The Epidemiology of Oral Health [Reprint 2014 ed.] 9780674423978, 9780674423961

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American Public Health Association VITAL AND HEALTH STATISTICS MONOGRAPHS

The Epidemiology of Oral Health

The Epidemiology of Oral Health Walter J . Pelton/John B. Dunbar/Russell S. McMillan/ Palmi Moller/Albert E. Wolff

1969/HARVARD UNIVERSITY PRESS

Cambridge, Massachusetts

© C o p y r i g h t 1969 by the P r e s i d e n t a n d F e l l o w s of H a r v a r d C o l l e g e All rights reserved D i s t r i b u t e d in G r e a t Britain by O x f o r d University Press, L o n d o n T h i s m a t e r i a l has been c o p y r i g h t e d to i n s u r e its a c c u r a t e q u o t a t i o n a n d use. P e r m i s s i o n t o r e p r i n t m a y be g r a n t e d u p o n p r e s e n t a t i o n of an a d e q u a t e s t a t e m e n t c o n c e r n i n g the m a t e r i a l t o b e used a n d the m a n n e r of its i n c o r p o r a t i o n in o t h e r texts. L i b r a r y of C o n g r e s s C a t a l o g C a r d N u m b e r 77-88811 S B N 674-25885-1 P r i n t e d in t h e U n i t e d States of A m e r i c a

PREFACE

The working title of this monographic volume was "Dental Health." It is the obverse, of course, a compendium related to dental disease. Even though malocclusions and clefts are not diseases, they are important conditions that lend themselves to epidemiologic techniques similar to those used to study dental caries and periodontal disease. This text attempts to marshal, present, and document the essentials about the main problems in dentistry. Because the Statistics Section of the American Public Health Association is the sponsor for this publication, the authors perhaps paid undue attention to the statistical aspects of their respective topics. But some preoccupation with statistics is warranted because it has been only within the past few decades that dental data have become more than simple summations or averages. The present generation of dentists has seen dentistry advance from an empirical profession to one that has learned to apply statistical methods to most of its problems. Dentistry passed from an empiricism to a science in the early 1930's when two groups made a breakthrough by applying epidemiologic methods to dental caries studies. Between 1929 and 1932 records of dental examinations performed by a single examiner on 8,257 American Indian children were accumulated and analyzed by the first group, Klein and Palmer. 3 They attempted to determine (1) the difference in prevalence of dental caries among Indian population groups (number of children, per 100 children examined, having one or more decayed or missing, or filled teeth), (2) the "caries attack rates" (total number of decayed, missing, and filled permanent teeth [DMF] per 100 examined mouths), and (3) the severity of attack by caries (the number of DMF teeth per 100 mouths which have been attacked by caries). The second group, the American Dental Association collaborating with the Public Health Service, arranged to conduct a dental survey of elementary school children in 1933. During the following two years data were obtained from nearly a million and a half children residing in 26 states. 6 W. M. Gafafer, a senior statistician in the Public Health Service assigned to the project, developed an examination form which incorporated an assessment of current dental needs and pathology, with a record of past dental treatment. All the components of a DMF rate were tabulated for the permanent V

vi I PREFACE

dentition as well as for deciduous teeth, and thus age-, color-, and sex-specific data were presented by geographic location. By the late 1930's, the f o r m a t for examination forms and the method of processing data employed by the several dental research groups within the Public Health Service were but variations of a method described and published by Klein and Palmer. 4 F u n d a mentally, Klein and Palmer had expanded on a method of machine processing dental statistics entered on a " p u n c h c a r d , " which had been described by Hyatt and Lotka 1 eleven years earlier. In the meantime, Klein, Palmer, and K r a m e r 5 used the normal probability curve for expressing the age distribution of eruption of the permanent teeth. A little later (1943) Klein, 2 pressing for more understanding of the epidemiology of dental diseases, related tooth mortality to socioeconomic status. Interested in the way teeth survive, he used age-interval-specific tooth mortality rates and developed a "tooth-life" expectancy rate or life tables for teeth. The former article 5 was from a series of papers under the generic title "Studies of Dental Caries," nearly all of which appeared in print in 1938. They firmly established the DMF count as a valuable epidemiological tool. The DMF count as an index of dental caries experience has always puzzled the clinically oriented dentist because it in no way relates to the time or work required to repair teeth. A little more understanding came with analyses considering DMF tooth surfaces rather than DMF teeth. However crude and baffling the DMF tool may be, it satisfied the need for a numerical index of caries and it was accurate enough to quantify the difference between caries attack rates of children reared in fluoride and nonfluoride communities. Dean's studies proving the caries-fluorine hypothesis, cited in the text, are classic examples of dental epidemiology based on the use of DMF counts. The growing interest in applying statistical techniques to periodontal disease is well documented in the chapter on that subject. Within a little more than a decade considerable knowledge has been acquired by the acceptance and world-wide application of Russell's Periodontal Index. Neither Russell's Periodontal Index nor the DMF index is complicated; both can be readily used in the field and both provide objective assessments which are reproducable. Unfortunately, however, no similar breakthrough can be reported concerning an index for malocclusions. Perhaps what is

PREFACE | vii

needed now is for a leadership g r o u p to select the best of the methods already available and recommend its universal adoption. The study of cleft lip and palate does not seem to need an index at this stage of our knowledge. K e r n a h a n and Stark's classification of the various types of clefts, presented in Chapter 5, seems to be reasonable, handy, and fairly well accepted. Most of the statistical support for the material presented in the chapter on oral cancer depends largely on mortality rates, as do studies of many morbid conditions for which incidence and prevalence rates are rarely, if ever, attainable. The understanding of cancer morbidity has been aided by several states which have m a d e cancer a reportable disease. Cancer survival rates, usually thought of as the antithesis of mortality rates, have been helpful too. The difference between the statistical tools available to each subject-matter specialist contributing to this text has made some difference in the format of the several chapters. Although some standardization was attempted, individual a u t h o r s were free to develop the subject as they saw fit. Each m a d e certain judgments as to the source material to be used in developing his subject. All were encouraged to add a supplemental bibliography listing those papers reviewed and thought to be of interest, but not actually cited. As might be anticipated, the writing style of the a u t h o r s differs. It is hoped that this volume will serve all dentists, dental hygienists, and students, as well as other teachers and professionals frequently in contact with dental problems. May 1968

Walter J. Pelton

CONTENTS

Foreword by Berwyn Mattison

xv

Notes on Tables 1

Dental Caries

2

Periodontal Disease

xviii John B. Dunbar

1

Russell S. McMillan and Albert E. Wolff

3

Oral Cancer

4

Dentofacial Deformities: Malocclusion

5

Dentofacial Deformities: Cleft Lip and Palate

15

Walter J. Pelton

42

Palmi Moller

72

Palmi Moller

94

References

127

Index

163

ix

TABLES

1.1 Number of new pit and fissure cavities per child by selected age intervals and three tooth types for children born in 1945: Culemborg, Holland 1.2 Influence of sugar supplement on caries 1.3 Percentage distribution of children of selected ages by number of DMF teeth: Neosho, Missouri, 1953 1.4 A v e r a g e number of remaining sound teeth per person by age and sex, white adults: United States, 1960-62 1.5 DMF teeth per person by age: Baltimore, Maryland (white children), 1955 and Thailand, 1960 1.6 DMF teeth per person for 6 - 8 and 12-14-year-old children by color: Evanston, Illinois, 1946 and Tennessee, 1937-41 1.7 DMF teeth per person by age, color, and sex: United States, 1960-62 1.8 DMF teeth per person for people living in low-fluoride and adequate-fluoride areas: Colombia and Ecuador, 1960 1.9 DMF teeth per person for 12-year-olds: Grand Rapids and Muskegon, Michigan, 1944-54 1.10 Distribution of states by national rank in the proportion of persons drinking fluoride-containing water by region: United States, 1963 1.11 DMF teeth per person aged 20-24 years, selected civilian groups

2.1 Percent of adults, aged 25 through 74, edentulous according to health examination and health interview by sex 2.2

Percent of adults free of periodontal disease by sex

and age 2.3 Percent tooth mortality or morbidity by cause for various studies cited 2.4 Dentist/population ratios for countries included in study 2.5 Criteria for the Periodontal Index 2.6 Percentage of children with " s e v e r e " gingivitis (Great Britain) or with one or more obvious periodontal pockets (United States)

TABLES | xi

2.7 Average Periodontal Index of white and N e g r o adults by age and sex 2.8 Periodontal scores by years of school completed: Birmingham, A l a b a m a , 1957 2.9 Relative scoring of Periodontal Index for two groups of children in a junior high school: M a r y l a n d , 1955 3.1 Deaths and death rates caused by malignant neoplasms of buccal cavity, pharynx, bones of face, skin, connective tissue, skull, maxillary sinus, and lower j a w : United States, 1965 3.2 Death rates for malignant neoplasms of buccal cavity and pharynx by 10-year age groups, color, and sex: United States, 1965 3.3 Deaths from malignant neoplasms of buccal cavity and pharynx by race: United States, 1959-61 3.4 Urban-rural ratios of age-adjusted cancer incidence rates for all sites, for buccal cavity and pharynx, and lip by sex: Connecticut, 1947-51; Iowa, 1950; and metropolitan and nonmetropolitan bounties of New York exclusive of New York City, 1949-51 3.5 Standardized mortality ratios for all sites of cancer combined and for cancer of buccal cavity and pharynx, by broad occupational group: white male population of United States aged 2 0 - 6 4 , 1950 3.6 Age-adjusted cancer incidence rates and mortality rates, by sex: New York State exclusive of New York City, 1941-43 and 1958-60 3.7 N u m b e r of buccal cavity cancer cases with stage stated and percentage distribution according to stage at diagnosis: New York State exclusive of New York City, by years specified 3.8 Consolidation of Table 3.7 3.9 Probability of eventually developing cancer, by age and selected sites, based on cancer morbidity reports: New York State exclusive of New York City, 1957-59 3.10 Observed survival rates for lip cancer in males, number of cases diagnosed, all stages, for years following diagnosis during period specified: California, Connecticut, and New York

30 32 37

46

48 49

52

54

54

55 56

57

58

xii I TABLES

3.11 Percent surviving 1, 3, and 5 years, by sex, cases of all sites and cases of buccal cavity and pharynx: cases diagnosed in Connecticut, 1935-40, 1941-46, and 1947-51 3.12 Outline of prospective studies of smoking and mortality 3.13 Expected and observed deaths and mortality ratios of current smokers of cigarettes only for selected cancer sites, all other sites, and all causes of death; each prospective study and all studies 3.14 Comparison of two groups living and well for three or more years following treatment for s q u a m o u s cell carcinoma of mouth or throat 3.15 Age distribution of 2,758 patients with m o u t h lesions 3.16 Specific site of 315 primary mouth cancers 4.1 Prevalence of malocclusion in the deciduous dentition (Angle's classification) 4.2 Prevalence of malocclusion in the mixed and permanent dentitions 4.3 The prevalence of malocclusion in Negroes and Caucasians 4.4 Prevalence of malocclusion in children with adverse oral habits 4.5 Central tendency (M) and variability (s.D.) of carious and filled surfaces (third molars excluded) for 106 individuals selected for good occlusion and 87 with severe malocclusion 5.1 Classification of cleft lip and palate 5.2 Incidence of cleft lip and palate in various locations in the United States 5.3 Incidence of cleft lip and palate in various locations outside the United States 5.4 Distribution of clefts by groups 5.5 Incidence by cleft groups 5.6 Distribution of clefts according to sex and cleft group 5.7 Percentage distribution of all clefts 5.8 Incidence of cleft lip and palate by race: rate per population sample 5.9 Seasonal incidence of cleft births

