmented gingival cyst, and nutritional deficiencies

166

C H A PT ER 20 C LIN IC A L FEATU R ES O F G IN G IV IT IS

FIGURE 20.1

TABLE 20.1

Normal healthy gingiva.

FIGURE 20.2 Generalized pigmentation.

Color Changes in Inflamed Gingival Tissues

Acute

Chronic (Fig. 20.2)

Is red because of increased vascularity in the inflamed site and due to decrease in the degree of keratinization. It can also change to pale pink due to decreased vascularity, increased fibrosis, and increased keratinization. It can become dull gray due to tissue necrosis

Bluish hue is seen in the gingiva, which is present due to venous stasis

TABLE 20.2

167

Endogenous and Exogenous Causes for Color Changes

Endogenous pigmentation

Exogenous pigmentation

Iron, bilirubin, melanin, and bile pigments • Hemochromatosis: iron deposition; blue gray pigmentation • Jaundice: bile pigments; yellowish color • Melanin: physiologic; in certain ethnic groups such as Africans

From atmospheric irritants, e.g., coal and metal dust, coloring agents added in foods, tobacco, and amalgam tattoo

Pathological: Addison disease, Peutz-Jeghers syndrome, Albright syndrome (polyostotic fibrous dysplasia), von Recklinghausen disease (neurofibromatosis)

Heavy metals such as bismuth, mercury, lead, and silver produce a line in the marginal gingiva or are seen as patches in the attached gingiva Metallic pigmentation: only in areas of gingival inflammation; systematically absorbed metal sulfides get precipitated in the perivascular area in the subepithelial connective tissue. This happens due to increased vessel permeability seen in inflammation

Melanin Melanin, a nonhemoglobin-derived brown pigment, is the most common of the endogenous pigments and is produced by melanocytes present in the basal layer of the epithelium. Melanin accumulates in the cytoplasm, and the melanosome is transformed into a structureless particle no longer capable of melanogenesis. The number of melanocytes in the mucosa corresponds numerically to that of skin; however, in the mucosa their activity is reduced. Various stimuli can result in an increased production of melanin at the level of mucosa including trauma, hormones, radiation, and medications.

The gingivae are the most frequently pigmented intraoral tissues. Microscopically, melanoblasts are normally present in the basal layers of the lamina propria. The most common location is the attached gingiva (27.5%) followed in decreasing order by the papillary gingiva, the marginal gingiva, and the alveolar mucosa. The total number of melanophores in the attached gingiva is approximately 16 times greater than that in the free gingiva. The prevalence of gingival pigmentation was higher on the labial part of the gingiva than on the buccal and palatal/lingual parts of the arches. The shade of pigment was classified as very dark brown to black, brown, and light brown-yellow. Melanin pigmentation of the oral tissues usually does

168

SECTION IV PERIODONTAL PATHOLOGY

• Idiopathic thrombocytopenic purpura and coagulation disorders - hemophilia and Christmas disease Clinical Significance Objective signs offer the best diagnostic methods of disease severity. In this case, bleeding on probing is an objective method for examining gingival connective tissue inflammation. Ulceration of the periodontal pocket wall epithelium causes bleeding, but bleeding in and of itself is not diagnostic for a specific form of disease.

Size

FIGURE 20.3 Bleeding on probing.

not present a medical problem, but patients complain of black gums.

Bleeding on Probing The first clinical sign of gingivitis is bleeding subsequent to careful probing (Fig. 20.3). A blunt periodontal probe is inserted at the bottom of the gingival pocket and is moved gently along the lateral wall of gingiva. If bleeding is provoked by this instrumentation, the site is considered inflamed. Causes • Gingivitis Poor oral hygiene Inadequate plaque removal Calculus accumulation • Periodontitis (advanced forms of gingivitis) • Anticoagulants such as coumarin and heparin • Self-inflicted oral trauma, such as toothbrush abrasion and improper flossing • Infection, which can be either tooth- or gum-related • Vitamin C deficiency • Vitamin K deficiency • Hormonal changes during pregnancy • Chemical irritants such as aspirin • Leukemia • Placement of new dentures leading to denture sores/ irritations TABLE 20.3

The sum total bulk of all cellular and extracellular components comprises the size of gingiva. Gingival swelling or edema is a clinical feature of the inflamed gingival tissues. Edematous gingival enlargement is caused by accumulation of fluids in the inflamed connective tissue. The fluid is primarily serum that has emerged from the blood vessels with increased permeability because of local inflammation. Recognition of gingival edema is easy when it is marked. But in the early stages this edema is confined to the marginal gingiva and involves changes in the contour, shape, surface texture, and consistency.

Contour and Shape The normal contour of gingiva is scalloped and knife edged (Table 20.3). Morphology of the teeth and embrasures, arch position, alignment in the arch, and the location of the proximal contact determine the shape and contour of the gingiva. This knife-edged margin is lost in gingivitis. McCall festoons and Stillman cleft were earlier considered to be due to trauma from occlusion but presently they are considered to represent the changes seen in inflammation of marginal gingiva.

Consistency Normal consistency of gingiva is firm and resilient (Table 20.4). Collagen in the underlying lamina propria and its continuation with the mucoperiosteum along with the gingival group of fibers give gingiva its firmness and resiliency.

Contour Changes During Gingival Inflammation

Gingivitis

ANUG (Fig. 20.4)

Stillman cleft

McCall festoons

The margins become round, rolled, and blunt, and the adjacent tissues are somewhat enlarged and puffy

Reverse contour is seen when there is loss of the interdental papilla as in ANUG

Is a narrow, triangular-shaped gingival recession, which exposes cementum as the recession progresses apically

They are rolled, thickened margins of gingiva seen near canine when recession progresses till the mucogingival junction

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FIGURE 20.4 Necrotizing ulcerative gingivitis. FIGURE 20.5 TABLE 20.4

Generalized recession in lower anterior teeth.

Changes in Consistency During Gingival

Inflammation Acute gingivitis

Chronic gingivitis

It is seen as soft and edematous (destructive), i.e., infiltration by inflammatory fluid and degeneration of connective tissue

It is fibrotic because of fibrosis and epithelial proliferation associated with long-standing inflammation

The consistency of gingiva is checked using the back side of a periodontal probe and gently applying pressure in the surface of gingiva. Recession is the apical shift in the position of gingiva exposing the root surface (Fig. 20.5). • Actual position is the level of epithelial attachment. • Apparent position is the level of crest of marginal gingiva (Table 20.5).

Surface Texture Attached gingiva shows small depressions on the surface. The depressions named stippling give the appearance of orange peel (Fig. 20.6). Surface texture is checked by drying the gingiva with a piece of gauze. The changes in the surface texture during gingival inflammation is described in Table 20.5.

FIGURE 20.6 Stippling seen on attached gingiva.

cavity, the margin and sulcus are at the tip of the crown; as eruption progresses, they are seen closer to the root. Actual position of gingiva is more important than the apparent position as it shows the loss of attachment that has taken place. At certain times this denuded root surface is hidden by the inflamed pocket wall. This part of root surface is known as hidden recession and the part that is visible clinically is called visible recession.

Position of Gingiva

Etiology of Gingival Recession

It refers to the level at which the gingival margin is attached to the tooth. When the tooth erupts into the oral

• Faulty brushing technique: It includes scrub technique of brushing or use of a hard -bristle toothbrush.

TABLE 20.5

Surface Texture Changes During Gingival Inflammation

Acute gingivitis

Chronic desquamative gingivitis

Drug-induced gingival enlargement

The surface texture becomes smooth and shiny due to infiltration by inflammatory fluid. This appearance is also seen in atrophic gingivitis

Peeling of the epithelial surface occurs

If the reparative changes predominate, the surface becomes firm and nodular

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TABLE 20.6

Classification of Gingivitis

Acute gingivitis

Subacute gingivitis

Recurrent gingivitis

Chronic gingivitis

Acute gingivitis is of sudden onset and short duration and can be painful

A less severe phase of the acute condition has been termed subacute

Recurrent gingivitis reappears after having been eliminated by treatment or disappearing spontaneously

Chronic gingivitis is slow in onset and of long duration, and is painless, unless complicated by acute or subacute exacerbations

• Tooth malposition: Susceptibility to recession is influenced by position of the tooth in the arch, the root bone angle, and mesiodistal curvature of the tooth surface. In rotated, tilted, and labially placed teeth, the labial plate is thinned and reduced. • Gingival ablation: It refers to pressure from soft tissues such as the tongue and buccal mucosa. • Gingival inflammation causes gingival recession. • Iatrogenic causes: These include clasp of ill-fitting denture, overhang restoration, and margins of restoration violating the biologic width. • Abnormal frenum attachment causes gingival recession.

FIGURE 20.7

Chronic generalized marginal gingivitis.

FIGURE 20.8

Chronic generalized diffuse gingivitis.

Clinical Significance Gingival recession can lead to dentinal hypersensitivity, root caries, abrasion, or erosion of cementum and aesthetics.

Gingival Exudate Presence of gingival exudation signifies the presence of disease activity or phase of active destruction taking in the tissue. It does not indicate the depth of the pocket or severity of the lesion. It is checked by placing the ball of the index finger along the lateral aspect of marginal gingiva with a rolling motion toward the crown.

Classification (Table 20.6) Course, Duration, and Distribution • Localized gingivitis is confined to the gingiva of a single tooth or group of teeth. • Generalized gingivitis involves the entire mouth.

• Marginal gingivitis (Fig. 20.7) involves the gingival margin and may include a portion of the contiguous attached gingiva. • Papillary gingivitis involves the interdental papillae and often extends into the adjacent portion of the gingival margin. • Diffuse gingivitis affects the gingival margin, the attached gingiva, and the interdental papillae (Fig. 20.8).

KEY POINTS • The normal color of the gingiva is described as coral pink or salmon pink. The factors determining the color of gingiva are vascular supply, the thickness and degree of keratinization of the epithelium, and melanin pigmentation. • Bluish hue is seen in the chronic gingivitis, which is present due to venous stasis.

• Pathological endogenous pigmentation can be due to Addison disease, Peutz-Jeghers syndrome, Albright syndrome (polyostotic fibrous dysplasia), and von Recklinghausen disease (neurofibromatosis). • Drugs that cause gingival pigmentation are antimalarials, antimicrobials, minocycline, amiodarone, chlorpromazine, ACTH, zidovudine, ketoconazole, methyldopa, busulfan,

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KEY POINTS (cont'd) menthol, contraceptive pills, and heavy metal exposure (gold, bismuth, mercury, silver, lead, copper). • The first clinical sign of gingivitis is bleeding subsequent to careful probing. • Reverse contour is seen when there is loss of the interdental papilla as in acute necrotizing ulcerative gingivitis (ANUG). • McCall festoons and Stillman cleft were earlier considered to be due to trauma from occlusion, but presently

QUESTIONS 1. Define gingival recession. Enumerate the causes. 2. Describe the clinical and microscopic features of

chronic gingivitis. 3. Define gingival bleeding. What are the causes? 4. What are McCall festoons and Stillman clefts?

they are considered to represent the changes seen in inflammation of marginal gingiva. • Actual position of the gingiva is the level of epithelial attachment. • Apparent position of gingiva is the level of crest of marginal gingiva. • Gingival recession can lead to dentinal hypersensitivity, root caries, abrasion, or erosion of cementum and aesthetics.

Suggested readings 1. Hassel MH. Periodontal tissue structure and function. Periodontology 2000;3:1993. 2. Lindhe J. Clinical Periodontology and Implant Dentistry. 5th ed. Copenhagen: Blackwell Munksgaard; 2008. 3. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Carranza's Clinical Periodontology. 10th ed. St. Louis: Saunders; 2006. 4. Rose LF, Mealey BL, Genco R. Periodontal Medicine, Surgery and [mp/ants. 1st ed. St. Louis: Elsevier; 2004.

CHAPTER

21 Gingival Enlargement CHAPTER OVERVIEW Alteration in the size of the gingiva is one of the clinical features of periodontal disease. Increase in the size of gingiva, which is termed gingival enlargement or gingival overgrowth, is a common clinical sign of gingival disease and a matter of great clinical concern. Increase in the size alters the physiologic contour of the gingiva, creates areas of plaque accumulation, interferes

CLASSIFICATION Depending on the involvement of components of gingiva and its distribution, gingival enlargement is designated as follows: • Localized: Limited to the gingiva adjacent to a single tooth or group of teeth • Generalized: Involving the gingiva throughout the mouth • Marginal: Confined to the marginal gingiva • Papillary: Confined to the interdental papilla • Diffuse: Involving the marginal and attached gingiva as well as papillae • Discrete: An isolated sessile or pedunculated tumorlike enlargement

with regular oral hygiene procedures, and creates aesthetic problems; in severe cases, it interferes with mastication and phonation. In children, gingival enlargements may impede the eruption of teeth. Enlargement may involve one or more components of the gingiva. It may be confined to a limited area or may involve all the teeth.

Increase in the size of the gingiva is a result of interaction between host and a variety of other factors. Depending on etiology and pathogenesis, gingival enlargements are classified as follows: 1. Inflammatory enlargement

2.

3.

4.

The degree of gingival enlargement can be scored as follows: • Grade 0: No signs of gingival enlargement • Grade I: Enlargement confined to interdental papilla • Grade II: Enlargement involving papilla and marginal gingiva • Grade III: Enlargement covering three quarters or more of the crown

5.

6.

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a. Chronic b. Acute Fibrotic enlargement a. Drug-induced enlargement b. Hereditary or idiopathic gingival enlargement Combined enlargement (inflammatory+ fibrotic) Enlargements associated with systemic conditions a. Conditioned enlargement - Pregnancy - Vitamin C deficiency - Diabetes-induced gingival enlargement - Nonspecific conditioned enlargement (granuloma pyogenicum) b. Systemic diseases causing gingival enlargement - Leukemia - Granulomatous diseases (Wegener granulomatosis, sarcoidosis, and so on) Neoplastic enlargement (gingival tumors) a. Benign tumors b. Malignant tumors False enlargements

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INFLAMMATORY GINGIVAL ENLARGEMENT Inflammatory gingival enlargement is the most common type of overgrowth, which manifests because of the increase in volume of gingival tissue in response to local microbial irritation. Inflammatory enlargement may be acute or chronic.

Chronic Inflammatory Gingival Enlargement It results from long-standing local irritation of gingiva. Overgrowth can be localized, generalized, or discrete. Clinical Features Early signs of overgrowth are seen in the interdental area as the ballooning of papilla and thickening of gingival margin, giving gingiva a characteristic lifesaver-like form around the teeth (Fig. 21.1). It may be localized to a few teeth or may be generalized. It is a painless and slowly progressing lesion, which bleeds on provocation. Discrete lesions may be sessile or pedunculated and arise from interdental papilla, marginal gingiva, or attached gingiva. Occasionally painful ulceration may occur in the fold between the growth and gingiva. Etiology Bacterial plaque is the prime cause of inflammatory gingival enlargement. Factors that favor plaque accumulation and retention, such as calculus, carious lesion and overhanging margins of dental restorations, improperly designed prosthesis, malaligned teeth, and orthodontic appliances, indirectly contribute to the pathogenesis of chronic inflammatory overgrowth. Drying of gingiva due to mouth breathing also is reported to cause chronic inflammatory gingival overgrowth.

FIGURE 21.1 Chronic inflammatory gingival overgrowth.

Histologic Features Lesions that are soft and friable are smooth and shiny on the surface. They have a preponderance of inflammatory cells and fluid with vascular engorgement, new capillary formation, and associated degenerative changes. Lesions that are firm and resilient have a greater fibrotic component and abundance of fibroblasts and collagen fibers. The epithelium is thickened with acanthosis. Treatment Treatment consists of patient education, instructions in home care and meticulous plaque control regimen, removal of dental deposits (plaque, calculus, stains), and correction of plaque retention factors. If overgrowth persists, surgical correction of gingival contour is necessary by either gingivectomy or flap surgery.

Acute Inflammatory Gingival Enlargement Gingival Abscess A gingival abscess is a purulent infection localized to the marginal gingiva. CLINICAL FEATURES

An abscess is a suppurative inflammation associated with pyogenic organisms. It is a localized, painful, rapidly expanding lesion that is usually of sudden onset and lies confined to interdental papilla or marginal gingiva. Enlargement appears smooth and shiny (Fig. 21.2). Teeth adjacent to it become sensitive to percussion. Abscess usually is pointed and ruptures in 1 or 2 days to drain on its own. ETIOLOGY

Acute gingival overgrowth results by traumatic interruption of the epithelial surface and implantation of bacteria in gingival tissue usually from toothbrush bristles,

FIGURE 21.2 relation to 15.

Gingival enlargement associated with abscess in

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seeds, cornhusks, apple core, fish bone, dental procedures, and trauma from occlusion.

TABLE 21. 1

HISTOLOGIC FEATURES

Anticonvulsants

Drugs Associated with Gingival Enlargement

Group of drug

Agent

Lesion shows purulent focus in the connective tissue surrounded by diffuse infiltration of acute inflammatory cells, edematous tissue, and vascular engorgement. Surface epithelium shows intracellular and extracellular edema, leukocytic infiltration, and ulceration.

Hydantoins

Ethotoin Mephenytoin Phenytoin

Succinimides

Ethosuximide Methsuximide Phensuximide

TREATMENT

Valproic acid

Valproic acid

Cause of the injury should be eliminated. Warm saline mouth rinses may be advised along with systemic antibiotics, but if there is a periodontal pocket, it should be treated with curettage or gingivectomy.

Immunosuppressant Calcium channel blockers Dihydropyridine derivatives

Amlodipine Felodipine Nicardipine Nifedipine Nimodipine Nisoldipine Nitrendipine

Benzothiazine derivatives

Diltiazem

Phenylalkylamine derivatives

Verapamil

FIBROTIC GINGIVAL ENLARGEMENT Noninflammatory fibrous gingival overgrowth is believed to be the result of genetic predisposition or an adverse effect of a drug. A large number of drugs and genetic disorders are associated with occurrence of gingival overgrowth in susceptible individuals. They may be

Cyclosporine Tacrolimus

1. Drug-induced gingival enlargements 2. Idiopathic gingival enlargements

Drug-Induced Gingival Enlargement The drugs that are reported to be associated with gingival overgrowth are anticonvulsants, immunosuppressants, and calcium channel blockers (Table 21.1). Despite their pharmacological diversity all these drugs have a similar mechanism of action at cellular level. They are known to inhibit intracellular calcium ion influx. Therefore, the action of these drugs on calcium and sodium influx may prove to be the key to understand why these groups of dissimilar drugs have a common side effect on a secondary target tissue such as gingiva in susceptible individuals. The clinical features of gingival overgrowth induced by these agents and even the histologic appearance are reported to have common characteristics such as increase in extracellular ground substance, number of fibroblasts, and acanthosis of epithelium.

acid, phenobarbitone, primidone, mephenytoin, and ethosuximide. Valproic acid has a broad spectrum of antiepileptic activity compared with other anticonvulsants. It is established that sodium valproate carries a relatively low risk for developing gingival overgrowth and may be a reasonable treatment alternative to phenytoin. The clinical and microscopic features of valproic acid-induced gingival overgrowth are comparable to phenytoin-induced overgrowth. CLINICAL FEATURES

Phenytoin-induced gingival overgrowth is characterized by initial enlargement of the interdental papillae, and

Anticonvulsants Phenytoin has been used to control seizure disorders in patients with epilepsy and in management of neuralgias. Patients have been reported to develop gingival enlargement in the first 6 months of intake of the drug (Fig. 21.3). Since then numerous investigations have been conducted to study its effect on gingival tissue. Anticonvulsant drugs that have been associated with gingival overgrowth, other than phenytoin, are valproic

FIGURE 21.3

Phenytoin-induced gingival overgrowth.

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is less frequently accompanied by increased thickening of the marginal tissue. Affected tissues typically present a granular or pebbly surface, with the enlarged papilla extending facially and/ or lingually covering the tooth surfaces. Affected papillae may become enlarged such that they contact resulting in the clinical appearance of pseudoclefts. The facial gingiva of the anterior sextants is more commonly affected.

Immunosuppressants Cyclosporine is a widely used immunosuppressant drug to prevent rejection of organ transplant and for treating a variety of autoimmune diseases. Its exact mechanism of action is not clearly understood, but it appears to selectively and reversibly inhibit helper T cells and NK cells, which play a role in cellular and humoral immune responses. Inhibition of these cells is believed to be based on the blocking of calcium channels of the cells. Prevalence of cyclosporine-induced gingival overgrowth varies from 25 to 70% according to various investigators and it seems to be dose dependent. Dosage more than 50 mg/ day has been reported to induce gingival overgrowth. Overgrowth is greater in patients who are medicated with cyclosporine along with calcium channel blockers. Cyclosporine-associated overgrowth resembles phenytoin-induced gingival overgrowth; however, it is reported to be more vascularized than phenytoin-induced gingival overgrowth. Tacrolimus is another immunosuppressant drug that is used because of its less severe side effects and is also reported to cause gingival overgrowth. However, the enlargement is less when compared with cyclosporine.

Calcium Channel Blockers These are drugs used in the management of a variety of cardiovascular conditions including hypertension, angina pectoris, coronary artery spasm, and cardiac arrhythmias. They act like phenytoin and cyclosporine by inhibiting calcium ion influx across the cell membrane of the heart and smooth muscle cells, blocking its cellular mobilization of calcium. Calcium channel blockers associated with gingival overgrowth are amlodipine, felodipine, nicardipine, nifedipine, nimodipine, nisoldipine, and nitrendipine. Nifedipine is most commonly used and widely studied drug. The incidence of overgrowth in patients on nifedipine is about 20%. Nifedipine-induced gingival overgrowth is reported to be dose dependent, and dose reduction is shown to have reduced the volume of gingival overgrowth (Fig. 21.4). Clinical and histologic features of nifedipine-induced gingival overgrowth are comparable to those of phenytoin-induced gingival overgrowth.

FIGURE 21.4

Nifedipine-induced gingival overgrowth.

Other Drugs The ability of sex hormones to induce hyperplastic gingivitis has been well established. Association of gingival overgrowth with the use of contraceptives (estrogen/ progesterone) has been reported. There is an interesting case report implicating antibiotic erythromycin with gingival overgrowth. HISTOLOGIC FEATURES

Histologic features of all drug-induced gingival overgrowths are comparable. They consist of connective tissue with an overlying multilayered parakeratinized epithelium with varying thickness and long rete pegs. Lamina propria is characterized by proliferation of fibroblasts and an increase in collagen formation accompanied by an increase in noncollagenous matrix proteins. Focal accumulation of infiltrative inflammatory cells within connective tissue has been demonstrated. PATHOGENESIS

Pathogenesis of drug-induced gingival overgrowth has not been clearly understood. It has been suggested that gingival overgrowth could possibly be due to inhibition of apoptosis. Calcium ion plays a significant role in apoptosis. Despite their pharmacological diversity all three types of drugs have a similar mechanism of action at cellular level, where they inhibit intracellular calcium ion influx. Available evidence suggests the direct effect of the involved drug on specific subpopulation of fibroblasts in gingival connective tissue, intercellular calcium metabolism and exchange, molecular mechanisms [various cytokines such as epidermal growth factor (EGF), platelet-derived growth factor (PDGF)], inactivation of collagenases, genetic predisposition, and inflammation induced by plaque. These dynamic variables may act on gingival milieu individually or collectively to alter the hemostatic state resulting in gingival overgrowth.

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PREVENTION AND TREATMENT

Significant correlations between the occurrence and/ or severity of drug-induced gingival overgrowth and the presence of plaque and plaque retentive factors have been reported. Hence, patients should be encouraged to perform meticulous oral hygiene and frequent recall visits for removal of local deposits and professional assistance. Physician should be advised to refer the patient scheduled to receive a drug associated with gingival overgrowth to a dentist for baseline evaluation and control of local causal factors. If gingival overgrowth occurs, the causative drug may be substituted if possible with a suitable noninductive drug in consultation with the patient's physician. Despite drug substitution if the growth persists, surgical intervention may be necessary. If small areas without attachment loss and adequate keratinized gingiva are involved, gingivectomy is indicated. Whenever larger areas are involved with attachment and bone loss, flap surgery may be performed. Placement of pressure appliances after surgical correction of overgrowth to prevent or reduce tendency for recurrence has been reported. Management of drug-induced gingival overgrowth should be a team approach involving the physician, the dentist, and the health care professionals, for prevention, early diagnosis, and effective treatment.

Idiopathic Gingival Enlargement It is a fibrotic gingival enlargement of rare occurrence and unknown etiology. It is called by synonyms such as hereditary gingival fibromatosis, hereditary gingival hyperplasia, elephantiasis gingivae, fibromatosis gingivae, idiopathic fibromatosis, and diffuse fibroma. Unlike drug-induced gingival overgrowth, idiopathic overgrowth is diffuse and involves marginal papillary and attached gingiva (Fig. 21.5).

Gradual enlargement of entire gingiva is noticed during the eruption of permanent dentition, but occasionally it may also be observed during eruption of deciduous dentition. Overgrowth may interfere with eruption of teeth. It has been observed on both facial and oral aspects of maxilla and mandible. Involvement may be localized or generalized and limited to either of the jaws. In severe cases overgrowth covers the entire crown, disfigures the patient's face, and interferes with speech and mastication. The gingiva is of normal color, firm, and of leathery consistency. Surface of the gingiva demonstrates pronounced stippling, giving it a characteristic pebbled appearance. It is painless without bleeding unless secondarily infected. The overgrowth regresses and disappears after extraction of teeth. There is a case report of occurrence of overgrowth in an edentulous jaw under a complete denture. Gingival enlargements have been associated with various syndromes. A genetic abnormality may be implicated with this type of presentation (Table 21.2).

Etiology Etiology is not clearly understood. Some cases have a hereditary basis, but the genetic mechanisms involved are not completely understood. A study of several families found the mode of inheritance to be autosomal recessive and some autosomal dominant. In some cases family history of inheritance cannot be established. The enlargement usually begins with eruption of primary or secondary dentition and regresses after extraction of teeth, suggesting the possibility of plaque being the initiating factor. It may be accompanied by other systemic disorders and syndromes.

Histologic Features Microscopic appearance of idiopathic gingival overgrowth is comparable to drug-induced overgrowth. There is acanthosis of epithelium with deep rete pegs. There is an increase in the amount of connective tissue, which is relatively avascular. Inflammatory changes are seen immediately in crevicular lining.

Treatment Surgical removal of enlarged tissue is necessary for functional and aesthetic reasons. This could be accomplished by gingivectomy or flap operation. Recurrence of the overgrowth, to a greater extent, depends on the patient's oral hygiene status. With meticulous oral hygiene maintenance, recurrence can be rendered very slow.

COMBINED ENLARGEMENT

FIGURE 21.5

Idiopathic gingival enlargement.

Fibrotic gingival enlargement produces conditions favorable for plaque accumulation by interfering with effective oral hygiene measures. This leads to secondary

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TABLE 21.2

177

Syndromes Associated with Fibrotic Gingival Enlargement

Name of syndrome

Characteristic features

Rutherford syndrome

Gingival fibromatosis with hypertrichosis, epilepsy, and mental retardation

Zimmermann-Laband syndrome

Gingival fibromatosis with defects of ears, nose, bones, nails, and terminal phalanges

Tuberous sclerosis

Gingival fibromatosis with triad of epilepsy, mental deficeincy and cutaneous angiofibromas

Murray-Puretic-Drescher syndrome

Gingival fibromatosis with multiple fibromas of head trunk, and extremities

Cross syndrome

Gingival and alveolar enlargement, microphthalmia, cloudy corneas, hypopigmentation, and athetosis

Ramon syndrome

Gingival fibromatosis, hypertrichosis, cherubism, mental retardation, and epilepsy: characteristic perivascular fibrosis in gingival biopsy specimens

inflammatory changes in existing fibrotic enlargements. This type of enlargement is known as combined enlargement. In such enlargement, the removal of local factors results in reduction in size by eliminating inflammatory component. However, the fibrotic component persists and requires surgical correction.

PREGNANCY,ASSOCIATED GINGIVAL ENLARGEMENT

inflamed gingiva forms discrete tumor-like mass referred to as pregnancy tumors.

Histologic Features It is nonspecific, vascularizing, and proliferating inflammation. There is marked inflammatory cell infiltration with edema and degeneration of the epithelium and connective tissue. The epithelium is hyperplastic with accentuated rete pegs, decreased keratinization, and extracellular edema. Connective tissues show engorged capillaries and infiltration of leukocytes.

Clinical Features The prevalence of pregnancy gingivitis ranges from 35 to 100%. The gingiva shows increased levels of inflammation often characterized by edema, color and contour change, and propensity to bleed on gentle stimulation. The marginal and interdental gingivae are enlarged (Fig. 21.6). They pit on pressure, appear smooth and shiny, and are soft and pliable giving the gingiva raspberry-like appearance. The gingival changes are usually painless unless complicated by acute infection. In some cases the

VITAMIN C DEFICIENCY The oral effects of vitamin C deficiency in humans occur chiefly in the gingival and periodontal tissues. The interdental and marginal gingiva appears bright red with a swollen, smooth, shiny surface. The gingiva becomes boggy, ulcerates, and bleeds. Sometimes, the enlarged tissue may cover the clinical crowns of the teeth. In severe chronic cases there is loss of bone and associated tooth mobility.

PYOGENIC GRANULOMA

FIGURE 21.6 Pregnancy-associated gingival enlargement.

It is considered a nonspecific conditioned gingival enlargement. It appears as a localized mass of highly vascularized granulation tissue arising as an exaggerated response to plaque. It commonly arises from the proximal gingival tissues and has pedunculated base (Fig. 21.7). The surface of the lesion may show ulceration. Bleeding on mastication or even spontaneously may be present. Treatment includes excision of the lesion accompanied by thorough debridement of the tooth surface.

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originate in the interdental papilla. The lesions are deep red, nodular, and friable and have been referred to as strawberry gingivitis because of their resemblance to overripe strawberries.

Histologic Features The tissue shows vasculitis with zone of necrosis and fibrinoid deposits in a background of granulomatous changes. Eosinophils and multinucleated giant cells are also seen. FIGURE 21.7 Pyogenic granuloma.

LEUKEMIA Leukemia is a disorder of the leukocytes which demonstrates an abnormality in formation as well as functioning of the leukocytes. It manifests itself in the gingiva as an associated gingival enlargement in acute myeloid leukemia.

Clinical Features Oral lesions occur in both acute and chronic forms of all types of leukemia: myeloid, lymphoid, and monocytic types. In both acute and chronic leukemias, the gingival overgrowth occurs in 10% of the patients. The gingival hyperplasia, which may be one of the most constant features of the disease expected in edentulous patients, is usually generalized and varies in severity. The gingiva is boggy, edematous, and deep red. The gingival enlargement is due to the leukemic cell infiltration in areas of mild chronic irritation. In severe cases the teeth may be completely hidden.

SARCOIDOSIS It is a chronic disease affecting the skin, mucosal surfaces, salivary glands, lungs, and occasionally other organs. It consists of multiple noncaseating epithelioid granulomas and fibrosis of adjacent tissue.

Clinical Features Oral lesions appear as diffuse submucosal enlargements or focal firm nodules. Lesions are usually symptomless.

Histologic Features Tissue contains multiple granulomas in a nodular pattern, each consisting of an accumulation of epithelial cells, macrophages, and multinucleated giant cells. The periphery of each granuloma is composed of cellular fibrous connective tissue.

BENIGN LESIONS OF GINGIVA

Histologic Features

Focal Fibrous Hyperplasia (Irritation Fibroma)

Biopsy of enlarged gingivae will disclose the presence of leukemic infiltrate. It is differentiated from inflammatory gingival hyperplasia by the presence of mononuclear blast cells that show cytologic atypia.

Focal fibrous hyperplasia is most often encountered in adults and is primarily located on the gingiva. It is a nodular lesion and usually has a dome-like growth with a smooth surface of normal color. Surface hyperkeratosis is sometimes encountered. It is a slowly progressing lesion and may remain of same size for many years. It is sometimes referred to as peripheral fibroma.

WEGENER GRANULOMATOSIS

Histologic Features Wegener granulomatosis is an uncommon disease consisting of an inflammatory granulomatous process characterized by severe vasculitis and necrosis involving the respiratory system and kidneys. The head and neck are involved in 90% of cases and oral lesions are 2-5%.

The surface epithelium may be intact, exhibit hyperorthokeratosis, or show foci of ulceration. This epithelium overlies an underlying mass of dense fibrous connective tissue composed of significant amount of soft mature collagen in a scar-like pattern.

Clinical Features

Peripheral Ossifying Fibroma

The oral lesions are most commonly described as granulomatous hyperplastic gingivitis that appears to

It is a gingival nodule consisting of a reactive hyperplasia of connective tissue containing focal areas of bone.

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179

The peripheral ossifying fibroma is a reactive fibrous proliferation, probably of periosteal or periodontal ligament origin.

and rarely results in a cluster of lesions. The lesion is of the same color as the adjacent normal mucosa. It can occur in free or attached gingival or interdental papilla.

Clinical Features

Histologic Features

It emanates from the interdental papillae, although occasionally it is seen to arise from the facial/lingual attached gingiva. The mass originates from within the periodontal ligament. The overlying mucosa may be smooth and of normal coloration, or there may be foci of surface ulceration.

Lesions are often small with the epithelial lining of two to five cells in thickness. They often exhibit neural thickening. Sometimes clear cells may be seen.

Histologic Features Within the connective tissue are diffuse sheets of fibroblasts with plump monomorphic nuclei. The overall picture is one of hypercellularity with hyalinized collagenous component. In focal areas, osteoid deposits can be identified. Rarely mature trabeculae of bone are seen.

Peripheral Giant Cell Granuloma The peripheral giant cell granuloma is a hyperplastic reaction of the gingival connective tissue in which the histiocytic and endothelial cellular components predominate.

Clinical Features Peripheral giant cell granuloma is found in all age groups with peak incidence in adults around 30 years of age. It is common in females and equally distributed between maxilla and mandible. It is most commonly found anterior to the molars. Lesions begin as a reddish or purplish dome-shaped swelling of the interdental papilla or alveolar ridge. Larger lesions usually encircle one or more teeth, often involving the periodontal ligament. These lesions produce loosening and movement of the teeth.

MALIGNANT LESIONS OF GINGIVA Squamous Cell Carcinoma Squamous cell carcinoma is defined as a malignant neoplasm that is derived from squamous epithelium. It is the most common malignant neoplasm of the oral cavity representing 90% of the oral cancers. Lesions of the gingival and alveolar ridges represent 4-6% of the intraoral carcinoma. Mandible is affected more than the maxilla and most of the lesions are present in posterior areas. Carcinoma of the gingiva is usually manifested as an area of ulceration. The growth may appear exophytic. It may or may not be painful. The attached gingiva is more commonly involved than the free gingiva. Metastasis occurs in the submandibular or cervical lymph nodes.

Nodular Melanoma It is a form of malignant melanoma occurring in the skin and occasionally the mucosa. It appears as a raised mass with a limited radial growth phase and quickly invades, and metastasized lesion consists of a combination of pink, red, brown, and black nodules, which may be ulcerated.

Histologic Features

Histologic Features

Microscopic appearance reveals a nodular arrangement of giant cell tissue separated by fibrous septa. The giant cell tissue consists of a mixture of mononuclear giant cells with background of red blood cells (RBCs). Capillary vessels and sinusoidal spaces are usually present. Heavy deposits of hemosiderin are common.

Connective tissue is densely packed with tumor cells, which may be epithelioid, spindle-shaped, or lymphocyte-like. Melanin deposition is seen among the cells.

Gingival Cyst Gingival cyst develops in the gingival soft tissues outside bone and is derived from the cell rests of the dental lamina.

Kaposi Sarcoma It comprises macular or nodular vascular lesions occurring singularly or in multiples on the mucosa and skin of human immunodeficiency virus (HIV)-infected patients. The dominant locations within the oral cavity are the palate and maxillary gingiva. The lesions are reddish to deep purple and may be macular or nodular. Large gingival lesions often interfere with mastication.

Clinical Features Gingival cyst occurs as a firm, compressible, fluid-filled swelling on the facial gingiva usually in the anterior or premolar region. It usually develops as a solitary lesion

Histologic Features Lesions exhibit a proliferation of hyperchromatic spindle-shaped or oval endothelial cells arranged in an

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irregular vascular pattern. Extravasated red blood cell and hemosiderin deposits are characteristically present.

FALSE GINGIVAL ENLARGEMENT

a picture of gingival enlargement. Lesions of the bonelike central giant cell granuloma, Paget disease, and fibrous dysplasia cause expansion of the cortical plates of the jaws, which may give a false appearance of gingival enlargement. Unerupted teeth, usually in the children, appear as localized enlargements.

Gingival contour may be altered by changes in the underlying bone or the dental tissues. Lesions of the bone or the underlying dental hard tissues may clinically give

KEY POINTS • The increase in the size of gingiva is termed gingival enlargement or overgrowth. • Increase in the size alters the physiologic contour of the gingiva, creates areas of plaque accumulation, interferes with regular oral hygiene procedures, and leads to aesthetic problems. • An abscess is a suppurative inflammation associated with pyogenic organisms. • The drugs that are reported to be associated with gingival overgrowth are anticonvulsants, immunosuppressants, and calcium channel blockers.

QUESTIONS 1. Classify gingival enlargements. Describe the

2. 3. 4. 5. 6. 7.

etiopathogenesis of drug-induced gingival enlargements. Classify gingival enlargements. Add a note on conditioned gingival enlargements. Describe tuberous sclerosis. Describe false gingival enlargements. Describe pyogenic granuloma. Describe idiopathic gingival enlargements. Describe gingival enlargements associated with pregnancy.

• Anticonvulsant drugs that have been associated with gingival overgrowth are phenytoin, valproic acid, phenobarbitone, primidone, mephenytoin, and ethosuximide. • Synonyms of idiopathic gingival enlargement are hereditary gingival fibromatosis, hereditary gingival hyperplasia, elephantiasis gingivae, fibromatosis gingivae, idiopathic fibromatosis, and diffuse fibroma.

Suggested readings 1. Alderer MJ, Bartold PM. Genetic disorders of gingivae and periodontium. Periodontal 2000 1998;18:7-20. 2. Carranza FA, Hogan EL. Gingival enlargement. In: Carranza's Clinical Periodontology. 10th ed. Philadelphia: Elsevier; 2000: 373-390. 3. Carranza Jr FA. Gingival enlargement. Clinical Periodontology. 8th ed. Prism Books Pvt. Ltd. Bangalore, India; 1996. p. 233-49. 4. Hallmon WW, Rossmann JA. The role of drugs in the pathogenesis of gingival overgrowth - a collective review of current concepts. Periodontal 2000 1999;21:176-96.

CHAPTER

22 Acute Gingival Infections CHAPTER OVERVIEW Acute gingival infections are those that can occur with sudden onset and are of short duration. They can be also very painful. The conditions that can be included under

this category are necrotizing ulcerative gingivitis, primary herpetic gingivostomatitis, and pericoronitis.

NECROTIZING ULCERATIVE GINGIVITIS Definition

2.

Necrotizing ulcerative gingivitis (NUG) is a microbial disease of the gingiva in the context of an impaired host response, which is characterized by the death and sloughing of gingival tissues and presents with characteristic signs and symptoms. Previously known as acute necrotizing ulcerative gingivitis (ANUG), it was renamed as necrotizing ulcerative gingivitis. It is also known as trench mouth because of its prevalence in the soldiers working in trenches during World War I. Vincent first described the bacteria associated with these infections; hence, the disease was also known as Vincent angina.

Clinical Features It usually presents as an acute disease. Sometimes it resolves on its own and has milder symptoms leading to a subacute stage.

3.

4. 5.

the marginal gingiva (Fig. 22.1). There is a rare involvement of attached gingiva and oral mucosa. Gray, pseudomembranous slough covers the gingival craters. It is demarcated from the healthy gingiva by a pronounced linear erythema. Lesion may be denuded of the pseudomembrane, exposing red, shiny, and hemorrhagic gingival surface in some cases. The lesion will bleed on slight provocation. There is fetid odor and increased salivation.

Oral Symptoms 1. Patient complains of a constant radiating, gnawing pain that is aggravated by eating spicy and hot foods and on chewing. 2. There is metallic foul taste and a pasty saliva.

Extraoral and Systemic Signs and Symptoms 1. Local lymphadenopathy and mild fever are the

symptoms.

History Symptoms are sudden in onset. Patients may have an episode of debilitating disease or acute respiratory tract infection; also change in habits, continuous work without rest, poor nutrition, tobacco use, and psychological stress are frequent features.

These systemic signs and symptoms are more severe in children.

Oral Signs The following are the characteristic signs:

Clinical Course

1. There are punched-out, crater-like depressions

at the crest of the interdental papillae; it may involve

2. In severe cases, high fever, increased pulse rate,

leukocytosis, loss of appetite, and general lassitude are the most common systemic signs.

NUG may lead to necrotizing ulcerative periodontitis (NUP) if untreated.