59 61

62

66 67 68

79 80 84 86

88 98 107 108 110 112 113 114 116 119

T A B L E S | xiii

5.10 Congenital malformations associated with cleft lip and palate: percentage of cleft cases with other congenital malformations

120

FIGURES 2.1 Periodontium in a normal and a b n o r m a l state 2.2 Civilian Periodontal Index, Oral Hygiene Index, Calculus Index, and Debris Index for Burma civilian males, ages 10-50 and over 2.3 Mean PI scores based on available world-wide data for 4 0 - 4 9 year age g r o u p 2.4 Distribution of Periodontal Index scores based on available world-wide data for 4 0 - 4 9 year age g r o u p 2.5 Percent of men and women edentulous by age 2.6 Relative PI scores of military and civilian males aged 2 0 - 2 9 years, nine ICNND surveys 3.1 Trends in age-adjusted mortality rates for selected cancer sites by sex in the United States, 1930-60 5.1 C o m m o n types: cleft lip, cleft lip and cleft alveolar process 5.2 C o m m o n types: clefts of soft and hard palate; clefts of primary and secondary palate

xiv

16

30 31 33 34 35

47

96 97

FOREWORD R a p i d advances in medical a n d allied sciences, changing p a t t e r n s in medical care a n d public health p r o g r a m s , an increasingly healthconscious public, a n d the rising concern of v o l u n t a r y agencies a n d g o v e r n m e n t at all levels in meeting the health needs of the people necessitate c o n s t a n t evaluation of the c o u n t r y ' s health status. Such an evaluation, which is required not only for an a p p r a i s a l of the current situation, but also to refine present goals a n d to g a u g e o u r progress t o w a r d them, d e p e n d s largely u p o n a study of vital a n d health statistics records. O p p o r t u n i t y to study mortality in d e p t h emerges when a n a t i o n a l census furnishes the requisite p o p u l a t i o n d a t a for the c o m p u t a t i o n of d e a t h rates in d e m o g r a p h i c and g e o g r a p h i c detail. Prior to the 1960 census of p o p u l a t i o n there h a d been no c o m p r e h e n s i v e analysis of this kind. It seemed a p p r o p r i a t e , therefore, to develop for intensive study a substantial b o d y of death statistics for a three-year period centered a r o u n d t h a t census year. A detailed e x a m i n a t i o n of the c o u n t r y ' s health status must go b e y o n d an e x a m i n a t i o n of mortality statistics. M a n y c o n d i t i o n s such as arthritis, r h e u m a t i s m , a n d m e n t a l diseases are m u c h m o r e i m p o r t a n t as causes of m o r b i d i t y t h a n of mortality. Also, an e x a m i n a t i o n of health status should n o t be based solely u p o n current findings, b u t should t a k e into a c c o u n t t r e n d s a n d whatever pertinent evidence has been assembled t h r o u g h local surveys a n d f r o m clinical experience. T h e p r o p o s a l for such an evaluation, to consist of a series of m o n o g r a p h s , was m a d e to the Statistics Section of the A m e r i c a n Public Health Association in O c t o b e r 1958, a n d a C o m m i t t e e on Vital a n d H e a l t h Statistics M o n o g r a p h s w a s a u t h o r i z e d . T h e m e m bers of this C o m m i t t e e a n d of the Editorial A d v i s o r y S u b c o m m i t t e e created later are:

Committee

on Vital and Health Statistics

M o r t i m e r Spiegelman, C h a i r m a n Paul M . Densen, D . Sc. Robert D. Grove, Ph.D. XV

Monographs

William H . Stewart, M . D . (withdrew J u n e 1964) Conrad Taeuber, Ph.D.

xvi I F O R E W O R D

Clyde V. Kiser, P h . D . Felix M o o r e George Rosen, M.D., Ph.D.

Editorial Advisory

Paul W e b b i n k Donald Young, Ph.D.

Subcommittee

M o r t i m e r Spiegelman, C h a i r m a n Duncan Clark, M . D . E. G u r n e y C l a r k , M . D . Jack Elinson, P h . D .

Eliot F r e i d s o n , P h . D . (withdrew F e b r u a r y 1964) Brian M a c M a h o n , M.D., Ph.D. Colin White, P h . D .

T h e early history of this u n d e r t a k i n g is described in a p a p e r that was presented at the 1962 A n n u a l C o n f e r e n c e of the M i l b a n k M e m o r i a l F u n d . 1 T h e C o m m i t t e e on Vital a n d H e a l t h Statistics M o n o g r a p h s selected the topics to be included in the series a n d also suggested c a n d i d a t e s for a u t h o r s h i p . T h e f r a m e of reference was extended by the C o m m i t t e e to include other topics in vital a n d health statistics t h a n mortality and m o r b i d i t y , namely fertility, m a r r i a g e , a n d divorce. C o n f e r e n c e s were held with a u t h o r s to establish general guidelines for the p r e p a r a t i o n of the m a n u s c r i p t s . S u p p o r t for this u n d e r t a k i n g in its preliminary stages was received f r o m the Rockefeller F o u n d a t i o n , the M i l b a n k M e m o r i a l F u n d , a n d the H e a l t h I n f o r m a t i o n F o u n d a t i o n . M a j o r s u p p o r t for the required t a b u l a t i o n s , f o r writing a n d editorial w o r k , a n d f o r the related research of the m o n o g r a p h a u t h o r s was p r o v i d e d by the U n i t e d States Public H e a l t h Service (Research G r a n t C H 00075, formerly G M 08262). A c k n o w l e d g m e n t should also be m a d e to the M e t r o p o l i t a n Life I n s u r a n c e C o m p a n y for the facilities a n d time that were m a d e available to M r . Spiegelman, now retired f r o m its service, w h o p r o p o s e d a n d administered the u n d e r t a k i n g a n d served as general editor. T h e N a t i o n a l C e n t e r for H e a l t h Statistics, under the supervision of D r . G r o v e a n d Miss Alice M . Hetzel, u n d e r t o o k the sizable tasks of planning a n d carrying o u t the extensive mortality t a b u l a t i o n s for the period 1959-1961. D r . T a e u 1 Mortimer Spiegelman, "The Organization of the Vital and Health Statistics Monograph Program," Emerging Techniques in Population Research (Proceedings of the ¡962 Annual Conference of the Milbank Memorial Fund; New York: Milbank Memorial Fund, 1963), p. 230. See also Mortimer Spiegelman, " T h e Demographic Viewpoint in the Vital and Health Statistics Monographs Project of the American Public Health Association," Demography, vol. 3, No. 2 (1966), p. 574.

FOREWORD | xvii

ber arranged for the cooperation of the Bureau of the Census at all stages of the project in many ways, principally by furnishing the required population data used in computing death rates and by undertaking a large number of varied special tabulations. As the sponsor of the project, the American Public Health Association furnished assistance through Dr. T h o m a s R. H o o d , its Deputy Executive Director. Because of the great variety of topics selected for m o n o g r a p h treatment, a u t h o r s were given an essentially free h a n d to develop their manuscripts as they desired. Accordingly, the authors of the individual m o n o g r a p h s bear the full responsibility for their m a n u scripts, and their opinions and statements do not necessarily represent the viewpoints of the American Public Health Association or the agencies with which they are affiliated. Berwyn F. Mattison, M . D . Executive Director American Public Health Association

NOTES ON TABLES 1. Regarding 1959-61 mortality data: a. D e a t h s relate to those occurring in the United States (including Alaska and Hawaii); b. D e a t h s are classified by place of residence (if pertinent); c . Fetal deaths are excluded; d. D e a t h s of u n k n o w n age, marital status, nativity, or other characteristics have not been distributed into the known categories, but are included in their totals; e . Deaths were classified by cause according to the Seventh Revision of the International Statistical Classification of Diseases, Injuries, and Causes of Death (Geneva: W o r l d Health Organization, 1957); f. All death rates are average a n n u a l rates per 100,000 population in the category specified, as recorded in the United States census of April 1, 1960; g. Age-adjusted rates were c o m p u t e d by the direct method using the age distribution of the total United States population in the census of April 1, 1940 as a standard. 1 2. Symbols used in tables of data: — D a t a not available; ... Category not applicable; - Quantity zero; 0.0 Quantity more than zero but less than 0.05; * Figure does not meet the standard of reliability of precision: a) R a t e or ratio based on less than 20 deaths; b) Percentage or median based on less than 100 deaths; c) Age-adjusted rate c o m p u t e d from age-specific rates where more than half of the rates were based on frequencies of less than 20 deaths. 3. G e o g r a p h i c classification: 2 a . S t a n d a r d Metropolitan Statistical Areas (SMSA's): except in the N e w England States, " a n S M S A is a county or a g r o u p of contiguous counties which contains at least one city of 50,000 inhabitants or more or 'twin cities' with a combined population of at least 50,000 in the 1960 census. In addition, contiguous counties are included in an S M S A if, according to specified criteria, they are (a) essentially metropolitan in character and (b) socially and economically integrated with the central city or cities." In New England, ' M o r t i m e r Spiegelman and H. H. Marks, "Empirical Testing of Standards for the Age Adjustment of Death Rates by the Direct Method," Human Biology, 38:280 (September 1966). 2 National Center for Health Statistics, Vital Statistics Mortality, Part A, sec. 7, p. 8.

xviii

of the United States, 1960, vol. II,

NOTES O N TABLES | xix the Division of Vital Statistics of the N a t i o n a l C e n t e r for H e a l t h Statistics uses, instead of the definition j u s t cited, M e t r o p o l i t a n State E c o n o m i c A r e a s ( M S E A ' s ) established by the Bureau of the C e n s u s , which are m a d e u p of c o u n t y units. b. M e t r o p o l i t a n a n d n o n m e t r o p o l i t a n : " C o u n t i e s which a r e included in S M S A ' s or, in N e w E n g l a n d , M S E A ' s are called m e t r o p o l i t a n counties; all other counties are classified as n o n m e t r o p o l i t a n . " c . M e t r o p o l i t a n counties m a y be s e p a r a t e d into t h o s e c o n t a i n i n g at least o n e central city of 50,000 i n h a b i t a n t s or m o r e or twin cities as specified previously, a n d into m e t r o p o l i t a n c o u n t i e s w i t h o u t a central city. 4. Sources: In a d d i t i o n to any sources specified in the figures, text tables, a n d a p p e n d i x tables, the d e a t h s a n d d e a t h rates for t h e period 1959-61 are derived f r o m special t a b u l a t i o n s m a d e at the N a t i o n a l C e n t e r for Health Statistics, Public H e a l t h Service, U . S. D e p a r t m e n t of H e a l t h , E d u c a t i o n , a n d Welfare, for the A m e r i c a n Public H e a l t h A s s o c i a t i o n .

The Epidemiology of Oral Health

1/DENTAL CARIES JOHN B. DUNBAR Dental caries is a widely spread chronic disease. A recent national survey 39 estimates that half the teeth of the average American have become carious by the age of 25 to 34 years. In the 45- to 54-yearold group, only about 10 or 11 teeth per person remain undamaged, and approximately half of 55- to 65-year-old persons have no remaining permanent teeth. Sognnaes 48 gave a different perspective to the problem in estimating that it would take 10 years work by two and one-half times as many dentists as exist in the United States just to repair present, ordinary dental defects. Whatever the approach, findings have documented the vastness of the problem and have brought about equally vast increases in support of research and research training relating to caries, largely by the National Institute of Dental Research. The Institute, beginning in 1948 with a modest funding of 33 thousand dollars, dispensed approximately 23 million dollars in 1968 for the support of extramural research and training programs related to all dental diseases.

The Teeth There are 28 teeth in the typical, healthy, adult mouth. This number is exclusive of the four wisdom teeth (third molars) whose history of appearance and whose physical form frequently are erratic.* Of the 28 teeth, there are eight molars and eight premolars (bicuspids) which serve to crush food and to mix it with saliva before swallowing. The remaining 12 teeth are incisor types which serve a cutting and tearing function. The molars and premolars are box-like in shape, hence they have five surfaces exposed to the oral environment. The incisor types are pointed or blade-like and thus have but four broad surfaces exposed. Of the permanent teeth, first molars are the first to erupt, generally around the age of six years. The first molars are followed by * S o m e dental researchers summarize their results on the basis of 32 permanent, adult teeth, e.g. Pelton et al.'10

1

21 THE EPIDEMIOLOGY OF ORAL HEALTH

the incisors at age 7-8, the bicuspids at age 9-11, and the second molars and cuspids around age 12. Teeth are made up of enamel, dentin, cementum, and dental pulp. Enamel, the hardest of all body tissues, is the exposed part (the crown) of the tooth. A thin layer of cementum covers the root surface while the bulk of the tooth is made up of dentin. A channel running from inside the tooth crown to the root opens out into the encasing bone at the root tip. The channel houses the pulp which consists of nerves, blood vessels, and other vital tissues.

Dental Caries Most commonly, caries begins as a small lesion on the enamel tooth surface; if the lesion is untreated it penetrates deeper, finally, progressing into the pulp chamber. Once the decay has reached the pulp chamber, inflammation occurs and an abscess forms at the apex of the tooth. Such inflamed teeth often can be saved by cleaning out the pulp canals and completely filling them ( " r o o t canal work") but the operation is time-consuming and expensive. Caries begins at typical points on the tooth and generally develops first in those teeth which have irregular surfaces. Most susceptible are the chewing (occlusal) surfaces of the molars. Characteristically, the enamel on these surfaces bears pits and fissures which tend to hold food particles. Fermentation of these food particles by bacteria is the essential mechanism of tooth decay.* Tongue (lingual) and cheek (buccal) tooth surfaces are much less susceptible to decay except where enamel faults exist. The spaces between adjoining teeth also hold food particles, making these contact surfaces (proximal surfaces) susceptible to decay. Decay along the gum line is more typical of older persons. Because susceptibility to caries is related to surface type and it, in turn, is related to tooth type, classifications of teeth have arisen based on observed order of susceptibility to caries. One classification was developed by Klein and Palmer: 32 Class

I II

Mandibular 1st and 2nd molars Maxillary 1st and 2nd molars

*It has been shown that caries will not develop unless foods c o m e in direct contact with the teeth. In an illustrative experiment, two groups of rats were fed a standard, cariesproducing diet. One group ate ad libidum. The other was fed through a stomach tube. The first group developed caries, the second developed none. 3 1

DENTAL CARIES ¡3 III

M a n d i b u l a r 2nd p r e m o l a r s , maxillary 1st a n d 2nd p r e m o l a r s a n d maxillary central and lateral incisors IV Maxillary canines a n d m a n d i b u l a r 1st premolars V M a n d i b u l a r central a n d lateral incisors a n d m a n d i b u l a r cuspids Class I contains the most susceptible teeth. It is interesting t h a t this o r d e r a p p e a r s to hold for different levels of caries experience. T h u s , in C h i n a with a very low caries experience, caries a p p e a r s p r e d o m i n a n t l y in the first m o l a r s . In A f o n s k y ' s study of Chinese students, no caries was observed in the f r o n t teeth. 1 On the o t h e r h a n d Icelanders, with a high decay rate, frequently show caries of the lower f r o n t teeth (least o r d e r of susceptibility). 9 In general it can be said that persons having little decay will have most or all of it in the m o l a r s . If the lower f r o n t teeth are decayed, it is a l m o s t certain that all teeth have experienced decay. T h e B a c k e r - D i r k s 3 study of D u t c h children, s u m m a r i z e d in T a b l e 1.1, illustrates the p a t t e r n : at age six only first m o l a r s are e r u p t e d a n d subject to decay; at age 12 bicuspids (erupting at ages 9 - 1 1 ) h a v e begun t o decay. Table 1.1.

Age in years

5 - 7 7 - 9 9-11 11 - 13 13 - 15

Source: a

Number of new pit and fissure cavities per child by selected age intervals and three tooth types for children born in 1945: Culemborg, Holland

Number new cavities per child3 First Molars Second Molars Bicuspids

1.8 3.2 1.0 0.5 0.2

... 0.4 1.9 2.1

0.1 0.2 1.0 0.7

Backer-Dirks (3).

Figures were estimated from a graph.

A m o n g the various foodstuffs, s o m e f o r m s of c a r b o h y d r a t e s have been especially implicated in the p r o d u c t i o n of caries. F o r example, there is the 1949-51 study b y G u s t a f s s o n a n d c o - w o r k e r s , " 1 2 w h o s e findings agree with those of Bibby 5 a n d Volker. 5 1 T h e G u s t a f s s o n study involved 436 institutionalized persons in Vipeholm, Sweden. T h e usual diet of these p e r s o n s is said to have been like t h a t of an

4 | THE EPIDEMIOLOGY OF ORAL HEALTH

ordinary Swedish family. Three experimental subgroups were taken from the major group of 436: a control group left on the usual diet; a group whose diet was supplemented by a sugar solution at all meals; a third group whose diet was supplemented by sticky toffee consumed throughout the day, including between-meal periods. For both test groups the amount of sugar or sugarequivalent supplied was over 100 pounds per year. Table 1.2 shows Table 1.2.

Influence of sugar supplement o n caries

Group

Control diet Control plus in liquid Control plus as sticky

Number of subjec ts

sugar forma sugar toffeea

Source: a

Tooth surfaces becoming carious per p e r s o n per year

60

0.30

57

0.67

48

4.02

Gustafsson (12); table as adapted by Volker

(51).

T h e s e groups consumed comparable amounts of sugar, over pounds per person per year.

100

that the caries rate in the subgroups was related strongly to the form of sugar and the daily frequency of ingestion. From such findings, it seems clear that candies, cookies, and ice cream have high caries-producing potential, while vegetables, fruits, and fruit juices have minimal potential. It would appear, therefore, that the property of a sweet form, to be retained in the mouth for an extended period, is more important in producing caries than the amount of sugar consumed.* This finding may explain why some primitive peoples have little caries even though their diet is high in fermentable carbohydrates. Sugar was severely restricted in most European countries during World War II. Sognnaes 47 analyzed reports from 10 European countries and found that the caries rate became significantly lower approximately two years after rationing was imposed. The caries rate did not return to the prewar levels until two years after the end * Russell 4 3 estimates t h a t sugar c o n s u m p t i o n in t h e F a r East ranges f r o m 6 to 16 kg. per person annually, in t h e N e a r East f r o m 13 to 19 kg., and in tropical S o u t h A m e r i c a f r o m 23 to 44 kg. Sugar c o n s u m p t i o n in t h e United States a n d in W e s t e r n E u r o p e averages 40 t o 45 kg. per person annually, DMF averages for the g e o g r a p h i c a l subdivisions are directly related t o these estimates of sugar intake.

DENTAL CARIES | 5

of rationing. Norwegian children were typical. Toverud 4 9 presents evidence that the intake of fermentable carbohydrates, particularly candies, was greatly reduced during the war. In 1935 the number of carious surfaces per 100 teeth of 8-year-olds was 80; in 1945 the low rate of 43 was reached; and by 1955 the caries rate was only 53, still considerably below the prewar level of 80. A striking example of the impact of modern refined foods on dental health involves the population of Tristan da C u n h a , a small volcanic island in the South Atlantic Ocean. Holloway 1 4 noted that in 1938 all persons under 20 years of age had sound p e r m a n e n t molars. In 1962 fully half of the corresponding teeth for the same age g r o u p were carious. In the interim a canteen selling modern foods had been established on the island. F r o m 1952 to 1962 each islander was estimated to have consumed a b o u t one-half a kilo of sugar a week, in contrast to the essentially sugar-free, austere diet of locally obtained foods prevailing until the late 1930's. Efforts are sometimes m a d e to translate access to fermentable carbohydrates and high caries rates into socioeconomic terms. For example, MacGregor 3 5 observed in G h a n a that recent high imports and consumption of sugar (a luxury) have produced a unique situation: children of higher income families have more dental decay than their parents (36 percent of 12-year-olds and 23 percent of adults). Poorer families without access to the expensive sweets had the least decay. Klein and Palmer, 3 3 however, in a United States study, found no evidence of a relationship between socioeconomic status measured by family income and caries prevalence. The low cost and ready accessibility of sweets in the United States may very well explain the departure from the G h a n a pattern. It may even be that high income (and concomitant high education) families tend to follow better nutrition and oral hygiene regimens with resulting lower caries prevalence than lower income a n d education groups exhibit—an entirely inverse relationship. The association between annual income and a m o u n t of sweets used by some Minnesota farm families is compatible with this view. F a r m families with incomes less than $1,000 in 1950 used 4.6 pounds of sugars and sweets in one week, from $1,000 to $1,999 used 5.2, f r o m $2,000 to $2,999 used 6.1, from $3,000 to $3,999 used 7.8, and those with incomes equal to or greater than $4,000 used 6.5 p o u n d s (sweets include sugars, syrups, jellies, jams, candy and ice cream). 6

6 | THE EPIDEMIOLOGY OF ORAL HEALTH Measurement of Caries In the introduction, reference is made to the magnitude of the caries problem. A commonly used index of this magnitude is the DMF index or count, where D represents the number of permanent teeth decayed, M the number missing, and F the number filled. The DMF index is the simple sum of these components. In younger people (with permanent teeth) the DMF tooth index closely reflects the number o f teeth damaged by caries. In older people many teeth may be lost for reasons other than caries, for example periodontal disease, and removal to permit construction of complete artificial dentures.* This being so, the DMF index is more difficult to interpret in older people. Also there is the question, already noted, of whether to include the four wisdom teeth (third molars) in a DMF study. This decision usually is determined by the character of the examination. On visual examination alone (such as Russell 4 2 ) it is impossible to determine whether an absent third molar has been extracted or remains unerupted, and hence such data usually are reported on the basis of 28 teeth. With X-ray films (as in a clinical setting such as described by Pelton et al. 4 0 ), the status of third molars is determined more readily. Such studies frequently are reported on the basis of 32 teeth. Other practical problems arise in using the DMF index, especially insofar as the decayed tooth count is concerned. It is not always easy to detect cavities, especially incipient ones. For this reason examiners using different methods and criteria may differ on the number of carious teeth observed in a given population. The F count is not always an accurate index o f decay prevalence. A sound tooth, for example, may be fitted with a metal filling to support an adjoining artificial tooth. Grainger 1 0 seems to have summed up the situation properly in his comment that the difficulties of measuring decay by counting cavities are " a s complicated as a study of chicken pox based on the number of pox per child." In spite of these problems, the DMF index is widely used as a measure of caries experience, and considerable effort is being expended in trying to arrive at international standards. 4 * J a c k s o n 3 0 had 6 0 dentists in Leeds, E n g l a n d , collect over 2 , 0 0 0 extracted teeth which were examined for caries. Ninety-seven percent o f all extracted m o l a r s and 21 percent o f lower incisors were carious. These figures are illustrative only. T h e i r magnitude would be wholly different for other localities.