181

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SECTION IV PERIODONTAL PATHOLOGY

Stage 5 Necrosis involving the buccal and labial mucosa (6%) Stage 6 Necrosis exposing alveolar bone (1 %) Stage 7 Necrosis perforating skin of the cheek (0%) (Fig. 22.2). According to Homing and Cohen, stage 1 is NUG, stage 2 may be either NUG or NUP because attachment loss may have occurred, stages 3 and 4 would correspond to NUP, stages 5 and 6 would correspond to necrotizing stomatitis, and stage 7 would be noma.

Relation of Bacteria to the Characteristic Lesion FIGURE 22.1

Necrotizing ulcerative gingivitis - crater-like depressions of the interdental papilla.

When there is bone loss along with NUG, the condition is termed NUP. Stages in progression of NUG are described by Pindborg et al. The lesion starts as 1. Erosion of the tip of the interdental papilla 2. The lesion involving all of the papilla and also involving

the marginal gingiva 3. The attached gingiva also involved 4. Exposure of the bone with complete loss of interdental

papilla, marginal gingiva, and the attached gingiva Homing and Cohen extended the staging as follows: Stage 1 Stage 2 Stage 3 Stage 4

Necrosis of the tip of the interdental papilla (93%) Necrosis of the entire papilla (19%) Necrosis of the marginal gingiva (21 %) Necrosis extending to the attached gingiva (1 %)

The characteristic lesion of NUG is studied under light microscopy and electron microscopy to study the relation of the bacteria in the lesion. Listgarten described the following zones in the lesion, which may overlap with one another; all zones may not be present at the same time: Zone 1 (bacterial zone): The most superficial zone composed of various types of bacteria and few spirochetes of the small, medium, and large types Zone 2 (neutrophil-rich zone): Contains numerous leukocytes, predominantly leukocytes with bacteria, including spirochetes of various types interspersed in between the leukocytes Zone 3 (necrotic zone): Consists of disintegrated tissue cells, fibrillar material, remnants of collagen fibers, and numerous intermediate and large types of spirochetes, with few other bacteria Zone 4 (zone of spirochetal infiltration): Consists of well-preserved tissue infiltrated with intermediate and large spirochetes, without other organisms

FIGURE 22.2 Necrosis perforating skin of the cheek (noma). (Courtesy: Nairobi Dental College, Kenya, East Africa.)

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C H A PT ER 22 A C U T E G IN G IV A L IN FEC T IO N S

Psychological stress and anxiety

i

Preexisting gingivitis

Increased corticosteroid production • . I mmunosuppression

i

Increased bacteria growth and invasion lmmunosuppression

+

Viral infection

Necrotizing ulcerative gingivitis HIV infection

+

Candida infection

l

Linear gingival erythema---..........

l

i eficient nutritioJ

Noma

,.

Viral infections rotozoal infections ~

Necrotizing ulcerative periodontitis

Necrotizing stomatitis

FIGURE 22.3

Necrotizing ulcerative gingivitis: possible etiologic mechanisms and sequelae.

Etiology (See Fig. 22.3) 1. Bacteria: Plaut (1894) and Vincent (1869) introduced

the concept that NUG is caused by specific bacteria: fusiform bacillus and spirochetal organism. Rosebury et al. described a fusospirochetal complex which consists of the following bacteria: Treponema microdentium, intermediate spirochetes, vibrios, fusiform bacilli, and filamentous organisms, and Borrelia sp. Loesche et al. described a constant flora composed of Prevotella intermedia, Fusobacterium, Treponema and Selenomonas spp., and Bacteroides melaninogenicus. Borrelia, gram-positive cocci, ~-hemolytic streptococci, and Candida albicans have been isolated from the lesions of human immunodefeciency virus (HIV)-associated NUG. 2. Predisposing factors: These can be divided into local predisposing factors and systemic predisposing factors. a. Local predisposing factors: These include preexisting gingivitis, deep periodontal pockets, and pericoronal flaps, which favor the proliferation of anaerobic fusiform bacilli and spirochetes. There is localized area of gingival trauma usually due to trauma by an opposing tooth in malocclusion. Frequency of NUG increases with smoking and tobacco use.

b. Systemic predisposing factors: Immunodeficient patients are most commonly affected by NUG. Immunodeficiency could be caused by nutritional deficiencies (e.g., vitamin C, vitamin B2), fatigue caused by chronic sleep deficiency, habits such as alcohol or drug abuse, and systemic diseases, e.g., diabetes. Other debilitating diseases that may predispose patients to NUG include chronic diseases such as syphilis and cancer, severe gastrointestinal disorder, leukemia, anemia, and acquired immunodeficiency syndrome (AIDS). c. Psychosomatic factors: The disease is often associated with stressful situations, e.g., school examination, induction into armed forces, patients with depression or other emotional disorders, and patients feeling inadequate at handling life situations. Psychiatric disturbances, e.g., trait anxiety, depression, psychopathic deviance, and the impact of negative life events, may lead to activation of the hypothalamicpituitary-adrenal axis. This activation elevates the level of serum and urine cortisol levels and in turn causes depression of lymphocyte and polymorphonuclear leukocyte (PMN) function, which facilitates bacterial invasion and damage. Increased cortisol level may also reduce gingival microcirculation and salivary flow and enhance nutrition of P. intermedia, which is a constant flora in NUG.

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Epidemiology and Prevalence

Diagnosis

NUG occurs at all ages, with the highest incidence reported between ages 20 and 30 years, and ages 15 and 20 years. It is not common in children in the United States, Canada, and Europe, but it has been reported in children from low socioeconomic groups in underdeveloped countries. In India, 54 and 58% of the patients in two studies were under age 10 years. In a random school population in Nigeria, NUG occurred in 11.3% of children between the ages of 2 and 6 years, and in a Nigerian hospital population, it was present in 23% of children under 10 years of age. It has been reported in several members of the same family in low socioeconomic groups. NUG is more common in children with Down syndrome than in other children with mental deficiencies. NUG is described as transmissible but not communicable or contagious disease. Communicability refers to the capacity for the maintenance of infection by natural modes of spread, such as direct contact through drinking water, food, and eating utensils; the airborne route; or by means of arthropod vectors. The disease is transmissible if it has the capacity for the maintenance of an infectious agent in successive passage through a susceptible animal host. A classical experiment by King: In an attempt to spread NUG among humans, King traumatized an area in his own gingiva and inoculated debris from a patient with severe case of NUG. There was no response until he fell ill shortly thereafter, and subsequent to his illness, he observed the characteristic lesion of NUG. This experiment demonstrated the role of predisposing factors along with the bacterial role.

Diagnosis is primarily made based on the clinical findings of gingival pain, ulceration, and bleeding. Microscopic examination of a bacterial smear or a biopsy specimen does not give specific picture. The histologic picture greatly resembles marginal gingivitis, periodontal pockets, pericoronitis, or primary herpetic gingivostomatitis. However, bacterial smears can be useful in differentiating from specific infections of the oral cavity, such as diphtheria, thrush, actinomycosis, and streptococcal stoma ti tis. Biopsy specimen can be used to differentiate NUG from specific infections such as tuberculosis or from neoplastic disease. NUG should be differentiated from other conditions such as herpetic gingivostomatitis, chronic periodontitis, and desquamative gingivitis (Tables 22.1 and 22.2).

Treatment Objectives of treatment of NUG include the following: 1. Resolution of acute phase 2. Treatment of the chronic disease either underlying the

acute involvement or elsewhere in the oral cavity 3. Alleviation of generalized symptoms such as fever and

malaise 4. Correction of the systemic etiologic factors, e.g.,

smoking and stress NUG is managed in a systematic sequence of three clinical visits. Vincent angina is a fusospirochetal infection of the oropharynx and throat. In this condition patients have a

TABLE 22.1

Differentiation Among Necrotizing Ulcerative Gingivitis, Chronic Desquamative Gingivitis, and Chronic Periodontal Disease

Necrotizing ulcerative gingivitis

Desquamative gingivitis

Chronic destructive periodontal disease

Bacterial smears show fusospirochetal complex

Bacterial smears reveal numerous epithelial cells, few bacterial forms

Bacterial smears are variable

Marginal gingiva affected

Diffuse involvement of marginal and attached gingiva and other areas of oral mucosa

Marginal gingiva affected

Acute history

Chronic history

Chronic history

Painful

May or may not be painful

Painless if uncomplicated

Pseudomembrane

Patchy desquamation of gingival epithelium

Generally no desquamation, but purulent material may appear from pockets

Papillary and marginal necrotic lesions

Papillae do not undergo necrosis

Papillae do not undergo noticeable necrosis

Affects adults of both genders, occasionally children

Affects adults, most often women

Generally in adults, occasionally in children

Characteristic fetid odor

None

Some odor present, but not strikingly fetid

C H A PT ER 22 A C U T E G IN G IV A L IN FEC T IO N S

TABLE 22.2

185

Differentiation Between Primary Herpetic Gingivostomatitis and Necrotizing Ulcerative Gingivitis Primary herpetic gingivostomatitis

Necrotizing ulcerative gingivitis

Etiology

The main causative organism is a virus (HSV-1)

The interaction between the host and bacteria (fusospirochetal complex)

Clinical features

Diffuse erythema and vesicular lesions, which rupture leaving slightly depressed area of ulcers Diffuse involvement of the gingiva

A necrotizing condition, with punched-out gingival margins covered by a pseudomembrane that peels off Involvement of marginal gingiva only

Age

Children and adolescents are more commonly affected

Occurrence in children is a rare case

Course

It has a course of 7-10 days

No definite duration

Immunity and contagion

Acute episodes lead to development of immunity and it is contagious

It does not develop an immunity and is not contagious

painful membranous ulceration of the throat with edema and hyperemic patches breaking down to form ulcers. First Visit • Complete evaluation of the patient regarding medical history and history of recent illness is done. • Dietary history, history of smoking, risk factors for HIV, and psychological factors are evaluated. • General examination should be performed to examine the vital signs and palpation of lymph nodes, especially submaxillary and submental nodes. Patient should also be examined for the skin lesions. • Treatment of the acute lesion is the primary goal. A topical anesthetic is applied to the affected area. The area has to be swabbed with moist cotton pellet to remove the pseudomembrane and nonattached surface debris. • Supragingival scaling with ultrasonic instruments can be performed. • Subgingival scaling and curettage is contraindicated because it may lead to extension of infection into the deeper tissues and can cause bacteremia. • Periodontal surgery and extractions are postponed until the patient is symptom free. The time period usually required is 4 weeks for a patient to be symptom free. • Patient has to be placed on the following antibiotic regimen: amoxicillin 500 mg orally every 6 h for 10 days; if allergic to amoxicillin, erythromycin 500 mg every 6 h or metronidazole 500 mg twice daily for 7 days can be prescribed. INSTRUCTIONS TO THE PATIENT a. Avoid tobacco, alcohol, and condiments. b. Patient is advised to rinse with 3% hydrogen peroxide mixed with equal amount of warm water every 2 h or twice daily with 0.2% chlorhexidine mouthwash. c. Avoid overzealous toothbrushing and use of interdental cleaning devices. An ultrasoft toothbrush may be used to clean the surface debris.

d. Patient is advised to get adequate rest and avoid strenuous exercise such as swimming and playing games, which requires a greater physical activity. e. An analgesic such as nonsteroidal anti-inflammatory drug can be prescribed for pain control. Second Visit • It is usually 1 or 2 days after the first visit. • Patient has to be examined for resolution of systemic signs and symptoms. • The area of the lesion will be erythematous but with marked reduction of necrotic tissue. Scaling may be reperformed. • Patient should follow the instructions as given during the first visit. Third Visit • After approximately 5 days of the second visit, patient is evaluated for the resolution of symptoms and complete protocol for the periodontal management is planned. • A hydrogen peroxide rinse will be discontinued; chlorhexidine mouthwash can be continued for 2 or 3 weeks. • A repeat scaling and root planing can be performed if required. • The patient should be reinstructed to follow the appropriate plaque control measures. • The patient is further counseled on nutrition, smoking cessation, and other habits associated with possible recurrence. • Appointments should be scheduled for the treatment of chronic gingivitis, periodontal pockets, and pericoronal flaps, as well as for the elimination of all local irritants including defective restorations. • Patient is reevaluated after 1 month for oral hygiene maintenance, health habits, psychosocial factors, and determination of the need for reconstructive or aesthetic surgery.

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SECTION IV PERIODONTAL PATHOLOGY

Additional Treatment Considerations CONTOURING OF GINGIVAL MARGIN

In cases of NUG when there is a severe loss of interdental gingiva as well as bone, healing results in the formation of shelf-like gingival margin, which is conducive to plaque accumulation and is an aesthetic concern too. This can be corrected by a periodontal plastic surgery or by reshaping the gingiva surgically so that the normal gingival architecture is restored. NUTRITIONAL SUPPLEMENTS

Nutritional supplements may be indicated along with local treatment in conditions where the patient is unable to take food due to pain. Patient may be given a standard multivitamin preparation along with therapeutic dose of vitamins B and C. PERSISTENT OR RECURRENT CASES

The following factors play a role in causing persistent disease or recurrence: 1. Diseases that resemble NUG, e.g., desquamative

diseases of the gingiva 2. Patients with underlying systemic diseases, e.g., HIV

infection 3. Inadequate local therapy and patient compliance

PRIMARY HERPETIC GINGIVOSTOMATITIS Primary herpetic gingivostomatitis is an infection of the oral cavity affecting mostly infants and children younger than 6 years of age. The causative organism is herpes simplex virus type 1 (HSV-1). Males and females are equally affected.

Clinical Features In most cases the primary infection is asymptomatic. After primary infection, the virus ascends through

FIGURE 22.4 Primary herpetic gingivostomatitis - vesicle formation and erythema seen on the gingiva.

sensory and autonomic nerves and persists as latent HSV in the neuronal ganglia that innervate the site. HSV-1 most commonly resides in the trigeminal ganglion. Secondary manifestation occurs as a result of various stimuli, such as sunlight, trauma, fever, and stress. Secondary manifestations include herpes labialis, herpetic stomatitis, herpetic genitalis, ocular herpes, and herpetic encephalitis. Secondary herpetic stomatitis can occur as a result of dental treatment. It presents as a characteristic vesicle at a site away from the site of treatment.

Oral Signs • It involves both the gingiva and the oral mucosa. In the initial stage, it is characterized by the presence of discrete, spherical gray vesicles on the gingiva, labial and buccal mucosa, soft palate, pharynx, sublingual mucosa, and the tongue. • After approximately 24 h, the vesicles rupture and form painful, small ulcers with a red, elevated, halo-like margin and a depressed, yellowish or grayish white central portion. The ulcers may occur in clusters or can be widely separated (Fig. 22.4).

Primary infecti_on by a virus

Virus ascends through sensory and autonomic nerves

Remains latent at trigeminal ganglion

L

Secondary manifestation

unlight Trauma Fever tress

187

C H A PT ER 22 A C U T E G IN G IV A L IN FEC T IO N S

• Occasionally primary herpetic gingivitis may occur without overt vesiculation. The clinical picture consists of diffuse erythematous, shiny discolouration and edematous enlargement of the gingiva with a tendency towards bleeding. • The lesion resolves on its own by 7-10 days. It heals without scarring.

TABLE 22.4 Differentiation Between Primary Herpetic Gingivostomatitis and Desquamative Gingivitis Primary herpetic gingivostomatitis

Desquamative gingivitis

Etiology

Viral

Bacterial forms

Sites involved

Diffuse involvement of gingiva without peeling Acute condition

Diffuse involvement of gingiva and varying degrees of peeling are seen Chronic condition

Oral Symptoms • Patient complains of soreness of mouth with difficulty in eating and drinking. • The lesions are painful and sensitive to touch, changes in temperature, and food and beverages, especially spicy foods and fruit juices and to the action of coarse foods. • Infants usually refuse to eat food due to pain. These oral signs and symptoms are accompanied by the following constitutional signs and symptoms: cervical adenitis, high-grade fever, and generalized malaise.

Diagnosis The diagnosis in most cases can be established by history and clinical examination. Confirmatory tests include virus culture and immunologic tests using monoclonal antibodies or DNA hybridization techniques.

Differential Diagnosis The lesion resembles the following conditions (Tables 22.3 and 22.4): • • • • • •

Necrotizing ulcerative gingivitis Desquamative gingivitis Recurrent aphthous stomatitis (RAS) Erythema multiforme Stevens-Johnson syndrome Bullous lichen planus

TABLE 22.3

Differentiation Between Primary Herpetic Gingivostomatitis and Recurrent Aphthous Stomatitis Primary herpetic gingivostomatitis

Recurrent aphthous stomatitis

Etiology

Viral etiology

Etiology is unknown; suspected immunopathologic mechanism

Sites involved

Diffuse erythematous involvement of the gingiva

No diffuse involvement of gingiva; isolated ulcers are seen

Healing

Lesion heals by scarring

Lesions less than 1 cm will heal without scarring

Other conditions resembling acute herpetic gingivostomatitis are • Erythema multiforme: It can be differentiated from primary herpetic gingivostomatitis as follows: It has extensive involvement of the tongue and skin lesions with large vesicles. Duration of erythema multiforme may be prolonged by more than a week. • Stevens-Johnson syndrome: It is a rare form of erythema multiforme with hemorrhagic vesicular lesions in the oral cavity, skin, and eyes. • Bullous lichen planus: Prolonged indefinite course of a disease Painful condition with large blisters on the tongue and cheeks, and ruptures resulting in ulceration Oral lesions coexistent with skin lesions

Treatment Previously treatment of acute herpetic gingivostomatitis consisted of only supportive care. Recently an antiviral therapy with 15 mg/kg of an acyclovir suspension given five times daily for 7 days has been implicated to reduce the course of disease. This antiviral therapy reduces symptoms such as fever, difficulty in eating, and also the appearance of new extraoral lesions. It is found to be effective only if the lesions are diagnosed within 3 days of onset. The patients reporting after 3 days of onset should be given a palliative care that includes • Removal of plaque and food debris • Administration of nonsteroidal anti-inflammatory drug (NSAID) to reduce fever and pain • Nutritional supplements or topical anesthetic before eating to aid in proper nutrition • Periodontal therapy postponed until the acute symptoms subside to prevent exacerbation Herpetic gingivostomatitis is contagious at certain stages such as when vesicles are present. Herpetic infection called herpetic whitlow, infection on the finger, can occur if a seronegative clinician becomes infected with a patient's herpetic lesions.

188

SECTION IV PERIODONTAL PATHOLOGY

PERICORONITIS It refers to the inflammation of the gingiva or a pericoronal flap of an incompletely erupted tooth. The most commonly involved tooth is the mandibular third molar. The major factor responsible for involvement of the mandibular third molar is the space between the erupting tooth and the overlying flap. The involvement of the mandibular third molar can be explained as given in Fig. 22.5.

Clinical Features • The pericoronal flap (Fig. 22.6) will be red and swollen with presence of exudate. • Patient complains of pain radiating to the ear, throat, and floor of the mouth. • Patient will be unable to open the jaws and will complain of foul taste. • Lymphadenitis may be present. • Systemic symptoms such as fever and malaise are also present.

22.6

Pericoronal flap in relation to third molar.

• Cellulitis • Ludwig angina

Treatment Treatment largely depends on the following factors:

Complications • Pericoronal abscess • Peritonsillar abscess Space between crown and pericoronal flap

J

Site for accumulation of food debris Area neglected by patients while brushing

i Area for bacterial colonization

i Inflammation and ulceration of the flap

i

Increased bulk of the flap due to inflammatory edema

i Exacerbation of inflammation and ulceration

FIGURE 22.5

FIGURE

Pericoronitis: involvement of mandibular third molar.

• Severity of inflammation • The systemic involvement • The possibility of retaining the tooth The acute pericoronitis is treated to relieve the acute symptoms that consist of the following: • Gentle irrigation of the area is performed with warm saline to remove debris and exudates. • Occlusion is evaluated to determine if an opposing tooth is occluding with the pericoronal flap. Occlusal adjustment is necessary in case of opposing tooth traumatizing the flap. • Antibiotics are administered in severe cases with involvement of lymph nodes. • Drainage can be established if the swelling is fluctuant by using a no. 15 blade. After resolution of the acute symptoms, the tooth should be evaluated for possibility of erupting to a functional position. If the tooth is to be retained, the pericoronal flap should be surgically excised using the periodontal knives. The surgical procedure to remove the operculum is called operculectomy (Fig. 22.7). The operculum can also be removed by electrosurgery. The removal of the flap should result in a site that can be easily maintained by the patient. To ensure this the flap covering the occlusal surface as well as the tissue distal to the tooth has to be removed.

C H A PT ER 22 A C U T E G IN G IV A L IN FEC T IO N S

FIGURE 22. 7

189

Operculectomy.

KEY POINTS • Necrotizing ulcerative gingivitis is a microbial disease of gingiva that can be attributed to various predisposing factors. • Primary herpetic gingivostomatitis is caused primarily by HSV-1 and it is a communicable disease.

QUESTIONS 1. Describe the clinical features of ANUG. 2. What are the acute gingival infections? Describe any

one in detail. 3. Discuss the management of ANUG. 4. What is pericoronitis? Discuss its management.

5. What are the clinical features of acute herpetic gingivostomatitis? 6. What are the complications of acute pericoronitis?

Suggested readings 1. Carranza Jr FA, Newman MG. Carranza's Clinical Periodontology. 8th ed. Philadelphia: Saunders; 1996.

• Pericoronitis is the inflammation of gingiva around an incompletely erupted tooth, which when untreated can lead to various complications.

2. Ellen RP, Galimanas VB. Spirochetes at the forefront of periodontal infections. Periodontal 2000 2005;38:13-32. 3. Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry. 5th ed. Oxford: Blackwell Munksgaard; 2006. 4. Newman MG, Takei HH, Klokevold PR, Carranza FA. Carranza's Clinical Periodontology. 10th ed. St. Louis: Elsevier; 2006. 5. Rivera-Hidalgo F, Stanford TW. Oral mucosa! lesions caused by infective microorganisms. Viruses and bacteria. Periodontal 2000. 1999;21:106-24. 6. Rowland RW. Necrotizing ulcerative gingivitis: abstract. Ann Periodontol 1999;4:65-73. 7. Seymour RA, Heasman PA, Macgregor IDM. Drugs, Diseases and the Periodontium. Oxford: Oxford University Press; 1992.

CHAPTER

23 Desquamative Gingivitis CHAPTER OVERVIEW Desquamative gingivitis is a clinical term to describe red, painful, glazed, and friable gingiva, which may be a manifestation of some mucocutaneous conditions such as lichen planus or the vesiculobullous disorders. It is important to be aware of this rare clinical entity so as to distinguish desquamative gingivitis from plaque-induced gingivitis, which is an extremely common condition. Chronic desquamative gingivitis was first recognized and reported in 1894 by Prinz. The term chronic desquamative gingivitis was coined in 1932 to describe a peculiar condition characterized by intense erythema, desquamation, and ulceration of the free and attached gingiva. Generally, lesions appear erythematous or ulcerative, but in some cases, hyperkeratotic. The condition was originally believed to represent a hormonally mediated disorder most commonly found in women. Subsequently improved diagnostic techniques have demonstrated that chronic gingival desquamation may be associated with a wide variety of diseases and disorders including vesiculoulcerative disorders and adverse reaction to medication. Approximately 75% of desquamative gingivitis (DG) cases have a dermatologic origin and are mainly associated with

mucous membrane pemphigoid (MMP), lichen planus (LP), and, to a lesser degree, pemphigus vulgaris (PV). However, chronic ulcerative stomatitis, bullous pemphigoid, linear IgA disease, lupus erythematosus, and dermatitis herpetiformis can also present as desquamative gingivitis. McCarthy et al suggested that desquamative gingivitis was not a specific disease entity but a gingival response associated with a variety of conditions. Difficulties are sometimes encountered in establishing a definitive diagnosis of desquamative gingival diseases. An effective diagnostic protocol can be established that will lead to correct identification of most oral diseases and disorders. This protocol includes a thorough medical and dental history, personal and family history of related diseases, a complete clinical oral examination, and, when indicated, the appropriate use of biopsies to perform histopathologic and direct immunofluorescence examination. Therefore, to properly diagnose the condition responsible for desquamative gingivitis, clinical examination coupled with a thorough medical history and routine histologic and immunofluorescence studies is required.

CLASSIFICATION OF DISEASES THAT CLINICALLY PRESENT AS DESQUAMATIVE GINGIVITIS • Derma tologic Lichen planus Mucous membrane pemphigoid Bullous pemphigoid Pemphigus vulgaris Chronic ulcerative stomatitis Linear IgA disease Lupus erythematosus • Allergic reaction

Dental restorative materials Food (reaction to oral hygiene products, chewing gum, food) Drug-induced mucocutaneous disorder • Traumatic lesions Physical injury Chemical injury Thermal injury • Miscellaneous conditions

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DERMATOLOGIC LESIONS Lichen Planus Lichen planus is the most common inflammatory mucocutaneous disease involving mucosa (oral cavity, genital tract, and skin), also manifesting on the gingiva. It is an immunologically mediated disorder in which host T lymphocytes play a major role. The prevalence of oral lichen planus in various populations has been found to be 0.1-4%. This disease may affect patients at any age, and has a female predilection in the ratio of 2:1. Clinical Features Oral lichen planus (OLP) presents in different forms of lesions: reticular, patch papular, atrophic, erosive, and bullous. The disease runs a chronic course with periods of quiescence and exacerbations. Any area of the oral mucosa may be affected by OLP, but the lesions often change in clinical type and extension over years. These changes are clinically indistinguishable from oral leukoplakia. More than 50% show skin-associated lesions. The most common forms are reticular and erosive. Reticular: The most characteristic clinical manifestation of the disease and the basis of clinical diagnosis are white papules and white striations that often form reticular patterns. They appear as striated, particularly reticular form, linear papular lesions whose edges have fine striae called the "Wickham striae." They form lacelike interlacing, or annular forms, usually bilaterally symmetrical, that commonly involve the cheek and tongue, but can occur anywhere. Erosive: These manifest as atrophic, erythematous, and ulcerated areas. Fine, white, radiating striations are seen bordering these zones. These lesions are sensitive to hot, acidic, and spicy food. Atrophic and ulcerative lesions are associated with moderate to severe pain, whereas papular, reticular lesions usually do not give rise to significant symptoms. Gingival lichen planus comprises 7-10% of oral lichen planus cases. Four patterns are seen: • Keratotic white lesions: Linear, papular, reticular, and plaque-like • Erosive/ulcerative: Hemorrhagic areas that can be focal or diffuse • Vesicular /bullous: Fluid-filled lesions that rupture and leave ulcerations on the gingiva • Atrophic: Epithelial thinning that results in erythema of gingiva (Fig. 23.1) Histologic Features 1. Microscopically, it shows hyperkeratosis, hydropic

degeneration of basal layer. 2. Rete ridges have "sawtooth configuration."

FIGURE 23.1

Lichen planus.

3. Dense "band-like" infiltrates, primarily of T lymphocytes, in the lamina propria are observed. 4. Colloid bodies (Civatte bodies) may be seen at the epithelium-connective tissue interface. A correlation between clinical, histopathologic, and immunofluorescence findings has to be made to arrive at a diagnosis of lichen planus. Diagnosis of oral lichen planus is direct in keratotic forms, and therefore biopsy should be obtained from these areas. But in ulcerative forms of lichen planus histopathologic diagnosis is difficult to make. Direct immunofluorescence shows linear deposits of fibrin in the basement membrane. Indirect immunofluorescence is negative. Immunohistochemical studies show higher T4/T8 ratio of lymphocytes in epithelium of lamina propria in lichenoid lesions. Differential Diagnosis • • • • • • • • • • • •

Lupus erythematosus Chronic ulcerative stomatitis Cicatricial pemphigoid Pemphigus vulgaris Linear IgA diseases Leukoplakia Electrogalvanic mucosal lesions Linea alba buccalis Leukoedema Ectopic geographic tongue Squamous cell carcinoma White sponge nevus

Treatment Keratotic lesions of oral lichen planus are asymptomatic and do not require any treatment. Patients need to be followed for any clinical change and erosive component every 6-12 months. The erosive, bullous, or ulcerative lesions of oral lichen planus can be treated with topical steroids such as 0.05%

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fluocinonide ointment three times daily. A gingival tray can also be used to deliver 0.05% clobetasol propionate with 100,000 IU /mL of nystatin in Orabase. However, 3-5 minutes application of this mixture daily appears to be effective in controlling erosive lichen planus. Intralesional injections of triamcinolone acetonide, 10-20 mg, also prove to be helpful. Short-term regimens of 40 mg of prednisone daily for 5 days followed by 10-20 mg daily for an additional 2 weeks have been used in more severe cases. Because of the potential side effects patients need to be monitored. A promising therapeutic agent tacrolimus 0.1 % twice daily is effective. Topical antifungal agents should be included in the symptomatic oral lichen planus therapy. Other modalities include retinoids, cyclosporine, hydroxychloroquine, azathioprine, and cyclophosphamide. Free gingival graft has also been used in a few cases.

Mucous Membrane Pemphigoid Mucous membrane pemphigoid, also known as cicatricial pemphigoid, is a group of putative autoimmune, chronic inflammatory, subepithelial blistering diseases predominantly affecting mucous membrane, with or without clinically observable scarring. It predominantly affects women in the fifth decade of life. Although rare, it has been reported in young children. Mucous membrane pemphigoid is characterized by an immune reaction involving autoantibodies directed against basement membrane zone, followed by complement activation and subsequent leukocyte recruitment. Proteolytic enzymes release and dissolve the basement membrane zone. Cicatricial pemphigoid involves the oral cavity conjunctiva and mucosa of the nose, vagina, rectum, esophagus, and urethra. The most common intraoral presentation is desquamative gingivitis. There might be areas of erythema, desquamation, ulceration, and vesiculation of the attached gingiva. Bullae have thick roof and rupture in 2-3 days to leave ulcers that heal in up to 3 weeks. Other oral mucosal sites involved are buccal mucosa, palate, alveolar ridge, and tongue. Rarely intact bulla is seen intraorally, the more common presentation being fibrin-covered superficial erosions with irregular margins; oral lesions tend to heal without scarring. The eyes can be affected in 25% of cases, with 15% developing permanent blindness as a result of subconjunctival scarring; symblepharon is also observed. Less commonly, strictures may form in the larynx, esophagus, and genital mucosa with serious complications (Fig. 23.2). Histology Biopsy needs to be taken from areas with intact epithelium. Microscopically, there is subepithelial clefting with separation of the epithelium from the underlying lamina

FIGURE 23.2

Cicatricial pemphigoid.

propria, leaving an intact basal layer. A mixed inflammatory infiltrate consisting of lymphocytes, plasma cells, neutrophils, and scarce eosinophils is observed in stroma. Direct immunofluorescence reveals deposits of immunoglobulin G (IgG) and C3 restricted to the basement membrane. Less than 25% of patients showed positive indirect immunofluorescence finding. Treatment It can be controlled with topical corticosteroid application. If DG is present, custom-made trays can be used for delivery of fluocinonide (0.05%) three times a day for 6 months with clobetasol propionate. Oral hygiene must be improved, and regular professional cleaning should be emphasized. Irritation from dental prosthesis should be minimized. If ocular sites or skin is involved, then more potent medications such as systemic corticosteroids, azathioprine, sulfapyridine, or dapsone are used. Some authors also advocated sulfonamides and tetracyclines as the drug of choice for treatment of mucous membrane pemphigoid. Connective tissue grafting can also be considered as treatment of choice to improve the aesthetics and surface sensitivity. Differential Diagnosis • • • • • • •

Bullous pemphigoid Linear IgA dermatosis Bullous lichen planus Erythema multiforme Dermatitis Epidermolysis bullosa acquisita Herpetiformis.

Bullous Pemphigoid The term pemphigoid applies to a number of cutaneous, immune-mediated, subepithelial bullous diseases that are characterized by a separation of basement membrane zone. Bullous pemphigoid is a chronic autoimmune

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Treatment Treatment is directed toward controlling signs and symptoms. Localized lesions are treated with highefficacy topical steroids or tetracycline with or without nicotinamide. Primary treatment is a moderate dose of systemic prednisone.

Pemphigus Vulgaris

FIGURE 23.3

Bullous pemphigoid (fluid-filled blisters and erosion).

subepidermal bullous disease with tense bullae that rupture and become flaccid. Developing bullae are subepithelial, unlike pemphis vulgaris where they are found to be intraepiteal. Bullous pemphigoid predominantly affects the skin, but oral mucosa! involvement may occur.

Clinical Features In 40% of cases desquamative or erosive oral lesions are seen. Any area of oral mucosa may be involved, but the main manifestation is desquamative lesion of the gingiva presenting intensely erythematous attached gingiva. The inflammatory changes, as always when not caused by plaque, may extend over the entire gingival width and even over the mucogingival junction. The rubbing of the gingiva may precipitate bullae formation. This denotes positive Nikolsky sign and is caused by destroyed adhesion of epithelium to the connective tissue at the junction, resulting in exposed vessels inside the bullae. Usually, the eruption of bulla rapidly leaves fibrin-coated ulcers (Fig. 23.3).

Histologic Features The vesicles and bullae in this disease are subepidermal and nonspecific. Direct immunofluorescence of normal and perilesional tissues reveals typical stratified epithelium-specific antinuclear antibodies. It consists of deposits of IgG and complement 3 with a speckled pattern mainly in the basal epithelial cell layer. In addition, fibrin deposits are visualized at the epithelium-connective tissue interface. Indirect immunofluorescence also reveals the presence of circulating stratified epithelium-specific antinuclear antibodies in stratified epithelium.

Differential Diagnosis • • • •

Erosive lichen planus Pemphigus vulgaris Cicatricial pemphigoid Linear IgA disease

Pemphigus is one of the very few potentially fatal mucocutaneous diseases characterized by intraepithelial bullous formation. It is an uncommon condition and usually affects females in their fourth to fifth decade of life. PV is the most important subtype to occur in the mouth, and it can be the initial sign of presentation in 50% of cases. In pemphigus vulgaris, autoantibodies are produced against pemphigus vulgaris antigens, which are glycoproteins of desmoglein family present on the keratinocytes. Damage to these cell-to-cell structures leads to epidermal and mucous membrane blisters.

Clinical Features Oral pemphigus vulgaris presents as bullae that break down rapidly to leave persistent, irregular, ragged-edge, painful erosions. Gingival involvement may manifest as desquamative gingivitis, though less commonly than pemphigoid. Bullae on the gingiva rupture, leaving painful eroded areas. Gentle pressure on the epithelium may result in its separation; that is, Nikolsky sign is positive and mastication becomes extremely painful for the patient. Other sites that can be involved are esophagus, pharynx, larynx, and nasal and genital mucosa. Microscopically, PV lesions demonstrate a characteristic intraepithelial clefting above the basal cell layer giving a characteristic tombstone appearance to the basal cell also called suprabasilar split. Acantholysis is also seen. Rounded acantholytic "Tzanck cell" is often visible in the cleft. Direct immunofluorescence demonstrates deposition of IgG and C3 intercellularly in a fishnet pattern. Circulating autoantibodies can usually be detected by immunofluorescence, and such antibodies usually correspond to disease activity and severity.

Treatment PV is treated with systemic corticosteroids. Therapies combine small doses of steroids and immunosuppressive agents such as azathioprine, cyclophosphamide, cyclosporine, dapsone, gold, and methotrexate. When the patients respond well, the dose of systemic steroids can be reduced. Topical antifungal application may be needed to eliminate iatrogenic candidiasis, which often arises when topical steroids are used intraorally. Other treatment strategies include photoplasmapheresis and plasmapheresis. Rituximab is an anti-CD20 monoclonal

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antibody aimed to remove desmoglein-reactive autoantibodies that is currently being evaluated as an adjunct to treat pemphigus vulgaris. Maintenance of oral hygiene is essential. In addition, fit and design of prosthesis should also be checked for irritation that can lead to inflammation.

Chronic Ulcerative Stomatitis Chronic ulcerative stomatitis (CUS) clinically presents with ulceration and has a predilection for women in the fourth decade of life.

Oral Lesions The oral lesions consist of small blisters and erosions with surrounding erythema and pain mainly on the gingiva and lateral border of the tongue. The hard palate may also present similar lesions.

Histology Microscopically, it resembles erosive lichen planus. Direct immunofluorescent finding is typical stratified epithelium with specific antinuclear antibodies.

Treatment Mild cases of chronic ulcerative stomatitis are treated with topical steroids (fluocinonide, clobetasol propionate); topical tetracycline may also be used. Recurrence is common. A dose of systemic corticosteroids may be used to achieve transient remission. Hydroxychloroquine sulfate at a dosage of 200-400 mg/ day seems to be the treatment of choice for long-lasting remission. The initial response to the chloroquine may end after several months or years of treatment. In those cases a combined therapeutic approach of corticosteroid and chloroquine might be indicated.

Linear lgA Disease Linear IgA disease (LAD) is a rare subepithelial vesiculobullous disease characterized by deposition of IgA autoantibodies in a linear pattern along the basement membrane zone. It clinically presents as a pruritic vesiculobullous rash usually during middle to late age, with more predilection in women. The face and perineum may also be affected. Mucosal involvement including the oral mucosa ranges from 50 to 100% of the cases published.

Oral Lesions Oral lesions consist of vesicles, painful ulcerations or erosions, and erosive gingivitis/ cheilitis. The hard and soft palates are more commonly affected. Tonsillar pillar, buccal mucosa, tongue, and gingiva follow in frequency. In addition, oral lesions of LAD and desquamative gingivitis are also reported.

Histopathology Lesions are similar to erosive lichen planus.

Immunofiuorescence: Linear deposits of IgA are observed at the epithelial-connective tissue interface.

Differential Diagnosis • • • • •

Erosive lichen planus Chronic ulcerative stomatitis Bullous pemphigoid Pemphigus vulgaris Lupus erythematosus

Treatment Linear IgA disease can be treated with combination of sulfones and dapsone. Small doses of prednisone (1030 mg/ day) can be given. Tetracycline (2 g/ day) combined with nicotinamide (1.5 g/ day) has shown promising results. Recently, mycophenolate [1 g twice daily (bid)] combined with prednisolone (30 mg daily) resulted in the resolution of refractory ulcerations associated with LAD.

Lupus Erythematosus Lupus erythematosus is a group of autoimmune connective tissue disorders in which autoantibodies form to various cellular constituents including nucleus, cytoplasm, and membrane. The etiology of lupus erythematosus is unknown, but deposits of antigen-antibody complexes appear to play a role in tissue damage. Lupus erythematosus includes two major clinical forms: • Systemic lupus erythematosus (SLE) • Discoid lupus erythematosus (OLE)

Systemic Lupus Erythematosus It occurs in third and fourth decades. It is characterized by repeated remission and exacerbation, with common sites being face, neck, upper arm, shoulders, and fingers. The cutaneous lesions consist of erythematous patches on the face, which coalesce to form symmetrical pattern over the cheek and across the bridge of the nose. Hence, this lesion has a butterfly distribution. This condition may involve a range of organ systems including kidney, heart, and bone marrow. The most common intraoral sites are buccal mucosa, lip, and palate. It begins as erythematous area, sometimes slightly elevated with hyperemia and edema. The lesions have a greater tendency to bleed and form petechiae, suspected ulcerations surrounded by red halo. The intraoral lesion is composed of central depressed, red atrophic areas surrounded by 2-4 mm elevated keratotic zone.

Discoid Lupus Erythematosus It occurs in third and fourth decades. The most common sites are face, oral mucosa, chest, and extremities.

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Cutaneous lesions are slightly elevated, red or purple macules that are often covered by gray or yellow adherent scales. The lesions increase in size by peripheral growth. Periphery of the lesion appears pink and red, while the center exhibits an atrophic scar. Butterfly distribution on macular region and across the bridge of the nose is seen. The most common intraoral sites are buccal mucosa, tongue, palate, and vermillion border of the lip. It begins as erythematous area, slightly elevated but more often depressed with induration and typically with white spots. Occasionally, superficial painful ulceration may occur with crusting or bleeding. There may be burning and tenderness, which may be intermittent or disappears if the lesion becomes inactive. Central healing may result in depression.

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Differential Diagnosis • • • • • • • • •

Aphthous stomatitis Contact dermatitis or stomatitis Acute necrotizing ulcerative gingivitis Pemphigus Dermatitis herpetiformis Bullous lichen planus Herpes zoster Chicken pox Toxic epidermal necrolysis

Treatment Oral antihistamines are given to treat the lesions of erythema multiforme. Topical steroids, analgesics, local skin care, and soothing mouthwashes in the form of chlorhexidine are also recommended.

Treatment • Patients with SLE and OLE should be treated with antibiotic prophylaxis before dental treatment in order to avoid bacteremia. Topical steroid application is needed for symptomatic lesions to be resolved. For patients resistant to topical therapy, systemic antimalarial drugs may be used with good results. • Cyclophosphamide and azathioprine are recommended for severe cases. • Nonsteroidal anti-inflammatory drugs (NSAIDs) are advised for inflammatory conditions. • Plasmapheresis alone, or with steroids, is also shown to be useful. • Recently, rituximab has been utilized and produced dramatic long-term remissions.