DENTAL CARIES I 7 Demographic Factors Relating to Caries Age is strongly a n d positively associated with DMF scores. T a b l e 1.1, already referred to, a n d Tables 1.3, 1.4, a n d 1.5 illustrate the age p a t t e r n . A study by K n u t s o n 3 4 of U n i t e d States Public H e a l t h Table 1.3.

Number of DMF teeth

13. 5 14. 4 25. 2 18. 9 27. 0 0. 9

13 10 14 15 30 7 3 1

7 3 8 9 8 9 4 1

— —

1 1 1 1

1.9 3.9 5.9 5.9 3.9 5.9 9.8 9.8 3.9 5.9 11.8 1.9 3.9 7.8 7.8 3.9

1.9 3.9

Source: Table 1.4.

Age in years

-

Percent of children having given number of DMF teeth Age Agi Age Age 14 6 8 10

42.0 27.3 17.9 6.3 6.3

0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22

18 25 35 45 55 65 75

Percentage distribution of children of selected ages by number of DMF teeth: Neosho, Missouri, 1953

24 34 44 54 64 74 79

Presnell (41). Average number of remaining sound teeth per person by age and sex, white adults: United States, 1960-62

Average number of sound teeth Male Female

17.6 14.7 12.7 10.4 6.6 5.1 3.2

Source: National Center for Health Statistics (39).

16.9 12.8 11.2 9.2 5.8 4.1 2.2

81 THE EPIDEMIOLOGY OF ORAL HEALTH Table 1.5.

DMF teeth per person by age: Baltimore, Maryland (white children), 1955 and Thailand, 1960

Age in years 5 10 15 20 30 40 50

DMF teeth per person Baltimore Thailand 0.2 0.6 1.0 0.8 1.0 2.9 10.6

2.5

- 9 - 14 - 19 - 29 - 39 - 49 and over

11.9 14.0 15.9 18.3 22.3

Source: Interdepartmental Committee on Nutrition for National Defense (24), McCauley and Frazier (36).

Service data on caries among school children in nine communities during 1937-55, and data from the National Health Survey 39 covering the 18-79-year-old group, also are illustrative of the relationship between age and DMF scores. Knutson found that the percentage of persons with one or more DMF teeth rises rapidly from ages 6 through 9 and continues to rise, though less rapidly, up to age 15. The National Health Survey data, combined with the Knutson data, show that DMF rates tend to rise sharply through the teen ages; the rates continue to rise though more slowly through the remaining years. Race or ethnic background appears to be relevant only when it involves differentials in cultural patterns and socioeconomic status and hence the type of diet, health care, and so on. In this country, white children tend to have more caries than Negro children of the same age, but the differences vary irregularly at all ages. Table 1.6 Table 1.6.

Age in years

DMF teeth per person for 6-8- and 12-14-yearold children by color: Evanston, Illinois, 1946 and Tennessee, 1937-41

White

Negro

White

Tennessee 3

Evanston, Illinois 6 - 8 12 - 14

1.6 10.1

Source: a

1.4 9.4

Hill (13), Sebelius (46).

Deciduous (baby) teeth included.

Negro

4.9 3.2

4.0 2.4

DENTAL CARIES ¡ 9 illustrates the difference in t w o unrelated studies; T a b l e 1.7 is m o r e detailed a n d m a k e s possible a c o m p a r i s o n by sex as well as race. In his study of DMF c o u n t s for U n i t e d States military inductees by race or nationality of parents, Hyde 1 5 f o u n d the Chinese a n d N e g r o to have the lowest c o u n t s a n d the Irish a n d English the highest. Table 1.7.

DMF teeth per person by age, color and sex: United States, 1960-62 White

Age in years

Male

Female

Male

18 25 35 45 55 65 75

14.1 16.8 18.4 18.8 21.5 22.7 24.4

14.8 18.4 19.5 20.4 22.5 23.4 25.0

8.1 8.4 9.2 13.6 15.2 19.0 24.0

- 24 - 34 - 44 - 54 - 64 - 74 and over

Negro Female 9.2 12.3 13.8 13.7 16.8 14.6 27.3

Source: National Center for Health Statistics (39).

Certain cultural practices may affect the caries rate. F o r example, D o n n e l l y 8 noted t h a t children of the Seventh D a y Adventist C h u r c h have less caries t h a n a control g r o u p . H e a t t r i b u t e d the difference to a churchwide e d u c a t i o n a l p r o g r a m emphasizing g o o d dietary habits. M e n a n d w o m e n differ little in their experience with decay, alt h o u g h DMF scores for w o m e n seem to be consistently higher t h a n t h o s e for men. Y o u n g girls develop t o o t h decay a p p r o x i m a t e l y six m o n t h s before boys of the s a m e age; the difference is explained in p a r t by the earlier e r u p t i o n of female teeth. 3 7 Also, at the m o r e a d v a n c e d ages, w o m e n tend to b e c o m e e d e n t u l o u s s o m e w h a t earlier t h a n men. 3 9 Fluoridation It has been shown t h a t , for any given age a n d diet, intake of small a m o u n t s of fluoride lowers caries rates as m u c h as 60 percent w i t h o u t d e m o n s t r a b l e side effects. Russell, 4 3 in r e p o r t i n g on s o m e of the studies of the I n t e r d e p a r t m e n t a l C o m m i t t e e on N u t r i tion for N a t i o n a l Defense 19,21 (concerning p e r s o n s d r i n k i n g fluoridated water), indicated t h a t findings in C o l o m b i a a n d E c u a d o r (Table 1.8) were typical; the lower rates for p e r s o n s drinking water with " a d e q u a t e " fluoride levels are u n m i s t a k a b l e .

101 THE EPIDEMIOLOGY OF ORAL HEALTH T a b l e 1.8.

Age in years

D M F teeth per person for people living in lowfluoride and adequate-fluoride areas: Colombia and Ecuador, 1960

Drinking water Low-fluoride A d e q u a t e - fluoride

Colombia 5 - 9 10 - 14 15 - 19

1 27 4 43 11 30

0 99 2 71 4 82 Ecuador

5 10 15 20 30 40 50

- 9 - 14 - 19 - 29 - 39 - 49 and over

1 3 8 10 13 21 22

01 33 16 10 18 12 12

Source: Russell (43), Interdepartmental o n N u t r i t i o n for National Defense (19,21).

0 1 1 4 8 9 14

08 39 63 20 33 73 68

Committee

T h e r e are, however, u p p e r a n d lower limits for fluoride. A t t o o low c o n c e n t r a t i o n s , the caries-inhibiting qualities a r e negligible; at t o o high c o n c e n t r a t i o n s , fluorosis (pitting a n d mottling) of the t o o t h enamel occurs. 7 A p p r o x i m a t e l y 1 p p m ( p a r t per million) of fluoride has been f o u n d an " i d e a l " average. W h e r e water supplies are artificially fluoridated, the level of fluoridation is raised if average water intake is low (colder climates), or the level of fluoridation is lowered if average water intake is high ( w a r m e r climates). W h a t e v e r the practical p r o b l e m s of a d m i n i s t e r i n g the fluoride, it is p r o d u c t i v e to consider T a b l e 1.9, s u m m a r i z i n g d a t a by A r n o l d et al. 2 DMF rates for 12-year-olds, for 1944-54, for t w o M i c h i g a n cities are c o m p a r e d . In o n e of the cities, G r a n d R a p i d s , t h e drinking water was fluoridated at a p p r o x i m a t e l y 1 p p m beginning in 1944 45. i n the other city, M u s k e g o n , water was left u n t r e a t e d . T h e children of b o t h cities h a v e been e x a m i n e d every year since 1944-45; the p r o n o u n c e d i m p r o v e m e n t following fluoridation is clear. Caries and Geographical Location Caries rates vary considerably a m o n g regions in the U n i t e d States. Massler a n d Ludwick 3 8 a n d Schlack et al., 45 reporting o n

DENTAL CARIES | 11 Table 1.9.

DMF teeth per person for 12-year-olds: Grand Rapids and Muskegon, Michigan, 1944-54

Average DMF per child Grand Rapids Muskegon

Year

1944 1945 1946 1947 1948 1949 1950 1951 1952 1953 1954

8 1 9 5 7 6 7 0 8 3 7 0 7 1 5 9 5. 0 4. 8 3. 9

Source:

8.7 -

8.4 6.8 7.8 7.2 6.9 7.7 7.0 6.5 6.1

Arnold and co-workers (2).

the dental experience of the military, f o u n d the highest caries levels in the Northeast, the lowest in the South and West, and intermediate experiences in the N o r t h Central region. Regional differences are difficult to explain fully. Because Negroes show a lower DMF index than whites, it might be expected that the South, with a larger proportion of Negroes, would show a lower index than the N o r t h e a s t . Yet the study of Massler and Ludwick 3 8 confirmed the regional difference because it was based exclusively on an examination of whites. The study also indicated a tendency for higher rates in urban areas, perhaps explaining some part of the regional caries differences. Regional differences in income and dietary habits also exist and may explain some part of regional differences in caries levels. Further, a United States Public Health Service study 50 estimates the p r o p o r t i o n of the total population in each state that consumes fluoride-containing drinking water. Table 1.10 shows an irregular association between the proportion of the population consuming fluoride-containing water and the caries level. Lack of weighting for lengths of time of fluoridation and for population mobility might explain some of the irregularity. C o m p a r i s o n s a m o n g other areas of the world are possible but may be misleading due to the considerable demographic, cultural, social, and economic differences a m o n g these areas a n d to lack of comparability a m o n g the studies. Nonetheless, a large n u m b e r of surveys were reviewed. The DMF levels appear to be generally

121 THE EPIDEMIOLOGY OF ORAL HEALTH Table

1.10.

Distribution of states by national rank in the proportion of persons drinking fluoride-containing water by region: United States, 1963

Number of s tates Highest Middle Lowest third 3 third third

Region

United States

16

16

16

38.0

1 7 6 2

2 4 7 3

6 1 3 6

22.0 56.0 44.0 19.0

Northeastern states North central states Southern stateg Western states

Source:

Percentage of persons drinking fluoridecontaining water

United States Public Health Service (50).

a Highest third means the 16 continental states with the largest proportion of persons drinking fluoride-containing water.

^Excluding Alaska and Hawaii.

lowest for A f r i c a n and Asian countries, and highest for Western civilizations. Table 1.11, based on more comparable data produced by trained dentists from the N a t i o n a l Institute o f Dental Research, provides a reliable summary of findings among 15 widely separated groups. O f the 15 groups listed, the eight with the lowest DMF are N o r t h A f r i c a n , Asian, or isolated. T h e highest Table 1.11.

DMF teeth per person aged 20-24 years, selected civilian groups

Groups

DMF per person

Ethiopia Vietnam - Hill Tribesmen Burma Thailand Vietnam - Vietnamese

0. 5 0. 7 1. 0 1. 2 1. 7

Palestinian Refugees Lebanon Alaska - Primitive Eskimos U.S. Negro Ecuador

2. 0 4. 0 6. 5 8. 5 9. 0

Chile Colombia Alaska - Urban Eskimos Iceland U.S. White Alaska - Aleuts

12. 0 13. 0 13. 5 14. 8 15. 0 18. 0

Source: Russell (43,44), Dunbar and others (9), Interdepartmental Committee on Nutrition for National Defense (16 - 29).

DENTAL CARIES [ 13 DMF figures are t h o s e for N o r t h a n d S o u t h A m e r i c a n s a n d

for

A l a s k a n E s k i m o s w h o h a v e t a k e n up the white m a n ' s ways.

Summary D e n t a l caries is a c h r o n i c , destructive disease o f teeth which begins very early in life* a n d , if untreated, generally results in loss o f the affected teeth. A l t h o u g h caries h a s been present in h u m a n p o p u l a t i o n s for t h o u s a n d s o f years, m a s s i v e a n d r a m p a n t t o o t h destruction by caries is c h a r a c t e r i s t i c o f recent times. F o r e x a m p l e , on the average m o r e than 14 teeth per person o v e r 18 years old in the U n i t e d S t a t e s are in need o f repair o r r e p l a c e m e n t . T h i s vast a c c u m u l a t i o n o f dental needs c o n s t i t u t e s a great c h a l l e n g e to the c o u n t r y ' s r e s o u r c e s b o t h for t r e a t m e n t a n d f o r research a n d prevention. T h e DMF index, a c o u n t o f the d e c a y e d , missing, o r filled teeth in a p e r s o n ' s m o u t h , is a widely used m e a s u r e o f the i m p a c t o f c a r i e s on a p o p u l a t i o n . S i n c e the DMF index is based on evidences o f past decay (filled o r missing teeth), it is a m e a s u r e o f a p e r s o n ' s lifetime e x p e r i e n c e with decay. It is m o r e effective for y o u n g e r t h a n for older people, since m u c h t o o t h loss in older people m a y be due t o r e a s o n s o t h e r t h a n caries. T h e i n t e r p r e t a t i o n o f DMF d a t a is beset with s u b s t a n t i a l difficulties due t o lack o f s t a n d a r d i z a t i o n a m o n g e x a m i n e r s , but m u c h effort has g o n e i n t o presurvey t r a i n i n g in an effort t o e l i m i n a t e e x a m i n e r differences. N o t only are there p r o n o u n c e d age differences in caries levels ( m e a s u r e d by the DMF index), but sex differences also are t y p i c a l — females tend to have a s o m e w h a t higher DMF e x p e r i e n c e than m a l e s . A l s o , older females are m o r e apt to be e d e n t u l o u s than m a l e s o f the s a m e age. T h e earlier eruption ( a p p e a r a n c e in the m o u t h ) o f female teeth a n d their longer e x p o s u r e m a y a c c o u n t for s o m e o f the differences. * M a n y children at age 6 - 7 years develop caries in the first permanent tooth even before it is fully erupted. Approximately one-fifth o f 6-year-olds in the United States have one or m o r e decayed, missing or filled (DMF) permanent teeth. At age 12, only 10 percent o f the young people have all o f their permanent teeth intact. Another measure shows an average o f o n e DMF tooth per child in the 6 - 7 - y e a r - o l d group and five DMF teeth per child at age 12. By age 18, the average per child is 10 DMF t e e t h — n e a r l y 4 0 percent o f the permanent teeth in the mouth (excluding the wisdom teeth).

141 THE EPIDEMIOLOGY OF ORAL HEALTH

Race, probably as a result of socioeconomic differences, finds whites with more caries than Negroes. One result of the concern with dental caries has been the discovery of the beneficial effect of small quantities (1 part per million) of fluorides in drinking water. In those areas in which fluoridation of water supplies is natural, it has been found that heavy overdoses may produce mottling and pitting of the teeth (fluorosis). Finally, there is a great variation in caries experience a m o n g different places. Of the countries for which studies were selected and reported, those of N o r t h Africa tend to have the lower DMF, those of South America have intermediate experiences, while those of England, N e w Zealand, Scandinavia, and N o r t h America have the higher rates. There is considerable variation f r o m section to section in this country as well. Northeastern residents have shown the highest number of DMF teeth per person, while southern and western residents have a lower n u m b e r . These differences are difficult to explain. It is pertinent, in this connection, that u r b a n residents tend to have more caries than rural-living persons a n d that the N o r t h east as a region still has the larger p r o p o r t i o n of persons living in urban places. The differences between the N o r t h e a s t and the South persist when whites only are considered. This comparison would not be as valid if all persons were considered, since adult Negroes have less caries than whites and the South has a larger p r o p o r t i o n of them than other regions.

2 / PERIODONTAL DISEASE RUSSELL s . MCMILLAN A N D ALBERT E. WOLFF Periodontal disease is an inexact term used to designate a variety of conditions of the supporting structures of teeth. It is ordinarily referred to by laymen as " p y o r r h e a . " Alveolar bone loss, a sequela of the more severe forms of the disease, was prevalent in the jaws of Egyptian mummies 1 6 of 4,000 years ago. Icelandic skulls 17 dating from A.D. 874-980 also have been found which display various stages of periodontal disease. The development, acceptance and widespread use of the DMF index as a measure of dental caries incidence and prevalence, described in the Preface and in the previous chapter, have led to comparable attempts to quantify periodontal disease. The early epidemiologic efforts lacked uniform criteria but recently considerable agreement has been attained toward standardized methods. In addition, limited studies on special population groups have given way to assessments of the pathology or relative severity of pathology occurring in larger segments of the population. Epidemiologic methods, as in many other health fields, are expected to contribute to knowledge a b o u t the etiology of periodontal disease, to assist in its treatment and control, and, one hopes, to aid in its ultimate prevention. Thus, the primary purpose of this chapter will be to present, as fully as possible, a picture of worldwide periodontal pathology and to point out meaningful and significant differences where they seem to occur. Since consideration of periodontal disease must necessarily relate to the periodontium, a description of the normal periodontal structures is desirable. The gingivae and the periodontal ligament in normal and abnormal states were described at the Sixth Annual Postgraduate Course in Periodontal Diseases in Tennessee in July 1948.75 The published results of this conference are utilized in the introductory portion of this chapter. Appreciation is extended to Dr. Wallace V. M a n n , D e p a r t m e n t of Periodontics, University of A l a b a m a , for Figure 2.1, which depicts the periodontium in a normal and a b n o r m a l state. Anatomical terms used in this chapter to describe the periodontium are identified in that figure. 15

16 | THE EPIDEMIOLOGY OF ORAL HEALTH

Fig. 2.1. Periodontium in a normal and abnormal state: MG, marginal gingiva; AEC, attached epithelial cuff; GP, gingival pocket; AB, alveolar bone; c, cementum; PL, periodontal ligament fibers; CE, crevicular epithelium; GS, gingival sulcus; GF, gingival fibers. T h e o r a l c a v i t y is lined by m u c o u s m e m b r a n e , a n e p i t h e l i a l m e m b r a n e w h i c h lines all c a v i t i e s a n d c a n a l s of t h e b o d y t h a t c o m m u n i c a t e w i t h t h e e x t e r n a l a i r . T h e m u c o u s m e m b r a n e of t h e o r a l c a v i t y f u s e s w i t h t h e skin a t t h e lips a n d w i t h t h e m u c o u s m e m b r a n e of t h e p h a r y n x . T h e p e r i o d o n t i u m is t h e s u p p o r t i n g s t r u c t u r e of t h e t o o t h a n d includes the gingivae, periodontal ligament, c e m e n t u m , and alveolar bone. T h a t p a r t of t h e m u c o u s m e m b r a n e w h i c h s u r r o u n d s t h e t e e t h a n d is a t t a c h e d t o a l v e o l a r b o n e is k n o w n as t h e g i n g i v a e . This tissue is s u b j e c t e d t o m u c h f r i c t i o n in m a s t i c a t i o n of f o o d a n d in t o o t h b r u s h i n g . T h e g i n g i v a e a r e n o r m a l l y of a p i n k u n i f o r m c o l o r , firmly a t t a c h e d t o t h e i r u n d e r l y i n g tissues a n d s o m e w h a t s t i p p l e d . T h e m o s t i m p o r t a n t p o r t i o n of t h e g i n g i v a e , f r o m t h e p e r i o d o n tal v i e w p o i n t , is t h e i r a r e a of a t t a c h m e n t t o t h e t e e t h , t h e e p i t h e l i a l a t t a c h m e n t , o r epithelial cuff. T h e t o p of t h e e p i t h e l i a l cuff a n d t h e

PERIODONTAL DISEASE | 17 crevicular epithelium (Figure 2.1) are the points of attack in gingivitis. The gingival sulcus surrounds the tooth as a potential space. The epithelial cuff extends around the tooth, forming the lateral border of the sulcus. The normal gingival sulcus is from zero to two millimeters deep, varying from tooth to tooth and from place to place on the same tooth. When the sulcus is involved by a pathologic condition and deepened, the term gingival pocket is used instead of gingival sulcus. The Periodontal Ligament The primary functions of the periodontal ligament are to support the tooth in its bony socket and to maintain gingival tone. The principal fibers of the ligament are nonelastic fibers arranged in bundles running from the cementum to the alveolar bone, to adjacent teeth, and to the gingivae. These fibers support the teeth so that pressure on them is transferred to the bone as a pull rather than as pressure, and the gingival tone is maintained. The periodontal ligament is the vital, active organ that maintains the cementum and alveolar bone and that acts to repair those structures after injury. The Cementum The cementum forms a foundation for attachment of the fibers into the teeth. These fibers must be reattached constantly by the formation of new thin layers of cementum. The A Iveolar Bone The alveolar bone which lines the socket affords attachment for the fibers on the bone side of the ligament. The bone is subject to changes with stress. Bone resorbs on the side of stress (physiologic or pathologic) and rebuilds on the side of pull. If the fibers are destroyed, the alveolar bone disappears. Loss of alveolar bone, in different forms, is seen in periodontitis and periodontosis. In broad terms, periodontal disease can be said to range from a simple inflammation of the gingivae (gingivitis) to the more progressive stages of periodontitis and periodontosis. Brief definitions of the principal aspects of periodontal disease are given in the following paragraphs.

18 | THE EPIDEMIOLOGY OF ORAL HEALTH

Gingivitis T h e r e is a g r a d u a l change f r o m clinically n o r m a l gingivae to this early pathological state. Gingivitis is recognized by signs of inflammation which may be manifest by presence of o n e or m o r e of the following: redness, swelling, bleeding, e x u d a t i o n , a n d infrequently pain.

Periodontitis Periodontitis is an i n f l a m m a t o r y disease of the gingiva a n d the deeper structures of the p e r i o d o n t i u m . T h e disease is considered a direct extension of gingivitis a n d it is characterized by pocket form a t i o n and alveolar b o n e loss. Clinically, it is often difficult to distinguish between gingivitis a n d early periodontitis.