Erythema Multiforme Erythema multiforme is an acute self-limiting dermatitis characterized by a distinctive clinical eruption manifested as the iris or target lesion. The oral mucous membrane lesions are not usually a significant feature of the disease except for the pain and discomfort. The hyperemic macules, papules, and vesicles may become eroded or ulcerated and bleed profusely. The tongue, palate, buccal mucosa, and gingiva are commonly affected sites.

Histopathology Intracellular edema of the spinous layer of the epithelium and edema of the superficial connective tissue which may produce subepidermal vesicles are seen. Shklar described a zone of severe liquefaction degeneration in the upper layer of the epithelium, intraepithelial vesicle formation, and thinning with frequent absence of the basement membrane.

ALLERGIC REACTIONS Several mechanisms may be involved in allergy, which are exaggerated immune reactions. Oral mucosal reactions are type I reactions, which are mediated by immunoglobulin E (IgE), or more often they are type IV mediated by T cells.

Dental Restorative Materials The oral mucosal reactions to restorative materials include reaction to mercury, nickel, gold, zinc, chromium, palladium, and acrylics.

Clinical Features The lesions are reddish or whitish, sometimes ulcerated lesions. They clinically resemble oral lichen planus or leukoplakia, but resolve after removal of the offending material. In case of dental amalgam restoration, clinical manifestation is confined to the area of contact with offending restorative material.

Treatment Elimination of the offending agent usually leads to resolution of the lesion within a week.

Reaction to Oral Hygiene Products, Chewing Gum, and Food Contact allergy rarely occurs after use of toothpaste and mouthwashes. The constituents responsible for allergic reactions are additives, preservatives, or flavoring agents. Desquamative gingivitis has been documented due to calculus control agents such as pyrophosphates and flavoring agents such as cinnamon compounds.

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Clinical Features Diffuse, fiery red, edematous gingivitis, sometimes with ulcerative lesions, may appear on labial, buccal, and tongue mucosa. The lesions resolve after cessation of the use of the allergen containing the agent. Allergic reaction attributable to food may manifest as both type I and type II reactions. The type I reaction occurs with severe swelling after intake of the food component. Another food allergy results in gingivitis or gingivostomatitis. The lesions resolve after removal of the allergen. Treatment The treatment involves thorough clinical history and removal of the causal agents. This leads to resolution of the gingival lesions soon. If removal of the offending medication is not possible, topical corticosteroids and topical tacrolimus can be used to treat the lesions.

Drug, Induced Mucocutaneous Disorder A number of drugs show reverse effects in the oral mucosa. Common drugs that cause gingival hyperplasia are phenytoin, sodium valproate, cyclosporine, and dihydropyridines. These lesions, to some extent, are plaque dependent. Azathioprine is an antimetabolite used for immunosuppression in the treatment of autoimmune and other types of diseases and to prevent rejection of transplants. The mode of action is through inhibition of purine base synthesis, resulting in suppression of nucleic acid and protein synthesis. As a side effect this may cause oral ulcerations, which even include gingiva. Other drugs that cause oral stomatitis are antineoplastic drugs used in cancer therapy and methotrexate used in leukemia. Clinical Features Epithelial atrophy, superficial sloughing, intense erythema, and ulceration are characteristic findings in the oral mucosa of gingiva. The ulcerative lesions are frequently portals of entry for microorganisms via oral route, which might lead to systemic complications.

Drug Eruptions Hypersensitivity to drugs sulfonamides, barbiturates, and various antibiotics is seen. The drug acts as an allergen, sensitizes the tissues, and then causes allergic reactions. Stomatitis medicamentosa: Eruptions in the oral cavity due to sensitivity to drugs taken orally and parenterally Stoma ti tis venenata/ contact stoma ti tis: Local reaction due to medicament in the oral cavity, such as aspirin and topical penicillin Forms seen due to reactions to drugs are vesicular, bullous, pigmented, and nonpigmented macular lesions.

MISCELLANEOUS CONDITIONS: MIMICKING DESQUAMATIVE GINGIVITIS A group of heterogeneous conditions may masquerade as desquamative gingivitis. Candidiasis, graft versus host disease, Wegener granulomatosis, and foreign body gingivitis can divert the attention of the clinician and result in a diagnostic challenge. Wegener granulomatosis is a disease of unknown etiology which involves the vascular, renal, and respiratory systems. Involvement of the oral cavity occurs with considerable frequency in Wegener granulomatosis. In reported cases, involvement of the gingiva has been the most common and characteristic manifestation and is termed "strawberry gingivitis." Brooke, in reviewing reported cases with oral lesions of this nature, has pointed out that the gingival lesions may be ulcerations, friable granular lesions, or simply enlargements of the gingiva. The inflammatory process starts in the interdental papilla and spreads rapidly to the periodontal structure and leads to bone loss and tooth mobility. Israelson reported a case characterized by hyperplastic gingivitis. Cyclophosphamide and prednisone have provided a good prognosis for this condition. Rarely, candidiasis may be limited to the gingival tissue and may stimulate desquamative gingivitis. Foreign body gingivitis is clinically characterized by red or white chronic lesions that may be painful and are reminiscent of desquamative gingivitis.

KEY POINTS • Desquamative gingivitis is a clinical term to describe red, painful, glazed, and friable gingiva, which may be a manifestation of some mucocutaneous conditions such as lichen planus or the vesiculobullous disorders.

• The term chronic desquamative gingivitis was coined in 1932 to describe a peculiar condition characterized by intense erythema, desquamation, and ulceration of the free and attached gingiva (by Prinz).

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KEY POINTS • Approximately 75% of DG cases have a dermatologic origin and are mainly associated with MMP, LP, and, to a lesser degree, PV. • To properly diagnose the condition responsible for desquamative gingivitis, clinical examination coupled with a thorough medical history and routine histologic and immunofluorescence studies is required. • Gingival lichen planus comprises 10% of oral lichen planus cases. Four patterns are seen: keratotic, erosive/ ulcerative, vesicular /bullous, and atrophic. • In lichen planus rete ridges have "sawtooth configuration."

QUESTIONS 1. What is desquamative gingivitis? Enumerate the lesions causing desquamative gingivitis. 2. Discuss differential diagnosis of desquamative gingivitis. 3. Classify desquamative gingivitis. 4. Write a note on Nikolsky sign. 5. Write a note on management of oral lichen planus. 6. Explain "Tzanck test."

Suggested readings 1. Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry, 4th ed. Oxford: Munksgard 2003.

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(cont'd)

• Cicatricial pemphigoid involves the oral cavity, conjunctiva and mucosa of the nose, vagina, rectum, esophagus, and urethra. • Lupus erythematosus includes two major clinical forms: systemic lupus erythematosus and discoid lupus erythematosus. • Stomatitis medicamentosa refers to eruptions in the oral cavity due to sensitivity to drugs taken orally and parenterally. • Stomatitis venenata/contact stomatitis refers to local reaction caused due to medicament in the oral cavity, such as aspirin burn and topical penicillin.

2. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Clinical Periodontology. 10th ed., 11th ed. Philadelphia: Saunders; 2006. 3. Nisengard RJ, Neiders M. Desquamative lesions of gingiva. J Periodontol 1981;52:500-510. 4. Nisengard RJ. Periodontal implications: mucocutaneous disorders. Ann Periodontol 1996;1:401-38. 5. Rose LF, Mealey BL, Genco RJ, Cohen W. Periodontics: Medicine, Surgery and Implants. 2nd ed. St. Louis: Mosby; 2004. 6. Scully C, Porter SR. The clinical spectrum of desquamative gingivitis. Med Surg 1997;16:308. 7. Wary RD. A sign of mucocutaneous disorders - a review. Aust Dent J 2003;48:4. 8. Rajendran R, Shivapathasundaram B, Shafer W G, Shafer's Textbook of Oral Pathology. 6th ed. New Delhi: Elsevier; 2009.

CHAPTER

24 Periodontal Diseases in Childhood and Adolescents CHAPTER OVERVIEW Periodontal disease in adults is at least in part precipitated by gingival inflammation in the formative years of childhood and early adolescence. The exchange of dentition

PERIODONTIUM OF DECIDUOUS DENTITION

• Eruptive stage • Posteruptive stage.

1. Shallower sulcus depth -2.1 mm. 2. Interdental gingiva broad buccolingually and narrow

3.

4. 5. 6. 7.

mesiodestally to confirm to morphology of deciduous dentition. Attached gingiva varies in width anteroposteriorly being the widest in the incisor area, narrowing over the cuspids and widening again over the posterior molars. Free gingiva has fewer collagen bundles and is more easily retracted away from deciduous tooth surface. Radiographically, lamina dura is prominent with a wider periodontal space. Marrow spaces of bone are larger and crests of interdental bony septa are flat. Bony crests are within 1-2 mm of cementoenamel junction.

Physiologic Gingival Changes Associated with Tooth Eruption Gingival changes that occur during the eruption of tooth can be studied by dividing the eruption into three stages, as follows: • Preemptive stage

from primary to permanent, and the hormonal changes associated with puberty bring about many changes in the periodontium.

Preeruptive Stage Before eruption of the permanent tooth the gingiva reveals a bulge that is firm and pink or blanched secondary to the underlying permanent crown (Fig. 24.1).

Eruptive Stage • This stage is associated with formation of gingival margin. • Marginal gingiva and sulcus develop as the crown penetrates the oral mucosa. • In the course of eruption, the gingival margin is usually edematous, rounded, and slightly reddened. • During the period of mixed dentition, it is normal for marginal gingiva around the permanent teeth to be quite prominent, particularly in the maxillary anterior region. At this stage in tooth eruption, the gingiva is still attached to the crown, and appears prominent when superimposed on the bulk of the underlying enamel (Fig. 24.2).

Posteruptive Stage The gingiva reduces in bulk and becomes thinner, tighter, and more firmly attached around the cervical portion of the tooth (Fig. 24.3).

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CHA PTER 24 PERIO DONTAL DISEA SES IN CHILDHOO D AND ADOLESCENTS

Health Plaque

Gingivitis Stress, smoking, and other factors

Drug therapy Hormones Puberty gingivitis

Necrotizing ulcerative gingivitis and periodontitis

Gingival overgrowth

Plaque

Host susceptibility

Periodontitis

Systemic diseases

Slow progression

Systemic disease forms of periodontitis

Rapid progression

Incipient (adult) periodontitis

Early onset periodontitis

~ t Prepubertal

Localized prepubertal periodontitis

Localized early onset periodontitis

Generalized early onset pe riodontitis

Incidental early onset periodontitis

Generalized prepubertal periodontitis

FIGURE 24.1

Periodontal diseases that can occur in children.

FIGURE 24.2

Gingival changes seen in the preemptive stage.

FIGURE 24.3

Gingival changes seen in the eruptive stage.

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GINGIVITIS • It is the inflammatory involvement of gingival tissue. • Microscopically, it is characterized by the presence of inflammatory exudate and edema and destruction of collagenous gingival fibers. • Ulcerations of the epithelium are also seen.

4. Changes in surface texture of the gingiva

a. Loss of surface stippling is an early sign of gingivitis. b. Chronic inflammation c. The surface is smooth, shiny, or firm, and nodular depending on whether changes are exudative or fibrotic.

Etiology of Gingival Diseases Stages of Gingivitis Stage I: Initial Lesion 1. Time period is 2-4 days. 2. Vascular dilatation and vasculitis is seen. 3. Junctional and sulcular epithelium are seen infiltrated by polymorphonuclear cells. 4. It is associated with mild change in color. Stage II: Early Lesion 1. Time period is 4-7 days. 2. There is increased vascular proliferation. 3. Junctional and sulcular epithelium is seen infiltrated by polymorphonuclear cells, rete peg formation, and atrophic areas. 4. Lymphocytes are predominant. 5. There is loss of collagen. 6. Clinical findings include erythema and bleeding on probing. Stage III: Established Lesion 1. Time period is 14-21 days. 2. There is increased vascular proliferation and blood 3.

stasis. Changes seen in the junctional and sulcular epithelium are more severe compared with Stage II. Plasma cells are predominant. There is severe loss of collagen. Clinical findings include changes in color, size, and texture.

1. Local irritating factors

a. Bacterial plaque b. Predisposing factors like materia alba, food debris, malalignment of teeth, dental calculus, etc. 2. Local functioning factors a. Malocclusion b. Habits: Mouth breathing, tongue thrusting c. Eruption of teeth 3. Systemic factors a. Puberty b. Vitamin or protein deficiency c. Drugs and chemicals d. Pregnancy e. Hereditary f. Metabolic disorders g. Hematologic disorder h. Viral, bacterial, and fungal infections

TYPES OF GINGIVAL DISEASES IN CHILDHOOD Eruption Gingivitis

1. The lesion extends into alveolar bone. 2. It is characterized by periodontal breakdown.

• It is seen during the eruption of teeth and subsides soon after eruption. • Greatest incidence is 6-7 years when permanent teeth begin to erupt. • Reason for this is the lack of protection to the gingiva from the coronal contour of the tooth. • It may be painful and may develop into pericoronitis or pericoronal abscess. • Management includes improving oral hygiene. Some severe cases may require antibiotic therapy.

Clinical Features of Gingivitis

Gingivitis Associated with Poor Oral Hygiene

1. Gingival bleeding

• Oral hygiene and gingivitis are directly related. • Adequate oral hygiene practice, leading to thorough plaque removal, and eating raw fiber vegetables and fruits have beneficial effect on reducing gingivitis. • It can be grouped as early, moderate, and advanced gingivitis. • Early gingivitis is quickly reversible and treated with good tooth brushing and flossing. • Moderate and severe gingivitis requires more elaborate measures.

4. 5. 6.

Stage IV: Advanced Lesion

Two earliest symptoms of gingival inflammation are: a. Increased gingival fluid production rate b. Bleeding from gingival sulcus on probing 2. Change in the color of gingiva a. Normal color is coral pink. Inflamed tissue is red or bluish red. 3. Changes in consistency of gingiva a. In chronic inflammation, both destructive (edematous) and reparative (fibrotic) changes coexist.

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Gingivitis Associated with HSV I Infection • It is caused by the herpes simplex virus (HSV). • Herpetic stomatitis is a common oral disease, which develops in both children and young adults. • It rarely occurs before the age of 6 months, apparently because of the presence of circulating antibodies in the infant, derived from the mother. The disease occurring in children is usually the primary attack. • It is characterized by the development of fever, irritability, headache, pain upon swallowing, and regional lymphadenopathy. • Within a few days, the mouth becomes painful and the gingiva intensely inflamed. • The lips, tongue, buccal mucosa, palate, pharynx, and tonsils may also be involved. • Shortly yellowish, fluid-filled vesicles develop. These rupture and form shallow, ragged, extremely painful ulcers covered by a gray membrane and surrounded by an erythematous halo. • They heal spontaneously within 7-14 days and leave no scar. • Treatment is symptomatic such as application of topical anesthetic agents on the ulcers, soft diet, and adequate fluids.

Gingivitis Associated with Aphthous Stomatitis

201

interproximal necrosis and ulceration and the rapid onset of gingival pain. • Viral infections (including HIV), malnutrition, emotional stress, lack of sleep, and a variety of systemic diseases are the common predisposing factors • Treatment involves mechanical debridement, oral hygiene instruction, and careful follow-up. • If the patient is febrile, antibiotics may be an important adjunct to therapy. Metronidazole and penicillin have been suggested as drugs of choice.

Gingivitis Associated with Acute Bacterial Infection • It is caused by streptococci group of bacteria. • The gingiva is painful and bleeds easily. • Papilla is enlarged with associated gingival abscess. Treatment includes broad-spectrum antibiotics, improvement of oral hygiene, and chlorhexidine mouthwash.

Chronic N onspecifi.c Gingivitis • It has no specific etiology. May be triggered by hormonal imbalance seen in the preteenage and teenage children. • It may be localized to the anterior region or may be more generalized. • It is rarely painful, but persists for a longer period of time. • Since the cause is nonspecific, the treatment is limited to maintaining the oral hygiene and regular professional prophylaxis.

• It can be triggered due to any stress, gastrointestinal disturbance, nutritional deficiency, hormonal imbalance, infection, allergy, etc. • Of the three types of apthous, minor aphthae are common. • Prodromal phase of paresthesia at the site of ulceration is observed. The ulcers appear in crops of two or three and are less than 10 mm in diameter. They are painful and discrete or confluent. • It persists for about 12 days and heals with no scar formation. • Treatment is symptomatic. Chlorhexidine, nystatin, or tetracycline can be prescribed if they are infected.

Puberty Gingivitis

Acute N ecrotizing Ulcerative Gingivitis

Hereditary Fibromatosis Gingival Enlargement

• Acute necrotizing ulcerative gingivitis (ANUG) is caused by Borrelia vincentii and spirochetes. • Severe ulcerating gingivitis involving the interproximal papillae, covered by a psuedomembrane, is seen. • It is associated with fetid odor. • Recovery promptly occurs within 36 h after penicillin therapy and application of hydrogen peroxide • This can progress into necrotising periodontal disease (NPD) if left untreated • The two most significant findings used in the diagnosis of necrotising periodontal diseases are the presence of

• It is characterized by slow, progressive, benign enlargement of the gingiva. • The surface is normal appearing. • It appears as soon as the deciduous teeth erupt in the oral cavity and cover the teeth completely. • They are fibrous tending to displace the teeth and are nonpainful. • They regress only if the teeth are extracted. • Surgical excision is the treatment of choice but may recur to the original condition within a period of few years.

• It occurs in the prepubertal and pubertal periods. • Gingival inflammation is confined to the anterior segment and may be limited to single arch only. • Gingiva on the lingual aspect is relatively uninvolved concerned with maintenance of adequate oral hygiene, removal of local irritants, and restoration of caries.

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Drug- Induced Hyperplasia • Phenytoin, an anticonvulsant drug, is the commonly seen to be the cause of hyperplasia of the gingiva. • Other drugs that induce hyperplasia are cyclosporine and nifedipine. • It appears as early as 2-3 weeks after initiation of the phenytoin therapy and peaks at 18-24 months. • They cause painless enlargement of the gingiva especially on the interproximal aspect. • Buccal and anterior segment are more often affected than the lingual and posterior segment. • Gingiva appears pink and firm unless infected. • They normally do not bleed readily. • There is formation of pseudopockets. • There are associated problems during mastication, speech, etc. • Management includes adequate oral hygiene maintenance, change of drug or dosage, and surgical excision.

Scorbutic Gingivitis • It is associated with vitamin C deficiency. • Involvement is limited to marginal tissue and papillae. • It is associated with severe pain and spontaneous hemorrhage. • Management includes replacement of ascorbic acid and oral hygiene maintenance.

TYPES OF PERIODONTAL DISEASES Prepubertal Periodontitis • Normally it is generalized, but when it occurs in deciduous dentition, it is localized. • Loss of attachment and alveolar bone loss are seen in deciduous dentition in the molar and incisor regions. • Plaque accumulation is minimum. Gingival inflammation may be present. • It is seen soon after the eruption of the primary teeth. Premature loss of teeth is common and all teeth may be lost by 3 years of age. • Actinobacillus actinomyceteomcomitans, bacteroids, and Fusobacterium are found in the gingival pocket. • Management includes early diagnosis, dental curettage, prophylaxis, removal of severely mobile teeth, and broad-spectrum antibiotics.

AGGRESSIVE PERIODONTITIS • Aggressive periodontitis may be more common in children and adolescents, whereas chronic periodontitis is more common in adults. • The important features of aggressive periodontitis include a history of rapid attachment and bone loss with familial aggregation. • The other features include phagocyte abnormalities and a hyperresponsive macrophage phenotype. Aggressive periodontitis can be localized or generalized. • Localized aggressive periodontitis (LAgP): These patients have interproximal attachment loss on at least two permanent first molars and incisors, with attachment loss on no more than two teeth other than first molars and incisors. • Generalized aggressive periodontitis (GAgP): These patients exhibit generalized interproximal attachment loss including at least three teeth that are not first molars and incisors. • In young individuals, the onset of these diseases is often circumpubertal.

Localized Aggressive Periodontitis • It is seen in otherwise healthy children. • It is characterized by rapid and severe loss of alveolar bone around more than one permanent tooth involving the first molars and incisors. • It appears self-limiting. • No tissue inflammation is seen, and little plaque or calculus is present. • Bone loss is three to four times faster than adult periodontitis. • It is caused by Actinobacillus actinomyceteomcomitans and bacteroid-like organisms. • Management includes early diagnosis, dental curettage, prophylaxis, removal of severely mobile teeth, and broad-spectrum antibiotics.

Generalized Aggressive Periodontitis 1. It is seen at around puberty. 2. It affects the entire dentition. 3. It is caused by nonmotile, facultative, anaerobic, gramnegative rod Porphyromonas gingivalis. 4. Management includes early diagnosis, dental curettage, prophylaxis, removal of severely mobile teeth and broad-spectrum antibiotics.

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203

KEY POINTS • Various physiologic changes are associated with tooth eruption. • The different types of gingival lesions seen in children are eruption gingivitis, gingivitis associated with poor oral hygiene, acute gingival inflammation, chronic nonspecific gingivitis, puberty gingivitis, fibromatosis,

QUESTIONS 1. Define eruption gingivitis. 2. Enumerate various periodontal diseases in childhood.

3. Define localized aggressive periodontitis.

Suggested readings 1. Albandar JM, Buischi AP, Mayer MP, Axellson P. Long term effect of two preventive programs on the incidence of plaque and gingivitis in children. J Periodontol 1994;65:605.

phenytoin-induced gingival overgrowth, and scorbutic gingivitis. • Periodontal lesions seen in children are prepubertal periodontitis, chronic periodontitis, aggressive periodontitis, and periodontitis as a manifestation of systemic diseases.

2. Loe H, Anerud A, Bousen H. The natural history of periodontal disease in man: prevalence, severity and extent of gingival recession. J Periodontol 1992;63:489. 3. Mattson L. Development of gingivitis in preschool children and young adults: a comparative experimental study. J Clin Periodontal 1978;5:24. 4. Molder T, Wondimu B. Periodontal disease in children and adolescents. Dent Clin North Am 2000;44:633. 5. Oh TJ, Eber R, Wang HL. Periodontal disease in the child and adolescents. J Clin Periodontal 2002;29:400.

CHAPTER

25 Periodontal Pocket CHAPTER OVERVIEW A periodontal pocket is defined as a pathologically deepened gingival sulcus and is one of the important clinical features of periodontal disease.

CLASSIFICATION Pockets are classified according to morphology and their relationship to adjacent structures as follows: 1. Gingival pocket (relative/ false) (Fig. 25.1)

3. Complex: It is a spiral pocket that originates on one tooth surface and twists around the tooth to involve one or more additional surfaces. Their only communication with the gingival margin is at the surface where the pocket originates. It is more commonly observed in furcation areas (Fig. 25.3A-C).

It is formed by gingival enlargement without destruction of the supporting tissues of the periodontium. There is no apical proliferation of the epithelial attachment. 2. Periodontal pocket (absolute/true) It is formed by pathologic deepening of the gingival sulcus due to destruction of the supporting tissues of the periodontium and apical proliferation of the epithelial attachment. True pockets are further subclassified into the following categories (Fig. 25.2A, B): • Suprabony pocket (supracrestal/ supra-alveolar) • Infrabony pocket (intrabony, subcrestal) The differences between suprabony and infrabony pocket are depicted in Table 25.1. Periodontal pockets can also be classified according to the number of surfaces involved as follows: 1. Simple: It involves only one tooth surface (Fig. 25.3).

2. Compound: Two or more tooth surfaces are involved. The base of the pocket is in direct communication with the gingival margin along each of the involved surfaces (Fig. 25.3).

CLINICAL FEATURES Signs • Enlarged bluish-red marginal gingiva with rolled-out edge separated from the tooth surface • Reddish-blue vertical zone from the gingival margin to attached gingiva/ alveolar mucosa • Break in faciolingual continuity of interdental gingiva • Shiny discolored puffy gingiva • Gingival bleeding • Purulent exudate from the gingival margin in response to digital pressure • Looseness, extrusion, migration of teeth • Development of diastema where none had previously existed.

Symptoms • Localized pain or sensation of pressure after eating, which gradually diminishes • Foul taste in localized areas

204

205

CHA PTER 25 PERIO DONTAL PO CKET

FIGURE 25.1

(A)

Gingival pocket.

(B)

FIGURE 25.2 (A) Suprabony pocket; (B) infrabony pocket.

TABLE 25.1

Differences Between Suprabony and lnfrabony Pockets

Suprabony pockets

Infrabony pockets

1.

Base of the pocket is coronal to the crest of the alveolar bone

Base of the pocket is apical to the crest of the alveolar bone; hence, bone is adjacent to the soft tissue wall

2.

Bone destructive pattern is horizontal

Vertical/ angular pattern of bone destruction

3.

Interproximally, the transseptal fibers are restored horizontally during progressive periodontal disease in the space between the base of the pocket and alveolar bone

Interproximally, the transseptal fibers are restored obliquely, from the cementum beneath the base of the pocket over the crest of the cementum of adjacent tooth

4.

On the facial and lingual surfaces, the periodontal ligament fibers beneath the pocket follow their normal course between the tooth and the bone

On the facial and lingual surfaces the periodontal fibers beneath the pocket follow the angular pattern of the adjacent bone

(A)

FIGURE 25.3

(B)

(A) Simple pocket; (B) compound pocket; (C) complex pocket.

(C)

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SECTION IV PERIODONTAL PATHOLOGY

• Tendency to suck material in the interdental areas • Radiating pain deep in the bone • Gnawing feeling or itching in the gingiva and urge to dig a pointed instrument into the gums and relief obtained from resultant bleeding • Food sticks in between the teeth or teeth feel loose • Sensitivity to heat and cold • Toothache in absence of caries.

PATHOGENESIS Periodontal pockets are caused by microorganisms and their products, which produce pathologic changes that lead to deepening of the gingival sulcus. The deepening may occur by: • Movement of the gingival margin in the direction of the crown (produces a gingival pocket) • Migration of the junctional epithelium apically and its separation from the tooth surface • A combination of the aforementioned processes. Changes involved in the transition from the normal gingival sulcus to the pathologic pocket are associated with increased number of spirochetes and motile rods. • Inflammatory changes are observed in the connective tissue wall of the sulcus. Several zones have been described in the process of destruction of connective tissue attachment. • Apical to the junctional epithelium, an area of destroyed collagen fibers develops and is occupied by inflammatory cells and edema. Immediately apical to this is a zone of partial destruction and then an area of normal attachment. • Two hypotheses have been proposed in regards to the mechanism of collagen loss: Collagenases and other lysosomal enzymes from PMNLs and macrophages become extracellular and destroy collagen. Fibroblasts phagocytize collagen fibers by extending cytoplasmic process to the ligament interface and by resorbing the inserted collagen fibrils and fibrils of the cementum matrix. • As a consequence of the loss of collagen, the apical portion of the junctional epithelium proliferates along the root, extending like projections 2-3 cells in thickness. • Extension of junctional epithelium along the root requires the presence of healthy epithelial cells. Marked degeneration or necrosis of the junctional epithelium retards rather than accelerates pocket formation. • The coronal portion of the junctional epithelium detaches from the root as the apical portion migrates. This is due to loss of cohesiveness of the junctional

epithelium as a result of rapidly proliferating bacteria, bacterial enzymes, and the relative volume of PMNs (60% or more of the junctional epithelium). Thus, the base of the gingival sulcus shifts apically and the sulcular epithelium is replaced by the pocket epithelium. The transformation of the gingival sulcus into a periodontal pocket creates an area where plaque removal becomes impossible, and the following feedback mechanism is established.

Plaque Gingival inflammation More plaque formation

j Pocket formation

Thus with continued inflammation, crest of the gingival margin extends coronally and the junctional epithelium continues to migrate apically along the root and separates from it.

HISTOPATHOLOGY • The connective tissue is edematous and densely infiltrated with plasma cells (approximately 80%) and lymphocytes and a scattering of PMNs. • Blood vessels are increased in number, dilated, and engorged; single or multiple necrotic foci are occasionally present. • Connective tissue also shows proliferation of the endothelial cells with newly formed capillaries, fibroblasts, and collagen fibers. • The junctional epithelium at the base of the pocket is usually much shorter than that of a normal sulcus. The coronoapical length of the junctional epithelium is 50-100 µm. • The most severe degenerative changes in the periodontal pocket occur along the lateral wall. Epithelial buds or interlacing cords of epithelial cells project from the lateral wall into the adjacent inflamed connective tissue and frequently extend farther apically than the junctional epithelium. • Progressive degeneration and necrosis of the epithelium leads to ulceration of the lateral wall, exposure of the underlying marked inflamed connective tissue, and suppuration. • The severity of the degenerative changes is not necessarily related to pocket depth. Ulceration of the lateral wall may occur in shallow pockets, and

CHA PTER 25 PERIO DONTAL PO CKET

deep pockets are occasionally observed in which the lateral epithelium is relatively intact and shows slight degeneration. • The epithelium at the gingival crest of a periodontal pocket is generally intact and thickened with prominent rete pegs. • Filaments, rods, and coccoid organisms with predominant gram-negative cell walls have been found in the intercellular space initially under exfoliating epithelial cells, but they are also found between deeper epithelial cells and accumulating on the basement lamina. • Some bacteria may traverse the basement lamina and invade the subepithelial connective tissue.

MICROTOPOGRAPHY OF THE GINGIVAL WALL OF THE POCKET The following areas have been noted in a scanning electron microscope (SEM) study to analyze the salient features of the soft tissue wall in deep periodontal pockets: 1.

2.

3.

4.

5.

207

6. Area of ulceration: It is occasionally seen surrounded by areas of hemorrhage. The bottom of the ulcer shows exposed collagen fibers and various connective tissue cells. 7. Areas of hemorrhage: Numerous erythrocytes are present.

Periodontal Pockets as Healing Lesion The condition of the soft-tissue wall of the periodontal pocket results from the interplay of destructive and constructive tissue changes. The destructive changes are characterized by the associated degenerative changes initiated by plaque bacteria. The reparative changes consist of the formation of blood vessels in an effort to repair the tissue damage caused by inflammation. Complete healing does not occur because of persistence of local irritants, which continue to stimulate fluid and cellular exudates, which in turn causes degeneration of the new tissue elements formed in the continuous effort at repair. The balance between destructive and reparative changes determines clinical features such as color, consistency, and surface texture of the pocket wall (Table 25.2).

Area of relative quiescence: A relatively flat surface with minor depressions and mounds and occasional shedding of cells. Areas of bacterial accumulation: Appear as depressions on the epithelial surfaces, with abundant debris and bacterial clumps penetrating into the enlarged intercellular spaces. Cocci, rods, and filaments with few spirochetes were the main bacteria and appeared covered by a loose, intercellular, fibrillar substance. Areas of emergence of leukocytes: Leukocytes appear in the pocket wall through holes located in the intercellular spaces. Areas of leukocyte-bacterial interaction: Numerous leukocytes are present and covered with bacteria in an apparent process of phagocytosis. Area of intense epithelial desquamation: It shows semiattached and folded epithelial squames with one end usually attached to the pocket wall surface and the other end free toward the pocket space.

TABLE 25.2

Pocket Contents Periodontal pockets contain debris consisting principally of microorganisms and their products (enzymes, endotoxins, and other metabolic products), gingival fluid, food remnants, salivary mucin, desquamated epithelial cells, and leukocytes.

Significance of Pus Formation Pus is a common feature of periodontal disease but it is only a secondary sign. The presence of pus or the ease with which it can be expressed from the pocket merely reflects the nature of the inflammatory changes in the pocket wall. It is not an indication of the depth of the pocket or the severity of the destruction of the supporting tissues. Extensive pus formation may occur in shallow pockets, whereas deep pockets may exhibit little or no pus.

Correlations of Clinical Features and Histopathologic Features

Clinical features

Histopathology features

1

Bluish-red color discoloration Flaccidity Smooth shiny surface Pitting on pressure

Circulatory stagnation Destruction of the connective tissue fibers Edema and atrophy of the epithelium Edema and degeneration of the connective tissue

2

Pink and firm gingival soft tissue wall

Fibrotic changes predominate over exudation and degeneration

3

Bleeding elicited by gentle probing

Increased vascularity, engorgement of blood vessels, and thinning and ulceration of the sulcular epithelium

4

Inner aspect of the pocket wall is painful on probing

Ulceration of the inner aspect of the pocket wall

5

Pus expressed on digital pressure

Suppurative inflammation of the inner wall of the pocket

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SECTION IV PERIODONTAL PATHOLOGY

Root Surface Wall Changes The root surface wall of the periodontal pocket often undergoes changes that are significant because they may perpetuate the periodontal infection, cause pain, and complicate periodontal treatment. Structural, chemical, and cytotoxic changes occur in the root cementum.

Calculus

Attached plaque

Structural Changes 1. Presence of pathologic granules: They represent areas of collagen degeneration or areas where collagen fibrils have not been fully mineralized. 2. Increased mineralization: It is a result of an exchange, on exposure to the oral cavity, of minerals and organic components at the cementum-saliva interface. 3. Areas of demineralization: It is commonly related to root caries. Exposure of oral fluid and bacterial plaque results in proteolysis of the embedded remnants of the Sharpey fibers; the cementum may be softened and may undergo fragmentation and cavitation. Active root caries appear as well-defined, yellowish or light brown area, are frequently covered by plaque, and have a softened or leathery consistency on probing. Inactive lesions are well-defined darker lesions with a smooth surface and a harder consistency on probing. Involvement of the cementum is followed by bacterial penetration of the dentinal tubules resulting in destruction of dentin.

Unattached plaque

Junctional epithelium Partially lysed CT fibers

Intact CT fibers

FIGURE 25.4 Morphology of the tooth wall.

5. Zone of semidestroyed connective tissue fibers apical to the JE: Zones 3, 4, and 5 compose the so-called plaque-free zone seen in extracted teeth.

Chemical Changes The mineral content of the exposed cementum is increased, e.g., calcium, magnesium, phosphorus, and fluoride. Microhardness, however, remains unchanged.

Cytotoxic Changes Bacterial endotoxins have been demonstrated in the cementum of untreated periodontally involved teeth. Thus cementum may act to perpetuate the destructive effects of periodontal disease, by acting as a reservoir for potentially destructive products.

MORPHOLOGY OF THE TOOTH WALL The following zones can be seen at the bottom of a periodontal pocket (Fig. 25.4):

Cementum covered by calculus: It exhibits all the aforementioned root surface changes. 2. Attached plaque: It covers calculus and extends apically from it to a variable degree, probably 100-500 µm. 3. Zone of unattached plaque: It surrounds attached plaque and extends apically. 1.

4.

Zone of attachment of functional epithelium to the tooth: In normal sulci, its extension is more than 500 µm but is usually reduced in periodontal pockets to less than 100 µm.

Relation of Loss of Attachment and Bone Loss to Pocket Depth Pocket formation causes loss of attachment and denudation of the root surface. The severity of attachment loss is generally not always correlated to pocket depth. This is because the degree of attachment loss depends on the location of the base of the pocket on the root surface, whereas pocket depth is the distance from the base of the pocket and the crest of the gingival margin. Pockets of same depth may be associated with different degrees of attachment loss (Fig. 25.5), and pockets of different depths may be associated with the same amount of attachment loss as observed in Fig. 25.6. Severity of bone loss is generally correlated with pocket depth, but not always extensive bone loss may be associated with shallow pockets and slight bone loss may occur in deep pockets.

Concept of Site Specificity The microflora, the anatomy, and the local immune response at one site around one tooth may be totally different from those at an adjacent site of the same tooth. This results in periodontitis at some sites next to sites with little or no periodontal destruction, which is referred to as the concept of site specificity of periodontal disease.

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FIGURE 25.5

209

Variable attachment loss with similar levels of probing depth.

Effect of Periodotal Pocket on the Dental Pulp

FIGURE 25.6

Variable pocket depths with similar levels of

attachment loss.

Accessory /lateral canals and the apical foramen may serve as a portal for the spread of infection from the periodontal pocket to the dental pulp. These changes may cause painful symptoms in the dental pulp. Although inflammatory changes have been reported adjacent to accessory canals exposed to periodontal pockets, periodontitis rarely produces significant changes in the dental pulp. Severe breakdown of the pulp is usually seen only when the periodontal pocket extends to the tooth apex.

KEY POINTS • A periodontal pocket is defined as a pathologically deepened gingival sulcus and is one of the important clinical features of periodontal disease. • True pockets are further subclassified into suprabony pocket (supracrestal/ supra-alveolar) and infrabony pocket (intrabony, subcrestal). Simple: It involves only one tooth surface. Compound: Two or more tooth surfaces are involved. Complex: It is a spiral pocket that originates on one tooth surface and twists around the tooth to involve one or more additional surfaces.

• Structural, chemical, and cytotoxic changes occur in the root cementum exposed to pocket environment. • Accessory /lateral canals and the apical foramen may serve as a portal for the spread of infection from the periodontal pocket to the dental pulp. • Periodontal pockets contain debris consisting principally of microorganisms and their products (enzymes, endotoxins, and other metabolic products), gingival fluid, food remnants, salivary mucin, desquamated epithelial cells, and leukocytes.

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SECTION IV PERIODONTAL PATHOLOGY

QUESTIONS 1. Define and classify periodontal pocket. 2. Describe in brief the pathogenesis of pocket formation. 3. Describe the microtopography of the soft tissue wall. 4. Explain in detail the root surface wall changes in a periodontal pocket. 5. Write a short note on periodontal disease activity. 6. What are the differences between suprabony and infrabony pockets?

Suggested readings 1. Adriaens PA, De Boever JA. Ultra structural study of bacterial invasion in roots of periodontally diseased, caries free human teeth. J Dent Res 1986;65:770. 2. Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry. 5th ed. Blackwell Munksgaard Publication; 2008. 3. Muller-Glauser W, Schroeder HE. The pocket epithelium: a light and electron microscopic study. J Periodontol 1982;53:133. 4. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Carranza's Clinical Periodontology. 10th ed. Philadelphia: Saunders; 2006. 5. Page RC, Schroeder HH. Structure and pathogenesis. In: Schluger S, Youdelis R, Page R, editors. Periodontal Disease. Philadelphia: Lea and Febiger; 1977. 6. Takada T, Donath K. The mechanism of pocket formation; a light microscopic study of undecalcified human material. J Periodontal 1988;59:215.

CHAPTER

26 Bone Loss in Periodontal Disease CHAPTER OVERVIEW Untreated cases of chronic generalized periodontitis leads to the loss of tooth due apical spread of infection. This results when the alveolar bone support is lost and it is an important characteristic feature of destructive periodontal disease. Loss of alveolar bone support is one of the characteristic signs of destructive periodontal

disease. The different architectures created due to the loss of osseous tissue result in the development of the ecological niches that are site-specific risk factors of periodontal disease progression. The amount and severity of loss of alveolar bone is assessed by clinical and radiographic evaluation.

ETIOLOGY OF BONE DESTRUCTION

The destructive periods result in loss of collagen and alveolar bone with deepening of the periodontal pocket. Following changes are associated with periods of activity or destruction:

Pathologic microorganisms elicit a host response that leads to periodontal hard tissue destruction, i.e., the alveolar bone and cementum. The immunoinflammatory host response along with the acquired and genetic risk factors modifies the probable development as well as progression of periodontal disease. Bone destruction in periodontal disease is caused by local and systemic factors. Local factors fall into the following groups: • That cause gingival inflammation • That cause trauma from occlusion Reduction in the height of alveolar bone is caused by extension of gingival inflammation, whereas trauma from occlusion (TFO) causes bone loss lateral to the root surface.

Bone Destruction Caused by Extension of Gingival Inflammation

1. Bursts of destructive activity are associated with

subgingival ulceration and an acute inflammatory reaction, resulting in rapid loss of alveolar bone. 2. Bursts of destructive activity coincide with the conversion of a predominately I-lymphocyte lesion to one with a predominance of B-lymphocyte-plasma cell infiltrated lesion. 3. Periods of exacerbation are associated with an increase of the loose, unattached, motile, gram-negative, anaerobic pocket flora, and periods of' remission coincide with the formation of a dense, unattached, nonmotile gram-positive flora with a tendency to mineralize. 4. Tissue invasion by one or several bacterial species is followed by an advanced local host defense that controls the attack.

• The uninhibited progression of inflammation from the gingival margin into the supporting tissues leads to bone destruction. • The transition from gingivitis to periodontitis is associated with periods of destruction/ activity/ Exacerbation Periodontal destruction occurs in an episodic, intermittent fashion, with periods of inactivity or quiescence. 211

HISTOPATHOLOGY • Gingival inflammation extends along the fiber bundles and follows the course of the blood vessels. • Interproximally, inflammation spreads to the loose connective tissue around the blood vessels, through the fibers, and then into the bone through vessel channels that perforate the crest, side, or at the angle of the

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SECTION IV PERIODONTAL PATHOLOGY

interdental septum entering the bone. Less frequently, it spreads directly into periodontal ligament and then into interproximal bone. • Facially and lingually, inflammation from the gingiva spreads along the outer periosteal surface of the bone and penetrates into marrow spaces by vessel channels in the outer cortex. • After inflammation reaches the bone by extension from gingiva, it spreads into marrow spaces and replaces the marrow with a leukocytic and fluid exudate. • Multinuclear osteoclasts and mononuclear phagocytes increase in number, bringing about bone destruction. Bone surface appears to be lined by Howship lacunae.