Periodontosis Periodontosis is a degenerative disease which a t t a c k s the period o n t a l m e m b r a n e and the alveolar b o n e . T h e r e are degenerative changes which occur in the p e r i o d o n t a l ligament, interfering with c e m e n t u m a p p o s i t i o n . As a result, the fibers lose their a t t a c h m e n t to the teeth, their pull on the b o n e ceases, a n d the b o n e resorbs. I n f l a m m a t i o n a n d pocket f o r m a t i o n are later s y m p t o m s of the disease. W h e n these s y m p t o m s occur, the degenerative changes ( p e r i o d o n t o s i s ) m a y be o v e r s h a d o w e d by t h e s y m p t o m s of periodontitis.

Magnitude of the Problem D e n t a l caries a n d p e r i o d o n t a l disease, t w o of the chief causes of t o o t h mortality in h u m a n p o p u l a t i o n s , are u b i q u i t o u s entities, a n d no race has been reported to be entirely free f r o m either. In 1952, 62 the A m e r i c a n D e n t a l Association c o n d u c t e d a survey of dental care r e q u i r e m e n t s in the U n i t e d States. F o u r t h o u s a n d dentists each r e p o r t e d the t r e a t m e n t needs for ten consecutive patients, resulting in an a c c u m u l a t i o n of i n f o r m a t i o n on m o r e t h a n 37,911 patients. P e r i o d o n t a l t r e a t m e n t was required by 9.5 percent of males a n d 9.7 percent of females aged 15 years a n d over, with an average of 13.8 a n d 13.6 teeth per case, respectively. F o r male patients aged 35 years a n d over a n d females 40 years a n d over, " p e r i o d o n t a l disease was the reason for between t w o a n d three times as m a n y extractions as dental d e c a y . " It was estimated t h a t

PERIODONTAL DISEASE | 19

one-tenth of all adults in the United States required periodontal treatment with an average of 14 teeth involved. Valid studies to assess the relative importance of the two diseases in relation to tooth loss are limited. F r o m surveys which are available, however, some reasonable estimates can be made. According to a National Health Survey conducted in 1957,97 which recorded replies from respondents in a r a n d o m sample of the noninstitutionalized civilian population of the United States, 13 percent of the entire population of the country was edentulous due to loss of permanent teeth. M o r e recently, preliminary findings67 reporting the results of actual dental examinations of a small r a n d o m sample of the noninstitutionalized civilian population showed that about 20 percent of all adults at ages 18-79 years had lost all their permanent teeth. (See Table 2.1.) Table 2.1.

Sex

Percent of adults, aged 25 through 74, edentulous, according to health examination and health interview by sex

Examinai ion

Interview

Both sexes

19.6

20.5

Men

17.6

19.2

Women

21.5

21.6

Source:

Dental Findings for A d u l t s

(67).

Thus far, two points stand out. The first, for obvious reasons, is that there is remarkable consistency between reports concerning edentulousness, however caused, whether obtained by interview or examination. Secondly, there is no inconsistency between 13 percent of the total population and 20 percent of adults at ages 18-79 being edentulous. Below 15 years edentulousness seldom occurs; it is less than 1.4 percent in the 18-24-year-old group. This proportion increases in each succeeding age g r o u p . In the ten-year span 65-74, approximately 50 percent of the population is edentulous, and for all those 65 years and over, edentulousness of one or both j a w s occurs in 68 percent of the population. Only 26.1 percent (Table 2.2) of the adult population of the United States is free from some degree of periodontal disease as determined by the use of Russell's Periodontal Index. 76 The range

20 | THE EPIDEMIOLOGY OF ORAL HEALTH Table 2.2.

Percent of adults free of periodontal disease by sex and age

Both sexes

Age

Sex Male

Female

18-79

26

1

20 9

31.0

18-24 25-34 35-44 45-54 55-64 65-74 75-79

33 32 27 20 18 10 8

2 1 8 9 1 5 4

29 26 22 15 15 5 6

0 3

36.8 37.6 33.3 26.6 20.8 15.2

Source:

1

0 3 6 2

Dental Findings for Adults

11.0

(67).

is from 33.2 percent in the 18-24 year age g r o u p to 8.4 in the 75-79 year age group. F r o m a sample of the Boston area, Marshall-Day, Stephens, and Quigley 54 estimated in 1955 that persons who still had teeth at age 49-51 years had, on the average, only 50 percent of the n o r m a l complement. Only 40 percent of the natural teeth were present by age 60. In 1928-31, approximately the same situation prevailed according to studies conducted by the United States Public Health Service 13 and the American Dental Association." In 1929, Brekhus 8 listed the reasons for extraction of 13,909 teeth in 2,723 patients (Table 2.3). Brekhus concluded that "caries and periodontoclasia are the two diseases responsible (directly or indirectly) for 96.53 percent of extractions." Allen, 1 in 1944, studied 1,167 consecutive registrants at the University of Michigan Dental School Clinic. A b o u t one-third (353) required extractions. Of the eight classifications utilized by Allen, 89.5 percent fell into either the dental caries or periodontal disease class. Dental caries was responsible for 48.8 percent and periodontal disease for 40.7 percent. In India, in 1951, Subramanian 9 5 observed 1,992 patients referred for the extraction of 2,840 teeth. Periodontal disease was responsible for 69 percent of extractions and dental caries accounted for 31 percent. In 1954 Pelton et al.72 reported the tooth morbidity for a segment of the United States adult population. D a t a in this report were secured from records accumulated in United States Public Health Service hospitals. The percentage b r e a k d o w n by reason for extrac-

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ORAL CANCER | 63

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64 | EPIDEMIOLOGY OF ORAL HEALTH

atively large a n d together they include well over o n e million men between the ages of 35 a n d 89 years. T h e period of follow-up f r o m initiation of each study r a n g e d f r o m a b o u t 22 to 120 m o n t h s . T h e expected a n d observed d e a t h s a n d mortality ratios s h o w n in T a b l e 3.13 need s o m e e x p l a n a t i o n . Obviously, d e a t h rates of any g r o u p are m a r k e d l y affected by the age distribution of t h o s e c o m prising the g r o u p . T o c o m p a r e the d e a t h rate of t w o g r o u p s (smokers a n d n o n s m o k e r s ) , a s s u r a n c e is necessary t h a t age distributions are c o m p a r a b l e . In this instance, the mortality ratio used was obtained as follows: In each five-year age class, the age-specific death rate for non-smokers is multiplied by the number of person-years in the group of smokers. This product gives an expected number of deaths, which represents the number of deaths of smokers that would be expected to occur if the agespecific death rate were the same as for non-smokers. These expected numbers of deaths are added over all age classes, and their total is compared with the total number of observed deaths in the smokers. The mortality ratio is the ratio (total observed deaths in the smokers)/ (total expected deaths). A mortality ratio of 1 implies that the overall death rates are the same in smokers and non-smokers after this adjustment for differences in age distribution. It does not imply that the death rates of smokers and non-smokers were the same at each specific age. A mortality ratio higher than 1 implies that the group of smokers has a higher overall death rate than the non-smokers. 41 Of the eight specific cancer sites, t h a t is, the lung, larynx, oral cavity, e s o p h a g u s , urinary b l a d d e r , kidney, s t o m a c h , a n d p r o s t a t e , the mortality ratios indicate t h a t cigaret s m o k e r s h a v e 11 times the risk of n o n s m o k e r s in dying f r o m cancer of the lung or b r o n c h u s . Of significance is the finding t h a t of the r e m a i n i n g f o u r sites— larynx, oral cavity, e s o p h a g u s , a n d urinary b l a d d e r — h a v i n g a high cancer risk, cancer of the oral cavity, with a weighted m e a n m o r t a l ity ratio of 4.1, r a n k s second. T h e mortality ratios ranged f r o m 1.0 in the C a l i f o r n i a o c c u p a t i o n a l g r o u p , in which only seven cases h a d been observed, to 9.2 in the " M e n in 25 S t a t e s " study. C a n c e r d e a t h s related to the r e m a i n i n g sites—kidney, s t o m a c h a n d prost a t e — s e e m t o be relatively little affected by cigaret s m o k i n g . Lip Cancer Pipe s m o k i n g is associated with lip cancer in six studies in which this site a n d f o r m of t o b a c c o were analyzed. O n e a d d i t i o n a l study

ORAL CANCER | 65

reported an association with pipe and cigars combined. Of four other studies of lip cancer, chewing of tobacco a n d / o r snuff was associated in two. During the past thirty years, pipe smoking a m o n g males had decreased markedly in the United States. As already noted, there has been a concurrent decrease during the same period of cancers of the buccal cavity and pharynx, so that the decline in lip cancer a m o n g males is not necessarily incompatible with a strong association between that condition and pipe smoking. 4 1 As already noted in Table 3.9, cancer of the lip a m o n g females has never been an imp o r t a n t site. Tongue Cancer There is some indication of an association of tongue cancer with cigar smoking and, in one study, pipe and cigar smoking combined showed such an association. One large and adequately controlled study 37 established graded differences for lip cancer by numbers of pipefuls smoked per day, for tongue cancer by the a m o u n t of tobacco in pipes and cigars combined, and for other cancers of the oral cavity by numbers of pipefuls. N o gradient differences for cigarets were reported. Leukoplakia The long-suspected association of leukoplakia and use of tobacco and the concept that leukoplakia is a precursor to certain oral cancers received support but no confirmation from the studies included in the Advisory Committee's Report to the Surgeon General. 4 1 The conclusions from the report cited in the foregoing paragraphs are extremely conservative and may be summarized as follows: 1. Little doubt now exists of the causal relationship of pipe smoking to lip cancer. 2. The implication that the use of tobacco in other forms may produce oral cancers cannot be stated, although such a relationship is suggested 41

On the basis of additional evidence related to smoking, reported subsequently by the same agency, it was held that cigaret smoking is a significant factor in the causation of laryngeal cancer in the male. 42 As for smoking and cancer of the buccal cavity, pharynx,

66 | EPIDEMIOLOGY OF ORAL HEALTH

and esophagus, the same reviewers were less positive, stating that a "causative relationship seems likely." Recurrence Moore 2 7 has been concerned with oropharyngeal cancer (all of the squamous cell carcinomas arising from the mucosa of the mouth, pharynx, and larynx, excluding lips and nasopharynx), which he calls " m o u t h - t h r o a t " cancer. Briefly he reported the dismaying frequency of second or new carcinomas occurring later than three years after the control of the first cancer. In essence, 102 tobacco-smoking patients (moderate to heavy) who had been " c u r e d " of one mouth-throat cancer divided themselves into two groups after the first cancer; 37 patients had quit smoking and 65 continued to smoke. After an average interval of 5.67 years, 23 patients developed a second squamous cell cancer (not recurrence of first lesion), but only two of these belonged to the group that had stopped using tobacco. (See Table 3.14.) Table 3.14.

C o m p a r i s o n of two groups living and well for three or m o r e years following treatment for squamous cell carcinoma of m o u t h or throat (lip cancer excluded)

Item

Total

102

Number Sex ratio M e a n age

(male:female) (years)

Stopped

smoking

37

Continued

smoking

65

3.4:1

3.6:1

3.3:1

58.1

59.1

57.6

M e a n a m o u n t smoked (packages/day)

1.39

1.40

1.38

No. of second cancers

23

2

21

Source:

Moore

(27).