Radius of Action • Radius of action is the range of effectiveness within which bacterial plaque can induce bone loss. • It is postulated to be 1.5-2.5 mm. Beyond that there is no effect. • Angular defects can appear only in spaces that are wider than 2.5 mm as marrow spaces will be destroyed completely. In periodontitis, interproximal bone typically is resorbed faster than the dense facial or lingual/ palatal cortical plates. Osseous plates measuring between 1.5 and 2 mm are vulnerable to be completely destroyed by microbial plaque causing horizontal bone resorption; in contrast, osseous plates thicker than 2 mm will develop vertical bone defects.

Periodontal pathogens (LPS)

lmcrlcukin-1 (IL-I) Tumor-necrosis factor-alpha (NF-a) l'Gt;2 Hydrolytic enzymes

lmerleukm-l(IL-1) Lymphotoxin (LT)

Interleukin- I (IL-I) Carhcpsins

Enhanced proinflammatory and catabolic acnvines

Periodontal tissue breakdown

• Host mediated: prostaglandins, leukotrienes, heparin, thrombin, bradykinin, cytokines, interleukin-1,6, tumor necrosis factor, transforming growth factor [3, platelet-derived growth factor.

Bone Formation in Periodontal Disease MECHANISM OF BONE DESTRUCTION The cascade of events leading to the connective breakdown is initiated by the interaction between the microbial plaque activating the host defense cells which release a wide array of mediators. The first step in the initiation of these events are the components of the dental plaque which have the inductive capacity for the infiltration and recruitment of the host inflammatory cells such as PMNs, lymphocytes, and macrophages. The lipopolysacchrides (LPS) from the bacterial cell wall stimulates the macrophages to synthesize and secrete a wide range of molecules like interleukin-l(IL-1), tumor necrosis factor-a (TNF-a), PGE2, cytokines, and other hydrolytic enzymes. The LPS of the bacterial cell wall activates the Tlymphocytes that produce IL-1 and lymphotoxin (LT), a molecule which possess similar properties as TNF-a. These cytokines have potent pro-inflammatory activity and catabolic nature, thus they ensue periodontal tissue destruction. • Bacteria mediated: lipopolysaccharides, lipoteichoic acids, peptidoglycan, capsular and surface-associated material, muramyl dipeptide, lipoprotein.

Areas of bone formation are also found adjacent to the sites of active bone resorption and along the trabecular surfaces at a distance from the inflammation in an effort to reinforce the remaining bone (buttressing bone formation). The response of alveolar bone to inflammation is not simply a destructive process but results from preponderance of resorption over formation.

Bone Destruction Caused by Trauma from Occlusion Bone destruction resulting from trauma from occlusion may occur in the presence as well as absence of inflammation. When there is no gingival inflammation the changes caused by trauma from occlusion may vary from increased compression and tension of the periodontal ligament and increased osteoclastic activity in the alveolar bone to necrosis of the periodontal ligament and resorption of bone. These changes are reversible if the offending forces are corrected. However, persistent trauma from occlusion results in funnel-shaped widening of the crestal portion of the periodontal ligamentl with resorption of the adjacent

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CHAPTER 26 BONE LOSS IN PERIODONTAL DISEASE

bone. These changes, which may cause the bony crest to have an angular shape, represent adaptation of' the periodontal tissues aimed at "cushioning" increased occlusal forces, but the modified bone shape may weaken tooth support and cause tooth mobility. The presence of gingival inflammation trauma from occlusion aggravates the bone destruction caused by the inflammation and results in the formation of bizarre bone patterns.

Bone Destruction Caused by Systemic Disorders When a generalized tendency toward bone resorption exists, bone loss initiated by local inflammatory processes may be magnified. This systemic influence on the response of alveolar bone has been termed the bone factor in periodontal disease. Periodontal bone loss may also occur in generalized skeletal disturbances (e.g., hyperparathyroidism, leukemia, or Langerhan cell histiocytosis) by mechanisms that may be totally unrelated to the usual periodontal way of destruction. Osteoporosis is a physiologic condition of postmenopausal women, resulting in loss of bone mineral content and structural bone changes. Periodontitis and osteoporosis share a number of risk factors (e.g., aging, smoking, diseases, and medications that interfere with healing). There are studies giving evidence of increased severity of bone loss if periodontitis is superimposed on osteoporosis.

TOPOGRAPHY OF THE ALVEOLAR BONE The tips of the interdental papillae are situated more coronally than the facial or lingual/ palatal height of the marginal gingival. In health, the alveolar crest also follows a similar wave-like pattern which is approximately 2 mm apical to the cementoenamel junction (CEJ). This scalloped configuration is called "positive architecture." It is more pronounced in the anterior regions of the jawbones than the posterior where it sometimes assumes an almost "flat architecture." "Negative architecture" (a.k.a "reverse architecture") exists, when either the gingiva or the bone is destroyed in the interproximal regions resulting in interdental areas being apical to the level of' the adjacent facial or lingual/ palatal gingiva or bone, respectively, for example, as seen in necrotizing ulcerative perlodontitis (NUP) and in area of chronic food impaction. In health, the bone and gingiva. run in parallel waves and probing depths are minimal (1-3 mm). In periodontitis, interproximal bone typically is resorbed faster than the dense facial or lingual/palatal cortical plates. Resorption occurs at alveolar crest. Once it is destroyed, the underlying bone marrow resorbs at a faster rate than the dense buccal and lingual cortical plates

FACTORS DETERMINING BONE MORPHOLOGY IN PERIODONTAL DISEASE • Normal variation in alveolar bone: The normal morphologic features of alveolar bone affect the bone-destructive pattern in periodontal disease. The thickness of the compact cortical labial plates varies. In the incisor, canine, and premolar regions, the buccal cortical plate is thin and may be associated with fenestrations and dehiscence of the cortical plates. The shape of the interdental septa follows the alignment of adjacent CEJs. When the teeth are in close approximation, the interdental septum is narrow or sometimes completely nonexistent; in such areas progression of periodontal disease is faster. In the anterior region, there is a fusion of inner and outer cortical plates; trabecular bone here is often minimal. The interdental septum of posterior teeth is wide and contains relatively more trabecular bone. However, the proximity of roots of "stacked" maxillary molars allows for only a very thin plate of interproximal bone as shown in Fig. 26.1. The restricted access for cleaning between stacked molars makes these sites susceptible to plaque accumulation and the very thin interproximal alveolar bone is rapidly resorbed. Root, root trunk morphology, and the position of the root in alveolar process are the other factors affecting the pattern of resorption of alveolar bone. • Exostoses: Bony projections of various shapes and sizes. They can be in the form of nodules, sharp ridges, or spikes. • Trauma from occlusion: A vertical bone loss of interdental septum is seen. Buttressing bone formation is seen as a reparative process associated with TFO. This can be seen as a pronounced bulge in the contour of the facial and lingual bone or as a shelf-like thickening of alveolar margin referred to as "lipping." • Aggressive periodontitis: Angular bone loss is seen around the first molars and incisors. Bone defects

FIGURE 26.1

Stacked molars - thin interproximal bone.

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SECTION IV PERIODONTAL PATHOLOGY

(A)

(B)

FIGURE 26.2 (A) Generalized horizontal bone loss; (B) generalized vertical bone loss.

FIGURE 26.3 Surgical exposure demonstrating horizontal bone loss.

FIGURE 26.4 Surgical exposure demonstrating vertical bone loss with respect to mandibular left central incisor.

are wider than what are usually seen in chronic periodontitis.

They are also called as infrabony or intrabony defects (Fig. 26.4). The number of walls in the apical portion of the defect may be greater than that in its occlusal portion, in which case the term combined osseous defect is used. Onewalled osseous defect is also called as the hemiseptum (Fig. 26.5). As horizontal or vertical bone loss takes place, a variety of bony lesions or configurations result. They include:

BONE LOSS PATTERNS IN PERIODONTAL DISEASE Bone loss can be in either a horizontal or a vertical manner. This loss may be generalized (most teeth in a quadrant are affected) or localized to one or two isolated tooth/teeth (Fig. 26.2). Horizontal bone loss shall be characterized as horizontal bone loss if it shows resorption pattern as being parallel to the line joining the CEJs of the involved adjacent teeth. Although the bone height is reduced, but the bone margins remain almost perpendicular to the tooth surface (Fig. 26.3). It is also called the suprabony defect where the base of the defect is located coronal to the alveolar crest. Vertical bone loss is characterized by maintenance of crestal bone height with loss of periodontal ligament and supporting structure adjacent to the tooth root. They are hollowed-out triangles in the bone alongside one or more denuded root surfaces, enclosed by one, two, or three bone walls called as one-, two-, or three-walled defect. The base of the defect is apical to the residual alveolar bone.

a. Interproximal Crater: It is the classic form of periodontal defect especially in the posterior regions. Between

(

FIGURE

~

26.5

Hemiseptal defect as a result of vertical bone loss.

215

CHAPTER 26 BONE LOSS IN PERIODONTAL DISEASE

FIGURE 26.6

Interproximal crater.

FIGURE 26. 7 Furcation involvement of molar teeth in advanced periodontal disease.

the dense buccal and lingual cortical plates lies a cancellous core that is a vascular lattice-like structure. Once the crestal cortical plate is destroyed by periodontitis, the central bone marrow resorbs more quickly than the buccal and lingual cortical plates and an interproximal crater is formed. The boundaries of the crater on the mesial and distal are the roots of the adjacent teeth (Fig. 26.6). It is the most frequently noted osseous lesion in periodontal disease, i.e., one-third of all osseous defects. They are more common in the posterior region. Following reasons have been suggested for the high frequency of interdental craters: 1. The interdental area between the posterior teeth is somewhat difficult to clean as it requires a good deal of manual dexterity, and cancellous bone is more reactive and has a rapid turnover than cortical bone. 2. The shape of interdental bone in mandibular molars has a flat or concave architecture buccolingually that may result in increased prevalence of osseous craters. 3. Because of the presence of interdental col and the specific arrangement of capillaries in this region, inflammation results in midplane bone resorption, with buccal and lingual plates being affected much less as the buccolingual dimension is far greater than the mesiodistal dimension. b. Ledges: Plateau-like bone margins caused by resorption of thickened bony plates. c. Reverse architecture: Formed due to loss of interdental bone including the facial and lingual bone without the concomitant loss of radicular bone. It is found more commonly in maxilla. d. Furcation involvement: Invasion of the bifurcation and trifurcation of multirooted teeth by periodontal disease. It is a phase in the apical extension of periodontal

pocket. Osseous destructive pattern in furcation-involved teeth varies and depends on the degree of involvement. Pattern of bone loss around the individual roots can be horizontal or vertical (Fig. 26.7).

DIAGNOSIS A thorough clinical examination with radiographs is the key to diagnosis and treatment planning of osseous defects. 1. Clinical examination and probing: This will determine the presence and the depth of the pocket on any surface of the tooth. Transgingival probing under local anaesthesia can give general sense of the bony topography. 2. Radiographs: In periodontal disease, the alveolar bone undergoes changes that affect the lamina dura, the crestal radiodensity, and the height and contour of interdental bone. Radiographs do not reveal the extent of involvement on the facial and lingual surfaces or the presence of fenestration and dehiscence. It is obscured by the dense root structure. Dense cortical bones on the facial and lingual surfaces of interdental septa obscure defects in the intervening cancellous bone. Thus it is possible to have a deep interdental crater without having any radiographic evidence of it. Also a minimum of 30% bone loss should occur to be visible radiographically. Periodontal diseases are more extensive than what they appear on the radiograph. 3. Surgical exposure: Direct observation during flap surgery is the only definitive method for determining the architecture of a bony deformity. Normally, the crestal lamina dura extends to a point approximately 1-2 mm from the CEJ. The bone crest

216

SECTION IV PERIODONTAL PATHOLOGY

FIGURE 26.8 Horizontal bone loss proximal to the posterior teeth.

FIGURE 26.9 Intrabony - one walled.

FIGURE 26. 10 Surgical exposure demonstrating vertical bone loss with respect to maxillary second premolar and first molar.

running from the mesial of one tooth to the distal of the adjacent tooth appears flat and parallel to the imaginary line drawn from the CEJs of the same two teeth. Horizontal bone loss proximal to the posterior teeth: Bone loss is considered horizontal when the crest of the proximal bone remains parallel to an imagi-

nary line drawn between the CEJs of adjacent teeth (Fig. 26.8). Vertical (angular) bone loss mesial to the maxillary molar: Bone loss is considered vertical when the crest of the proximal bone is not parallel to an imaginary line drawn between the CEJs of adjacent teeth (Figs 26.9 and 26.10).

KEY POINTS • Periodontal destruction occurs in an episodic, intermittent fashion, with periods of inactivity or quiescence. • Interproximally, inflammation spreads to the loose connective tissue around the blood vessels, through the fibers, and then into the bone through vessel channels

that perforate the crest, side, or at the angle of the interdental septum entering the bone. • Radius of action is the range of effectiveness within which bacterial plaque can induce bone loss. It is postulated to be 1.5-2.5 mm. When combined with inflammation, trauma

CHAPTER 26 BONE LOSS IN PERIODONTAL DISEASE

KEY POINTS from occlusion aggravates the bone destruction caused by the inflammation and causes bizarre bone patterns. • Topography of alveolar bone can be positive, negative, or flat architecture.

QUESTIONS 1. Explain osseous craters. What are the procedures for

eliminating osseous craters? 2. What are the various osseous defects?

3. Write a short note on radius of action. 4. Write a note on reverse architecture 5. Classify osseous defects. 6. Describe infrabony defects.

217

(cont'd)

• Ledges are plateau-like bone margins caused by resorption of thickened bony plates. • Osseous defects can be diagnosed by transgingival probing, radiographs, or surgical exposure.

Suggested readings 1. Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry. 5th ed. Oxford: Blackwell Munksgaard; 2008. 2. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Carranza's Clinical Periodontology. 10th ed. St. Louis: Elsevier; 2006.

CHAPTER

27 Periodontitis: Chronic, Refractory, and Necrotizing Ulcerative CHAPTER OVERVIEW Chronic periodontitis is the most prevalent form of periodontitis. It is considered to start as plaque-induced gingivitis, if left untreated progresses into chronic periodontitis. It was formerly known as adult periodontitis or slowly progressing periodontitis. In the presence of systemic or environmental

CHRONIC PERIODONTITIS Epidemiologic data and clinical experiences have suggested that the adult form of periodontitis commonly seen in older individuals can also be seen in children and adolescents. Therefore, it was concluded that it would be more accurate to adopt a nonspecific term such as chronic periodontitis to characterize this constellation of periodontal disease. Traditionally, this form of periodontitis has been characterized as a slowly progressive disease. However, there are also data indicating that in presence of factors like diabetes, smoking, and stress, some patients may experience short periods of rapid progression. Chronic periodontitis has been defined as an infectious disease resulting in inflammation within the supporting tissues of teeth, progressive attachment loss, and bone loss.

Clinical Features The following are the most common clinical findings associated with chronic periodontitis (Fig. 27.1): • Slightly to moderately swollen gingiva with alteration in color ranging from pale red to magenta. • Loss of gingival stippling with blunted or rolled gingival margins and flattened or cratered papilla. • Gingival bleeding either spontaneous or in response to probing.

factors such as diabtetes, smoking, or stress, disease progression may become aggressive. Chronic periodontitis lesions include loss of attachment and bone, and are regarded as an irreversible condition. Although this disease is seen more commonly in adults, it can occur in children and adolescents also.

• Exudation of crevicular fluid and suppuration from the pocket. • Abscess formation in some cases when the pocket occludes (Fig. 27.2). • Thickened fibrotic marginal tissues obscuring the underlying inflammatory changes in cases of longstanding, low-grade inflammation. • Supragingival and subgingival plaque accumulation (frequently associated with calculus formation). • Presence of suprabony or infrabony pocket formation. • Loss of clinical attachment. • Tooth mobility in advanced cases.

Radiographic Features • Chronic periodontitis is diagnosed radiographically by the evidence of bone loss. • Pattern of bone loss observed may be vertical or horizontal (Fig. 27.3). • Vertical bone loss is when attachment and bone loss on one tooth surface is greater than that on an adjacent surface and is usually associated with angular bone defects and intrabony pocket formation. • When attachment and bone loss occurs at a uniform rate on the majority of tooth surfaces, it is called horizontal bone loss and is usually associated with suprabony pockets.

218

CHA PTER 27 PERIO DONTITIS: CHRONIC, REFRACTORY, AND NECROTIZING ULCERATIVE

(A)

219

(B)

FIGURE 2 7. 1

Clinical features of chronic periodontitis: (A) increased amount of calculus, redness, swelling, and edema of gingival margin; (B) gingival recession with visible exudate and gingival stippling has been lost.

Fusobacterium nucleaium, Actinobacillus actinomycetemcomitans, Treponema, and Eubacterium species. Symptoms • Chronic periodontitis is usually painless unless associated with caries due to exposed roots that are sensitive to heat, cold, or both. • Localized dull pain sometimes radiating deep into jaw; areas of food impaction and gingival tenderness can be found. • Usually patient notices that their gums bleed while brushing or eating; spaces appear between their teeth or teeth start moving. FIGURE 2 7 .2 Periodontal abscess.

Disease Distribution According to area of disease distribution chronic periodontitis may be classified as localized and generalized.

• Localized periodontitis: Periodontitis is considered localized when less than 30% of sites assessed in the mouth demonstrate attachment loss and bone loss. • Generalized periodontitis: Periodontitis is considered generalized when more than 30% of sites assessed in the mouth demonstrate attachment loss and bone loss.

Disease Severity FIGURE 2 7 .3 Pattern of bone loss seen in chronic periodontitis.

Microbiologic Features • Chronic periodontitis is associated with a variable microbial pattern. • The microorganisms commonly found are

Porphyromonas gingivalis, Bacteroides Jorsythus, Prevotella iniermedia, Campylobacter recius, Eikenella corrodens,

According to disease severity chronic periodontitis may be classified as slight (mild), moderate, or severe.

• Slight (mild) periodontitis: When no more than 1-2 mm of clinical attachment loss has occurred.

• Moderate periodontitis: When 3-4 mm of clinical attachment loss has occurred.

• Severe periodontitis: When 5 mm or more of clinical attachment loss has occurred.

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SECTION IV PERIODONTAL PATHOLOGY

Disease Progression The rate of disease progression in chronic periodontitis is slow but sometimes may be modified by systemic or underlying factors. Several models have been proposed to describe the rate of disease progression • Continuous paradigm • Random burst model • Asynchronous multiple burst model

• Continuous model implies slow, continuous, and progressive destruction of periodontium over time.

Plaque retentive factors are those that facilitate plaque accumulation or prevent the removal of plaque by routine oral hygiene procedures. They retain plaque microorganisms in proximity to the periodontal tissues, providing an ecologic niche for plaque growth and maturation. Among the plaque retentive factors the most important is calculus because of its ability to retain and harbor plaque bacteria on its rough surface. Other factors that are known to retain plaque or prevent its removal are subgingival carious lesions, furcations exposed by loss of attachment and bone, crowded and malaligned teeth, root grooves, and concavities.

• Random burst model proposes that progression of disease

Systemic Factors

occurs at short periods of active destruction, which are followed by periods of remission that occurs randomly with respect to site in an individual. • In asynchronous multiple burst model the majority of destructive disease takes place within a definite period of the individual's life then followed by prolonged periods of inactivity.

In plaque-induced chronic periodontitis, the rate of progression is considered to be slow. But when this type of periodontitis occurs in a patient who also suffers from a systemic disease that influences host response, the rate of destruction is significantly increased. Diabetes type II or noninsulin-dependent diabetes mellitus (NIDDM) is considered as the most important systemic factor that can lead to increased periodontal destruction. The synergistic effect of plaque accumulation and modulation of an effective host response through the effects of diabetes can lead to severe and extensive periodontal destruction that may be difficult to manage with standard clinical techniques without controlling systemic condition

Differentiation Characteristics of Chronic Periodontitis • • • • •

Prevalent in adults but can occur in children. Amount of destruction consistent with local factors. Associated with variable microbial pattern. Subgingival calculus frequently found. Slow to moderate rate of progression with possible periods of rapid progression. • Possibly modified or associated with the following: Systemic diseases such as diabetes mellitus and HIV infection. Local factors predisposing to periodontitis. Environmental factors such as cigarette smoking and emotional stress.

Risk Factors for Chronic Periodontitis Local Factors Plaque accumulation is the primary initiating factor in periodontal destruction. In addition to this, plaque retentive factors are also important in the development and progression of chronic periodontitis. Plaque that accumulates on the tooth and gingival surfaces at the dentogingival junction is considered to be the main etiologic factor in periodontal destruction. Increase in the proportion of gram-negative organisms such as Poprphromonas gingivalis, Tanarella forsythia, and Treponema denticola (known as red complex) are associated with the ongoing attachment and bone loss in chronic periodontitis. It has been found that these bacteria may impart a local effect on the cells of the inflammatory response and cells and tissues of the host resulting in a local, site-specific disease process.

Environmental and Behavioral Factors Smoking is one such factor that has been found to increase the severity and extent of periodontal disease. It is seen that smokers with chronic periodontitis have more attachment and bone loss, more furcation involvements, and deeper pockets compared with nonsmokers. The reasons behind this effect can be changes in subgingival microflora between smokers and nonsmokers in addition to effects of smoking on host response. Emotional stress can also influence the extent and severity of chronic periodontitis because of the effect of stress on immune function.

Genetic Factors Periodontal destruction frequently seen among family members and across different generations suggests the possibility that there is an underlying genetic factor that plays a role in periodontal disease. Recent data indicate that a genetic variation or polymorphism in the genes encoding interleukin-la (IL-la) and IL-113 is associated with an increased susceptibility to a more aggressive form of chronic periodontitis.

Treatment Considerations in Chronic Periodontitis Clinical judgment is an integral part of the decisionmaking process. Many factors affect the decisions for

CHA PTER 27 PERIO DONTITIS: CHRONIC, REFRACTORY, AND NECROTIZING ULCERATIVE

appropriate therapy and expected therapeutic results, Patient-related factors include systemic health, age, compliance, therapeutic preferences, and patient's ability to control plaque, Other factors include the clinician's ability to remove subgingival deposits, prosthetic demands, and the presence and treatment of teeth with more advanced chronic periodontitis. Treatment considerations can be divided into initial therapy, compromised therapy, and periodontal surgical procedures as discussed in subsequent sections.

Initial Therapy

221

monitored, demonstrate additional attachment loss at one or more sites, despite well-executed therapeutic measures and patient's efforts to stop the progression of disease. The recent concept is that the refractory can be applied to all forms of destructive periodontal disease that appear to be nonresponsive to treatment, e.g., refractory chronic periodontitis and refractory aggressive periodontitis. Refractory periodontitis is completely different from recurrent periodontitis; as in the latter, a complete remission occurs after therapy followed by recurrence of disease due to local factors.

1. Elimination, alteration, or control of risk factors like

2. 3.

4. 5.

diabetes, smoking, certain periodontal bacteria, genetic predisposition, systemic diseases and conditions, stress, nutrition, HIV infection, and medications that may contribute to chronic periodontitis should be attempted. Consultation with the patient's physician may be indicated in such cases Instruction, reinforcement and evaluation of the patient's plaque control should be performed. Supra- and subgingival scaling and root planing should be performed to remove microbial plaque and calculus. Antimicrobial agents or devices may be used as adjuncts to the routine periodontal therapy. Local factors contributing to chronic periodontitis should be eliminated like removal of restorative overhangs and overcontoured crowns, correction of ill-fitting prosthetic appliances, restoration of carious lesions, and occlusal trauma should be corrected.

Compromised Therapy In certain cases, because of severity and extent of disease and the age and health of the patient, initial therapy may become end point that should include timely periodontal maintenance.

Periodontal Surgical Procedures In patients with chronic periodontitis with advanced loss of periodontal support, a variety of periodontal surgical treatment modalities can be considered: 1. Flap surgery 2. Gingivectomy

3. Periodontal plastic surgery 4. Regenerative therapy with bone grafts/ GTR membranes 5. Osseous resective surgery 6. Root resective therapy

REFRACTORY PERIODONTITIS According to American Academy of Periodontology, the term refractory periodontitis refers to destructive periodontal diseases in patients who, when longitudinally

Etiology Refractory periodontitis occurs when conventional periodontal therapy has failed to eliminate microbial reservoirs of infection or has resulted in the emergence or superinfection of opportunistic pathogens. It may also occur as a result of a complexity of unknown factors that may compromise the host's response to conventional periodontal therapy. The causative factors for refractory periodontitis can be: • Abnormal host response • Resistant periodontopathic microorganisms • Failure to eliminate morphologic conditions such as furcation involvement and irregular root surface • Smoking and systemic diseases On the basis of causative factors, two types of refractory periodontitis have been considered. The first type comprises those with refractory sites, i.e., patients with adult periodontitis in whom anatomic conditions favor the proliferation of periodontopathic microorganisms. The second type of refractory periodontitis is due to severe PMN defects or other immunologic problems, e.g., aggressive periodontitis associated with Papillon-Lefevre syndrome. The subgingival microbiota in refractory periodontitis mainly consists of elevated levels of red complex species and orange complex species. They include B. forsythus, P. gingivalis, Fusobacterium, Campylobacter, Prevotella, and Peptostreptococcus spp., and S. intermedius.

Clinical Features The primary feature of refractory periodontitis is the occurrence of additional attachment loss and bone loss after repeated attempts to control the infection with conventional periodontal therapy. Refractory periodontitis should be diagnosed only after the conclusion of conventional active periodontal

222

SECTION IV PERIODONTAL PATHOLOGY

therapy and in patients who follow a rigorous program of periodontal maintenance and comply with recommended oral hygiene procedures.

Treatment The goal of therapy for refractory periodontitis is to stop or slow the progression of the disease. Due to complexity and many unknown factors a reasonable treatment objective is to slow the progression of the disease. Once the diagnosis is made the following steps are indicated in the treatment planning: 1. Collection of subgingival microbial samples from

selected sites for analyses, possibly including antibiotic sensitivity testing 2. An appropriate antibiotic regimen should be selected 3. Along with administration of antimicrobial regimen, use of conventional periodontal therapies 4. Periodontal maintenance program

SYSTEMIC ANTIBIOTIC THERAPY IN THE MANAGEMENT OF REFRACTORY PERIODONTITIS Systemic antibiotic therapy is administered to reinforce mechanical periodontal treatment and support the host defense system in overcoming the infection by killing subgingival pathogens that remain after conventional mechanical periodontal therapy. The antibiotics that are commonly found effective are: • 250 mg of tetracycline hydrochloride four times daily for minimum of 1 week • 250 mg of amoxicillin and 125 mg of clavulanate potassium three times daily for 14 days • 500 mg of metronidazole three times daily for 7 days • 150 mg of clindamycin hydrochloride four times daily for 7 days • Combination of metronidazole-amoxicillin, metronidazole-doxycycline, and metronidazoleciprofloxacin

Clinical Features Most of the clinical features are same as that seen in necrotizing ulcerative gingivitis, i.e., necrosis and ulceration of tips of interdental papilla or gingival margin, which gets covered by pseudomembrane. Ulcerated margins are surrounded by erythematous halo. The lesions are extremely painful and bleed on slight manipulation. The distinguishing feature of NUP is destructive progression of the disease that includes periodontal attachment and bone loss. Deep interdental osseous craters typify periodontal lesions of NUP. The most striking feature of this lesion is absence of deep conventional pockets. This is because ulcerative and necrotizing nature of this lesion destroys the marginal epithelium resulting in gingival recession. Advanced lesions of NUP lead to severe bone loss, tooth mobility and ultimately tooth loss. In addition to these intraoral manifestations, NUP patients may present with oral malodor, fever, malaise, or lymphadenopathy.

NECROTIZING ULCERATIVE PERIODONTITIS IN HIV/AIDS PATIENTS Necrotizing ulcerative periodontal lesions seen in HIVpositive/ AIDS patients are much more destructive and result in complications that are rarely seen in non-HIV/ AIDS patients (Fig. 27.4). Periodontal attachment and bone loss associated with these types of NUP are extremely rapid (10 mm of bone loss over a 62-month period). Many of these lesions have resulted in tooth loss. The major complication seen is progression of lesions to involve large areas of soft tissue necrosis with exposure of bone and sequestration of bone fragments. These lesions when extend to the vestibular area and palate are termed as necrotizing ulcerative stomatitis (NUS).

Etiology

NECROTIZING ULCERATIVE PERIODONTITIS

Bacterial pathogens, specifically a mixed fusiformspirochete bacterial flora, play a key role in the etiology of NUP. Numerous predisposing factors have been attributed including poor oral hygiene, preexisting periodontal diseases, smoking, viral infections, immunocompromised status, psychosocial stress, and malnutrition.

When necrotizing ulcerative gingivitis (NUG) progresses to the underlying periodontal structures, it results in attachment and bone loss. This condition is referred to as necrotizing ulcerative periodontitis (NUP). According to the World Workshop of Periodontics, NUG and NUP can be collectively referred to as necrotizing periodontal diseases.

Microbial Flora Microbiologic studies of NUP have demonstrated the presence of an anaerobic flora consisting of Treponema and Selenomonas spp., Fusobacterium nucleatum, Prevotella intermedia, and Porphyromonas gingivalis. It was also found that there was significantly greater prevalence of opportunistic fungus Candida albicans and a

CHA PTER 27 PERIO DONTITIS: CHRONIC, REFRACTORY, AND NECROTIZING ULCERATIVE

(A)

FIGURE 2 7 .4

223

(B)

Necrotizing ulcerative period on ti tis (there is complete necrosis of interdental papilla).

higher prevalence of Actinobacillus actinomycetemcomitans, P. intermedia, P. gingivalis, F. nucleatum, and Campylobacter species in HIV-associ-ated NUP patients.

Immunosuppression It has been seen that some form of immune dysfunction exists in NUP patients. The main reason for this immunosuppression is likely reduced CD4+ cell counts, black females > white females > white males

FIGURE 28.1

Distolabial migration of maxillary central incisors

noticed in LAP.

Generalized Aggressive Periodontitis (GAP) • Blacks are at much higher risk than whites • Male teenagers > female adolescents Important Epidemiological Studies The important LAP-related epidemiological studies conducted in different parts of the world have been summarized in Table 28.2.

LOCALIZED AGGRESSIVE PERIODONTITIS Localized aggressive periodontitis is formerly called localized juvenile periodontitis. Aggressive forms of periodontal disease show some primary and secondary features as follows (Lang, 1999):

TABLE 28.2

Prevalence of Localized Aggressive Periodontitis

Geographic location

Investigators

Prevalence (%)

Africa

Mac Gregor (1980)

0.80

Brazil

Gjermo et al (1984)

3.70

Chile

Saxby (1987)

0.32

UK

Saxby (1987)

0.10-0.80

Japan

Kowashi (1988)

0.47

USA

Loe and Brown (1991)

0.14-2.05

India • Chennai • Mumbai • Mumbai

Miglani et al (1949) Marshall Day and Shourie (1965) Rao and Tewani (1968)

0.10 17.60 6.80

C H A PT ER 28 A G G R ESSIV E PER IO D O N T IT IS

227

Primary Features • Noncontributory medical history • Rapid attachment loss and bone destruction • Familial aggregation of cases Secondary Features • Amount of microbial deposits inconsistent with the severity of periodontal tissue destruction • Elevated proportions of Aggregatibacter actinomycetomcomitans (Aa) and in some far east populations,

Prophyromonas gingivalis • Phagocyte abnormalities • Hyperresponsive phagocyte, including elevated production of PGE2 and IL-113 in response to bacterial endotoxins • Progression of attachment loss and bone loss may be self-arresting • Age of onset: Around puberty, but there are no fixed or arbitrary upper age limits • The patients are otherwise systemically healthy. • The progression of disease: The loss of clinical attachment in patients with aggressive periodontitis is about three to four times faster. There are many factors that influence how rapidly the periodontium is destroyed. • Familial pattern: There is tendency of cases to aggregate in families. • Presence of local factors and periodontal destruction: There is minimal amount of dental plaque (i.e., biofilm) present on the affected teeth but the periodontal destruction is extensive. Hence, the amount of plaque deposit is inconsistent with the magnitude of bone destruction which seems quality of plaque is a significant factor in patients with LAP. • Distribution: Localized to first molar/ incisor presentation with interproximal attachment loss on at least two permanent teeth, one of which is a first molar, and involving no more than two teeth other than first molars and incisors. • Causative/specific microorganisms: The plaque contains elevated levels of A actinomycetomcomitans, however, in Far East Asian country, the microorganism detected was P. gingivalis (Pg.). • Robust serum antibody response to the infecting microorganism (A actinomycetomcomitans). • Gingival inflammation: There is low level of clinical gingival inflammation despite the presence of deep periodontal pocket and advanced alveolar bone loss (Fig. 28.2). • Pathological migration: There is distolabial migration of maxillary incisors resulting in diastema formation (Fig. 28.3). • Tooth mobility: Increasing mobility of incisors and first molars. • Single or multiple periodontal abscess: Formation with lymph node enlargement. • Pain: Deep, dull, radiating pain during the mastication.

FIGURE 28.2 Clinical view showing deep periodontal pocket in relation to #12.

FIGURE 28.3 Distolabial migration of maxillary incisors with diastema formation.

• Dental hypersensitivity: Patient may complain of sensitivity of denuded root surfaces to thermal and tactile stimuli. • Burnout phenomenon: In many cases of LAP, the rate of disease progression slows down or stops entirely and disease appears to be self-limiting. The attachment loss and bone destruction do not spread to other teeth. This phenomenon of self-limitation of disease activity with advancing age is called as "burn-out" phenomenon. This can be explained by the possibility that the periodontal disease merely goes into remission and can become active sometime in the future. • Incidental attachment loss: There are isolated areas of attachment loss in otherwise healthy dentitions including the recessions associated with: Traumatic injuries Tooth position Impacted third molars Endodontic infection

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SECTION IV PERIODONTAL PATHOLOGY

FIGURE 28.4

Radiograph illustrating arc shaped bone loss in mandibular molar region.

Root fractures Subgingival caries Subgingival restoration. The patient showing this clinical finding can be categorized under high risk for aggressive periodontitis or chronic periodontitis. It is necessary to understand that to assign a diagnosis or classify the disease, not all the features/ characteristics must be present. The diagnosis of disease may be based on the clinical, radiological, historical data and laboratory testing.

Radiographic Features The presence of vertical/ angular bone loss around the first molars and incisor teeth (see Figs 28.4 and 28.5). "Arc shaped" alveolar bone loss around first molars extending from the distal surface of second premolars to the mesial surface of second molars. This bilateral "arc shaped" bone loss is mirror image and characteristic of LAP (Figs 28.4 and 28.5).

The first molars and the incisors are the first permanent teeth to erupt in the oral cavity, and get exposed to microorganisms, deposits, and their toxins for a longer period of time. Hence, these teeth are more susceptible to periodontal tissue destruction. After the initial invasion of the periodontal tissues by the causative organism A. actinomycetomcomitans, there is increased antibody formation to neutralize these microorganisms. Hence, the spread of the disease to other teeth may be arrested. There may be possible colonization of some other microorganisms considered to be antagonistic to the main causative organisms, thus localizing the A. actinomycetemcomitans infection and tissue destruction. Due to the unknown etiology, the causative organism, i.e., A. actinomycetemcomitans, may lose its ability to produce the virulence factors such as leukotoxins. This phenomenon may arrest the existing disease activity and prevents further colonization of microorganisms. Some defects on the cemental surface (cemental hypoplasia or aplastic cementum) may be responsible for the localization of the lesion in LAP.

Microbiology of LAP l. Aggregatibacter actinomycetemcomitans (Aa.) (about 90%) 2. P. gingivalis (Pg.) 3. Capnocytophaga spp. 4. Eikenella corrodens 5. Campylobacter rectus 6. Fusobacterium nucleatum 7. Bacteroides capillus 8. Capnocytophaga spp. 9. Eubacterium brachy 10. Spirochetes 11. Viruses: Human Cytomegalovirus,

Epstein-Barr virus-I,

Herpes virus. Area-Specific (First Molar/Incisor) Distribution in Localized Aggressive Periodontitis Although the exact etiology for the area-specific distribution of LAP is not known, it can be explained as follows:

FIGURE 28.5

Radiograph showing angular bone loss.

A. Actinomycetemcomitans (Aa.) This organism was first isolated in 1912 by Klinger (a German microbiologist) from the lesions of cervicofacial actinomycosis. Since the organism was isolated together with Actinomyces israelii, the species name stands actinomy-

C H A PT ER 28 A G G R ESSIV E PER IO D O N T IT IS

cetemcomitans (together with Actinomyces). Furthermore, in the genus name Actinobacillus, actino refers to starshaped internal morphology of the colonies and bacillus refers to the cell shape. Recently, Niels Norskov-Lauritsen and Mogens Kilian (2006) renamed this bacterium as Aggregatibacter (rod-shaped bacterium that aggregate with others) actinomycetemcomitans. A. actinomycetemcomitans is a fastidious, facultatively anaerobic, nonmotile, nonsporing, short cocco-bacilli, small gram-negative rod, 0.4-0.5 lm x 1.0-1.5 lm in size that has been strongly implicated in LAP (Zambon, 1983). Various studies have shown that A actinomycetemcomitans is the key microorganism found in more than 90% of patients diagnosed with LAP. A. actinomycetemcomitans is a human pathogen that can cause severe extraoral infections including infective endocarditis, brain, facial and thyroid abscess, osteomylitis, meningitis, and urinary tract infection (UTI). In LAP, certain A actinomycetemcomitans serotypes and corresponding serotype antigens may be related to specific sites of infection. Six serotypes (a, b, c, d, e, and f) of A actinomycetemcomitans have been identified. However, in LAP, serotype-b is significantly elevated in the subgingival plaque.

A. actinomycetemcomitans (Aa.) As a Key Etiologic Agent in LAP There are several lines of evidence that incriminate A

actinomycetemcomitans a key etiologic agent in LAP. These are summarized hereunder: • This organism is found in high numbers in periodontal lesions in LAP patients. However, it is either absent or present in low numbers in healthy sites in the same patient. • Over 90% of patients with LAP patients have high titers of serum IgG antibodies to A actinomycetemcomitans. • This organism possesses several potent virulence factors responsible for neutrophil dysfunction and bone destruction in LAP. • Sites with evidence of disease progression often show elevated levels of A actinomycetemcomitans. • Elimination of A actinomycetemcomitans from periodontal lesions by therapeutic measures is associated with clinical improvement.

Virulence Factors Produced by

A. actinomycetemcomitans A. actinomycetemcomitans produces a variety of factors that can damage the periodontal tissues in LAP: • A leukotoxin that can destroy polymorphonuclear leukocytes (PMNs) and macrophages • Cytolethal distending toxin causes apoptosis of cells • Chemotactic inhibition factor • A bone resorption-inducing toxin

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• Surface-associated material (SAM), which stimulates bone resorption • Lipopolysaccharide (LPS), which can also cause bone resorption • Proteases that degrade immunoglobulins • Collagenase, which may degrade connective tissue collagen • The RANKL/OPG ratio is increased in the gingival crevicular fluid • Extracellular outer membrane vesicles • Factors affecting the immune response may inhibit IgG and IgM production • Factors damaging host cells including epithelial cells and fibroblasts

Immunologic Factors The host immune response is crucial to neutralize effectively the periodontal pathogens and their by-products. In aggressive periodontitis, the following immune defects have been implicated in its pathogenesis. • Human leukocyte antigens (HLA), HLA-A9 and B15 antigens are consistently associated with aggressive periodontitis. • HLA-A2 and HLA-B5 polymorphisms demonstrate negative association to aggressive periodontitis. • Functional defects of PMN s or monocytes or both result into defective chemotaxis and phagocytosis. • On exposure to microbial lipopolysaccharides, the monocytes become hyperresponsive and produce proinflammatory product prostaglandin E2 (PGE2) ultimately responsible for the increased connective tissue and bone destruction. • Receptors for IgG2 antibodies monocyte Fc-yRII are immensely increased in patients with aggressive periodontitis. In generalized aggressive periodontitis, autoimmunity plays an important role. Host antibodies to collagen, DNA, and IgG may be observed in patients with aggressive periodontitis.

Genetic Factors • Aggressive periodontitis tends to occur in families, suggesting a genetic basis to the disease. • The precise nature of any immune defect or the specific gene that is inherited in families is not apparent presently. • Familial clustering of neutrophil abnormalities has been observed in LAP. • The specific gene, which is inherited in families, varies in different populations and ethnic groups. • It is believed that the response of antibody to the causative organism (A actinomycetemcomitans) is under genetic control and may be race dependent.

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• The true heterogeneity in disease susceptibility may be present. • Various single nucleotide polymorphisms of a specific gene (e.g. Pc-v receptor Illb/Ilbgenes) can also be responsible for development of AgP. • The segregational and linkage analyses have shown that a major gene plays a role in LAP and it is transmitted through the autosomal dominant mode of inheritance. • At present, the existence of a gene of major effect is accepted, although it is considered unlikely that all forms of aggressive periodontitis are due to same genetic variant.

Environmental Factors Recent evidence has indicated that besides genetic influences, environmental factors may affect the clinical expression of aggressive periodontitis. • Cigarette smoking is an important environmental risk factor for developing a more severe periodontal breakdown in patients with localized and generalized AP. • The frequency and duration of smoking are the important variables that can influence the extent of destruction in GAP. • Smokers with GAP have more affected teeth and greater attachment loss than the nonsmoker GAP patients. Smokers also demonstrate poorer clinical response to treatment compared with nonsmokers. • The protective antibody (IgG2) response to A. actinomycetemcomitans in GAP patients with smoking habits is significantly depressed. • Psychological stress and depression have also been proposed to act as an environmental risk factor for AgP.

Other Features of GAP • Unlike LAP, there is marked plaque and calculus accumulation and clinical signs of gingival inflammation are evident. • It is a heterogeneous condition, and as such it is difficult to determine its presence. • The familial nature of the GAP is unclear. • The subgingival flora of GAP is much more complex than seen in LAP. • The microbial flora in GAP unlike LAP is not diagnostic, since these pathogens can be isolated from other forms of periodontal disease. • The loss of attachment and alveolar bone destruction are episodic in nature. • Antibody level to the causative organism is elevated but not diagnostic, since this immune response is not evident in all patients. • Neutrophil dysfunction may play a key role in the pathogenesis of GAP. Reports have shown that the neutrophils from these patients may exhibit decreased chemotaxis. • Because of the similarities between the LAP and GAP, it is presumed that the generalized form may be the continuation of the localized disease process.

Radiographic Feature of GAP Radiographic picture can range from severe bone loss associated with minimal number of teeth to advanced bone loss affecting majority of the teeth in the dentition (Fig. 28.6).

Microbiology of GAP 1. P. gingivalis

GENERALIZED AGGRESSIVE PERIODONTITIS (GAP) It was formerly called generalized juvenile periodontitis or rapidly progressive periodontitis.

Tannerella forsythia A. actinomycetemcomitans 4. Campyobacter rectus 5. Eubacterium spp. 6. Treponema spp. 2. 3.

• Usually the individuals are younger than 30 years of age, but older patients may also be affected • Poor serum antibody response to infecting agents • Pronounced episodic nature of the attachment loss and alveolar bone destruction • Generalized interproximal attachment loss affecting at least three permanent teeth other than the first molars and incisors.

Epidemiology of GAP The prevalence of GAP has been estimated to be 0.13% varying according to geographic location, ethnicity, and race.

FIGURE 28.6 periodontitis.

Severe bone loss seen in generalized aggressive

C H A PT ER 28 A G G R ESSIV E PER IO D O N T IT IS

7. Microbes from the Archaea domain 8. Selenomonas spp. 9. Treponema lecithinolyticum

Risk Factors Although patients suffering from aggressive periodontitis show minimal amount of plaque accumulation, the specific organisms present in the plaque may be associated with extensive destruction of periodontal tissues. A consortium of multiple microorganisms living in biofilms participate in the events leading to periodontitis. However, it is clear that localized and generalized aggressive forms of periodontitis are not monoinfections. There is compelling evidence that some subgingival microorganisms are more important than others.

TREATMENT Early diagnosis of this disease is crucial because the successful treatment and prognosis of aggressive periodontitis is considered to be dependent on meticulous debridement of microbial plaque, elimination of causative microorganisms, and providing an environment conducive to long-term maintenance. The treatment of aggressive periodontitis must be pursued with a logical and regimented approach.

Nonsurgical Treatment Phase-L therapy: 1. Motivation and education of the patient 2. Oral hygiene instructions (OHi) 3. Counseling of the family members because of its familial pattern 4. Scaling and root planing 5. Correction of anatomical factors 6. Occlusal adjustment 7. Recall appointments for the maintenance. Full mouth disinfection: It has been observed that A. actinomycetemcomitans has a tendency of translocation from person to person and from site to site and may reinfect the treated sites by translocation from the infected sites in the oral cavity. Hence, to prevent it, Quirynen et al. proposed the concept of "Full Mouth Disinfection" which is carried out as follows: 1. Full mouth scaling and root planing (two visits within 24 h) 2. Brushing of dorsum of tongue by the patient for 60 s with 1 % chlorhexidine gel 3. Spraying of peritonsillar regions twice daily with chlorhexidine

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4. Subgingival application of 1 % chlorhexidine solution into the full depth of periodontal pockets, three times in 10 min 5. Rinsing of mouth with 0.2% chlorhexidine mouthwash for 2 min Antibiotic therapy 1. Elimination of A actinomycetemcomitans (main causative organism) is the mainstay of treatment of aggressive periodontitis. 2. The tissue invasive property by A actinomycetemcomitans in LAP markedly affects the overall treatment planning. 3. Systemic antibiotics such as tetracyclines are effective in the treatment of LAP, when administered as an adjunct to scaling and root planing or surgical therapy. 4. 250 mg ofTetracycline HCl QID for 14 days, (after systemic administration), shows 2-10 times more concentration in GCF than in serum. 5. Semisynthetic preparation of tetracycline, Doxycycline 100 mg/ day for 2 weeks, has also been successfully tried in conjunction with periodontal surgery in the treatment of LAP. 6. Metronidazole 200 mg, three times daily for 10 days, in combination with scaling and root planing has proven its efficacy in the eradication of A. actinomycetemcomitans. 7. The combination of metronidazole 500 mg three times daily plus amoxicillin 500 mg three times daily is probably the most popular antibiotic regimen in the current literature. 8. Deas and Mealy (2010) recommended that antibiotic therapy should be started 24 h before scaling and root planing. 9. Microbiological monitoring of the subgingival flora for A actinomycetemcomitans is a critical aid in the successful therapy of LAP. Local drug delivery system: This mode of drug administration, especially in LAP, is a useful alternative for systemic antibiotic therapy. The therapeutic advantages of local drug delivery are as follows: 1. It enhances the exposure of the target organisms with higher concentrations of the drug. 2. Smaller total doses of topical agents can be delivered inside the pocket, thereby avoiding the side effects of systemic antibacterial agents. 3. It helps in achieving the higher therapeutic level of medication. Host modulation: The current approach in the treatment of aggressive periodontitis includes the administration of agents that modulate the host response to the disease. The administration of subantimicrobial-dose doxycycline (SOD) may help to prevent the periodontal tissue destruction

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by controlling the activation of matrix metallo proteinases (MMPs). Photodynamic therapy (PDT): Recently, PDT has gained much popularity as one of the most effective broad-spectrum antibacterial therapy for aggressive periodontitis. This procedure involves the eradication of target cells, i.e., periodontal pathogens by reactive oxygen particles produced by means of photosensitizing compounds (e.g., toluidine blue) instilled in periodontal pocket that is activated by laser.

Extraction of the hopeless teeth. Implant therapy is a very useful treatment modality in aggressive periodontitis patients.

Dental Implants Initially, the use of dental implants was recommended with much caution in patients with aggressive periodontitis because of the fear of bone loss. Currently, it is suggested that use of dental implants must be considered in the overall treatment plan of patients with aggressive period on ti tis.

Surgical (Regenerative and Resective) Therapy Modified Widman flap surgery supplemented with systemic tetracycline therapy shows good results. Osteoctomy and osteoplasty: These are of limited value in LAP patients because of the severity of disease. Regenerative procedure: - Flap surgery+ bone graft+ antibiotic therapy+ maintenance therapy. - Flap surgery+ bone graft+ GTR membrane+ antibiotics+ maintenance therapy. Root resection/hemisection of the affected first molar tooth, depending on the indication. Autotransplantation: Extraction of the affected mandibular first molar and simultaneous autotransplantation of incompletely (90%) erupted third molar in the extraction socket.

Periodontal Maintenance Care Frequent recall visits of the aggressive periodontitis patients are very important factors in the control of the disease and to prevent its further progression or its recurrence. Each recall visit at every 3-4 months should include a thorough medical history review, a comprehensive periodontal and oral examination, thorough scaling and root planing, and reenforcement of oral hygiene instructions. Yearly radiographic examination of the teeth at risk should be taken.

• Localized recurrence: SRP + local drug delivery • Generalized recurrence: Full mouth SRP + systemic antibiotics + host modulation therapy • Extraction of teeth with progressive disease to preserve alveolar bone

KEY POINTS • Aggressive periodontitis is defined as the rare form of periodontitis occurring in an otherwise healthy young individual, and characterized by rapid loss of alveolar bone in about more than one tooth of permanent dentition. The amount of bone destruction is inconsistent with the amount of local factors. • There is a robust serum antibody response to the infecting microorganism (A. actinomycetemcomitans). • There is presence of vertical/ angular bone loss around the first molars and incisor teeth. • The prevalence of localized aggressive periodontitis varies in different parts of the world ranging from Oto 17%. • Neutrophil dysfunction may play a key role in the pathogenesis of GAP. Reports have shown that the neutrophils from these patients may exhibit decreased chemotaxis.

• The commonest microorganisms implicated in the GAP are as follows:

P. gingivalis A. actinomycetemcomitans Tannerella forsythia (formerly Bacteroides forsythus). • Actinobacillus actinomycetomcomitans was first isolated in 1. 2. 3.

1912 by Klinger. • Five serotypes (a, b, c, d, and e) of A. actinomycetemcomitans have been identified. However, in LAP, serotype-b is significantly elevated in the subgingival plaque. • Cigarette smoking is an important environmental risk factor for GAP. Metronidazole 500 mg + amoxicillin 500 mg three times per day for 7 days+ surgical therapy has shown promising results in the treatment of GAP.

C H A PT ER 28 A G G R ESSIV E PER IO D O N T IT IS

QUESTIONS 1. Describe the etiology and clinical features of aggressive

periodontitis. 2. Write a note on diagnosis and management of

aggressive periodontitis. 3. Describe the clinical and radiographic features of

aggressive periodontitis. 4. Describe the microbiology of aggressive periodontitis. 5. Write a note on current concepts in the management

of aggressive periodontitis.

Suggested readings 1. Armitage GC. Development of a classification system of periodontal diseases and conditions. Ann Periodontol 1999;4:l-6. 2. Baer PN. The case for periodontitis as a clinical entity. J Periodontal 1971;42:l-6. 3. Butler JH. Familial pattern of juvenile periodontitis (periodont). J Periodontol 1969;40:115-8. 4. Gottlieb B. The formation of the pocket: diffuse atrophy of alveolar bone. J Am Dent Assoc 1928;15:462-76. 5. Orban B, Weinmann JP. Diffuse atrophy of alveolar bone. J Periodontal 1942;13 :31. 6. Quirynen M, Bollen CM, Vandekerckhove BN, et al. Full vs. partialmouth disinfection in the treatment of periodontal infections: short term clinical and microbiological observations. J Dent Res 1995;74:1459. 7. Thoma KH, Goldman HM. Wandering and elongation of the teeth and pocket formation in paradontosis. J Am Dent Assoc 1940;27:335.

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8. Zambon JJ, Christersson LA, Slots J, et al. Actinobacillus actinomycetomcomitans in human periodontal disease: prevalence in patient groups and distribution of bio-types and serotypes within families. J Periodontol 1983;54:707-11. 9. Deas DE, Mealey BL. Response of chronic and aggressive periodontitis to treatment. Periodontal 2000 2010;53:154-66. 10. Lang NP, Bartold PM, Cullinan M, Jeffcoat M, Mombelli A, et al. Consensus report: aggressive periodontitis. Ann Periodontology 1999;4:53. 11. Loe H, Brown LJ. Early onset periodontitis in the United States of America. J Periodontal 1991;62:608-16. 12. Gjermo P, Bellini HT, Santos VP, Martens JG, Ferracyoli JR. Prevalence of bone loss in a group of Brazilian teenagers assessed in bitewing radiographs. J Clin Periodontol 1984;11:104-13. 13. Saxby MS. Juvenile periodontitis: an epidemiological study in the west Midlands of the United Kingdom. J Clin Periodontal 1987;14:594-8. 14. Macgregor ID. Radiographic survey of periodontal disease in 264 adolescent schoolboys in Lagos, Nigeria. Community Dent Oral Epidemiol 1980;8:56-60. 15. Kowashi Y. Prevalence of juvenile periodontitis among students at Nagasaki University. Adv Dent Res 1988;2:395-6. 16. Miglani DC, Sharma OP. Incidence of acute necrotizing ulcerative gingivitis and periodontosis among cases seen at the government hospital Madras, India. J All India Dent Assoc 1965;37:183-202. 17. Marshall-Day CD, Shourie KL. A roentgenographic survey of periodontal disease in India. J Am Dent Assoc 1949;39:572-88. 18. Rao SS, Tewani SV. Prevalence of periodontosis among Indians. J Periodontol 1968;39:27-34. 19. Lopez NJ, Rios V, Pareja MA, Fernandez 0. Prevalence of juvenile periodontitis in Chile. J Clin Periodontol 1991;18:529-33.

CHAPTER

29 Periodontal Abscess CHAPTER OVERVIEW A periodontal abscess is a localized purulent infection of the periodontal tissues that may lead to destruction of periodontal ligament and alveolar bone and is one of the

CLASSIFICATION

most frequently encountered dental emergencies. It is also referred to as a lateral or parietal abscess.

Depending on Number

According to Location 1. Abscess in the supporting periodontal tissues along

the lateral aspect of the root. 2. Abscess in the soft-tissue wall of the deep periodontal pocket.

1. Single periodontal abscess: They are usually related to local factors that contribute to the closure of the periodontal pocket. 2. Multiple periodontal abscess: They have been reported in diabetes mellitus and medically compromised patients.

ETIOLOGY

According to Onset or Course of Lesion 1. Acute periodontal abscess: It appears as a bright red

ovoid elevation of the gingiva, which may be relatively firm or pointed and soft. In most instances, pus may be expressed from the gingival margin by gentle digital pressure. It is accompanied by symptoms such as throbbing, radiating pain, sensitivity to percussion, tooth mobility, and, in some cases, lymphadenopathy and systemic effects such as fever and malaise. 2. Chronic periodontal abscess (Fig. 29.1): It usually presents a sinus that opens onto the gingival mucosa somewhere along the root length. It is usually asymptomatic. However, the patient may complain of intermittent exudation, dull gnawing pain, slight elevation of the tooth, and a desire to bite down on and grind the tooth. Acute lesions often subside but persist in the chronic state, whereas chronic lesions may exist without being acute. Chronic lesions frequently undergo acute exacerbation.

Periodontal abscesses have been associated either directly to periodontitis (periodontitis-related abscess) or to sites without the prior existence of a periodontal pocket (nonperiodontitis-related abscess).

Periodontitis-Related Abscess 1. The existence of tortuous pockets, with cul-de-sac that

eventually becomes isolated, may favor the formation of abscess. 2. The marginal closure of the periodontal pocket may lead to an extension of infection into the surrounding periodontal tissues due to the pressure of suppuration inside the closed pocket. 3. The development of periodontal abscess in periodontitis may occur at different stages during the course of the infection as an exacerbation of an untreated periodontitis, during periodontal therapy, in refractory periodontitis, or during periodontal maintenance. Also, fibrin secretions, leading to the local accumulation of

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released by the bacteria, and the concomitant inflammatory reaction leads to destruction of the connective tissues, the encapsulation of the bacterial infection, and the production of pus. Histologically, intact neutrophils are found surrounding a central area of soft-tissue debris and destroyed leukocytes. At a later stage, a pyogenic membrane composed of macrophages and neutrophils is organized. An acute inflammatory reaction surrounds the purulent area, and the overlying epithelium exhibits intracellular and extracellular edema and invasion of leukocytes. Gram-negative bacteria may be seen invading the pocket epithelium and the altered connective tissue.

DIAGNOSIS FIGURE 29.1

Chronic periodontal abscess.

pus, may favor the closure of gingival margin to the tooth surface. 4. Changes in composition of the microflora, bacterial virulence, or host defenses could also make the pocket lumen inefficient to drain the increased suppuration. 5. Treatment with systemic antibiotics without subgingival debridement in patients with advanced periodontitis may also cause abscess formation. 6. Abscess can form due to inadequate scaling which will allow calculus to remain in the deepest pocket area, whereas the resolution of the inflammation at the coronal pocket area will occlude the normal drainage, and entrapment of the subgingival flora in the deepest part of the pocket. Also, calculus might get dislodged and pushed into the soft tissue after procedures like scaling.

N onperiodontitis- Related Abscess 1. Impaction of foreign bodies, such as a toothbrush bristle,

The diagnosis of the periodontal abscess requires correlation of the history, and clinical and radiographic findings. The dental history can provide information about previous periodontal treatments, endodontic therapy, and previous abscesses. The suspected area should be carefully probed (Fig. 29.2). Continuity of the lesion with the gingival margin serves as the clinical evidence that the abscess is periodontal. Other findings are ovoid swelling of the gingiva, pain, tooth mobility, tooth elevation, suppuration, either spontaneous or on digital pressure, and the presence of deep periodontal pockets. Radiographically, it appears as a discrete area of radiolucency along the lateral aspect of the root. However, lesions in the soft-tissue wall of a periodontal pocket are less likely to produce radiographic changes than those deep in the supporting tissues. Similarly abscesses on the facial or lingual surfaces are obscured by the radiopacity of the root. Also in the early stages, the acute periodontal abscess is extremely painful but presents no radiographic changes.

a piece of dental floss, orthodontic elastic, a dislodged cemental tear, food (such as fish bone) into the gingival tissue, etc., can result in abscess formation. Periodontal abscesses caused by foreign bodies, related with oral hygiene aids, have been named "oral hygiene abscesses". 2. Lateral perforation of the root during endodontic therapy and trauma to the tooth. 3. Local factors affecting morphology of roots such as cemental tears, external root resorption, invaginated tooth, and cracked tooth may predispose to periodontal abscess formation.

PATHOGENESIS AND HISTOPATHOLOGY The entry of bacteria into the soft-tissue pocket wall could be the first event to initiate the periodontal abscess. Inflammatory cells are then attracted by chemotactic factors

FIGURE 29.2

Diagnosis of periodontal abscess.

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TABLE 29.1

Differentiation Between Gingival and Periodontal

Abscess Gingival abscess

Periodontal abscess

It is confined to the marginal gingiva

It involves the supporting periodontal structures

It often occurs in former diseasefree areas

It occurs in the course of chronic destructive periodontitis

It is an acute inflammatory response that results when a foreign object (apple core, lobster fragment) is forcefully embedded into the gingiva

The occlusion of the orifice of a preexisting periodontal pocket prevents drainage of the purulent material leading to abscess formation

Treatment involves only drainage and irrigation

Treatment involves drainage, irrigation, and pocket elimination procedure

Thus, the radiographic examination may reveal a normal appearance or some degree of bone loss ranging from a widening of the periodontal space to a dramatic radiographic bone loss especially with interproximal lesions.

DIFFERENTIAL DIAGNOSIS The differential diagnosis of periodontal abscesses should be made using different signs and symptoms, such as pulp vitality, the presence of dental caries versus TABLE 29.2

Differentiation Between Periapical and Periodontal

Abscess Periapical abscess

Periodontal abscess

Pain may be sharp, intermittent, throbbing, severe, and diffuse

The pain is usually dull, steady, and continuous

Pain is not always localized, and the patient may not be able to locate the offending tooth

The pain is localized, and the patient usually can locate the offending tooth

Vitality test does not show vital pulp

Vitality test shows vital pulp

The tooth is painful to percussion or with movement

The tooth is usually not as painful to percussion or with movement

The abscess may be associated with deep restoration

The abscess is associated with a preexisting periodontal pocket, caries, or both

Swelling usually present in apical area and sinus tract formation is common

Swelling usually includes gingival tissue and fistula tract is uncommon

Clinically may have no periodontal pocket, or if present, probes as narrow defect

Unclinically there is presence of periodontal pocket; and radiographically there is presence of vertical or argular bone loss or fuscation radiolucency

periodontal pockets, the location of abscess, and a careful radiographic examination. It is differentiated from gingival abscess (Table 29.1) and periapical abscess (Table 29.2), which are the other abscesses found in the oral cavity that have similar appearance and symptomatology, although their etiologies are different.

TREATMENT Periodontal abscesses most often present as a painful dental emergency. The patient should be treated immediately to relieve pain and resolve the infection, which may spread and lead to periodontal attachment loss.

Treatment of Acute Periodontal Abscess It usually includes two stages: 1. The management of the acute lesion. 2. The appropriate treatment of the residual lesion, once the acute situation is under control. Establishing drainage of the lesion is one of the first lines of treatment of the acute abscess. The affected area is anesthetized, and a flat instrument or probe is carefully introduced into the pocket in an attempt to distend the pocket wall. A small curette can then be gently used to penetrate the tissues and establish drainage. The root surface is then thoroughly root planed to eliminate plaque and calculus. When drainage cannot be easily established via the pocket or when the abscess can be seen pointing through the gingiva, an external incision is indicated. With a No. 11 BP blade, a vertical incision is made at most fluctuant point. After the initial extravasation of blood and pus, the area is irrigated with an antiseptic agent and the incision is gently spread to facilitate drainage. After therapy, the patient is instructed to rinse with warm saline and be examined for resolution of the abscess after 24-48 h. In the absence of systemic symptoms, antibiotic therapy is seldom recommended. Systemic antibiotics should be considered only if the patient has lymphadenopathy, fever, and/ or malaise. The symptoms invariably disappear by 1 week and the lesion is ready for the usual treatment of a chronic periodontal abscess.

Treatment of Chronic Periodontal Abscess The chronic periodontal abscess is usually asymptomatic and the treatment is similar to the elimination of a periodontal pocket by flap technique.

CHAPTER 29 PERIODONTAL ABSCESS

PERIODONTAL CYST The lateral periodontal cyst is an uncommon but wellrecognized type of developmental odontogenic cyst. The pathogenesis is still not very clear. It could be due to three reasons: the dental lamina, the epithelial cell rests of Malassez, and the reduced enamel epithelium. The most common location of the cyst is the mandibular premolar area

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followed by the anterior maxilla. It does not present distinct clinical symptoms except sometimes as a localized tender swelling in the gingiva. The tooth is vital unless it is secondarily infected; hence, the lesion is often reported mainly on routine radiographic examination. Radiographs depict a well-circumscribed, ovoid or round, radiolucent zone surrounded by a sclerotic border, which cannot be sometimes differentiated from the periodontal abscess.

KEY POINTS • A periodontal abscess is a localized purulent infection of the periodontal tissues and is one of the most frequently encountered dental emergencies. • In a periodontal abscess, the pain is usually dull, steady, and continuous.

QUESTIONS 1. Differentiate between periodontal and periapical

abscess. 2. Write a short note on gingival abscess. 3. Describe etiological factors considered in a

periodontal abscess. 4. Write a short note on periodontal cyst.

Suggested readings 1. Corbet EF. Diagnosis of acute periodontal lesions. Periodontology 2000 2004;34:204.

• Treatment of acute periodontal abscess usually includes two stages: the management of the acute lesion and the appropriate treatment of the residual lesion once the acute situation is under control.

2. Dahlen G. Microbiology and treatment of dental abscess and periodontal-endodontic lesions. Periodontology 2000 2002;28:206. 3. Gillette WB, Van House RL. Ill effects of improper oral hygiene procedures. J Am Dent Assoc 1980;101:476-81. 4. Herrera D, Roldan S, Sanz M. The periodontal abcess: a review. J Clin Periodontal 2000;27:377. 5. Herrera D, Roldan S, Gonzalez I, Sanz M. The periodontal abscess. Clinical and microbiologic findings. J Ciin Periodontal 2000;27:287. 6. Herrera D, Silvia Rolda'N, Sanz M. The periodontal abscess - a review. J Clin Periodontal 2000;27:377-86. 7. Lindhe J, Lang N, Karring T. Clinical Periodontology and Implant Dentistry. 5th ed. Blackwell Munksgaard; 2008. 8. Meng HX. Periodontal abscess. Ann Periodontol 1999;4:79. 9. Newman MG, Takei HH, Klokkevold PR, Carranza FA, eds. Carranza's Clinical Periodontology. 10th ed. Philadelphia: W.B. Saunders Company; 2006.

CHAPTER

30 AIDS and Periodontium CHAPTER OVERVIEW In December 1981, there was a report about a group of 7 men who had severe infections with microorganisms that had previously infected only profoundly immunologically compromised individuals. Soon this disease came to be known as the acquired immunodeficiency syndrome (AIDS). The first report on AIDS appeared in June 1981, in the Morbidity and Mortality Weekly Report. However, cases of AIDS before 1981 have been identified in retrospect. A Danish woman who had evolved as a surgeon in Zaire since 1972 was flown home to Denmark in 1977 with an undetermined illness characterized by chronic diarrhea and lymphadenopathy, and after a few months, she died. Her lung disease afterward proved to have been a Pneumocystis carinii infection, and it is suggested that she had AIDS. There was also a report on a Norwegian sailor who had possible HIV-associated symptoms in 1966 and died in

DEFINITION OF AIDS According to the World Health Organization (WHO)/ Centers for Disease Control and Prevention (CDC) case definition of AIDS, a case of AIDS is defined as a reliably diagnosed opportunistic disease in an adolescent or an adult at least moderately indicative of underlying cellular immunodeficiency with no other known cause or any other reduced resistance reported to be associated with an opportunistic disease, including secondary immunodeficiencies associated with immunosuppressive therapy, lymphoreticular malignancy, or starvation.

HUMAN IMMUNODEFICIENCY VIRUS The appearance of truly new organisms is extremely rare. New infectious agents do not arise in a vacuum but evolve from preexisting ones, usually among

1976 with lesions typical of AIDS. His wife had signs suggestive of HIV infection since 1967 and she died of AIDS in 1976. Their daughter, born in 1967, got symptoms in 1969 and died in 1976. Frozen serum samples of all three were positive for HIV type 1 (HIV-1). In May 1983, a new T-lymphotropic retrovirus was isolated by French investigators from a patient with lymphadenopathy. It was called lymphadenopathy-associated virus (LAV). Some months later, American investigators isolated a virus from AIDS patients, which they named human T-cell lymphotropic virus type III (HTLV-III). Subsequent studies have shown that LAV and HTLV-III are the same virus. In 1986, the AIDS retroviruses were officially termed the human immunodeficiency virus, to be known in abbreviated form as HIV. The original form of HIV is now known as HIV-1, while the similar virus found predominantly in West Africa is known as HIV type 2 (HIV-2).

animal populations. It is not likely that HIV caused disease in humans for many years before the onset of the AIDS epidemic. Some links have been drawn between AIDS and the African green monkey, which carries a virus closely related to HIV that, however, does not cause disease in this species. As such the origin of HIV is not known, but a primate origin is suggested and appears likely, particularly for HIV2. The origin of HIV-1 is more difficult to understand. The existence of animal lentiviruses with a predilection for the CD4+ T lymphocytes strongly suggests an animal origin for this virus also. However, it has been proposed that the nonpathogenic precursor of HIV-1 has infected humans for a long period, and that relatively recently it mutated to become the pathogenic virus that causes AIDS. HIV belongs to the family of lentiviruses. As the name implies, infections caused by lentiviruses progress slowly with long incubation periods. After the initial recovery of viruses from lymph nodes, HIV was isolated from peripheral

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blood mononuclear cells (PBMCs) both in patients with clinical manifestations of AIDS and in patients without any clinical signs or symptoms. To distinguish between these two viruses, the initial HIV was named HIV-1, while the second virus was called HIV-2. The course of the disease appears to be much longer with HIV-2.

Life Cycle of HIV HIV is transmitted by exchange of blood or body fluids. Once inside the host, the virus seeks or binds to the CD4 molecule of T-helper cells and other target cells. These include bone marrow stem cells, macrophages, endothelial cells, glial cells, lymph nodes, dendritic cells, bowel enterochromaffin cells, cervical epithelium, and possibly Langerhans cells. However, it is the effects of HIV on T-helper cells that are the best known and that probably play a major role in the pathogenesis of HIV disease, including AIDS. Binding of HIV to CD4+ target cell involves interaction of the external envelope glycoprotein molecule gp120 with the CD4 molecule, although other cell receptors may be involved. This interaction can involve free viral particles, but direct cell-to-cell spread of HIV may also occur. The virus next enters the target cell, or is internalized, through fusion of the viral envelope with the target cell membrane. Next, the viral RNA is subjected to reverse transcription. This involves the production of a singlestranded DNA copy of the viral RNA and the destruction of the viral RNA. A second strand of DNA is then synthesized. The linear double-stranded DNA becomes circular and then integrates into host chromosomal DNA. Here the proviral DNA can remain latent for the lifetime of the host cell. Alternatively, it can generate new viral RNA and hence HIV virions. Virions are assembled in the cytoplasm and eventually bud from the cell surface. The processes of viral latency and replication are controlled in part by the HIV regulatory genes, acting directly or through the actions of host cell factors.

Stages of HIV Infection HIV infection can be described in four stages: 1. Primary infection: In this stage there is a rapid spread of

the virus through the blood and lymph nodes. There is a rapid decline of the CD4 cell count, which later comes back to normal when the virus is controlled by the immune system. This is referred to as seroconversion illness, and it usually resolves within weeks. 2. Early immune deficiency (CD4 cell count >500/mL): In this stage the patients are without any active symptoms

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of the disease as the immune system restricts the virus to the lymphoid tissues and hence the damaging capacity of the virus is limited. 3. Intermediate immune deficiency (CD4 cell count 200500 / mL): In this stage viral replication is very high and CD4 cell turnover is rapid. Signs and symptoms indicating a compromise of the immune system begin to appear. 4. Advanced immune deficiency (CD4 cell count .:::;200/mL): The virus overcomes the immune system and proliferates throughout the body. This results in the occurrence of opportunistic infections and malignancies which require medical intervention.

Human Cells/Cell Lines and Tissues Susceptible to HIV The extent of replication of HIV varies in different cells, although it can multiply in all the cells. • Hematopoietic system: In the hematopoietic system the virus affects "T" and "B" lymphocytes, macrophages, natural killer (NK) cells, megakaryocytes, dendritic cells, promyelocytes, stem cells, thymic epithelium, and follicular dendritic cells. • Brain: In the brain the cells affected are the oligodendrocytes, choroid plexus, ganglia, neurons, and capillary endothelial cells. • Skin: In the skin the fibroblasts and Langerhans cells are affected and in the bowel the columnar and goblet as well as the colon carcinoma cells are affected. • Others: The other cells which are affected include the cells of myocardium, prostate, testes, retina, synovial membrane, cervix epithelium, and placental trophoblasts.

Modes of Transmission of HIV The transmission of HIV still remains the primary concern for dental providers who treat infected patients. The fear of contracting HIV is also a major concern in the community at large, and providers need to be well informed regarding known modes of transmission. There are three principal modes of HIV transmission: through sexual contact, through exposure to infected blood and blood products, and through perinatal contact from infected mothers to their children. Other possible routes of transmission of concern to dental health care providers include saliva and cross-contamination with dental hand pieces.

Documented and Undocumented Modes of HIV Transmission • Documented modes of transmission: Sexual transmission Exposure to blood and blood products Vertical transmission from mother to fetus/ child

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• Undocumented modes of transmission Aerosol Dental rotary instrument Tears Urine Sweat Hepatitis B vaccine Insect bites Casual contact.

CLASSIFICATION AND STAGING In 1982 the CDC developed a surveillance case definition for AIDS based on the presence of opportunistic illnesses or malignancies secondary to defective cell-mediated immunity in HIV-positive individuals. This definition was further expanded in 1985, 1987, and 1993. The most significant change in the new CDC case definition was the inclusion of severe immunodeficiency (CD4-T4 lymphocyte count of less than 200/mm3 or a T4 lymphocyte percentage of less than 14% of total lymphocytes) as definitive for AIDS. This change was based on recognition that severe immunodeficiency results in increased risk for opportunistic life-threatening conditions.

CDC Surveillance Case Classification ( 1993) • Category A: It includes patients with acute symptoms or asymptomatic diseases, along with individuals with persistent generalized lymphadenopathy, with or without malaise, fatigue, or low-grade fever. • Category B: Patients have symptomatic conditions such as oropharyngeal or vulvovaginal candidiasis; herpes zoster; oral hairy leukoplakia; idiopathic thrombocytopenia; or constitutional symptoms of fever, diarrhea, and weight loss. • Category C: Patients are those with outright AIDS as manifested by life-threatening conditions identified by CD4+ T4 lymphocyte levels of less than 206/mm3. These staging categories reflect progressive immunologic dysfunction, but patients do not necessarily progress serially through the three stages, and the predictive value of these categories is not known.

ORAL AND PERIODONTAL MANIFESTATIONS OF AIDS AIDS, as we are aware, is a multiple disease complex syndrome affecting almost every system of the body. The oral cavity and periodontal structures have been found to be affected more frequently with various opportunistic infections that result from immunodeficiency caused by the virus. It is not surprising that nowadays, dental surgeons

are probably the first ones to suspect this infection in the patients because many of the oral manifestations may herald or form a hallmark diagnostic sign of this disease. Dental surgeons during their clinical practice can come across not only patients with AIDS but also cases with the AIDS-related complex (ARC) and those who are seropositive for HIV but are without any syndromes currently. As known today the HIV affects the CD4 receptors of the helper T lymphocytes, which form the major interlink between cell-mediated and humoral immunity, thus resulting in serious deficiency of these immune responses of the body. The oral mucosa and periodontal structures, which are under constant threat of infections, also get affected because of this deficient immune status. This occurs due to setting in of various opportunistic infections, and also exacerbations of existing infections leading to an increased pathological destruction of these otherwise healthy tissues.

GENERAL CLINICAL SIGNS IN AIDS PATIENT 1. Lymphadenopathy or swollen glands 2. Unexpected and unexplained loss of appetite and bodyweight 3. Weakness in the legs and difficulty in climbing the stairs 4. Unexpected fever of I-week duration or more 5. Night sweats 6. Persistent and unexplained diarrhea 7. Persistent dry cough that cannot be explained by smoking or seasonal allergic manifestation 8. White patches in the mouth 9. Hairy leukoplakia 10. Shingles 11. Lymphoma.

The following are the most common opportunistic infections: 1. Cryptococcal meningitis 2. CNS toxoplasmosis 3. P. carinii pneumonia 4. Cryptosporidiosis 5. Kaposi sarcoma 6. Tuberculosis 7. Herpes simplex viruses 8. Mycobacterium avium-intracellulare.

CLASSIFICATION OF ORAL LESIONS ASSOCIATED WITH HIV INFECTION The oral manifestations of HIV infection are classified based on the clinical appearance of the lesion and also on the basis of definitive criteria which is the result of investigations.

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Group 1: Lesions Strongly Associated with HIV Infection 1. Candidiasis: a. Erythematous

b. Pseudomembranous 2. Hairy leukoplakia 3. Kaposi sarcoma 4. Periodontal disease a. Linear gingival erythema

b. Ulcerative necrotizing gingivitis c. Ulcerative necrotizing periodontitis 5. Non-Hodgkin lymphoma.

Group 2: Lesions Less Commonly Associated with HIV Infection Infections of bacterial origin Hyperpigmentation of oral mucosa Ulcerative necrotizing stomatitis Oral conditions a. Decreased salivary flow leading to dry mouth b. Swelling of major salivary glands 5. Thrombocytopenic purpura 6. Nonspecific ulcerations 7. Infections of viral origin a. Herpes simplex virus b. Human papilloma virus c. Varicella zoster virus d. Herpes zoster virus e. Varicella virus.

1. 2. 3. 4.

ERYTHEMATOUS CANDIDIASIS

This form of candidiasis presents as red areas. It is occasionally mixed with white spots. High rate of occurrence is seen on the palate and dorsum of the tongue (Figs 30.1 and 30.2). PSEUDOMEMBRANOUS CANDIDIASIS

• The condition is characterized by presence of white or yellow spots or plaques. • When removed, it leaves a red bleeding surface. • Definitive criteria include response to antifungal therapy. • C. albicans is detected by smear culture. Angular Cheilitis • This is another form of oral candidiasis (Fig. 30.3). • It is seen as redness, cracking, or fissuring of the commissural region. It may be unilateral or bilateral and can be seen associated with other oral manifestations.

Group 3: Lesions which May Occur in HIV Infection Bacterial infections such as E.coli Adverse drug reactions Fungal infections of candidal origin Neurologic disturbances a. Facial palsy b. Trigeminal neuralgia 5. Recurrent aphthous stomatitis 6. Infections of viral origin such as a. Cytomegalovirus.

1. 2. 3. 4.

FIGURE 30.1

Candidiasis seen on the buccal mucosa in HIV patient.

FIGURE 30.2

Candidiasis seen on the gingiva in HIV patient.

Candidiasis • Oral candidiasis is a common early manifestation of HIV infection caused predominantly due to Candida albicans. Commonest forms of Candida infections are as follows: • Erythematous candidiasis • Pseudomembranous candidiasis • Angular cheilitis.

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FIGURE 30.3

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Angular cheilitis.

FIGURE 30.4 Necrotizing ulcerative gingivitis.

Periodontal Diseases

NECROTIZING ULCERATIVE PERIODONTITIS

HIV-related periodontal disease includes three conditions:

• NUP is characterized by generalized aggressive alveolar bone loss and attachment apparatus destruction (Fig. 30.5). • There is also deep-seated pain, spontaneous gingival bleeding, halitosis, and tooth mobility.

a. Linear gingival erythema b. Necrotizing ulcerative gingivitis (NUG) c. Necrotizing ulcerative periodontitis (NUP).

NUG, NUP, and necrotizing stomatitis (NS) may be collectively referred to as necrotizing gingivostomatitis (NG). STAGING OF NECROTIZING GINGIVOSTOMATITIS

Staging of NG infections was proposed by Pindborg, who described four stages: 1. Tip of the interdental papilla is affected. 2. Punched-out lesions of the interdental papilla are

confined to the marginal gingiva. 3. Lesions extend to the attached gingiva also. 4. Underlying bone is exposed.

Viral Infections HERPETIC GINGIVOSTOMATITIS

• Viral shedding into the oral environment is common in immunosuppressed patients. • The condition is characterized by gingival, palatal, dorsal tongue, and occasionally mucosal vesicles. These rupture and leave painful, irregular one to two ulcers often in clusters. VARICELLA ZOSTER INFECTIONS (HERPES ZOSTER AND VARICELLA)

• This disease manifests as a unilateral occurrence of vesicles or ulcers in the area which is innervated by the

LINEAR GINGIVAL ERYTHEMA

• This is characterized by red to bluish red, edematous gingival tissue. • It usually appears with enlarged interdental papillae and tendency to bleed easily. • Significantly more bleeding sites and destruction of interdental papillae are present in HIV-seropositive patients. NECROTIZING ULCERATIVE GINGIVITIS

• Necrotizing ulcerative gingivitis (NUG) in HIV patients is seen as fiery red and enlarged gingiva with necrosis and loss of interdental papilla (Fig. 30.4). • The condition has extremely fast rate of progression with destruction of the periodontal tissues and is associated with severe pain.

FIGURE 30.5

Necrotizing ulcerative periodontitis.

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branch of the trigeminal nerve. The disease extends to the bone leading to osteonecrosis, and is an extremely painful condition. MOLLUSCUM CONTAGIOSUM

• It is an infection of skin caused by a pox virus. • Lesions are shiny, white, and hemispherical, and grow up to 0.5 cm. • Facial skin is commonly involved. HAIRY LEUKOPLAKIA

• Hairy leukoplakia is seen in about one-fourth of HIVinfected persons (Fig. 30.6). • It is characterized by the presence of white to gray lesions. • It is seen on the lateral borders of the tongue usually bilaterally and cannot be scraped off. • The lesions can extend to the ventral and dorsal surfaces of the tongue, and may also involve the buccal mucosa. XEROSTOMIA

• Some HIV-infected persons in an early stage of infection experience xerostomia (Fig. 30.7). • The xerostomia may be a complication of the prescribed medications for the patients which may be xerostomic in nature. • HIV salivary gland disease in HIV patients has been described as Sicca-type syndrome. It is associated with diffuse infiltrative CDS lymphocytosis. KAPOSI SARCOMA

• It is a malignancy associated with HIV (Fig. 30.8). • Oral Kaposi sarcoma typically presents as red-bluish swellings with or without ulceration. • It is most common on the palate, gingiva, and dorsal tongue.

FIGURE 30.6

Hairy leukoplakia seen on the tongue.

FIGURE 30. 7

Xerostomia in an AIDS patient.

• Kaposi sarcoma is usually seen as a red purple or bluish patch, which later presents as nodules resembling hemangiomas or a peripheral giant cell granuloma. • It is initially seen in the subepithelial connective tissue. • As the tumor progresses, pathological changes can occur in the bone and other periodontal tissues.

INVESTIGATIONS HIV Antibody Diagnosis Testing for HIV antibodies invariably necessitates the availability of at least two different assays: • A screening test Nonquantitative detection Enzyme-linked immunosorbant assay (ELISA) • A confirmatory test Western blot assay DNA polymerase chain reaction (PCR) Viral culturing HIVDNAPCR

FIGURE 30.8

Kaposi sarcoma of palate.

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• Rapid HIV antibody test The single-use diagnostic system (SUDS) • Viral load Reverse transcriptase PCR (RT-PCR) Nucleic acid sequence-based amplification (NASBA).