Although there may have been reasonable homogeneity among the 102 patients, a wide variety of unrecorded differences undoubtedly existed among them. Regardless of such factors as cancer susceptibility or even susceptibility as to a single tissue site, use of alcohol and so on, the cessation of smoking appears to confer a remarkable protection against the recurrence of cancer of the buccal cavity.

ORAL CANCER | 67 Oral Cancer Detection

A giant step in the control of neoplasms was taken when Papanicolaou's work reported in the early 1940's, using exfoliative cells of the uterus as a diagnostic tool to discover unsuspected uterine cancer, became known and was accepted. 34 In 1951, Montgomery and Von Haam 25,26 and later other contributors 35,44145 pointed to the value of cytodiagnosis of cancer of the mouth even when first biopsies were negative. Oral examinations completed on 118,194 patients by the Veterans Administration over a three-year period ending in 1962 disclosed 2,758 patients with some kind of lesion or abnormality of the oral mucosa, and all of them submitted to an oral cytologic examination. Of the 2,758 patients, 277 were judged to be cancer free, while 315 had lesions which were confirmed by biopsies. The high rate of 2.6 oral cancer per 1,000 patients examined is a reasonable comparison with the current prevalence of mouth cancer in the United States of one per 1,000 males over 40 years of age.43 The age distribution of the 2,758 patients with oral lesions, in Table 3.15, shows also the number, type, and percent of mouth Table 3.15.

Patients with mouth lesions

Age

TOTAL 20-39 40-44 45-49 50-54 55-59 60-64 65-69 70-89 Unknown

Source:

Age d i s t r i b u t i o n

Not cancer

of 2,758 p a t i e n t s w i t h m o u t h

Confirmed by Cancer Invasive Total carcinoma

biopsy

Cancers per 100 mouth lesions

Carcinoma in situ

Sarcoma

2

11.3

1

2.4 4.9 11.6 15.4

2,758

277

315

285

28

458 327 310 254 166 355 512 302 74

33 35 24 31 15 39 61 28 11

11 16 36 39 32 54 83 39 5

9 16 30 36 28 49 79 34 4

1 0 6 3 4 5 4 4 1

Veterans Administration Cooperative

lesions

Study

-

-

1 -

19.3 15.2 16.2 12. 9 6.8

(43).

lesions that were cancer. At ages 40 to 44, one out of 20 lesions was found to be cancer, and at ages 55 to 59 the peak was reached, when one in five lesions was found to be cancer. Thereafter, the proportion declined to about one cancer in eight lesions for those 70 to 89 years of age.

68 | EPIDEMIOLOGY OF ORAL HEALTH Table 3.16.

Specific site of 315 primary mouth cancers

Carcinoma In situ

Invasive carcinoma

Total

Percent

TOTAL

28

287

315

100.0

Floor of mouth Tongue Oropharynx Alveolar ridge (mandible) Buccal mucosa Soft palate Lip, lower Tongue and floor of mouth Alveolar ridge (maxilla) Hard palate Lip, upper

10 6 6 0 2 0 2 1 1 0 0

59 57 53 33 20 17 15 16 7 6 4

69 63 59 33 22 17 17 17 8 6 4

21.9 20.0 18.7 10.5 6.9 5.4 5.4 5.4 2.6 1.9 1.3

Location

Source:

Veterans Administration Cooperative Study (43).

Table 3.16, classifying the location of the lesions, indicates that m o r e than two in five lesions occur on the floor of the mouth and on the tongue. Treatment of lesions in both these areas usually results in some disability. Frequently the prognosis is poor. These data suggest that cancer of the m o u t h may begin long before the lesions are recognized clinically and that the period between inception and recognition could be as long as 20 years. 43 The precise technic for taking a smear for cytological examination can be found elsewhere. 36,43 F o r present purposes it is enough to stress that the procedure is painless and simple. Its principal value is the ease with which it may be applied to unsuspected and harmless-appearing lesions without arousing the patient's fears unnecessarily. Russell 36 cautions that a negative cytology report does not preclude the existence of cancer but that a suspicious or positive report makes biopsy m a n d a t o r y . A biopsy should be skillfully done, without delay, and preferably by the clinician who will be responsible for the ultimate treatment plan. The chief lesson to be learned a b o u t the value of exfoliative cytology is that many innocent-appearing lesions ordinarily overlooked even by highly cancer-conscious examiners prove to be malignant. This fact suggests that for the benefits of cytodiagnosis to be fully effective a vast educational campaign a m o n g dentists at undergraduate and g r a d u a t e levels is in order. Cytodiagnosis is an i m p o r t a n t tool available to the dental profession, and its acceptance and widespread application can serve as the most i m p o r t a n t lifesaving technic ever offered to any profes-

ORAL CANCER | 69 sion. In view of t h e already r a t h e r f a v o r a b l e survival rates for lip a n d buccal cavity cancers u n d e r prior conditions, the early detection a n d t r e a t m e n t possible t h r o u g h cytodiagnosis offers a r a r e o p p o r t u n i t y for the dental profession to reduce significantly the death rates for cancers occurring on the lip a n d within the buccal cavity.

Cancer Treatment P e r h a p s little needs to be said here concerning the t r e a t m e n t of oral cancer, since the basic technics available a r e the s a m e as those in general use for cancer regardless of site. T h e r e is c o m m o n agreement, however, that n o great i m p a c t in the reduction of the n u m b e r of d e a t h s f r o m cancer m a y be expected f r o m f u r t h e r imp r o v e m e n t s in the technics of surgery a n d r a d i o t h e r a p y a l o n e . " Within the last twenty years, anticancer chemicals have increased the period of survival of patients with a d v a n c e d cancer, have reduced pain, a n d have permitted a small b u t g r o w i n g n u m b e r of patients to return to a condition a p p r o a c h i n g n o r m a l for a few m o n t h s a n d sometimes for years. F o r instance, nucleic acid inhibitors classified as a n t i m e t a b o l i t e s have been effective in controlling epithelial t u m o r s . Clinically, i m p o r t a n t t e m p o r a r y successes have been claimed for 1) Male and female sex h o r m o n e s , 2) Antimetabolites, including new applications of chemicals previously available, 3) Corticosteroids, 4) Nitrogen mustard and oral alkylating agents, 5) Antibiotics, particularly A c t i n o m y c i n C and D , 6) Plant extracts.

U n f o r t u n a t e l y , no chemical agent h a s been discovered c a p a b l e of destroying completely all evidence of cancer in every patient with cancer of any o n e kind. Nonetheless, in institutions concerned with cancer research a n d t r e a t m e n t , c h e m o t h e r a p y h a s been a d d e d to surgical a n d r a d i o t h e r a p y p r o c e d u r e s as soon as the diagnosis of a solid t u m o r was m a d e . Such action is based on the u n p r o v e n ass u m p t i o n that chemical agents w o u l d h a r m b u t n o t destroy a large t u m o r mass a n d might very well destroy small n u m b e r s of circu-

70 | EPIDEMIOLOGY OF ORAL HEALTH

lating cells or small tumor metastases. In addition, the rationalization that chemical agents might render an inoperable tumor operable or sensitize a radioinsensitive tumor seems to have become a possibility as cancer chemotherapy research has progressed." Still to be achieved, however, if cancers—or if some cancers—are actually intracellular chemical aberrations, is an inexpensive, simple, accurate, and rapidly performed diagnostic tool subject to mass application which will identify the biochemical disorder before a tumor is formed. Also to be achieved is the chemical (or other) agent necessary to correct the intracellular aberration and thus control or prevent the initiation of cancer. Indeed, both steps seem impossible, but they remain the ultimate goal of a preventive program.

Summary

The occurrence of cancer in any site is an unhappy event. It is particularly so of those advanced cancers which occur about the face and jaws because it is most difficult to correct or mask the mutilation of successful treatment. Difficulty with eating and communicating, even when disability is reduced by plastic surgery or a prosthesis, makes an oral cancer patient a most pathetic individual. There were 7,568 deaths in 1965 from cancers occurring in sites commonly under the supervision of dentists. This figure includes 6,501 deaths from neoplasms of the buccal cavity and pharynx, the classification which forms the basis for much of the data presented in this chapter. The pharynx is the leading site for oral cancers, followed by the tongue, and together they account for nearly two-thirds of all oral cancer deaths. Oral cancer occurs more frequently in adults. The death rates for males are three times those for females, and vary according to race, religion, income, region, urbanization, and country of origin. Educational efforts directed toward early detection and treatment of oral cancers have been disappointing (Table 3.8). The probability of developing cancer of the pharnyx following birth is four times greater for males than for females and ten times greater in the case of lip cancer. Once cancer of the buccal cavity and pharynx has occurred and treatment begun, the picture is much better than formerly. Survival rates have significantly improved

ORAL CANCER | 71

during the more recent years (Table 3.11), particularly when one considers that a cancer victim at the turn of the century had little hope of recovery. 10 The reduction of cigaret and pipe smoking may help improve the cancer incidence rates of the lung and perhaps other sites as well. Certainly there is little argument left about the relationship of tobacco to lip cancer. The small sample study (Table 3.14) of the recurrence of oral cancer in smokers who continued to smoke following treatment for one lesion is impressive indeed. As a diagnostic tool to uncover early cancer lesions of the oral cavity, the so-called " P a p " smear offers great possibilities to those attempting mass control programs as well as to alert dental clinicians. It seems self-evident that for the time being the case-finding technics so successfully applied in uterine cancer programs must be undertaken to control oral cancer. A cytodiagnostic tool has been available for the past 25 years with which it can be done. The dental profession, whose aim is to inspect the oral cavity of every person each year, is in a strategic position to contribute to further improvements in cancer survival rates by systematic use of cytodiagnosis, either routinely or through special screening programs. Although there is great hope that the tremendous sums of money and the large share of scientific workers being concentrated on cancer research and therapy will be effective, there appear to be voids in the attack. Epidemiology, clinical research, and control of environmental carcinogens have been named as examples where more emphasis is needed. 10 Returning to the opening statement in this chapter; compared to other diseases and conditions within the scope of dental practice, cancer is dealt with rather infrequently, yet, no disease affords a greater challenge and the prospect of doing so much solely by the early use of a simple diagnostic tool.

4

DENTOFACIAL DEFORMITIES: MALOCCLUSION PALMI MOLLER

Dental occlusion generally refers to the relationship of the teeth in the maxillary and mandibular alveolar arches when the jaws are closed. The term malocclusion has been defined as " t h a t condition in which dental structures are not in acceptable equilibrium with each other or with the facial structures a n d / o r the cranium, thus interfering with or posing a potential threat to normal tissue development and maintenance, effective function, or a physiological behavior problem." 3 7 Thus, this definition embraces irregularities of the individual teeth, alveolar arches, soft tissues, the neuromuscular system, the jaws, or any combination of these irregularities. That malocclusion has existed since the beginning of mankind is apparent from illustrations or reproductions of the skull of Neanderthal man. The earliest written report of irregularities of the dentition was made by Hippocrates (460-377 B.C.) in the sixth book of Epidemics. The first report on treatment or preventive orthodontics was made by Celsus (25 b.c.-a.d. 50). He wrote: "If a second tooth should happen to grow in children before the first had fallen out, that which ought to be shed is to be drawn out and the new one daily pushed toward its place by means of the finger until it arrives at its just position." 5 0 Although studies of the dentition in skulls from the Stone Age, Iron Age, and medieval times have indicated that malocclusion was not uncommon in those times, prevalence figures obtained from them have limited significance because of the small number of skulls discovered in any one location. Attempts at correction of malocclusion have been carried out for centuries. These, however, were based on the desire of patients for a more aesthetic appearance. Orthodontics did not emerge as a science until Angle developed a classification of malocclusion and established a school of orthodontics at the beginning of this century. In the last fifty years a vast body of written work concerning malocclusion has accumulated. The majority of these papers are chiefly concerned with the technical aspects of orthodontics, and relatively few reports have appeared which deal with the 72

MALOCCLUSION | 73 prevalence of malocclusion. W h e n one realizes that an estimated twenty to thirty million children, in A m e r i c a alone, suffer f r o m s o m e f o r m of malocclusion, it becomes a p p a r e n t that extensive a n d well-planned clinical surveys are needed to answer the m a n y stillexisting questions regarding the a n o m a l y . In this chapter an a t t e m p t will be m a d e to s u m m a r i z e the findings of several clinical surveys concerning the prevalence of the various types of malocclusion. T h e etiology of the a n o m a l y will be discussed briefly, with special attention to two of the m o r e c o m m o n e n v i r o n m e n t a l factors.