MANAGEMENT OF HIV/AIDS ANTIRETROVIRAL TREATMENT Antiretroviral drugs are agents that help to delay the progression of the disease from HIV to AIDS. This helps to increase the life span of patients and provide a good quality of life for them. Several advances have been made in the antiretroviral treatment protocols and their effectiveness has been well documented, during the last three decades.

Antiretroviral Drugs The antiretroviral agents act at different stages of the life cycle of the HIV: 1. By blocking binding of HIV to the target cell 2. By blocking the viral RNA cleavage 3. By inhibiting the enzyme reverse transcriptase.

Qualities of an Ideal Antiretroviral Drug 1. 2. 3. 4. 5. 6.

It should act on the specific organisms. It should reduce viral production from infected cells. It can be preferably administered orally. It should penetrate the blood-brain barrier easily. It should not develop resistance to the organism easily. It should not be toxic to the tissues.

However, none of the antiretroviral drugs available today fulfill all these properties.

Classification of Antiretroviral Drugs • Inhibitors of viral attachment • Recombinant soluble CD4 (rsCD4) or immunoglobulins • Reverse transcriptase inhibitors: Nucleoside analog RT inhibitors (NRTI) - Dideoxythymidine (AZT) or zidovudine (ZDV) - Dideoxycytidine (ddl) or didanosine - Dideoxyinosine (ddC) or zalcitabine - Dideoxyadenosine (ddA) - Didehydrodeoxythymidine (D4T) or stavudine - Deoxythiacytidine (3TC) or lamivudine Non-nucleoside analog RT inhibitors (NNRTI) - Nevirapine - Delavirdine - Thiobenzimidazoline derivatives - Efavirenz (Sustiva) • Protease inhibitors (Pl): Saquinavir

Ritonavir Indinavir Nelfinavir • Integrase inhibitors: Agents that block the assembling of the virus and their budding.

HAART Highly active antiretroviral therapy (HAART) is a type of treatment procedure where a combination of three or more antiretroviral drugs are given in combination, over a prolonged period of time in an effort to block the replication of the HIV virus and improve the immune status of the individual. NNRTI are used in combination with NRTI and PI. Although it was suggested initially that HAART should not be administered until significant immune suppression occurred, currently it is suggested that early treatment is more successful in HIV patients than delayed treatment. HAART has been shown as a very successful treatment protocol in reversing the immune suppression and increasing the life expectancy in many individuals using the therapy. However, HAART is seen to be not very effective in individuals with AIDS (before initiation of the therapy) and in those with a high viral load before initiation of the therapy, noncompliance with the drug regimen, injected drug abusers, patients with various bacterial, viral, or fungal infections, and various systemic diseases.

INFECTION CONTROL MEASURES WITH A FOCUS ON THE DENTAL SETTING Dental patients and dental health care personnel (DHCP) can be exposed to numerous pathogenic organisms, including the HIV. HIV can be transmitted in dental settings through 1. Direct contact, e.g., blood, oral fluids, or patient

materials 2. Indirect contact, e.g., contaminated objects such as

instruments and equipment 3. Contact of mucosal surfaces, nasal, oral, or conjunctiva!

with droplets containing microorganisms from an infected individual. Infection by any of the above mechanisms requires the following conditions: 1. Adequate number of pathogenic organisms having

sufficient virulence 2. An area or medium that allows the pathogen to multiply 3. A mechanism for transmission to the host 4. A source of entry into the host for the pathogen

5. A susceptible host.

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If these events occur, it leads to infection. Infection control strategies are designed to prevent disease transmission by interrupting one or more links in the chain, thus breaking the chain of infection and nullifying the virulence of the organisms.

PRECAUTIONS FOR DENTISTS All oral fluids such as saliva, gingival crevicular fluid (GCF), and also blood from dental patients should be considered infective. The following precautions should be taken for preventing transmission of blood-borne pathogens in dental practice: 1. Surgical gloves, surgical masks, and protective eyewear

during all dental procedures where splashing of saliva and blood is likely. Rubber dams and high-speed evacuation, and also proper patient positioning, should be used to minimize generation of droplets and spatter. 2. Handpieces should be flushed, cleaned with a chemical disinfectant, and then sterilized, after use with every patient. This is necessary as oral fluids such as saliva, GCF, and blood can be aspirated into the handpiece. Follow manufacturer's instructions for maintenance of dental waterlines. The above precautions should be followed for ultrasonic scalers and air/ water syringes also. 3. Oral fluids such as saliva and blood must be removed from the materials used in the mouth such as impression materials and also from intraoral devices such as acrylic appliances. These contaminated materials and

appliances should be cleaned and disinfected each time they are taken out from the patient's mouth and before being handled in the dental laboratory. The disinfection procedures for each material should be carried out in accordance with the manufacturer's instructions. 4. Dental light handles, X-ray unit heads, and other surfaces that are difficult to disinfect should be completely wrapped in an aluminum foil or a clean plastic wrap. After use with every single patient it should be discarded and a new covering must be put in its place.

STERILIZATION AND DISINFECTION The following are the methods to be used for sterilization: 1. Sterilization a. Boiling for 20-30 min

b. Dry heat at 170°C for 1 h c. Autoclaving at 121 °C, 15 lb pressure for 20 min 2. Chemical disinfection is done by the following procedures: a. Ethanol: 70% b. Formalin: 3-4% c. Glutaraldehyde: 2% for 30 min d. Povidone iodine e. Calcium hypochlorite: 1.4 g/L £. Sodium hypochlorite: 5 g/L g. Chloramine: 20 g/L.

KEY POINTS • HIV is transmitted by exchange of blood or body fluids. Once inside the host, the virus seeks or binds to the CD4 molecule of T-helper cells and other target cells. • Lesions strongly associated with HIV infection: 1. Candidiasis: a. Erythematous b. Pseudomembranous 2. Hairy leukoplakia 3. Kaposi sarcoma

4. Non-Hodgkin lymphoma 5. Periodontal diseases: a. Gingival erythema - linear b. Ulcerative necrotizing gingivitis c. Ulcerative necrotizing periodontitis • HIV-related periodontal disease includes three conditions: 1. Linear gingival erythema

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2. NUG 3. NUP

Testing for HIV antibodies invariably necessitates the availability of at least two different assays: 1. A screening test: a. Nonquantitative detection b. ELISA 2. A confirmatory test:

a. b. c. d.

Western blot assay DNAPCR Viral culturing HIV DNA PCR

3. Rapid HIV antibody test: a. The SUDS

4. Viral load: a. RT-PCR b. NASBA

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QUESTIONS 1. Describe in detail the oral and periodontal

manifestations in AIDS patients. 2. Short essays: a. Kaposi sarcoma b. Elaborate on the precautions to be taken when treating a patient with HIV infection.

Suggested readings 1. Axelsson P. Diagnosis and Risk Prediction of Periodontal Diseases, Vol 3. Chicago: Quintessence; 2002. p. 219-235. 2. Einstein E, Needleman HL, Karimbur N, Vandyke TE, editors. Periodontal and Gingival Health and Diseases: Children Adolescents and Young Adults. New York: Informa Healthcare; 2001.

3. Eley BM, Manson JD. Periodontics. 5th ed. Bristol: Wright; 2004. 4. Genco RJ, Goldman HM, Cohen DW. Contemporary Periodontics. St. Louis: Mosby-Year Book; 2004. 5. Laskaris G, Scully C. Periodontal Manifestations of Local and Systemic Diseases: Colour Atlas and Text. New York: Springer; 1990. 6. Lindhe J, Karring T, Lang NP. Clinical Periodontologu and Implant Dentistry. 4th ed. New York: Wiley-Blackwell; 2003. 7. Rateischak KH. Colour Atlas of Dental Medicine. Stuttgart: Thieme; 1989. 8. Rose LF, Genco RJ, Mealey BL, Cohen DW. Periodontal Medicine. Hamilton: BC Decker; 2000. 9. Rose LF, Mealey BL. Periodontics - Medicine, Surgery and Implants. St. Louis: Mosby; 2004. 10. Seymour RA, Heasman PA. Drugs, Diseases and the Periodoniium. New York: Oxford University Press; 1992. 11. Wilson TG, Kornman KS. Fundamentals of Periodontics. 2nd ed. New York: Quintessence; 2003.

CHAPTER

31 Halitosis CHAPTER OVERVIEW Breath ma/odor is an important social problem. Bad breath can be defined as the subjective perception after smelling one's breath. If unpleasant, the terms breath ma/odor, halitosis, or bad breath can be applied. If the odor has origin in the oral cavity, it is called oral ma/odor.

INCIDENCE Industrialized countries show an incidence of 50%. There is no gender predominance, and people between age 18 and 64 years may be equally affected. The most prevalent causes of oral malodor are gingivitis, periodontitis, and tongue coatings. Minority of patients showing breath malodor reveal underlying systemic conditions such as ear-nose-throat pathology, diabetes, hormonal problems, metabolic problems, hepatic renal conditions, bronchial carcinoma, or gastroenterologic pathology. Imaginary breath or halitophobia are terms given to patients who imagine they have breath malodor (Table 31.1).

ETIOLOGY Volatile sulfur compounds (VSCs) are the main cause of breath malodor. These mainly include hydrogen sulfide, methyl mercaptan, and dimethyl sulfide. Various other compounds have also been implicated in the etiology such as putrescine, indole, skatole, butyric acid, or propionic acid. The above-mentioned compounds are mostly formed by the degradation of compounds within the oral cavity by various proteolytic microorganisms. Various peptides present in saliva, food debris, oral epithelium, gingival crevicular fluid (GCF), plaque, postnasal drip, and blood are broken down to various chemicals mentioned above and contribute to oral malodor.

Transient conditions can produce momentary malodor (temporary/ transient oral malodor), and few examples are food intake, e.g., garlic, smoking, and morning breath experienced on awakening. These do not reveal any health problems. Any persistent breath malodor may reflect some underlying pathology, and diagnosis is important to treat the malodor.

Volatile fatty acids such as fumarate and valerate are also malodorous. These can be released through expired air or the GCF and can express themselves when they become volatile. Unpleasant breath can be due to intraoral or extraoral causes.

INTRAORAL CAUSES

Dental Causes Extraction wounds, carious cavities, and purulent discharge all can contribute to oral malodor. Interproximal food impaction and crowding of teeth cause accumulation of food debris, which can result in halitosis.

Periodontal Pathology Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Campylobacter rectus, and Tannerella forsythia are responsible for pathogenesis of periodontitis and production of VSCs. As the periodontal pocket depth increases, it is seen that the concentration of the malodorous chemicals increases. Deep pockets also cause the formation of putrescine and cadaverine. VSCs are themselves causative factors for aggravation of periodontitis. They increase the epithelial and pocket permeability and contribute to the direct contact of periodontal products to the tissues. Methyl mercaptan also

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TABLE 31.1

Classification of Halitosis

Classification

Treatment needs

I. Genuine halitosis A. Physiologic halitosis

Description Obvious malodor, intensity beyond socially acceptable level

TN-1

1. Due to putrefactive process in the oral cavity. No specific disease nor pathologic condition is found 2. Origin is dorsoposterior region of the tongue 3. Temporary halitosis due to dietary factors should be excluded

(i) Oral

TN-1 and TN-2

1. Caused by disease, pathologic condition, or malfunction of oral tissues 2. Halitosis derived from tongue coating, modified by pathologic condition (e.g., periodontal disease, xerostomia)

(ii) Extraoral

TN-1 and TN-3

1. Origin from nasal, and/or laryngeal regions 2. Origin from pulmonary tract or upper digestive tract 3. Disorders anywhere in the body, odor is blood-borne and emitted via the lungs (e.g., diabetes mellitus, hepatic cirrhosis)

II. Pseudo-halitosis

TN-1 and TN-4

1. Malodor is not perceived by others, patient stubbornly complains of its existence 2. Counseling and simple oral hygiene measures provide relief

III. Halitophobia

TN-1 and TN-5

1. After treatment for genuine halitosis or pseudo- halitosis, the patient still feels that he/ she has halitosis 2. Absence of physical or social evidence of halitosis

B. Pathologic halitosis

TN, treatment need. (Source: Modified from Yaegaki K, Coil JM. Classification and treatment of halitosis - clinical perspective. J Can Dent Assoc 2000;66:257-61; Modified from Miyazaki H et al. Tentative classification of halitosis and its treatment needs. Niigata Dent J. 1999;32: 7-11. Japanese).

can enhance the production of interstitial collagenases, interleukin-I, and cathepsin B. These further aggravate the periodontal breakdown. Malodorous compounds can also alter fibroblasts and cell migration and proliferation. Other conditions such as pericoronitis, acute necrotizing ulcerative gingivitis (ANUG), and oral ulcers can also contribute to oral malodor.

Crypts of the tonsils can also cause accumulation of microorganisms and putrefaction leading to oral malodor.

Lungs and Bronchus Chronic bronchitis, bronchiectasis, and bronchial carcinoma are also extraoral causes of oral malodor.

Xerostomia

Gastrointestinal Tract

Dry mouth can cause the VSCs to escape, and absence of saliva can cause an increase in the number of microorganisms that produce VSCs.

Various conditions that contribute to oral malodor are Zenker diverticulum, hernia, gastric regurgitation, and intestinal gas production. Other extraoral causes that contribute to halitosis are liver insufficiency, kidney insufficiency, type 1 diabetes mellitus (OM), and hereditary disorders such as trimethylaminuria. Menstrual breath due to progesterone levels in females and medications such as metronidazole also cause oral malodor.

Contribution of Tongue Dorsum of the tongue is irregular and can accommodate microorganisms and food debris. Desquamated calls and food remnants remain entrapped on the surface and are consequently decomposed and contribute to oral malodor. The dorsum of the tongue is considered to be the primary etiologic factor for oral malodor.

DIAGNOSIS 1. Self-evaluation: Involving the patient in the diagnosis

EXTRAORAL CAUSES Ear-Nose-Throat Purulent sinusitis, pharyngitis, tonsillitis, and postnasal drip are among the extraoral causes of oral malodor.

can be important especially when there is an intraoral cause. This helps to motivate the patient toward better plaque control methods. 2. Organoleptic method: This is the gold standard for assessing oral malodor. A trained judge sniffs the air expired, assesses whether or not it is unpleasant, and

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gives a rating. The judge smells a series of different air samples as follows: a. Oral cavity odor: The subject opens the oral cavity and refrains from breathing. Expression of VSCs by drying of the oral mucosa can relate to intraoral cause. b. Breath odor: The judge smells the expired air of the subject. The first part of the breath relates to intraoral causes while the latter part relates to factors from the respiratory system. c. Tongue coating: The judge takes a sample of tongue coating and examines and presents it to patient or relative to determine if the smell is similar to that experienced. d. Nasal breath odor: When the patient expires through the nose with the mouth closed and it is malodorous but the air expired from the mouth is not, a nasal cause can be suspected.

Electronic Nose A new device that is being developed and has the capacities of the human nose is referred to as the electronic nose.

TREATMENT ASPECTS OF ORAL MALODOR (Table 31.2) Tongue Cleaning Tongue cleaning has been recommended in patients with thick coatings on their tongue. Going as far posterior as possible is advised, as maximum load is seen in this area.

Toothpastes Gas Chromatography This is a device to test the saliva of the subject formalodorous substances. Recently, a portable machine OralChroma has been introduced for this purpose.

Portable Volatile Sulfide Monitor This machine helps to identify VSCs or methyl mercaptan. The commercially available monitor is Halimeter (Fig. 31.1).

Cleaning the dentition and the tongue with a dentifrice has shown to reduce the levels of VSCs.

Mouth Rinses In addition to tongue cleaning, the use of different mouth rinses has been advocated. Various mouth rinses containing cetylpyridinium chloride, triclosan, chlorhexidine, essential oils, chlorine dioxide, metal ions, etc., have been shown to be effective in controlling oral malodor.

Chewing Gum Saliva Incubation Test Incubating the saliva and testing for the various malodorous chemicals with the help of a Halimeter or gas chromatography also helps to identify various compounds that contribute to oral malodor.

Chewing gum containing metal salts such as fluorides or chlorhexidine helps in reducing the bacterial load and reducing the levels of malodorous chemicals from the oral cavity. Long-term studies using these agents are further needed.

TABLE 30.2

FIGURE 31. 1

Halimeter.

Description of Various Treatment Needs

Category*

Description

TN-1

Explanation of halitosis and instructions for oral hygiene ( reinforcement of a patient's own self-care for improvement of oral hygiene)

TN-2

Oral prophylaxis, and treatment for oral diseases

TN-3

Referral to a physician

TN-4

Explanation of examination data, education, and reassurance

TN-5

Referral to a clinical psychologist

TN, treatment need. * TN-1 is applicable to all cases requiring TN-2 to TN-5. (Source: Yaegaki K, Coil JM. Classification and treatment of halitosis - clinical perspective. J Can Dent Assoc 2000; 66: 257-61).

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SECTION IV PERIODONTAL PATHOLOGY

Masking the Malodor Treatment modalities using rinses, mouth sprays, and lozenges that contain pleasant volatile odors have only a short-term effect in controlling oral malodor. Drinking water at frequent intervals and chewing of gum can keep the VSCs in solution and prevent them from producing oral malodor.

Since the oral cavity is the main origin of halitosis or oral malodor, it is important for the dentist to be familiar with the diagnosis and treatment plan of the condition.

KEY POINTS • Bad breath can be defined as the subjective perception after smelling one's breath. If unpleasant, the terms breath ma/odor, halitosis, or bad breath can be applied. • Imaginary breath or halitophobia are terms given to patients who imagine they have breath malodor. • Volatile sulfur compounds are the main cause of breath malodor. These mainly include hydrogen sulfide, methyl mercaptan, and dimethyl sulfide. Various other compounds have also been implicated in the etiology, such

QUESTIONS 1. Classify halitosis. 2. Enumerate the etiologic factors in halitosis. 3. How do you go about the diagnosis of halitosis?

4. What is the role of halitosis in periodontal disease?

as putrescine, indole, skatole, butyric acid, or propionic acid. • Organoleptic method: This is the gold standard for assessing oral malodor. A trained judge sniffs the air expired, assesses whether or not it is unpleasant, and gives a rating. • Gas chromatography is a device to test the air saliva of the subject for malodorous substances. Recently, a portable machine OralChroma has been introduced for this purpose.

Suggested readings 1. Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry. 5th ed. Copenhagen: Blackwell Munksgaard; 2008. 2. Newman MG, Takei HH, Klokkevold PR, Carranza FA, eds. Carranza's Clinical Periodontology. 10th ed. Philadelphia: W.B. Saunders Company; 2006. 3. Yaegaki K, Coil JM. Classification and treatment of halitosis -clinical perspective. J Can Dent Assoc 2000;66:257-61.

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V

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CHAPTER

32 Clinical Diagnosis CHAPTER OVERVIEW Periodontal diagnosis is an important part of the overall diagnosis of the oral cavity. It is an important label a clinician places on a patient's periodontal condition, but the diagnosis should not be limited to giving name to the condition. It should find out the possible related etiological factors too. Diagnosis can be defined as the process of identifying a disease by its signs, symptoms, and the results of various biological assessments. Diagnostic procedures may be used to • Classify disease categories (classification) • Identify people at risk of developing disease (risk assessment)

IMPORTANCE OF DIAGNOSING THE PERIODONTAL CONDITION

• Detect early stage disease in clinically asymptomatic individuals (screening) • Predict likely responders to specific treatments (treatment planning) • Monitor treatment efficacy and detect disease recurrence (monitoring). Naming the disease or assigning the name carries with it the implication that the clinician has ruled out all other possible diseases it may resemble, with its signs and symptoms, but with few differences, a differential diagnosis.

Information Gathering

• To find out the cause of the disease or condition • To find out what periodontal disease or condition the patient may have, if it is generalized or localized, and how severe the problem is • For easy communication between the clinicians • For the development of well-designed and appropriate treatment plan • For ascertaining the prognosis of the particular condition. A clinician arrives at a diagnosis of condition of the patient by a systematic, methodical inclusion of the various components of periodontal examination.

COMPONENTS OF PERIODONTAL EXAMINATION • Information gathering • A thorough hands-on examination of extraoral and intraoral aspects, including periodontal examination.

Information gathering process begins with the collection of personal information, including name, age, sex, address, and phone number; most often this data collection can be done by a receptionist. It is important to know the proper name of the patient because it helps in identification of the patient; also if you call the patient by his or her name during conversation, the patient feels more comfortable and happy to render the details required for the diagnosis. Knowledge of the exact age of the patient helps not only in the diagnosis of the condition but also in assessing the prognosis. Predilection of certain periodontal condition in particular gender is the importance of recording the gender of the patient properly. Address and phone number are the two essential data to be recorded for future communication with the patient; they also give a clue regarding certain endemic diseases of the patient.

Chief Complaints The chief complaint of the patient should be recorded in his or her own words, as it gives an opportunity to

253

254 TABLE 32.1

SECTION V DIAGNOSIS, PROGNOSIS, AND TREATMENT PLANNING

Most Common Chief Complaints of the Patient

Bleeding from the gums or bleeding while brushing Bad breath Mobile tooth Increased spacing between the teeth Food gets stuck between the teeth Feel like sucking in between the teeth; get relief after that Pain, which increases immediately after having food Long appearance of the tooth Gummy smile Pain and inability to open the mouth, especially in 17- to 25-yearold patients Sensitivity of the teeth Dark gums (brown or black gums)

know the exact problem of the patient. A patient with periodontal disease often may not have any complaint at all; if told that he or she has a problem, the patient may be suspicious of any suggestions that disease is present. Nevertheless, the most common chief complaints of the patients are listed in Table 32.1.

Medical History A thorough and detailed medical history is relevant while diagnosing a periodontal condition. A definite format will be helpful in recording all possible information related to the patient, which is often neglected by a clinician. Patients do not reveal all the information, thinking that it is not necessary for a dentist to diagnose the oral conditions. Before taking a medical history its importance in diagnosing the oral and periodontal changes and its implications in treatment plan should be explained to the patient. IMPORTANCE

• Certain systemic diseases may require precautions to be taken before carrying out a treatment, for example, patients susceptible to infective endocarditis. • Periodontal disease may be aggravated in the presence of systemic condition/ diseases, for example, diabetes mellitus/pregnancy. • Systemic diseases may be having oral manifestations as the only manifestation, for example, skin diseases such as lichen planus. • Systemic disease may be modified by periodontal disease. A new branch of periodontology, periodontal medicine, is emerging. For example, insulin resistance in periodontitis patients, preterm low birth weight, stroke, and atherosclerosis is being related to the periodontal disease. • Patients may be taking medications that may have unwanted effects on the periodontium, for example, phenytoin and gingival overgrowth, and anticoagulants and bleeding from the gums. • Patients may be allergic to certain medications.

A questionnaire used for this purpose is useful in collecting all the data. It is also essential to review the same at subsequent visits of the patients. It is essential that the patient fill the form with the help of receptionist and sign it. This step is necessary prior to starting the procedure, to avoid medicolegal complications which may arise.

Dental History Recording dental history gives an opportunity to know the following: • How much the patient is aware of the dental treatment; future compliance of the patient can also be assessed by this. • A patient who has gone to several dentists for the same complaint may not easily get satisfied with the treatment provided by you. • It also gives a clue regarding the possible iatrogenic causes of the periodontal disease; for example, patients complain of pain immediate next day of the tooth restoration because of pulpal exposure or high filling. • Previous eventful dental appointment may also give information regarding the hidden systemic disease of the patient, for example, delayed healing of the socket and diabetes, uncontrolled bleeding during dental surgical procedures, and bleeding/ clotting disorders.

Personal History It should include the brushing habits; use of tobacco (smoking and nonsmoking); pan chewing, including gutka; parafunctional habits such as bruxism, clenching, and grinding; use of devices associated with the profession, for example, nail with the cobbler, needle with the tailor, wire opening with the electrician, and bobby pin opening with the girls; and consumption of alcohol.

Brushing Habits Method of brushing, type of brush used, and frequency of changing the toothbrush should be recorded. A note of the type of dentifrice used, paste, or powder may also be made. Uses of any type of interdental devices also should be noted. Tooth abrasion and gingival recession may be related to the wrong brushing technique and hard toothbrush. Patient's poor oral hygiene and gingival injuries may be related to a delay in changing the toothbrush after it is worn out. Patients may be asked to bring the toothbrush along with them to assess the status of the brush. It is also prudent to ask the patient to get the brush and tell him or her to demonstrate the brushing in front of us so that it is easy to correct the technique of brushing.

C H A PT ER 32 C LIN IC A L D IA G N O SIS

255

Tobacco Use

TM] Examination

Tobacco, with smoke or smokeless, is considered as a risk factor for periodontitis. Past smoking and current smoking activities should be recorded. Current smoking history should include number of cigarettes/beedies per day and number of years since smoking. Reverse smoking habits are associated with certain parts of the country. Palatal tissues are affected by this habit. Passive smoking is becoming common due to the work environment and other reasons. Recording the same may be necessary in selected cases.

Extra-auricular and/ or intra-auricular examination should be done to evaluate the changes in the TMJ, in the form of clicking, popping, deviation, etc. Bruxism, failure to replace the missing teeth, and related vertical dimension changes may result in the alterations of TMJ movement.

Pan Chewing Pan chewing habit is considered to be a risk factor for periodontal disease. Constant chewing increases the masticatory load applied onto the tooth. Increased prevalence of periodontitis is seen with the pan chewers, with or without tobacco (betel nut used alone). Frequency of gingival recession is also found to be more with this group of patients. Relation between pan chewing and oral carcinomas is well-known.

Parafunctional Habit Patients with parafunctional habit may not know that they have this habit. Proper history taking and associated oral and extraoral changes help in diagnosing bruxism or other habits.

Other Habits Periodontal disease may be worsened in case of habits such as keeping the needle between the teeth, opening of wire, bobby pin opening, etc. It also may be the cause of periodontal abscess.

Alcohol and Periodontal Disease Periodontal changes may not be directly related to the consumption of alcohol. Chronic alcoholism, and related changes in the liver, may be one of the factors for the gingival bleeding. Protein malnutrition occurs in this type of patients and may affect the periodontal tissues. After gathering the above-said information, hands-on examination should be started.

Extraoral Examination Examination of the symmetry of the face, lymph node, and temporomandibular joint (TMJ) should be done systema ti call y. Asymmetry of the face because of any periodontal conditions is not common. Rarely pericoronal abscess appears as an extraoral swelling at the angle of the mandible. Lymph node examination: Most commonly submandibular lymph nodes are palpated. It should be seen if it is tender and movable or fixed; if it is palpable and tender, it is suggestive of systemic spread of infection.

lntraoral Examination Mouth Odors or Halitosis Halitosis or fetor ex ore or bad breath is the most common chief complaint of the patient. Patient with this complaint should be assessed for the tongue coating, food impaction areas, pericoronal areas, deep pockets, and draining abscesses. History also should include the amount of water intake daily. Organoleptic measurement is a sensory test scored on the basis of a subject's oral malodor. Other available methods are gas chromatography, sulfide monitors such as Halimeter, and Tanita Breath Alert to assess the hydrogen sulfide and methyl mercaptan (see Chapter 31).

Oral Hygiene Assessment Prior to conducting the detailed periodontal examination, plaque and calculus should be evaluated. Assessment of plaque at the initial visit will help in understanding the oral hygiene status of the patient. Increase or decrease in the plaque scores at the subsequent appointment is suggestive of poor or good maintenance of the patients, respectively. A simple index system can be followed to assess the same (Simplified Oral Hygiene Index). O'Leary Plaque Control Record, etc., can be used. Disclosing solution should be used once the gingival examination is completed.

Soft Tissue Examination (Oral Mucosal Examination) Lips, vestibule, buccal mucosa, tongue (dorsal surface), palate (hard and soft), tongue (ventral surface), and floor of the mouth are examined for the change in the color, vesicle, bullae, ulcer, white and red lesions, etc. Angular cheilitis and swelling of the lips should be noted. Possible etiology for this should be related. White or red patches seen on the buccal mucosa may be suggestive of associated skin disease; there may be associated gingival change (chronic desquamative gingivitis). Changes in the tongue may be because of the underlying nutritional deficiency. Smoker's palate is a common feature of the chronic smokers. Ulcers not healed for a longer duration and with irregular borders may be suggestive of carcinoma. Referral to an oral and maxillofacial surgeon may be sought at that time for further evaluation and treatment.

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Overall assessment of periodontium - periodontal screening and recording (PSR) or basic periodontal examination (BPE) - a modification of CPITN (community periodontal index of treatment needs) index system, is depicted in Table 32.2. In many countries screening surveys have made use of a methodology largely derived from the CPITN. Periodontal screening and recording or basic periodontal examination is designed to assess the periodontal status of an individual, which gives a quick and general idea regarding the periodontal status and its etiological factors to an extent. Periodontal screening and recording system is a service mark of the American Dental Association. Similarly, BPE found its way into use in the United Kingdom and New Zealand, whereas the primary essential periodontal examination (PEPE) was used in Australia. The use of WH0-621 probe (CPI probe, Maryland probe) is a common feature in all of these methodologies.

Examination of the Gingiva Before conducting the gingival examination, it is necessary to have a good idea how a healthy periodontal TABLE 32.2

tissue looks like. Then only presence or absence of the disease can be identified. The gingiva should be examined for the color, size, contour, consistency, surface texture, position, bleeding, and exudate. Gingival inflammation usually has two types of tissue response; most common is the edematous tissue response, which is characterized by red, enlarged, soft, smooth, and glossy gingiva, which easily bleeds on probing. In another response, the gingiva is pink, enlarged, firm, and stippled, and may or may not easily bleed. Color and size changes in the gingiva should be examined; the parts of the gingiva involved are papillary, marginal, or diffuse. In chronic gingivitis, most often the involvement is seen with marginal and papillary gingiva alone. In contrast, in chronic desquamative gingivitis, diffuse involvement is observed. Drug-induced gingival enlargement is confined to marginal and papillary gingiva; in case of idiopathic gingival enlargement, diffuse enlargement is noted. The contour and shape of the gingiva change in the gingivitis. Scalloped border of the gingiva may remain the same, but it may be accentuated, or as seen in the

Periodontal Screening and Recording (PSR)

Instrument used: CPI probe, which is a specially designed probe that has a 0.5 mm ball at the tip and is color coded from 3.5 to 5.5 mm; other markings are at 8.5 and 11.5 mm While recording the index, the patient's mouth is divided into six sextants: Maxillary right (18-14)

Maxillary anterior (13-23)

Maxillary left (24-28)

Mandibular right (48-44)

Mandibular anterior (43-33)

Mandibular left (34-38)

Each tooth is probed with the clinician walking the probe around entire tooth to examine at least six points around each tooth: mesiofacial, midfacial, distofacial, and the corresponding lingual/palatal areas. The deepest finding is recorded in each sextant, along with other findings, according to the following codes: Code 0- In the deepest sulcus of the sextant, the probe's colored band remains completely visible. Gingival tissue is healthy and does not bleed on gentle probing. No calculus or defective margins are found. These patients require reinforcement of oral hygiene instructions Code 1 -The colored band of the probe is completely visible in the deepest sulcus of the sextant. No calculus or defective margins are found, but some bleeding after gentle probing is detected. These patients require supragingival and subgingival scaling and oral hygiene instructions Code 2 - The probe's colored band is still completely visible, but there is bleeding on probing and supragingival or subgingival calculus and/ or defective margins are found. Treatment consists of supragingival and subgingival scaling, correction of plaque retentive areas such as defective margins of restorations, followed by oral hygiene instructions Code 3 - The colored band of the probe is partially submerged. This indicates the need for a comprehensive periodontal examination and charting the affected sextant to determine the necessary treatment plan. If two or more sextants score code 3, a comprehensive full mouth examination and charting are indicated Code 4 - The colored band completely disappears in the pocket, indicating a depth greater than 5.5 mm. A comprehensive full mouth examination and charting and treatment are needed Code " - When any of the following abnormalities are seen, an asterisk(*) is entered: in addition to the code number furcation involvement, tooth mobility, mucogingival problem, or gingival recession extending to the colored band of the probe, which is equal to or more than 3.5mm The code finding of each sextant and the date are entered in the box and a record is maintained for the future Sextant score Month

Day

Year

C H A PT ER 32 C LIN IC A L D IA G N O SIS

FIGURE 32.1

Examining the consistency of the gingiva.

acute necrotizing ulcerative gingivitis (ANUG), it may be flat or in reverse architecture. The shape of the gingiva changes from knife edge border to rounded or blunt border. Specific changes such as McCall festoon and Stillman cleft should be noted, even though there is no special significance to this. Healthy gingiva is firm and resilient; the consistency of the gingiva is assessed by gently pressing the side of the probe against the gingival tissue for a few seconds and then removing it (Fig. 32.1). If the tissue is edematous, imprint of probe is seen. If the tissue is firm and fibrous, no imprint will be left. Before examining for the surface texture, gingiva should be wiped with cotton and then examined (Fig. 32.2). The presence of the stippling is suggestive of the absence of the disease; however, the absence of the stippling is not always suggestive of presence of the disease.

FIGURE 32.2 Examining the surface texture of the gingiva.

257

FIGURE 32.3 Examining the bleeding on probing.

Position of the gingiva, coronal or apical to cementoenamel junction (CEJ), should be recorded. Gingival recession, which is an apical shift in the position of the gingiva, if present, should be classified according to Miller classification. Coronal shift in the position occurs due to gingival enlargement, either inflammatory or drug induced; this becomes clinically important if it creates aesthetic problem, and it also makes plaque control difficult or interferes with the normal function. Altered passive eruption is another situation that results in short clinical crown and requires surgical correction for aesthetic reasons. Bleeding on probing is an important component of the gingival examination. It is an objective sign of gingival inflammation. Inflamed gingival tissue bleeds when gently probed because of minute ulceration in the pocket epithelium and the fragility of the underlying vasculature. A periodontal probe, which has a blunt tip, helps in finding out the bleeding sites. Periodontal probe is passed along the lateral wall of the gingival sulcus (it need not be to the depth of the pocket), followed by a wait for 30 s (Fig. 32.3). Index system with just absence or presence of bleeding or bleeding severity (grading 0, 1, 2, and 3) can be used (Mombelli Bleeding Index; Table 32.3). The percentage of sites that exhibit bleeding on probing prior to treatment is a clinically useful information to compare it with the posttreatment bleeding sites and judge the efficacy of the treatment rendered to the patient. It also reassures the patient regarding the treatment provided. Purulent exudate or suppuration is often seen at the sites with chronic periodontitis, which is neutrophil-rich exudate. Occasionally it is found at sites with gingivitis. Pus formation does not occur in all periodontal pockets. Presence of bleeding and exudate is suggestive of active disease site, a site that is inflamed and infected.

258 TABLE 32.3

SECTION V DIAGNOSIS, PROGNOSIS, AND TREATMENT PLANNING

Sulcus Bleeding Index

SCORING CRITERIA 0 - No bleeding when periodontal probe is passed along the gingival margin 1 - Isolated gingival spots visible 2 - Blood forms a confluent red line margin 3 - Heavy or profuse bleeding

The best way to detect the presence of pus is to gently apply digital pressure to overlying gingiva from mucogingival junction toward the marginal gingiva. In case of periodontal abscess, there is a localized enlargement of gingiva with collection of copious amounts of pus. It is often misunderstood that the presence of pus always means presence of an abscess. If there is no loss of attachment (gingival recession) or periodontal pocket, the case can be diagnosed as gingivitis according to the parts of the gingiva involved, the number of teeth involved, and association with the plaque or not; different diagnosis can be given (see the classification of periodontal diseases).

Assessment of Periodontal Status Periodontal examination includes examination of periodontal pocket, clinical attachment loss, furcation involvement, mobility, and pathological migration. Periodontal Pocket Pathological deepening of the gingival sulcus is one of the signs of pathological changes in the periodontium. Therefore, examination of the existence of such a pocket is considered to be an essential part of the periodontal examination. Examination of periodontal pocket must include the presence and distribution on each tooth surface, depth of the pocket, and identification of suprabony or infrabony type of pocket. Visual examination of the gingiva should be carried out to see the signs and symptoms of the pocket, before using a periodontal probe to detect the pocket. Area of the pocket may show the changes in clinical signs, such as bluish red marginal gingiva, bluish red vertical zone extending from the marginal gingiva to mucogingival junction, separated buccal and lingual interdental papilla, enlarged edematous gingiva, and rolled-out marginal gingiva, which can be easily separated from the tooth surface.

is a tapered rod-like instrument having a blunt end, so that tissue is not perforated. Most commonly used periodontal probe is University of Michigan "o" probe with Williams markings and WHO probe. Pocket depth recorded using a periodontal probe is considered as clinical probing depth. It is the distance between the base of the pocket and gingival margin. It is not the true depth of the pocket. Clinical studies carried out in the beagle dogs, regarding the probe penetration in different clinical situations, revealed that in healthy specimens, the probe penetrated the epithelium to about two-thirds of its length; in gingivitis specimens, it stopped at 0.1 mm short of its apical end; and in case of periodontitis, the probe tip went past the most apical cells of the junctional epithelium. So clinical probing depth may vary, but biological depth can be obtained in carefully prepared and adequately oriented histological preparation, where distance between the gingival margin and the base of the pocket (the coronal end of the junctional epithelium) is considered to be the true depth of the periodontal pocket. METHOD OF PROBING - PROBING POCKET DEPTH

Both probing depth and clinical attachment level should be recorded usually at six points around each tooth (conventional method). When measuring the pocket at a particular point, the probe is inserted with a firm gentle pressure to the bottom of the pocket (Fig. 32.4); the shank should be aligned parallel to the long axis of the tooth surface. Penetration should be stopped when soft tissue resistance is felt, which is nothing but base of the pocket. Pocket depth is recorded at the level of the gingival margin. For the interproximal pocket and to detect the interdental crater, it is necessary to angulate the probe beneath the contact area, from both the facial and lingual areas.

Measuring the pocket - clinical probing depth and histological or biological depth: A pocket measuring probe or otherwise periodontal probe is an ad hoc instrument used to measure the depth of the pocket. Several such conventional periodontal probes are available. The typical probe

FIGURE 32.4 Measuring the pocket.

C H A PT ER 32 C LIN IC A L D IA G N O SIS

If there is supragingival calculus observed during the initial visit, periodontal pocket recording can be postponed till the supragingival scaling has been carried out. If there are subgingival deposits noted, delicate handling of the probe must be employed. Delineation between suprabony and infrabony pockets can be made by simple clinical method or using some other devices. Probe is inserted parallel to the long axis of the tooth, and it is pulled toward the gingiva; if one feels bony resistance, pocket could be infrabony. Bony resistance felt is the bony wall of an infrabony pocket. For the research purpose, gutta-percha point or silver points can be used with the radiograph, to assist in determining the different levels of attachment of periodontal pocket. OTHER ALTERNATE METHODS

Walking probing method (also called stepping): In this technique, probe is inserted at the distal most surface of the tooth, and walked or stepped toward the mesial surface of the tooth, at 1 mm distance, without taking out the probe completely from the gingival sulcus. Measurement is recorded at each millimeter, and thus deepest penetrated area is recorded. The advantage of this technique over the conventional method is that one will not miss the deepest areas of involvement. However, the process is time-consuming. TRANSGINGIVAL PROBING, TRANSSULCULAR PROBING- SOUNDING

Easley, Tibbets, and Ochenbein and Ross (1969) described a sounding technique for plotting the morphological outline of the alveolar bone. This procedure performed with local anesthesia utilized the periodontal probe pushed through the gingival tissue as a sounding device till one feels the bony margin. This will determine the shape of the bony margin. This is also used to determine the biological width. Even though not done routinely, it is necessary to this procedure before planning the surgical crown lengthening. FACTORS AFFECTING ACCURACY OF THE PROBING THE SIZE OF THE PROBE Tip of the probe may vary from 0.3 to 0.8 mm, for the different periodontal probes. This variation will affect the measurement of the probing. ANGULATION OF THE PROBING Same angulation to be used at each appointment is a difficult task. For the research purpose, acrylic stent can be used to measure the pocket depth, at the same point each time.

Penetration of the probe may vary depending on the force of introduction. Probing force applied by different clinicians may vary from 30 to 130 g. Forces of 0.75 N have been found to be accurate and well THE PROBING FORCE

259

tolerated. Before probing the sulcus, one can practice applying probing force by keeping the probe in the nail bed; amount of force to be applied may vary according to the severity of inflammation. INFLAMMATORY STATUS OF THE TISSUE During gingival inflammation, connective tissue adjacent to pocket epithelium is filled with inflammatory fluid and cells. Pocket epithelium is also infiltrated with inflammatory cells and ulcerated. This allows easy penetration of the periodontal probe even with the lightest probing force, and in some cases, probe penetrates as far as the bone margin, which results in overestimation of the pocket depth. Conversely, in treated cases, reduction in the pocket depth is often misunderstood as gain in clinical attachment. Results achieved after therapy should be considered with caution. The contour of the tooth and root surface is also found to be affecting the probing pocket depth.

Clinical Attachment Loss and Relative Attachment Loss Clinical attachment loss (CAL) is the true measure of the periodontitis. It is the distance between the base of the pocket and a fixed point on the crown such as CEJ. If the CEJ is missing because it has been destroyed by dental caries or placement of a restoration or because of abrasion, another fixed reference point can be used to measure the loss of attachment. Such landmarks might include apical margin of restoration or incisal edge of a tooth or composite point placed on the crown. When attachment loss is taken other than from the CEJ, it is termed relative attachment loss (RAL). CAL or RAL is considered to be a better indication of the degree of periodontal destruction than that of the pocket depth. METHOD OF ASSESSING THE CLINICAL ATTACHMENT LOSS

As it is used in the pocket depth, probe is held parallel to the long axis of the tooth. At first, the probe is passed from the enamel (smoother surface) toward the cementoenamel junction (which is the first rough point). Measurement is taken from the CEJ to the base of the probeable crevice (till soft tissue resistance is felt), at six points around each tooth. A case in which the CEJ is not visible, at first measurement is taken from the crest of the gingival margin to the base of the pocket (recorded as A). After this, measurement is taken from the crest of the gingival margin to the CEJ (recorded as B). Then we get A- B = CAL. RELATION BETWEEN POCKET DEPTH AND CLINICAL ATTACHMENT LOSS

Pocket depth and CAL are two different entities. The relation between these two is explained as it is related to

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the gingival margin. When the gingival margin is located coronal to CEJ, pocket depth will be more than the clinical attachment loss (CAL= distance from the gingival margin to base of the pocket - distance from gingival margin to CEJ). When the gingival margin is at the CEJ, pocket depth and clinical attachment loss are same. When the gingival margin is located apical to the CEJ, CAL is more than the pocket depth. DIAGNOSIS OF PERIODONTITIS In the presence of CAL and/ or a true pocket, case can be diagnosed as periodontitis. If the amount of plaque correlates with the amount of periodontal destruction, the given case can be diagnosed as chronic periodontitis. If there are less than 30% sites involved, it is diagnosed as localized, and if there are more than 30% sites, the case is diagnosed as generalized. Furthermore, depending on the severity of CAL, it can be further classified as mild (less than 2 mm CAL), moderate (more than 2 mm, but less than 5 mm), and severe (more than 5 mm). If there is less plaque and severe destruction and rate of progression of disease is faster than normal, the case can be diagnosed as an aggressive periodontitis. If the involvement is confined to first molars and incisors, it can be diagnosed as localized aggressive periodontitis, and if it involves addition of two permanent teeth, other than the first molar and incisors, the periodontitis is diagnosed as generalized aggressive periodontitis.

Furcation Involvement Involvement of furcation of multirooted teeth is a sign of periodontitis. There are several types of classification available. Most commonly followed classification based on horizontal involvement is the Glickman classification and Hamp and coworkers' classification. To add to this, to assess the vertical involvement of the furcation, Tarnow and Fletcher classification is utilized. To assess the furcation involvement, most commonly used instrument is the Naber's probe. HOW TO IDENTIFY THE FURCATION INVOLVEMENT?

If the pocket depth is more than 5 mm, there are more chances of furcation involvement. Naber's lN probe, Naber's 2N probe, or a curette is commonly used. The curved shanks of the Naber's lN and 2N probes are expressly designed for furcation detection. In case of nonavailability of the Naber's probe, periodontal probe can be used (Fig. 32.5). The probe is inserted parallel to the long axis of the tooth, at the midbuccal surface of the tooth and approximately 5 mm from the CEJ. It is angulated to find out the possible bone loss in the furcation area. If there is minimal bone loss, furcation can be felt like a groove between the roots. If there is moderate bone loss, probe can be easily entered in the furcation area, but cannot pass through. If there is severe bone loss, probe can

FIGURE 32.5

Detecting the furcation involvement.

be passed through. For maxillary furcation detection, especially mesial and distal furcations, approach to the furcation differs from the usual. The Naber's lN probe is specifically designed for mesial and distal furcations on maxillary molars. Probing a maxillary molar furcation may require an extraoral handrest in order to keep the probe tip properly adapted. Approach any maxillary molar mesial furcation from the lingual aspect because this furcation is located two-thirds of the way across the mesial surface from the buccal aspect, or one-third of the way in from the lingual aspect. The distal furcation is located on the distal surface, halfway between the buccal and lingual aspect. Approach it first from the buccal aspect and then from the lingual aspect.

Mobility of the Tooth Mobility of teeth is one of the signs associated with periodontitis. Even though teeth mobility may have several causes other than the periodontal infections, loss of alveolar bone from periodontitis is a major cause of abnormal tooth mobility. It needs to be understood in detail because often this is the chief complaint of the patient. It is a visually perceptible movement of the tooth away from its normal position when a light force is applied. All the teeth have some degree of mobility. This physiological tooth mobility is the limited tooth mobility allowed by resilience of an intact periodontium on application of a normal force. Physiological (normal) tooth mobility basically occurs in two stages: initial/intrasocket stage, which occurs rapidly, in which tooth moves within the confines of periodontal ligament space. This is associated with the viscoelastic distortion of periodontal ligament, which

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C H A PT ER 32 C LIN IC A L D IA G N O SIS

progresses until the complete elongation of the fibers is achieved. The range of mobility is in the order of 0.050.10 mm, when forces of 100 lb are applied. In contrast, secondary stage occurs gradually, where elastic deformation of the alveolar bone takes place in response to forces of 500 lb. Range of tooth mobility varies from tooth to tooth (incisors, canines, premolars, molars). When forces are discontinued, teeth return to their original position in two stages: immediate spring-like elastic recoil and slow recovery movement. Several factors affect tooth mobility: number, shape, and length of the root; diurnal variation, greater mobility in the morning, which progressively decreases thereafter; and females having more tooth mobility than males. Greater tooth mobility in the morning is due to slight extrusion of tooth from the socket, which progressively decreases thereafter once masticatory forces are applied on the tooth. Females usually will have more tooth mobility compared with males probably due to hormonal variation.

Pathological Tooth Mobility (Abnormal) As the name designated, tooth mobility because of pathological processes within the periodontium is called pathological or abnormal tooth mobility. Mobility occurs beyond the physiological range. Principal causes for the pathological tooth mobility are loss of alveolar bone, inflammatory changes in the periodontal ligament, and trauma from occlusion. ALVEOLAR BONE LOSS (LOSS OF TOOTH SUPPORT)

This is the most common cause of the tooth mobility. Here mobility of the tooth occurs because of an apical shift in the fulcrum. The amount of tooth mobility depends on the severity and distribution of bone loss on individual tooth surface, length and shape of the root, and crown to root ratio. Same amount of bone loss at incisors and molars will have different severity of mobility. Even though bone loss is severe on one side of the root surface, teeth may not be having much mobility.

stages, funnel-shaped variation in the crest of the bone results in increased tooth mobility. Root resorption, which may occur especially when excessive force is applied in case of orthodontic treatment, also leads to increased tooth mobility. Mobility due to trauma from occlusion usually occurs in two stages: progressive hypermobility and permanent hypermobility. Sometimes, the term "adaptive tooth mobility" is used when the changes in mobility are retained for a long period of time. OTHER CAUSES OF TOOTH MOBILITY HORMONAL CHANGES Due to physicochemical changes in the periodontal tissues, increased capillary permeability, increased edema, and alteration in the collagen metabolism result in increased tooth mobility in case of pregnancy and oral contraceptive users. Similar changes are observed during menstrual cycle also. PATHOLOGICAL PROCESSES OF THE JAWS Cysts and tumors involving the maxilla and mandible, and other infections of the bone such as osteomyelitis, result in increased tooth mobility. PERIODONTAL SURGERY A transient increase in tooth mobility is found immediately after the surgery because normal arrangement of collagen fibers will form only after 72 days. METHOD OF ASSESSING THE TOOTH MOBILITY MANUAL METHOD Tooth is held firmly between handles of two metallic instruments and force is applied in the buccolingual direction (Fig. 32.6). Mobility is noted with the adjacent teeth. Common index used to measure the tooth mobility was tooth mobility index by Mulhemann, which was later modified by Grace and Smales (Table 32.4).

EXTENSION OF INFLAMMATION

Extension of inflammation from gingiva to the periodontal ligament, or from the periapical region to the periodontal region, may result in increased tooth mobility; periodontal abscess and periapical abscess are the typical examples for this. TRAUMA FROM OCCLUSION

Trauma from occlusion results in increased tooth mobility. During injury stage, loss of lamina dura results in widening of periodontal ligament space. In case of repair stage, attempt to strengthen the periodontal structures also results in widening of periodontal ligament space. Furthermore, in adaptive remodeling

FIGURE 32.6

Detecting the mobility of tooth.

262 TABLE 32.4

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Indices for Measuring the Tooth Mobility

Mobility index - Miller Grade 0-Normal tooth mobility Grade 1 - Slightly more than the normal Grade 2 - Moderately more than the normal Grade 3 - Severe mobility faciolingually and mesiodistally combined with the vertical displacement Mobility index - Grace and Smales Grade 1 - Mobility 2 mm buccolingually and/or vertical tooth mobility

FACTORS INFLUENCING THE PATHOLOGICAL MIGRATION The factors influencing pathological mi-

gration include weakened periodontal support, pressure from the tongue, abnormal occlusal contact, tooth with abnormal proximal contact, absence of an antagonist, pressure from food bolus during mastication, abnormal lip sucking habit, etc.

MUCOGINGIVAL PROBLEMS OR PROBLEMS RELATED TO PLASTIC PERIODONTAL SURGERY Inadequate or Adequate Attached Gingiva

Mobilometer, periodontometer, and Periotest measure the reaction of the periodontium to a defined percussion force applied to the tooth via a tapping instrument. MECHANICAL/ELECTRONIC EVALUATION

PATHOLOGICAL MIGRATION

Tooth displacement results when the balance among the factors that maintain physiological tooth position is altered by periodontal disease (Fig. 32.7). This may be the presenting complaint of the patient, especially in the anterior region, and is the early sign of localized aggressive periodontitis, commonly called wandering of the teeth. Pathological migration is usually accompanied by mobility and rotation; tooth may move in any direction. Pathological migration in incisal/ occlusal direction is called extrusion. CLINICAL DETECTION OF THE PATHOLOGICAL MIGRATION Clinically, one should look at the change

in the position of the tooth, and then observe for the presence of pocket or loss of attachment. If it is present, then change in the position of the tooth in the arch is due to the loss of bone, and it should be considered as pathological migration.

FIGURE 32. 7 Pathological migration of right central incisor.

When pocket or recession extends beyond the mucogingival junction, there is absence of an attached gingiva. Even though controversy exists regarding the need for the zone of attached gingiva, correction of such problems may be required for aesthetic and functional reasons. Steps in Measuring the Zone of Attached Gingiva The following are the steps to find out the mucogingival junction: 1. Clinical differentiation between the alveolar mucosa

and attached gingiva: Color difference (red and pink, respectively; Fig. 32.8). 2. Use of Schiller's potassium iodide solution to stain the mucosa and attached gingiva: This solution stains the glycogen content of the tissue, and glycogen is more in the alveolar mucosa than in the attached gingiva. Because glycogen is utilized for the process of keratinization in the attached gingiva, this stain gives dark brown color to the alveolar mucosa and light brown color to the attached gingiva. The differentiating line between these two colors is the mucogingival junction.

FIGURE 32.8 Difference in the color between alveolar mucosa and the attached gingiva.

C H A PT ER 32 C LIN IC A L D IA G N O SIS

263

FIGURE 32.9 Bunching of the tissue at the junction between alveolar mucosa and the attached gingiva.

3. Passing the probe horizontally from alveolar mucosa

to the attached gingiva: Since the probe is moved from the movable tissue to the firm tissue, bunching of the tissue occurs at the site of the mucogingival junction (Fig. 32.9). 4. Anesthetizing the area, which blows out the loose alveolar mucosa and leaves the firm attached gingiva and hence easily differentiates the mucogingival junction. 5. Once the mucogingival junction is marked, measuring the distance between the crest of the gingival margin and the mucogingival junction using a periodontal probe (A); then pocket depth is measured (B). A - B gives the width of attached gingiva.

Abnormal Frenal Attachment Placek and coworkers classified the frenal attachment into four types: mucosal, gingival, papillary, and papillary penetrating. In the presence of adequate attached gingiva, papillary and papillary penetrating types should be considered as abnormal because they not only make it difficult for an individual to keep the brush in that area, resulting in plaque accumulation, but also cause gingiva to move away from the tooth surface, making the area a plaque retentive site. Tension test: This test is performed to check the abnormal frenal attachment and the adequate attached gingiva. Here the lip is moved outward, upward for the upper and downward for the lower, and also moved sideward. If the marginal and/ or the interdental papilla moves away from the tooth surface, then the tension test is said to be positive. If not, the test is said to be negative (Fig. 32.10).

FIGURE 32.10 Performing the tension test.

Blanch test: Blanch test is performed to diagnose a fleshy labial frenum. It is done by pulling the upper lip outward. Presence of a thick and fleshy frenum is confirmed by the blanching of the tissue in the incisive papilla region palatal to the two central incisors.

Inadequate Depth of the Vestibule Normal depth of the vestibule helps in proper maintenance of oral hygiene and also the movement of food during mastication. In the absence of this, food accumulates on the marginal gingiva and gingival sulcular area, resulting in the progression of the periodontal disease.

Identification of the Deficient Alveolar Ridge Lack of sufficient bony and soft tissue may limit the aesthetic value and oral hygiene habits of the patient when prosthetic restorations are placed over the defective ridges. The prosthetic teeth that are placed frequently look like as if they are resting on top of the flattened ridge. At present ridge augmentation procedures are included under the periodontal plastic procedures. Siebert and Allen classification is used to classify the deficient alveolar ridge.

Identification of the Black Triangle or Loss of Interdental Papilla Black triangle or black hole appearance between the teeth, especially in the anterior region, is of great aesthetic concern. Patients often come with the complaint of unaesthetic appearance of this area. Identification of such problems can be dealt with Nordland and Tarnow (1998) classification, which helps in planning out the treatment plan and prognosis of such treatment.

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Exposed Root Surface or Gingival Recession - Need for Root Coverage Gingival recession is the apical shift in the position of the gingiva with the denudation of the root surface. It is of aesthetic or functional concern. Classification of such recession is necessary in order to develop the prognosis after the root coverage procedure. Miller classification of marginal tissue recession is helpful in identifying the type of gingival recession. Gingival Pigmentation This is one of the most common complaints of patients nowadays. There are many depigmentation procedures available. However, before undertaking the procedure pigmentation needs to be classified according to available classification [recent classification and gingival pigmentation index (GPI; Singh V, Bhat GS, Bhat KM, Kumar S, 2012)] and good-contrast photograph needs to be taken. GP! Index 0

Absence of pigmentation, pink color of the gingiva

1

Spots of brown to black pigmentation

2

Brown to black pigmentation, more than spots but not diffuse (patches of pigmentation)

3

Diffuse brown to black pigmentation involving papillary, marginal, and attached gingiva

Fremitus Test Fremitus is a measure of the vibratory patterns of the teeth when the teeth are placed in contacting positions and movements. To measure fremitus, a dampened index finger is placed along the buccal and lingual surfaces of maxillary teeth. The patient is asked to tap the teeth in the maximum intercuspal position and then grind systemically in the lateral and protrusive contacting movements and positions. The teeth that are displaced by the patient in these jaw positions are then identified (Fig. 32.11). Generally this is limited to the maxillary teeth; however, in case of edge-to-edge occlusion or when there is little overlap of the teeth, mandibular teeth can be assessed. The classification system used to differentiate different degrees of fremitus is as follows: • Class I fremitus - mild vibration or movement detected • Class II fremitus - easily palpable vibration but no visible movement • Class III fremitus - movement visible with the naked eye Fremitus is a guide to the ability of the patient to displace and traumatize the teeth. It differs from the mobility in that fremitus refers to tooth displacement created by the patient's own occlusal force.

Assessment of Tooth Loss Substance Hard Tissue Examination Hard tissue examination includes finding out the number of teeth present: missing teeth, carious teeth, and restored teeth. Especially proximal caries is considered because this acts as a plaque retentive area. Restored teeth should be examined for the overhanging margins, which may have encroached upon the biological width. Overhanging restorations can be evaluated with the dental floss. Other plaque retentive areas such as palatal grooves, cervical enamel projections, and enamel pearl may be associated with localized deep pocket formation, which needs correction during pocket elimination procedure.

Attrition, abrasion, erosion, and abfraction should be evaluated. For example, if there is erosion, history related to esophageal reflux and food habits must be evaluated. Final diagnosis of the periodontal changes is done with collective information available after the history, and

TEETH IN OCCLUSION Type of occlusion, deep bite or open bite, should be evaluated. Plunger cusp: It is a sharp cusp that forces the food into the periodontium. Food impaction is the forceful wedging of the food into the periodontium. Such a problem can be revealed with the patient complaint and the local tissue changes. The patient usually complains of the symptoms of pocket formation.

FIGURE 32.11

Performing the fremitus test.

C H A PT ER 32 C LIN IC A L D IA G N O SIS

gingival and periodontal examination. Once the diagnosis is made, risk factors for the existing condition should be evaluated. Differential diagnosis may not be always sought for the commonly existing periodontal conditions.

265

However, for few gingival and periodontal changes such as localized gingival enlargement, differential diagnosis may be required. Furthermore, prognosis and treatment plan are planned.

KEY POINTS • Periodontal probing is the important method for assess-

• Presence of trauma from occlusion can be assessed clini-

ing the periodontal status. • Bleeding on probing is the important sign and presence of bleeding is suggestive of periodontal disease. • Assessment of furcation involvement is necessary in periodontal diagnosis because maintenance and treatment of the furcation is essential in preserving the tooth.

cally by fremitus test. • Width of attached gingiva is measured simply by tension test.

QUESTIONS 1. List any five common chief periodontal complaints. 2. Discuss the method of probing at a given periodontal

site. 3. What are the factors affecting the accuracy of probing? 4. List the etiology of the tooth mobility. 5. Mention the steps in zone of attached gingiva.

Suggested readings 1. American Dental Association, American Academy of Periodontology. Periodontal Screening and Recording Training Manual. 1992 [reprinted with permission from American Dental Association]. 2. American Academy of Periodontology. Proceedings of the world workshop in periodontics. In: Annals of Periodontology. Chicago: American Academy of Periodontology, 1996. 3. Armitage GC, Svanberg GK, Loe H. Microscopic evaluation of clinical measurement of connective tissue attachment levels. J Ciin Periodontol 1977;1:173-5. 4. Bhlaji J. Orthodontics, Art and the Science. 1st ed. New Delhi: Arya Publications:chap 35. 5. British Society of Periodontology. Basic Periodontal Examination. 6. Butler RT, Kalkwarf KL, Kaldahl WB. Drug induced gingival hyperplasia: phenytoin, cyclosporine and nifedipine. J Am Dent Assoc 1987;114:56. 7. Carranza AF, Takei HH. Clinical diagnosis. In: Carranza's Clinical Periodontology. 10th ed. Philadelphia: Elsevier; 2007. 8. Dajani AS, Talbert KA, Wilson W. Prevention of bacterial endocarditis: recommendations by the American Heart Association. JAMA 1997;277:1794. 9. Dussault G, Sheiham A. Medical theories and professional development: the theory of focal sepsis and dentistry in early twentieth century. Br Soc Sci Med 1982;16:1405. 10. Easley J. Methods of determining the osseous form. J Periodontal 1967;38:112. 11. Edwards JG. The diastema, the frenum and the frenectomy: a clinical study. Am J Orthod 1997;3:489-508.

• Medical history taking is very important to prevent the complications during the treatment. • Walking probing is also called stepping, and transgingival probing or transsulcular probing (TSP) is also called sounding.

12. Genco RJ, Goldman HM, Cohen DW. Periodontal diagnosis. In: Contemporary of Periodontics. 2nd ed. St. Louis: Mosby, 1990. 13. Glickman I. Clinical Periodontology. Philadelphia: Saunders; 1953. 14. Green C, Vermillion J. Simplified oral hygiene index. In: Peter S, editor. Essentials of Preventive and Community Dentistru. 2nd ed. New Delhi: Arya Publishing House; 2004. p. 126-240. 15. Grace AM, Smales FC, editors. Mobility Index. Periodontal Control: An Effective System for the Diagnosis, Selection, and Treatment in General Practice. New York: Quintessence; 1989. p. 52. 16. Greenberg MS, Glick M. Burkett's Oral Medicine: L - Diagnosis and Treatment. 10th ed. India: Elsevier; 2003. 17. Hamp SE, Nyman S, Lindhe J. Periodontal treatment of multirooted teeth results after 5 years. J Clin Periodontol 1975;2:126. 18. Kalkwarf JJ, Kahldal WD, Patil KD. Comparison of manual and pressure controlled periodontal probing. Periodontologu 1989;57:467. 19. Listgarten MA, Mao R, Robinson PJ. Periodontal probing and the relationship of the probe tip to periodontal tissues. J Periodontal 1976;47:511. 20. Listgarten MA. Periodontal probing: what does it mean? J Clin Periodontol 1980;7:165. 21. Loe H. Periodontal changes in pregnancy. J Periodontol 1965;36:209. 22. Lozda-Nur F, Miranda C. Oral lichen planus: epidemiology, clinical characteristics and associated disease. Semin Cutan Med Sur 1997;16:273. 23. Miller Jr PD. A classification of marginal tissue recession. Int J Periodontics Restorative Dent 1985;5:9. 24. Mombelli A, Van Oosten MAC, Schurch E Jr, Lang NP. Sulcus bleeding index. In: Periodontal Control: An Effective System for the Diagnosis, Selection, Control, and Treatment in General Practice. Vol 52. London: Quintessence; 1989. 25. Morita M, Wang HL. Association between oral malodour and adult periodontitis: a review. J Clin Periodontal 2001;2:257-63. 26. Mulhemann HQ. Periodontometry: a method of measuring tooth mobility. Oral Surg Oral Med Oral Pathol 1951;4:1220-32. 27. Murata T, Yamuga T, Lida T, Miyazaki K. Classification and examination of halitosis. Int Dent J 2002;52:181-6. 28. Nordland P, Tarnow S. Classification system for the papillary height. In: Lindhe J, ed. Textbook of Clinical. 30. Lindhe J, Karring T, Lang NP. Clinical Periodontology and Implant Dentistry. 4th ed. Malden, MA: Blackwell Munskgaard; 2003:234-237.

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31. Ochsenbein C, Ross F. A primer for the osseous surgery. Int J Periodontics Restorative Dent 1986;6:9. 32. Parmar G, Sangwar P, Vashi P, Kulkarni P, Kumar S. Effect of chewing mixture of areca nut and tobacco on periodontal tissues and oral hygiene status. J Oral Sci 2008;50(1):57-62. 33. Pattison GA. Self inflicted gingival injuries: literature review and case report. J Periodontal 1983;54:299. 34. Placek and coworkers. Mandibular and maxillary midline frenum problem. In: Hoel E, ed. Textbook of Orthodontics and Periodontics. Quintessence. 35. Rees TD, Mealey BL. Periodontal treatment of medically compromised patients. In: Rose LF, Mealey BL, Genco RJ, Cohen DW, editors. Periodontal Medicine, Surgery and Implants. St Louis: Elsevier Mosby; 2004. 36. Sanz M, Roldon S, Herera D. Fundamental of breath malodour: review. J Contemp Dent Pract 2001;15(4):1-17. 37. Seibert JS. Reconstruction of deformed partially edentulous ridges using full thickness onlay grafts. Compend Conlin Educ Dent 1993. 38. Schulte W, Lukas D. The Periotest method. Int Dent J 1992;42:433--40.

39. Sumanth S, Bhat KM, Bhat GS. Periodontal health status in pan chewers with or without use of tobacco. Oral Health Prev Dent 2008;6(37):223-9. 40. Stottenberg JL, Osborn JB, Phlstorm BL. Association between cigarette smoking, bacterial pathogens and periodontal status. Periodontology 1995;64:1225. 41. Tarnow D, Fletcher P. Classification of the vertical component of furcation involvement. J Periodontal 1984;35:283. 42. Tibbets LS. Use of diagnostic probes for the detection of periodontal disease. J Am Dent Assoc 1969;78:549. 43. Van der Vaiden V. Probing forces and the relationship of the probe tip to periodontal tissues. J Clin Periodontal 1979;6:106. 44. Yegaki K, Coil JM. Examination, classification and treatment of halitosis: clinical perspective. J Can Dent Assoc 2000;66: 257-61. 45. Zambon JJ, Reynolds H, Fisher JB. Microbiological and immunological studies of adult periodontitis in patients with noninsulin dependent diabetes mellitus. J Periodontol 1988;59:23.

CHAPTER

33 Role of Radiology in the Diagnosis of Periodontal Diseases CHAPTER OVERVIEW Periodontal disease, an inflammatory condition affecting the tooth and primarily its supporting structures (destruction of periodontal ligament and alveolar bone), is undoubtedly still the only common cause for premature loss of teeth. In developing countries such as India the lack of awareness of the importance of high standards of oral health and its effect on systemic health and inadequate health care facilities compounds the problem. Periodontal diseases are clinically characterized by gingival inflammation, gingival recession, periodontal pockets,

RADIOGRAPHIC APPLICATION IN THE DIAGNOSIS AND TREATMENT PLANNING OF PERIODONTAL DISEASE

pus discharge from the gingival sulcus, tooth mobility, and pathologic migration. Apart from the classical clinical signs, periodontal diseases are also evident in radiographs in terms of alteration in periodontal ligament width and lamina dura, alveolar bone changes (interdental and alveolar), furcation involvement, root resorption, etc. Although a thorough clinical examination will aid in making a good working diagnosis, it is universally accepted that radiographs supplement clinical examination and they help in formulating an ideal treatment plan.

3. Evaluation of root fractures and cementa/ tears 4. Assessment of local jaw pathology and systemic conditions

causing bone destruction

Local and systemic conditions that influence the health of the periodontium can be assessed using intraoral and extraoral radiographs. The following are the conditions that can be radiographically assessed to a large extent: l. Assessment of local factors that predispose/aggravate periodontal disease (Figs 33.1-33.4): a. Calculus (primarily subgingival calculus) b. Overhanging restorations c. Ill-fitting/poorly contoured crowns d. Endo-perio lesions 2. Assessment of tooth morphology and supporting structures: a. Crown-root ratio b. Root morphology c. Width of the periodontal ligament space d. Integrity of lamina dura e. Bone in the furcation area £. Interdental bone (condition of crestal bone and extent/pattern of bone loss)

5. Assessment of bone quantity (especially important for implant placement) 6. Surgical planning and assessment of bone defects for

placement of bone grafts. Along with the inherent advantages of radiographs for diagnosis of periodontal diseases they have their limitations as listed in the next section.

LIMITATIONS OF RADIOGRAPHS 1. Early bone changes may not be evident on the

radiograph, as a minimum of 55-60% demineralization should have occurred. 2. Conventional imaging techniques such as the intraoral periapical, bitewing, and panoramic radiography provide only a two-dimensional view of the threedimensional bone structure.

267

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FIGURE 33.1

Intraoral periapical radiograph showing evidence of subgingival calculus and minimal interdental bone loss (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

FIGURE 33.3 Poorly contoured crown associated with interdental bone loss (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

FIGURE 33.2 Overhanging restoration (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

3. Conventional imaging may result in superimposition

and overlapped images, thereby making the radiograph occasionally nondiagnostic. 4. Soft tissue changes are not evident on conventional imaging techniques.

FIGURE 33.4

Endo-perio lesion associated with the maxillary canine (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

Conventional Radiography

RADIOGRAPHS USEFUL FOR DIAGNOSING PERIODONTAL DISEASE Both traditional and newer imaging modalities can be used for the diagnosis of periodontal disease. However, the clinician needs to judge the inherent advantages and limitations of each of the projections and employ them as required.

1. 2. 3. 4.

Intraoral periapical radiographs Bitewing radiographs Occlusal radiographs Orthopantomograms.

Newer Imaging Techniques Cone beam computed tomography

CHAPTER 33 ROLE OF RADIOLOGY IN THE DIAGNOSIS OF PERIODONTAL DISEASES

IMAGING CONSIDERATIONS FOR PERIODONTAL DISEASE Periodontal tissues encompass a wide range of structures with varying radiodensities from bone (cortical and cancellous) to cementum. In order to improve the diagnostic yield of the radiograph, an image with a wider gray scale is desirable.

Patient Selection It is always advisable that the clinician conducts a thorough clinical examination and takes into consideration patients' present symptoms and signs and their underlying systemic condition before embarking on radiographic investigations. It goes without saying that the periodontist should weigh the benefits of taking dental radiographs against the risk of exposing the patient to radiation. Radiographs should be advised only when the clinician feels that the additional diagnostic information obtained from radiographs will affect patient care.

269

shortened, or overlapped (Fig. 33.6). Paralleling technique along with the wire grid is the best technique to quantify the amount of bone loss (Fig. 33.7). This technique provides an image with the least amount of distortion. Bitewing radiographs (Fig. 33.8) are also useful alternatives for assessing early and initial destruction of interdental bone, assessing crestal bone contour and height, and evaluating poorly contoured restorations and prosthetic crowns that initiate and aggravate periodontitis. Traditionally horizontal bitewings are used for assessing interdental bone loss. However, moderate to severe bone destruction extending apically can be evaluated best with vertical bitewings (Fig. 33.9). A diagnostic-quality intraoral periapical radiograph should be able to exhibit the full crown, full length of the roots and at least 2 mm beyond the periapex and

Choice of Radiographic Projection Both conventional and specialized imaging may be used to image periodontal structures. Conventional imaging techniques are still widely used as they are more universally available and inexpensive. Newer imaging techniques such as Cone beam computed tomography (CBCT) are now finding their use in implant planning and detailed supporting bone assessment for periodontal surgery. If an overall view of the status of supporting bone is required, an extraoral radiograph such as the panoramic radiograph (Fig. 33.5) may be taken. However, if the clinician requires minute details such as the condition of the lamina dura, width of the periodontal ligament space, and height of the alveolar bone, area-specific intraoral periapical radiographs using either bisecting angle or paralleling technique can be used. Intraoral periapical radiographs, though widely taken using bisecting angle technique, may frequently provide images that are elongated, fore-

FIGURE 33.6 Intraoral periapical radiograph taken using bisecting angle technique revealing overlapped and elongated image (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

FIGURE 33. 7 FIGURE 33.5

Radiograph taken using paralleling technique along with a wire grid to assess the amount of bone destruction (Courtesy

Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

Panoramic radiograph taken as a screening radiograph to assess periodontal bone destruction (Courtesy Department of Oral

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SECTION V DIAGNOSIS, PROGNOSIS, AND TREATMENT PLANNING

FIGURE 33. IO Diagnostic quality intraoral periapical radiograph (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

FIGURE 33.8 Bitewing radiograph showing early interdental bone loss (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

The full mouth series consist of 17 periapical and 4 bitewing radiographs. These include maxillary centrals (1), maxillary laterals (2), maxillary canines (2), maxillary premolars (2), maxillary molars (2), mandibular central and lateral incisors together (2), mandibular canines (2), mandibular premolars (2), mandibular molars (2), and bitewing radiographs (4) consisting of premolars (2) and molars (2). Panoramic radiograph provides a broad coverage and view of the upper and lower teeth and the supporting bone. However, owing to its low resolution, it does not provide fine detail. Also, unequal magnification is another important limitation in panoramic radiographs. A study by Valchovic et al (1986) showed that the panoramic radiograph in comparison to full mouth series of intraoral periapical radiographs exhibited low specificity in detecting evidence of periodontal disease. However, the sensitivity was high and comparable to intraoral periapical films ranging from 87 to 96%.

Cone Beam Computed Tomography in the Detection of Periodontal Disease

FIGURE 33.9 Moderate amount of interdental bone loss evident on a vertical bitewing radiograph (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

proximal aspects of adjacent teeth (if present), and the interdental bone (Fig. 33.10). Likewise a diagnostic-quality bitewing should be able to display each proximal surface at least once. A full mouth series of intraoral radiographs will help in diagnosis and treatment planning for periodontal diseases.

Before the advent of cone beam computed tomography (CBCT), periodontal bone destruction was primarily assessed with conventional imaging and digital imaging such as radiovisiography (RVG) which has the inherent limitation of two-dimensional imaging. Since the introduction of CBCT in diagnostic radiography, various studies were carried out to evaluate its role in maxillofacial imaging including imaging of periodontal structures. CBCT is used to evaluate integrity of lamina dura, periodontal ligament space and periodontal bone defects (furcation defects; osseous craters; pattern, extent, and location of bone defects), and implant planning and postimplant assessment (Figs 33.11-33.16).

CHAPTER 33 ROLE OF RADIOLOGY IN THE DIAGNOSIS OF PERIODONTAL DISEASES

FIGURE 33.11 Axial section reveals loss of cancellous bone and labial cortical plate with respect to the edentulous region 13. Bone loss extends up to the mesial surface of the root of 14 labio-palatally (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

FIGURE 33.12 Coronal section revealing bone loss up to the apical one third of the 31, 32, 33 and 41 (Courtesy Department of Oral Medicine and Radiologi]. Manipal College of Dental Sciences, Mangalore).

There are still some conflicting reports with regards to a better imaging technique for visualizing periodontal ligament space. However, majority of the studies report that conventional intraoral periapical radiographs are superior to CBCT for assessing periodontal ligament space. However, in comparison to computed tomography (CT) scan, CBCT images provide more clarity. The only limitation

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FIGURE 33.13 Sagittal section shows bone loss extending to the middle one third of the distal surface of the distobuccal root of the first molar. Bone loss extending to the apical one third of the roots of the second molar involving the furcation. Bone loss extending up to the apical one third of the third molar (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

FIGURE 33.14 Sagittal section reveals labial and lingual bone loss extending up to the apical one third of the incisor.

with conventional imaging is a possibility of overlap of adjacent anatomical structures.

Choice of Image Receptor and Collimation Imaging can be performed using digital image receptors such as charge-coupled device (CCD), photostimulable

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phosphors (PSP), and complementary metal-oxide semiconductors (CMOS) or conventional analog films. In various studies to compare speed of film with patient exposure, F (Insight) speed film was shown to reduce patient exposure by about 20-50% when compared with E (Ekta) speed films and the slower D speed film caused 30-40% more patient exposure when compared with E speed films. Also digital receptors are known to cause the least patient exposure, reducing the exposure almost up to 60% when compared with conventional films. It is also preferable to use a rectangular collimator and a long cone technique (target to skin distance of 40 cm) to further minimize radiation exposure. Most of the dental X-ray machines in India have fixed tube voltage (kVp) and tube current (mA) settings between 60 and 70 kVp and 8 and 10 mA, respectively. However, wherever possible a higher tube voltage and a lower tube current produce a wide gray scale (low-contrast image) showing even the minor changes in the supporting alveolar bone and outlines of soft tissue, which is best suited for diagnosis of periodontal disease. FIGURE 33.15

Coronal section reveals bone loss up to the middle third of the distobuccal root of the molar on the buccal aspect and up to the apical third in relation to the palatal root. Mucosa! thickening is also evident at the floor of the maxillary sinus (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

Normal Periodontal Radiographic Anatomy Periodontal tissues include the gingiva, periodontal ligament, cementum, and alveolar bone. Of these, radiographically the periodontal ligament in terms of status of lamina dura (presence or absence) and the width; cementum in terms of the root width; and alveolar bone in terms of the morphology, location, pattern, and extent of destruction are routinely assessed.

Cementum The tooth root is covered with an extremely thin layer of cementum which is poorly mineralized when compared with dentine (just about 50% as that of dentine). This low mineral content makes it invisible on radiographs. In radiographic terms the contrast between dentine and the cementum is very minimal, thereby exhibiting the same radiodensity as that of dentine. However, excessive secondary cementum formation (Fig. 33.17) can lead to either a generalized uniform bulbous enlargement of the root (hypercementosis) or a localized mass of radiodensity at the apex (nodular type of hypercementosis).

Lamina Dura and Periodontal Ligament Space

FIGURE 33.16 Reconstructed 3D view reveals bone loss involving the furcation and middle third of the mesial root of the first molar. Presence of a periapical bone defect at the mesial root of the tooth (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

Lamina dura is a radiographic term used to describe the dense bone that forms the tooth socket (Fig. 33.18). Radiographically, on a two-dimensional image, it appears as a uniform radiopaque line that is in continuation with the alveolar crestal bone and surrounds the root of teeth. The integrity of the lamina dura, variation in the thickness, etc., are usually considered as associated with

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average thickness ranged between 0.22 and 0.54 mm. Studies have shown that the lamina dura is generally dense and relatively thicker for teeth under greater occlusal loading. Periodontal ligament space is the radiolucent space between the root of the tooth and the lamina dura. The ligament space is generally widest in the region approximating the alveolar crest and the periapical region of the tooth and relatively thinner at the middle third of the tooth. Histologically, the width of the periodontal membrane ranges from 0.15 to 0.38 mm.

Alveolar Bone ( Crestal, lnterdental, and Periapical)

FIGURE 33.17 IOPAR reveals bulbous roots of molar suggestive of hypercementosis (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

The alveolar crest is the term used to describe that part of the alveolar bone that extends interdentally toward the cervical margin of teeth and is continuous with the lamina dura of adjacent teeth. The alveolar crest is bounded by dense cortical bone. The presence of the dense cortical outline usually signifies healthy periodontium and absence of active disease process. The morphology of the crestal bone varies based on the location. In between the anterior teeth, the alveolar crest is pointed (Fig. 33.19) and in the region of the posterior teeth it is flat topped and located 1-1.5 mm below and parallel to an imaginary line joining cementoenamel junctions of adjacent teeth. In healthy individuals the junction between lamina dura and the alveolar crest forms a sharp angle (Fig. 33.20). Majority of the bone is cancellous /spongy/ trabecular in nature which is enclosed within dense buccal, lingual, and palatal cortical plates. The bone marrow trabeculae vary in the morphology and density in both the maxilla and mandible. Complete absence of the trabeculae or destruction/ abnormal morphology/ density of the trabecular pattern when compared with the opposite side may indicate a disease process.

Trabecular Pattern in the Maxilla

FIGURE 33.18 Photograph illustrating lamina dura surrounding the roots of teeth (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

pathologies. However, one should also be aware that the appearance of lamina dura also depends on the projection geometry of the X-ray beam. When the X-ray beam is directed tangentially, it may not show lamina dura very distinctly in spite of absence of disease. In a study by Hubar (1993) to quantify the thickness of lamina dura it was found that the lamina dura varied in thickness between anterior and posterior teeth and the

Trabecular pattern is relatively sparser in the mandible when compared with the coarse, dense trabeculae in the maxilla (Fig. 33.21A and B). However, individual trabeculae are dense when compared with the maxilla. In the anterior segment of the maxilla, the trabeculae are very slender and closely placed giving rise to numerous small marrow spaces. In the premolar-molar region the marrow spaces are slightly larger. However, the trabecular pattern remains the same.

Trabecular Pattern in the Mandible Compared with the maxilla the trabeculae are fewer and arranged in a set horizontal pattern with large marrow spaces (Fig. 33.22A and B). In the molar region the trabeculae are literally absent. It is believed that the stronger and tougher the cortical plates, more sparse is the trabeculae and vice versa.

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SECTION V DIAGNOSIS, PROGNOSIS, AND TREATMENT PLANNING

FIGURE 33.19 Pointed alveolar crest in the maxillary anterior region (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

CHARACTERISTIC RADIOGRAPHIC FEATURES OF PERIODONTAL DISEASES Chronic Periodontitis Early Stage Radiographic changes are usually evident almost 8-10 months after the initial occurrence of periodontal

FIGURE 33.21 Sparse trabecular pattern of the anterior and posterior parts of the maxilla (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Man galore).

disease. The earliest changes include widening of the periodontal ligament space at the lateral margin of the tooth approximating the cementoenamel junction and rounded appearance of the crestal margin. As the disease progresses, loss of the cortical margin of the crestal bone followed by mild erosion of the crestal bone is evident (Fig. 33.23).

Intermediate Stage As the disease progresses, bone defects become more obvious with resorption of the buccal and/ or lingual cortical plate or cancellous bone defects. The bone defects are usually evident on conventional imaging techniques as a horizontal pattern of bone destruction or angular/ vertical pattern of bone loss. FIGURE 33.20 Flat topped crestal margins of the posterior teeth (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

HORIZONTAL PATTERN OF BONE LOSS

Horizontal pattern of bone loss is the most common form of bone loss that occurs when the buccal, lingual,

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275

FIGURE 33.23 Loss of the cortical margin and mild erosion of the crestal bone (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

The exact location and pattern of the osseous defect is not possible to identify on a conventional two-dimensional image. There are four distinct patterns that are recognized as angular bone defects, namely: interproximal craters, interproximal hemiseptal defects, proximal intrabony defects, and inconsistent bony margins. Other less common defects include ledges and reversed architecture. INTERPROXIMAL CRATERS Like the name suggests interproximal craters are seen on radiographs as shallow saucer-shaped or crater-like defects located at the alveolar crests between two teeth. The apical extent of the defect is usually not clearly visualized. It is considered to be the most common osseous defect that is seen in moderately progressed form of periodontitis.

FIGURE 33.22 Bony trabecular pattern in the anterior and posterior region of the mandible (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

and cancellous bones interposed between have been uniformly resorbed. The bone loss either is localized to a few teeth or affects multiple teeth (Fig. 33.24). ANGULAR PATTERN OF BONE LOSS

The bone level is angulated when compared with an imaginary horizontal line drawn across the cementoenamel junction of adjacent teeth (Fig. 33.25). The base of the bone defect is typically located apical to the bone adjacent to it.

INTERPROXIMAL HEMISEPTAL DEFECTS lnterproximal hemiseptal defect is radiographically evident as a V-shaped defect. It results when bone is resorbed from either the mesial or distal aspect of the root. Many of these defects usually progress to involve the bone on the buccal aspect of teeth. PROXIMAL INTRABONY DEFECTS Proximal intrabony defect is a three-walled defect extending in an apical direction from the alveolar crest along the root length. It is bounded by the interdental septal bone (hemisepta) and the two cortical plates (buccal and lingual). On a radiograph it appears as a well-demarcated V-shaped defect. Use of a contrast agent such as a gutta-percha point may be used to track the full depth of the intrabony defect.

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FIGURE 33.26 Panoramic radiograph showing angular and horizontal bone defects in the advanced stage of periodontitis (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

FIGURE 33.24

Radiograph showing interdental horizontal bone loss (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

LEDGES When the thick cortical plates resorb, they may occasionally produce margins of bone that resemble plateaus, which are referred to as ledges. REVERSED ARCHITECTURE These forms of osseous defects are more frequently seen in the maxilla. In this form of defect, the radicular bone remains intact. However, the buccal, lingual, and interdental bones are resorbed, causing a reversal of normal bony architecture.

Advanced Stage In the advanced form of periodontitis there are both angular and horizontal bone defects. The involvement is more generalized and severe, resulting in tooth mobility, and as the disease progresses, teeth are lost (Fig. 33.26).

Aggressive Periodontitis

FIGURE 33.25

Intraoral periapical radiograph showing angular interdental bone loss extending up to the apical one third of the root (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

INCONSISTENT BONY MARGINS When either the lingual or buccal cortical plates are resorbed in an uneven or irregular fashion, an inconsistent crestal bony margin is formed. Radiographically they are evident as irregular coronal edges of the cortical plates superimposed over the root of the affected tooth.

Aggressive periodontitis was previously referred to as juvenile periodontitis. Although it has been reported to occur at any age, the term aggressive periodontitis is usually reserved for that form of periodontal disease which affects individuals younger than 30 years of age with no underlying systemic illness with a tendency to aggregate within families and cause extensive periodontal tissue destruction. The extent of periodontal destruction does not correlate with the amount of local irritants (calculus). There are two forms that are recognized based on the extent of involvement: localized aggressive periodontitis and generalized aggressive periodontitis. The localized form of aggressive periodontitis is characterized by clinically deep periodontal pockets and radiographically extensive bone defects (Fig. 33.27) affecting the incisors and molars. Bone destruction associated with the bilateral molars is described as "arcshaped mirror image." According to the consensus report on aggressive periodontitis reported by Lang et al (1999), the term generalized aggressive periodontitis is used when at least three permanent teeth are affected other than the first molars

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277

and incisors. The radiographic features usually cover the entire gamut of bone destruction from minimal crestal destruction to extensive bone destruction exhibiting both horizontal and angular defects.

Periodontal Abscess

FIGURE 33.27 Panoramic radiograph showing extensive bone loss associated with the incisors and molars in aggressive periodontitis (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

A periodontal abscess is typically formed due to entrapment of a foreign substance or debris such as loose fragment of calculus, etc., within a periodontal pocket and subsequently getting infected. Another possible etiology is closure of the marginal gingival over a localized infection within the periodontal pocket resulting in an area of increased pressure further causing a swelling (Fig. 33.28A and B). Based on the severity and duration radiographically the findings may vary from a normal interdental bone to widening of the periodontal ligament space, interdental bone loss, or in severe cases of chronic nature extensive bone loss extending up to and involving the apex of the tooth, occasionally resulting in a floating tooth appearance. As a thumb rule acute abscesses hardly exhibit any radiographic changes.

SYSTEMIC CONDITIONS INFLUENCING PERIODONTITIS 1

Papillon-Lel'evre syndrome

Periodontitis with palmar plantar keratosis

2

Chediak-Higashi syndrome

Oral ulcers with severe periodontal destruction

3

Down syndrome

Generalized gingival recession with periodontal pockets

4

Acquired immunodeficiency Necrotizing ulcerative gingivitis syndrome and periodontitis

5

Diabetes mellitus

Multiple periodontal abscesses, rapid destruction of alveolar bone

SYSTEMIC CONDITIONS MIMICKING PERIODONTITIS RADIOGRAPHICALLY

FIGURE 33.28

Photograph depicting palatal swelling in relation to the right premolar and molar. Intraoral periapical radiograph shows evidence of interdental bone loss extending to the apex of the molar. A broken toothpick is also seen on the mesial aspect of the molar (Courtesy Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Mangalore).

1

Systemic sclerosis

Widening of periodontal ligament space

2

Hyperpituitarism (gigantism, acromegaly)

Hypercementosis

3

Hyperparathyroidism

Complete or partial absence of lamina dura

4

Gaucher disease (lysosomal storage disease)

Widening of periodontal ligament space and loss of trabeculae

5

Gingival squamous cell carcinoma

Destruction of interdental bone

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KEY POINTS 1. A minimum of 55-60% demineralization of bone is required to be evident radiographically. 2. Radiographically an image with a wider gray scale is desirable of detection of periodontal disease. 3. Intraoral periapical radiograph using paralleling technique along with the wire grid is the best technique to quantify the amount of bone loss.

QUESTIONS 1. What are the indications for radiographs in periodontal diseases? 2. What are the limitations of radiographs in the assessment of periodontal disease? 3. Enumerate radiographic projections that can aid in diagnosis of periodontal disease. 4. Discuss various radiographic features of periodontal diseases. 5. Name some systemic conditions that can radiographically mimic periodontal disease.

Suggested readings 1. Valachovic RW, Douglass CW, Reiskin AB, Chauncey HH, McNeil BJ. The use of panoramic radiography in the evaluation of asymptomatic adult dental patients. Oral Surg Oral Med Oral Pathol 1986;61(3):289-96. 2. White SC, Pharoah MJ. Oral Radiology. Principles and Interpretation. 1st South Asia ed New Delhi: Elsevier 2014. 3. Hubar JS. Quantification of the lamina dura. J Can Dent Assoc 1993;59(12):997-1000.

4. Interproximal craters, interproximal hemiseptal defects, proximal intrabony defects, inconsistent bony margins, ledges and reversed architecture are various patterns of angular bone loss. 5. Bone destruction associated with bilateral molars described as "arc-shaped mirror image" is characteristic of aggressive periodontitis.

4. Stafne EC, Gibilisco J. Stafne's Oral Radiographic Diagnosis. 5th ed. Philadelphia: WB Saunders Company; 1985. 5. Corbet EF, Ho DKL, Lai SML. Radiographs in periodontal disease diagnosis and management. Aust Dent J 2009;54(1 suppl):S27-43. 6. Jervoe-Storm PM, Hagner M, Neugebauer J, et al. Comparison of cone-beam computerized tomography and intraoral radiographs for determination of the periodontal ligament in a variable phantom. Oral Surg Oral Med Oral Pathol Oral Radial Endod 2010;109(2):e95-e101. 7. Lang N, Bartold PM, Cullinan M. Consensus report: aggressive periodontitis. Ann Peridontol 1999;4:53. 8. Tugnait A, Clerehugh V, Hirschmann PN. The usefulness of radiographs in diagnosis and management of periodontal diseases: a review. J Dent 2000;28:219-26. 9. Akesson L, Hakansson J, Rohlin M. Comparison of panoramic and intraoral radiography and pocket probing for the measurement of alveolar bone level. J Ciin Periodontol 1992;19:232-326. 10. Pepelassi EA, Tsiklakis K, Diamanti-Kipioti A. Radiographic detection and assessment of the periodontal endosseous defects. J Clin Periodontol 2000;27:224-30. 11. Faculty of General Dental Practitioners (UK). Radiographs in periodontal assessment. In: Selection Criteria for Dental Radiography. London: Royal College of Surgeons; 1998:42-44. 12. Akesson L, Rohlin Hakansson J. Marginal bone in periodontal disease: an evaluation of image quality in panoramic and intraoral radiography. Dentomaxillofac Radiol 1989;18:105-12.

CHAPTER

34 Advanced Diagnostic Methods CHAPTER OVERVIEW Diagnosis is derived from the Greek word gnosis ("to know") and dia ("through"). Medical diagnosis has been

defined as the process of identifying a disease by its signs, symptoms, and results of various biological tests.

USES

CONVENTIONAL DIAGNOSIS

• Clinical utility • Research utility • Administrative utility.

Clinical Uses Diagnostic procedures may be used to: • • • • •

Identify people at risk Screen for disease Classify disease Treatment planning Monitor treatment efficacy and detect disease recurrence.

Periodontitis is an inflammatory process caused by host-parasite interactions, which lead to tissue destruction. This results in pocket formation, loss of connective tissue attachment, bone loss, tooth mobility, and tooth loss. Dentists have limited means to detect periodontal disease. Conventional diagnostic techniques have focused on attachment loss and estimating alveolar bone loss on radiographs, but these techniques have limitations as they measure only the past disease.

The Basis Classification helps in systematic study of diseases. It is the first step in the identification of disease. There are two approaches to classification: • Ontological approach • Physiological approach

Research Uses • Classification of disease helps to identify patterns of disease within populations and evaluate treatment. • Accurate diagnosis is essential for selection of samples from the population.

Administrative Uses • In developed nations, diagnosis is essential for claiming dental insurance. • Diagnosis is essential for effective communication between clinicians. The goal of periodontal diagnosis is to classify periodontal disease, provide optimal therapy, and give a realistic prognosis.

Ontological approach deals with the general concept of a disease. Physiological approach considers the particular case of illness in a specific patient. Both approaches are essential in identifying and treating diseases. Diagnosis should have both clinical and biological plausibility. Clinical utility means the diagnosis should dictate possible treatment options and suggest the likely course of the disease. Biological plausibility means the diagnosis should be able to distinguish between conditions that have similar clinical presentations but different etiologies.

Evaluating Diagnostic Tests Some amount of uncertainty exists in the formulation of diagnosis and the interpretation of all diagnostic tests.

279

280 TABLE 34.1

SECTION V DIAGNOSIS, PROGNOSIS, AND TREATMENT PLANNING

Evaluation of Diagnostic Tests

Results of test

Presence of disease

Absence of disease

Positive

True-positive (1)

False-positive (2)

Negative

False-negative (3)

True-negative (4)

Total

1+3

2+4

A diagnostic test can give a positive or negative result. When the result is correct, it is true-positive, and if incorrect, it is false-positive. Similarly, true-negative and falsenegative results may also exist (Table 34.1). • The sensitivity of a test is the proportion of subjects with the disease who test positive. • The specificity of a test is the proportion of subjects with the disease who test negative.

TRUE DISEASE STATUS Sensitivity and specificity help in choosing an appropriate test. Once the result has come, the probability that the test will be right is given by the predictive value. The probability that a person with a positive test has the disease is called positive predictive value and vice versa.

Diagnostic Sequence Collection of Data Accurate data collection by a systematic approach is necessary to arrive at a diagnosis. Organized and structured examination ensures that no aspect of the patient's status is overlooked. The medium for recording examination findings may be just charting or computerized medium.

Primary Diagnosis Formulating a primary or presumptive diagnosis is essential. The goal is to limit uncertainty. This helps the clinician change the diagnosis later if required.

involved the use of sense of touch, sight, smell, and even taste and hearing. Systematic diagnosis evolved in the sixteenth century.

Clinical Evaluation The periodontal probe was the first attempt to quantify the data and record severity of disease. GV Black was the first to describe the systematic use of a noncalibrated probe. Simonton developed the calibrated University of California periodontometer and also the method of charting. Till date the use of visual signs and periodontal probe to quantify and record severity of periodontal disease has been the most popular tool.

Limitations of Probing Probing depth does not necessarily correspond to pocket depth. Factors that affect probing are as follows: 1. Nature of soft tissues

2. 3. 4. 5. 6.

Probing force Angulation of the probe Pocket configuration Type and location of calculus Degree of healing with long junctional epithelium after treatment 7. Morphology of the tooth.

This resulted in a search for newer diagnostic aids to overcome the limitations. Specific indices have been developed for the assessment of other features such as gingival bleeding and tooth mobility. Miller proposed a graduated mobility scale to record lateral movement when a tooth was displaced between two instrument handles. Muhlemann developed a periodontometer for recording horizontal mobility with greater precision.

Histological Evaluation Disease Activity Disease activity is the loss of the clinical attachment caused by periodontitis. There is no practical method available that can predict attachment loss. The clinician has to rely on the record of attachment loss that has already occurred. Recording disease activity is essential because pretreatment disease severity plays an important role in determining response to therapy.

Janssens discovered the first microscope. GV Black described the principal fibers of periodontium and supported local inflammatory concept of periodontal disease. A group of Viennese researchers described in detail the anatomy of periodontium. Coolidge described the width of periodontium. Waerhaug described the nature of attachment of gingival epithelium and the role of plaque.

Early Approaches to Periodontal Diagnosis

Disadvantage of Histological Evaluation

Diagnosis is mainly based on understanding pathophysiology of periodontitis. So the earliest instruments

The disadvantage of histological evaluation is the invasive nature of biopsy technique.

C H A PT ER 34 A D VA N C ED D IA G N O ST IC M ET H O D S

Radiographic Diagnosis The first dental radiograph was taken by King. Edmond Kells was the first to use X-rays for diagnosis. Thoma noted the use of radiograph in periodontics. Neumann used radiopaque markers to record pocket topography. Updegreaves developed the standardized film holders. The use of conventional radiographic techniques has demonstrated certain limitations such as: 1. 2. 3. 4.

Image distinction Difficulty in reproducing the radiographs Inability to identify initial signs of disease activity Inability to identify etiologic factors. Newer diagnostic methods have offered some promise.

Application of Microbiological Techniques Antonie van Leeuwenhoek first described in 1683 five types of "animalculae" obtained from scrapings on human teeth. WD Miller described that periodontal infection was nonspecific. Base and Johns made the first attempt to postulate that a specific microorganism is responsible for periodontal disease. They demonstrated the use of smears of plaque collected from periodontal pockets, stained for amoeba as a diagnostic tool. Prinz used smears for Plaut-Vincent organisms. Keyes used phase contrast microscopy to identify bacterial morphotypes. Culture studies have been used to identify specific microorganisms. Newer techniques such as DNA probes have been used to identify several bacterial species associated with disease activity.

Measurement of Host Response in Periodontal Disease Metchnikoff was the first to describe the role of white blood cells in inflammation. Znamensky gave the observations that were similar to our current understanding of the pathogenesis of periodontitis. Bass and Johns recommended microscopic examination of GCF contents. Brill and coworkers described the contents and chemical composition of the gingival crevicular fluid (GCF). Earlier, the diagnosis of periodontal disease was mainly based on symptoms. Improvement in understanding and development of technology in various disciplines has resulted in the development of newer diagnostic procedures for early identification of the disease. This facilitates effective and least invasive intervention.

281

AIDS IN CLINICAL DIAGNOSIS • • • •

Gingival bleeding Gingival temperature Periodontal probing Tooth mobility.

Gingival Bleeding Color and texture changes are the visible signs of inflammation. However, there may be underlying structural changes without visible clinical signs. Gingival bleeding is a good indicator of presence of inflammatory infiltrate in the connective tissue. It is more objective, while color and texture assessment is more subjective. Gingival bleeding can be elicited by using a periodontal probe or wooden interdental aids such as toothpicks, but its relationship to disease progression is not clear. Bleeding on probing may indicate periodontal stability except in smokers.

Gingival Temperature According to Kung and coworkers, thermal probes are sensitive diagnostic devices used to measure early inflammatory changes in the gingival tissues. The Periotemp probe (Abiomed, Danvers, MA) is a commercially available system. It helps clinician detect pocket temperature difference to 0.1 °C from a referenced sublingual temperature. Healthy sites have lower temperature than reference sites. Temperature is increased in periodontal disease sites. Individual temperature differences are compared with those expected for each tooth and the results are shown by one of the three light-emitting diodes: • Green - inactive or low-risk site • Yellow - intermediate-risk site • Red - higher-risk site A natural temperature gradient exists in the dental arches. Posterior sites are warmer. Mandible is warmer. The reason why temperature increases with probing depth is not known. It could be because of increased cellular and molecular activities caused by increased periodontal inflammation. It is also found that subgingival temperature is elevated in areas showing attachment loss and periodontal pathogens. Variations in subgingival temperature have been observed in smokers as compared with nonsmokers.

Periodontal Probing Periodontal probing is a simple, yet an essential element of the intraoral examination. It is used to: 1. Measure probing depth 2. Determine attachment levels

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3. Measure gingival recession and width of attached

gingiva 4. Assess nature of soft tissue 5. Detect bleeding on probing 6. Detect presence of plaque, calculus, and defective

margin of restorations. The problems associated with the periodontal probes are lack of sensitivity and reproducibility of measurements. The disparity between measurements depends on: 1. 2. 3. 4. 5. 6.

Probing technique Probing force Size of the probe Angle of insertion of the probe Precision of the probe calibration Nature of the underlying soft tissues (whether inflamed or fibrotic).

Different probe prototypes have been developed since 1980s to overcome these limitations. The National Institute of Dental and Craniofacial Research (NIDCR) proposed the following criteria for an ideal probe: A precision of 0.1 mm A range of 10 mm A constant and standardized probing force Noninvasive, lightweight, and easy to use Easy to access any location around all teeth A guidance system to ensure proper angulation Complete sterilization of all portions entering the mouth; cold sterilization not acceptable 8. No biohazard from material or electric shock 9. Direct electronic reading and digital output.

1. 2. 3. 4. 5. 6. 7.

Periodontal probes may be divided into five generations:

• First-generation probes: Conventional manual (handheld) probes.

• Second-generation probes: Pressure-sensitive probes, e.g., true pressure-sensitive probes. Thirty grams of probing pressure is sufficient to determine the probing pocket depth. Fifty grams of probing pressure is required to detect alveolar bone defects. However, these probes lack tactile sensitivity. • Third-generation probes: Computerized probes, e.g., Florida probe (Fig. 34.1), Foster-Miller probe, and Toronto automated probes. Limitations of automated probes: • Reduced tactile sensitivity • Increased patient discomfort • Expensive. • Fourth-generation probes: These are under development. In these devices an attempt to extend linear probing in a serial manner is made to take account of the

FIGURE 34.1

Three types of Florida probe - cementoenamel junction (CEJ), stent, and disk. Courtesy: Sharad Pawar Dental College, Wardha.

continuous and three-dimensional topography of the pocket being examined. • Fifth-generation probes: They aim to identify the attachment level without penetrating it. These are noninvasive probes, e.g., ultrasound probe.

Tooth Mobility Assessment Tooth mobility is one of the important clinical manifestations of an advanced periodontal disease. It may be determined statically and dynamically. The static method measures the deviation of tooth position when a predetermined force is applied to the tooth at a defined point. The dynamic determination is used to gain information about the biophysical behavior of a tooth in its alveolus under the influence of changing forces. Miller described the most commonly used clinical method in which the tooth is held firmly between two instruments and moved back and forth. The mobility was scored from 0 to 3 as follows (Table 34.2): 0: There is no detectable movement when force is applied. 1: There is barely distinguishable tooth movement. 2: The crown of the tooth moves up to 1 mm. 3: The tooth can be depressed or rotated in its socket. Percussion test is another method. It provides qualitative information through the change in sound characteristics from "highly pitched" to "low pitched."

C H A PT ER 34 A D VA N C ED D IA G N O ST IC M ET H O D S

TABLE 34.2

AIDS IN RADIOGRAPHIC DIAGNOSIS

Miller's Evaluation of Tooth Mobility

Miller's original classification

MI

PTV

No movement distinguishable

0

-8 to +19

First distinguishable sign of movement

1

+10 to +19

Crown deviates within 1 mm of its normal position

2

+20 to +29

Mobility is easily seen and tooth moves 1 mm in any direction or can be rotated in its socket

3

+30 to +50

Ml, Mobility index; PTV, Periotest value.

Manual method helps the assessment only after a palpable mobility exists and not during the early stages of mobility. Periodontometer was introduced by Muhlemann to measure tooth mobility. Laser techniques using heliumneon gas laser were used by Ryden et al, but these methods were unsuitable for routine use. In 1982, Schutle and coworkers developed a simple and easy-to-manage, objective procedure called "Periotest" (Siemens AG, Germany; Fig. 34.2). Periotest measures the reaction of the periodontium to a predetermined percussive force applied to the tooth. It measures the damping characteristics of the periodontium. The instrument is similar in design and size to a dental handpiece. A metal rod is accelerated to a speed of 0.2 m/ s and maintained at a constant speed. On impact, the tooth is deflected and the rod deaccelerated. The contact time between the tapping head and tooth varies between 0.3 and 0.2 ms and is shorter for stable than for mobile tooth. The Periotest value ranges from -8 to 50 (Table 34.2).

283

Dental radiographs are the conventional methods used to assess the destruction of alveolar bone. They provide meaningful information on: • • • • • • • •

Interproximal bone levels Crown-root ratio Root length Root proximity Integrity of lamina dura Width of periodontal ligament space Presence of periapical lesions Height of remaining alveolar bone.

About 30% or more of alveolar bone should be lost before any detectable changes can be seen on the radiograph. The limitations of conventional radiographs are as follows: • Highly specific but lack sensitivity • Difficulty in reproducing radiographs due to the variable projection geometry, contrast, and density • Masking of bony changes by other anatomic structures • No information on buccal and lingual bony cortical plates. The variations in projection geometry can be overcome by using paralleling technique. Variation in contrast and density can be overcome to some extent by standardizing the film and other related radiologic accessories.

Digital Radiography Digital intraoral radiography can be used to overcome the variations in image quality. It allows the use of computerized images. These images can be stored, manipulated, and corrected for underexposure or overexposure. Digital intraoral radiography also reduces the radiation dose by one-half to one-third.

Subtraction Radiography

FIGURE 34.2

Periotest for implant mobility assessment.

Subtraction radiography relies on the conversion of serial radiographs into digital images. These serial digital images are then superimposed and the composite is viewed on a video screen. Changes in the bone density and volume can be seen. Bone gain is seen as lighter areas and bone loss as darker areas. Computer-assisted subtraction radiography helps in detecting changes from the baseline images. This technique helps in detection of minor changes in the bone by removing the unchanged anatomic structures from the image. Thus, it increases the sensitivity.

284

SECTION V DIAGNOSIS, PROGNOSIS, AND TREATMENT PLANNING

The main disadvantage is the need to get an identical alignment to obtain accurate sequential radiographs. To overcome this disadvantage a new technique called diagnostic subtraction radiography (DSR) has been introduced. This method combines a positioning device during film exposure and specialized software. This software corrects any minor changes of alignment.

Computer-Assisted Densitometric Image Analysis System In computer-assisted densitometric image analysis (CADIA) system a video camera measures the light transmitted through a radiograph and the signals are converted into grayscale images. The camera is connected to an image processor and a computer. Here the images are stored and mathematical manipulation of the images is done. This system has a higher sensitivity than other systems.

Computerized Tomography Computerized tomography (CT) gives an exact picture of the bone levels in all the three phases, namely coronal, axial, and sagittal planes in implant dentistry. A localized computerized tomography technique is also available.

Photodensitometric Image Analysis Technique This technique is used to evaluate bone resorption in furcation areas. Radiographic film absorbs a beam of light. Microdensitometer linked to a microcomputer enables the clinician to detect variations in bone density that cannot be detected by naked eye.

AIDS IN MICROBIOLOGICAL DIAGNOSIS Microbiological tests are used to identify putative pathogens. These tests are used to:

susceptibility testing can also be done. The disadvantages of this method are as follows: • Only live organisms can be grown. So strict sampling and transport conditions are required. • Fastidious organisms are not easy to culture. • Sensitivity is low. • Sophisticated equipment and experienced personnel are required. • It is relatively time-consuming and expensive.

Direct Microscopy Dark field or phase contrast microscopy can be used to assess the morphology and mobility of bacteria, but most of the periodontal pathogens are nonmotile. So its utility is limited.

AIDS USED IN IMMUNOLOGICAL AND BIOCHEMICAL DIAGNOSIS Immunodiagnostic Methods Immunological assays utilize antibodies that recognize specific bacterial antigens to detect target microorganisms. This principle is used in the following diagnostic procedures: Direct immunofluorescent microscopy assays Indirect immunofluorescent assays Flow cytometry ELISA 5. Membrane assay 6. Latex agglutination.

1. 2. 3. 4.

Direct Immunofluorescent Assays They use both monoclonal and polyclonal antibodies. These antibodies are conjugated to a fluorescent marker that binds with the bacterial antigen to form a fluorescent immune complex detectable under a microscope (Fig. 34.3). Indirect Immunofluorescent Assays

• Support the diagnosis • Serve as indicators of disease initiation and progression • Determine which periodontal sites are at high risk for active destruction • Monitor the healing response.

This procedure employs a secondary fluoresceinconjugated antibody that reacts with the primary antigen-antibody complex. Both direct and indirect immune fluorescent assays can detect the pathogen and measure the quantity of the pathogen directly in a given plaque smear (Fig. 34.3).

Bacterial Culturing

Flow Cytometry - It helps in rapid identification of bacteria. - Bacterial cells are labeled with species-specific antibody and then with fluorescein-conjugated antibody. - The suspension is then introduced into the flow cytometer. This separates the bacterial cells into single cell suspension by means of laminar flow through

Culture methods have been used to characterize the composition of supragingival plaque. They are still considered as the gold standard. Plaque samples are cultivated under anaerobic conditions. Selective and nonselective media are used. Several physical and biochemical tests are done to identify pathogenic microorganisms. Antibiotic

285

C H A PT ER 34 A D VA N C ED D IA G N O ST IC M ET H O D S

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a narrow tube. After incubation the cells are passed through a focused beam of laser. The cells then scatter the light at low and wide angles and the fluorescent emission can be measured by appropriate detectors. - However, it is very expensive. Latex Agglutination Assay This assay is based on the binding of protein to latex. Latex beads are coated with species-specific antibody. When it contacts antigen, cross-linking occurs. A visible precipitate is seen in 2-5 min. There are two types: (i) indirect assay; (ii) inhibition assay. 1. Indirect assay: Antibody is bound to latex. A suspension

of plaque sample is mixed and gently agitated for 3-5 min; if the test is positive, agglutination occurs. 2. Inhibition assay: Here the expected agglutination between known antigen and antibody is inhibited as a result of competition.

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FIGURE 34.4 ELISA. (A) A positive direct ELISA to detect antigens; (B) a positive indirect ELISA to detect antigens. Anti-HISG, Mouse monoclonal IgG2b antibody (commercially available antibody).

2. Require stringent sampling and transport methodology.

EVALUSITE

Enzymatic Methods

It is a membrane immunoassay. Here the immune complex is seen through a colorimetric reaction. It is designed to detect Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia.

P. gingivalis, T. forsythia, T. denticola, and Capnocytophaga species release a trypsin-like enzyme. These en-

ELISA Enzyme-linked immunosorbent assay (ELISA) is similar to other radioassays. Microwells are coated with antibody. Then test samples are added and incubated. After washing, another antibody labeled with an enzyme is added followed by a suitable substrate. The enzyme will break down the substrate to yield suitable color (Fig. 34.4).

zymes hydrolyze a colorless substrate called N-benzoylDL-arginine-2-naphthylamide (BANA). They release a chromophore ~-naphthylamide. This turns orange red when a drop of fast garnet is added to the solution. The commercially available diagnostic kit is called Perioscan. Disadvantage: It only detects a limited species of pathogens.

Diagnostic Methods Based on Molecular Biology Nucleic Acid Probes

Disadvantages of Immunological Assays 1. Cross-reactivity resulting in false-positive and falsenegative results

A nucleic acid probe is a molecule of either DNA or RNA from a specific microorganism. It is artificially synthesized and labeled with an enzyme or radioisotope.

286

SECTION V DIAGNOSIS, PROGNOSIS, AND TREATMENT PLANNING

POLYMERASE CHAIN REACTION (PCR) I

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These single-stranded nucleic acid hybridize (pair with complementary DNA strands to produce double-stranded nucleic acid) and thus detect the presence of target microorganism (Fig. 34.5). DNA probes may target whole genomic DNA or individual genes (whole genomic probes and oligonucleotide probes). Whole genomic probes have been developed to detect A. actinomycetemcomitans, P. gingivalis, P. intermedia, and T. denticola. Examples of commercially available probes are DMDx and Omnigene. However, disadvantage is cross-reactivity. Oligonucleotide probes have been developed. These probes are complementary to variable regions of 16s and 50s RNA bacterial genes.

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Effect of Tissue Temperature on Tissues

490

SECTION VI PERIODONTAL THERAPY

• Photoacoustic effect: Laser energy when absorbed by water present in hard tissue (hydroxyapatite) leads to vaporization of water. This increases pressure within the tissues leading to explosion. This photoacoustic effect forms the basis for hard tissue cutting by erbium lasers. • Fluorescence: When laser light is absorbed by certain biological pigments, it leads to fluorescence. This is helpful in detection of caries within teeth. • Biostimulation: When used in noncontact and lowerpower settings, lasers elicit beneficial cellular and biological responses. It is helpful in rapid tissue healing, pain relief, and increased collagen growth and has anti-inflammatory effect. This is also referred to as low-level laser therapy. Advantages of using lasers for periodontal therapy: • Precise surgical cutting • Less need for anesthesia • Better visualization of cutting (hemostasis and coagulation) • Detoxification of a wound • Minimal wound contraction and scarring • Minimal swelling • Minimal suturing required • Patient acceptance. Disadvantages: • Cost is high. • Use of lasers requires training and complete knowledge to attain all the benefits of lasers without collateral damage. • Modification of clinical technique may be required. • No single wavelength optimally treats all dental diseases. TABLE 54.6

Precautions to be taken while using lasers: • Use glasses provided by the manufactures (specific for wavelengths) for eye protection (patient, operator, and assistants). • Prevent inadvertent irradiation. • Avoid reflection from shiny metal surfaces. • The surgical environment should have a warning sign and limited access. • Ensure adequate high-speed evacuation to capture the laser plume.

LASER APPLICATION IN PERIODONTAL THERAPY Soft Tissue Surgical Application Soft tissue lasers are being widely used as a tool for gingival soft tissue procedures, i.e., gingivoplasty, gingivectomy, frenectomy, gingival depigmentation, second-stage exposure of implant, and soft tissue crown lengthening (Table 54.6). Nd:YAG, CO2, and diode lasers are used for soft tissue procedures. Nd:YAG laser was one of the first to be approved by the Food and Drug Administration (FDA). It has the disadvantage of deeper depth of penetration leading to damage to underlying tissue. Its use with peri-implant tissue is contraindicated as it may damage the implants. The diode laser has been introduced over the past few years for dental use, obtaining FDA safety clearance. The diode laser has been shown to have similar tissue effects as the Nd:YAG laser in comparable studies, with less thermal effects on the deeper tissues. The CO2 laser was also introduced long back for soft tissue application. It has the advantage of lesser depth of penetration, but more of charred tissues are formed which might delay wound healing.

Specific Uses of Dental Lasers Based on the Various Tissue Interactions

Laser medium

Wavelength (nm)

Dental uses

Argon

488-514

Tooth bleaching and advanced curing lights

Carbon dioxide (CO2 )

10,600

Gingivectomy / gingivoplasty, second-stage implant exposure, periodontal curettage (advocated but not evidence based)

Diode

655-980

Gingivectomy / gingivoplasty, oral medicine uses (aphthous ulcer therapy, biopsies, dentinal desensitizing), second-stage implant exposure, periodontal curettage (advocated but not evidence based)

Neodymium:yttriumaluminum-garnet (Nd:YAG)

1064

Gingivectomy / gingivoplasty, oral medicine uses (aphthous ulcer therapy, biopsies, dentinal desensitizing), second-stage implant exposure, periodontal curettage (advocated but not evidence based)

Erbium:YAG (Er:YAG)

2940

Gingivectomy / gingivoplasty, oral medicine uses (aphthous ulcer therapy, biopsies, dentinal desensitizing), second-stage implant exposure, periodontal curettage (advocated but not evidence based), hard tissue cutting (dentin and osseous)

Erbium, chromium:yttrium (Er, Cr:YSGG)

2780

Gingivectomy / gingivoplasty, oral medicine uses (aphthous ulcer therapy, biopsies, dentinal desensitizing), second-stage implant exposure, periodontal curettage (advocated but not evidence based), hard tissue cutting (dentin and osseous)

YSGG, yttrium scandium gallium garnet.

CHA PTER 54 RECENT ADVANCES IN PERIO DONTAL SURGICA L TECHNIQ UES

Erbium lasers can also be used for soft tissue surgery. They are absorbed only in superficial layer and are therefore advantageous. Their cost factor may be a limitation.

491

based on clinical attachment gain are needed to determine if laser-assisted SRP has a beneficial effect.

Surgical Pocket Therapy Nonsurgical Treatment of Periodontal Disease Laser-Mediated Sulcular/Pocket Debridement Diode and Nd:YAG lasers have been used for pocket debridement. Recent studies have shown that instrumentation of the periodontal pocket wall tissues with a diode laser leads to complete epithelial removal while instrumentation with conventional curettes may leave epithelial remnants. But based on clinical parameter of reduction of pocket depth or gain in clinical attachment level laser curettage has little to no benefit beyond scaling and root planing (SRP) as either monotherapy or adjunctive to SRP.

Reduction of Subgingival Bacterial Levels The bactericidal and detoxifying effect of laser treatment is advantageous in periodontal therapy. Diode laser and Nd:YAG laser are a good choice for pigmented bacteria. Diode lasers are found to be effective in suppression of A. actinomycetemcomitans in cases of aggressive periodontitis. But still lasers as a group have been found to be unpredictable and inconsistent in their ability to reduce subgingival microbial loads beyond that achieved by SRP alone. Photodynamic therapy has been used to reduce microbial load by free radicals produced during the therapy. The evidence for benefit of use of diode laser in photodynamic therapy in reduction of microbial load as monotherapy or adjunct to SRP is conflicting. Only a few studies have shown photodynamic therapy to be effective in reducing subgingival microbial load.

Scaling and Root Planing Nd:YAG lasers have deeper depth of penetration and carry the risk of intrapulpal temperature elevations during laser irradiation on the root surface. They also cause surface pitting, crater formation, and melting of root surface. The carbonization caused by CO2 laser inhibits the soft tissue attachment post-root planing. Thus, use of Nd:YAG and CO2 lasers is not advisable for calculus removal. Diode lasers are ineffective in removal of calculus. Nevertheless, erbium lasers have shown great potential for effective root debridement. In vitro studies have shown positive results in removal of calculus, reduction of endotoxin, and enhancement of fibroblast attachment. But during in vivo removal of calculus by erbium laser, there is potential for root damage as the healthy hard tissue may get lased along with calculus. With introduction of a new laser system combining diode laser-induced fluorescence with erbium-doped YAG (Er:YAG), calculus removal might be possible without risk of damaging root surface as the feedback system ensures the Er:YAG laser is inactivated once the calculus is removed. Further studies

Degranulation During Flap Surgery Lasers can be useful in debridement of areas with limited accessibility such as deep defects and furcation areas. Nd:YAG and diode lasers are generally not used for degranulation. CO2 lasers can be used for degranulation but cause carbonization of bone. Erbium lasers are most appropriate to be used for degranulation of bony defects as they do not have any harmful effect on bone. Further studies are required to establish additional benefits of laser application in flap surgery. Low-level laser therapy application during and after periodontal surgical and regenerative therapy has been shown to enhance the gingival fibroblast and periodontal ligament cell proliferation and release of growth factors in vitro. Studies have also suggested that low-level laser therapy (LLLT) can enhance new bone formation by promoting osteoblast proliferation.

Osseous Surgery Erbium lasers can easily be used for osseous contouring during flap surgery and in crown lengthening cases. Some studies have refuted their use as they may have lower cutting efficiency as compared with conventional instruments and lack of depth control may be a limitation. There has been limited evidence to support the use of lasers over conventional therapy in treatment of periodontal disease. Much of this uncertainty arises from not making proper comparisons in terms of the type of lasers utilized and the way that studies are designed.

Surgical Procedures in Implant Placement Erbium lasers can be used for implant site preparation, causing less damage than conventional bur drilling. Preparation time has also been found to be acceptable. Whether faster and superior osseointegration can be achieved using erbium lasers is yet to be established. Lack of depth control might be a limitation which can easily be overcome using advanced methods of imaging during implant procedures. Diode and erbium lasers can undoubtedly be used for second-stage implant exposure without causing any damage to underlying tissue and implant.

Treatment of Peri-Implantitis Nd:YAG laser is contraindicated in treatment of periimplantitis as it may damage the titanium implant surface. CO2 lasers are also not used as they may carbonize the adjacent bone. Diode lasers can be used. Erbium

492

SECTION VI PERIODONTAL THERAPY

lasers are preferred for degranulation and implant surface decontamination as they can be used for both hard and soft tissue ablation.

• gallium-aluminum-arsenide diode lasers (630-690, 830, or 906 nm); and • argon lasers (488-514 nm).

Treatment of Dentinal Hypersensitivity

High-level-energy laser irradiation is not used to activate the photoactive dye because relatively low-level exposure produces a high bactericidal effect.

Nd:YAG, CO2, erbium, and diode lasers have been tried in treatment of dentinal hypersensitivity. All the lasers are used at low-power settings. Nd:YAG laser irradiation causes melting and fusion of dentine and therefore the closure of exposed dentinal tubules. CO2 lasers are used for treatment of dentinal hypersensitivity by sealing or narrowing of dentinal tubules. Erbium lasers also reduce dentinal hypersensitivity by sealing of dentinal tubules, at lower settings; they seem to reduce fluid movement in dentin by evaporating the superficial layers of dentinal fluid. The diode laser relies on depressed nerve transmission changes within the dental pulp, rather than alterations in the exposed dentine surface. The diode laser may also stimulate the normal physiological cellular functions. At subsequent appointments, it stimulates the production of sclerotic dentin, thus promoting the internal obliteration of dentinal tubules. Lasers when used along with fluoride gel and varnishes may show better results.

Photosensitizer An ideal photosensitizer: 1. Should be nontoxic and should be activated on

illumination 2. Should bind with bacteria and plaque without staining the gingiva and other soft tissues 3. Should be acceptable to patients 4. Should have an access to pathogens present in deeper periodontal pockets. The various photosensitizers used are as follows: 1. Dyes:

Wound Healing Decreased swelling, scarring, pain, and faster healing response have been suggested with use of lasers. But the evidence regarding faster healing of wounds is conflicting. It is important to use the lasers with appropriate power settings to achieve better wound healing after surgical therapy. Low-level laser therapy using diode lasers with wavelengths 635-810 nm at low-power, noncontact mode can be used to promote wound healing, suppress inflammation, and stimulate cellular ATP.

PHOTODYNAMIC THERAPY Photodynamic therapy (PDT) is defined as the eradication of target cells by reactive oxygen species that are produced by means of a photosensitizing compound, and light of an appropriate wavelength. Photodynamic therapy basically involves three nontoxic ingredients: • Visible harmless light • A nontoxic photosensitizer • Oxygen.

Light Light sources of a specific wavelength are used and are mostly: • helium-neon lasers (633 nm);

2.

3.

4. 5.

a. Tricyclic dyes with different meso-atoms - methylene blue, toluidine blue 0, and acridine orange b. Phthalocyanines - aluminum disulfonated phthalocyanine c. Cationic Zn(II) - phthalocyanine Chlorines: chlorine e6, stannous(IV) chlorine e6, chlorine e6-2.5 N-methyl-o-glucamine (BLC1010), polylysine, and polyethyleneimine conjugates of chlorine e6 Porphyrins: hematoporphyrin HCl, photofrin and 5-aminolevulinic acid (ALA), benzoporphyrin derivative (BPD) Xanthenes: erythrosine Monoterpene: azulene.

PHOTODYNAMIC ANTIMICROBIAL THERAPY It is based on the principle that a photosensitizer binds to the target cells and can get activated by light of a suitable wavelength. Following this, singlet oxygen and other very reactive agents are produced which are extremely toxic to certain cells and bacteria. Two pathways explain the mechanism of action of antimicrobial photodynamic therapy. After irradiation with light of a specific wavelength (lasers), the photosensitizer at ground state is activated to a highly energized triplet state (Fig. 54.7). This triplet state has a longer lifetime and this enables the photosensitizer to interact with the surrounding molecules and generate cytotoxic species. The triplet-state photosensitizer follows two different pathways (types I and II) to react with biomolecules.

CHA PTER 54 RECENT ADVANCES IN PERIO DONTAL SURGICA L TECHNIQ UES

493

Ground state sensitizer Light

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