Possible Etiologic Factors T h e immense i m p r o v e m e n t in materials a n d techniques employed t o d a y by the o r t h o d o n t i s t has not been paralleled by increase in his knowledge of the causative factors of malocclusion. A l t h o u g h a great n u m b e r of studies have been u n d e r t a k e n a i m e d at clarifying the etiology of malocclusion, m a n y answers concerning its causes are still being s o u g h t . T h e likelihood t h a t most types of malocclusion are not caused by any one single factor but r a t h e r a complex c o m b i n a t i o n of various factors is p r o b a b l y the m a i n s t u m b l i n g block in the search for the answers. M o s t authorities on the subject agree t h a t the possible etiologic factors of malocclusion can be placed in two groups: genetic a n d e n v i r o n m e n t a l . This c o n v e n t i o n a l division of the etiologic factors does n o t signify that all types of malocclusion are caused exclusively by factors of o n e g r o u p or the o t h e r . M a n y of the a n o m a l i e s are m o s t likely caused by or associated with a c o m b i n a t i o n of inherited tendencies a n d o n e or m o r e e n v i r o n m e n t a l factors. A l t h o u g h genetic factors as etiologic agents in malocclusion are steadily gaining recognition, there are a n u m b e r of u n a n s w e r e d questions regarding the inheritance of such factors or their m o d e of transmission f r o m one generation to a n o t h e r . T h e o b v i o u s limitations of m a n as a genetic experimental subject m a k e the solution to these p r o b l e m s extremely difficult. F u r t h e r m o r e , it must be r e m e m b e r e d t h a t a l t h o u g h an a p p a r e n t cause-and-effect m e c h a n i s m h a s been implied in a n u m b e r of o r t h o d o n t i c publications, this mechanism m a y be only an association relationship. T h e following is a typical list of possible etiologic agents that a p p e a r s in a t e x t b o o k of o r t h o d o n t i c s edited by L u n d s t r o m : 3 0

7 4 | EPIDEMIOLOGY OF ORAL HEALTH a) Diseases or deficiency conditions afflicting the mother pregnancy, b) Birth injuries, c) Bottle f e e d i n g — b r e a s t f e e d i n g , d) Composition of diet, e) Consistency of diet, f) Thumb-sucking and other habits, g) Diseases of the ear, nose and throat; m o u t h breathing, h) Premature loss of deciduous teeth, i) Loss of p e r m a n e n t teeth, j ) T r a u m a , burns, etc.

during

Oral habits and premature loss of tooth structure are the two environmental factors that have received most attention; they will be considered later in more detail.

M e t h o d s of A s s e s s m e n t

A review of the literature exposes considerable disagreement among the published findings concerning the prevalence of malocclusion. Although a number of factors, such as difference in age, size, and racial background of the population studied, may account for some of these disagreements, the main lack of comparability appears to be caused by a variance in the criteria for assessing normal and abnormal occlusion. As some of the prevalence studies of malocclusion reviewed for this chapter utilized different methods for assessment of the problem, it is believed that a summary of some of these indexes would be helpful. A number of studies based their assessment of malocclusion on the classification suggested by Angle, 4 which in turn is based on the mesio-distal relation of the maxillary and mandibular first permanent molars. Angle listed three main classes of malocclusion: Class I (neutroclusion). Malocclusion in which there is a n o r m a l mesiodistal relationship of the mandible to the maxilla. There is, however, malocclusion of the individual teeth. Class II (distoclusion): Malocclusion in which there is a distal relationship of the mandible to the maxilla. Class II-Division 1: A Class II occlusion in which the maxillary incisor teeth are labially inclined. Class II-Division 2: A Class II occlusion in which the maxillary

MALOCCLUSION | 75 incisor teeth are near normal anteroposterior^ or slightly lingually inclined. Class III (mesioclusion): Malocclusion in which there is a mesial relationship of the mandible to the maxilla.

The unilateral deviations of Classes II and III were termed subdivisions by Angle. The Angle classification has withstood the test of time as a workable classification of malocclusion for the practicing orthodontist. But its subjectivity and the inability of others to convert the classification to numerical values for statistical manipulation have led to a search for a classification system having more objectivity, and one which is readily reproducable by investigators interested in applying epidemiologic techniques to the malocclusion problem. In a general way, and certainly not intended to be used in such a fashion, Angle's classification also may be used to categorize the severity of malocclusion as well as the difficulty of treatment. The range from Class I (the simplest of abnormalities, denoting only one or two malaligned teeth) to Class III (indicating complex abnormalities, some of which require surgical intervention for desirable results) also displays from the lowest to the highest the complexity of treatment procedures required. Moore 35 developed a classification of malocclusion to yield information directly related to treatment needs and the complexity of treatment, that is, the time required for correction. Such a classification would be most useful in planning and operating a program of dental service but proves too cumbersome for epidemiologic use. In 1951 Massler and Frankel 32 suggested an index based on the number of maloccluded teeth; that is, the individual tooth was used as "the unit of occlusion rather than a segment of the arch." This type of quantitative index approaches the now generally accepted DMF index utilized in most epidemiologic studies of the prevalence of caries. Pelton and Elsasser 40 studied dentofacial morphology and designed an anthropometric instrument, named the Facial Orthometer, for use in population studies. In order to analyze the measurements obtained by the Orthometer, they established a standard index, the Dentofacial Index (DFI). As described by Elsasser, 16 this index "is a measure of dentofacial morphology based upon the degree of departure of midline facial points from a vertical plane perpendicular to Frankfort horizontal and dropped

76 | EPIDEMIOLOGY OF ORAL HEALTH

through a point 20 mm. anterior to nasion." The index also included the proportion of upper facial height to total face height and the presence or absence of crossbite and crowded dental arches. Even though the index failed to distinguish between normal and Class I cases, the attempt to develop a standardized measuring device, such as the Facial Orthometer, contributed to decreasing the subjectivity which exists in most population studies of malocclusion. In an effort to improve Pelton and Elsasser's method of assessing malocclusion, Van Kirk and Pennell 49 proposed a simplified index using a small plastic measuring device as an instrument to obtain the individual scores. This index is based on the measurements of rotated and malaligned teeth. Each tooth is given a score of 0, 1, or 2, depending on the amount it deviates from the ideal arch line. The scores are summed for the anterior and the right and left posterior segments of each arch. The final malalignment index is arrived at by totalling the six segment scores. In an effort to arrive at a practical method of assigning priorities for orthodontic treatment in a publicly supported program, Draker 15 developed an index, "The Handicapping Labio-Lingual Deviations." This index includes nine basic observations: cleft palate, traumatic deviations, overjet, overbite, mandibular protrusion, open bite, ectopic eruption, anterior crowding, and labiolingual spread. Each factor was given a numerical score, and a total score of 13 or over was considered to represent a handicap and made the individual eligible for treatment under New York State's Dental Rehabilitation Program. In 1957 an index of occlusion, the Occlusion Feature Index (OFI), was developed by Poulton and Aaronson. 42 The OFI is based on the evaluation of the following features: (1) lower anterior arch crowding, (2) cuspal indigitation looking at the right premolar-tomolar area from the buccal aspect, (3) vertical overbite, measured by that portion of the lower incisors covered by upper central incisors in occlusion, and (4) horizontal overjet, measured in occlusion from labial surface of upper incisors to labial surface of lower incisors. A value is assigned to each of these features according to an established yardstick and a total score is obtained by adding them together. According to Poulton and Aaronson, a preliminary test has shown the Occlusion Feature Index to be a workable method of recording malocclusion in population studies. Close

MALOCCLUSION | 77 agreement was observed between the index values o b t a i n e d by t w o dentists w o r k i n g separately on the s a m e p o p u l a t i o n sample. C l o s e correlation also was observed between the OFI scores a n d a s e p a r a t e " n e e d for o r t h o d o n t i c t r e a t m e n t " rating. These results a p p e a r to w a r r a n t f u r t h e r study a n d testing of this index. In an effort to test the applicability of statistical tests to epidemiologic studies of malocclusion, Mills 34 f o u n d t h a t certain a n a t o m i c a l variables distribute n o r m a l l y , a n d the usual statistical procedures, based on the m e a s u r e m e n t s of those variables, p r o v e d efficient a n d practical. Mills considers the following variables: arch b r e a d t h , arch length, c r o w n diameters of a n t e r i o r teeth, a n d palatal height index. These findings m a y lead to the creation of a v a l u a b l e epidemiological tool for malocclusion studies in p o p u l a tion samples. T h e failure of the foregoing malocclusion indexes to satisfactorily meet epidemiologic needs should not deter the search f o r an a c c u r a t e a n d objective m e t h o d of assessing the prevalence of malocclusion. Such an index, if accepted a n d used by the m a j o r i t y of w o r k e r s concerned, would help solve o n e of the m a j o r p r o b l e m s preventing an organized attack on the p r o b l e m . T h e view of most researchers was aptly expressed by Salzmann: 4 6 American orthodontists should take steps to establish a classification of malocclusion that would be adequate for clinical, semantic, and public health purposes, without entailing subjective value judgments. There is a basic need for a system of classification of malocclusion that could be universally employed by those practicing the specialty throughout the world.

Utilizing an index of this type in c o n j u n c t i o n with a DMF assessm e n t a n d an index for p e r i o d o n t a l disease w o u l d u n d o u b t e d l y a d d to the overall picture of the oral health status of p o p u l a t i o n samples.

Prevalence A s suggested previously, the lack of an objective index for malocclusion a n d the lack of c o m p a r a b i l i t y a m o n g r e p o r t s on the prevalence of this a n o m a l y m a k e any a t t e m p t at establishing an overall picture of the prevalence of malocclusion a h a z a r d o u s u n d e r t a k i n g . Nonetheless, it has been estimated t h a t a b o u t half

78 | EPIDEMIOLOGY OF ORAL HEALTH the school-age population in the United States needs some kind of treatment, and that one in five children suffers from malocclusion that could be considered severe. 47 A number of clinical surveys have been undertaken to quantify the prevalence of malocclusion in various age groups, and the reports include not only the overall prevalence of malocclusion but also the prevalence of the various types of the anomaly. The majority of the examiners relied on Angle's classification when the prevalence of the different types of malocclusion were considered. In a number of these studies the age grouping of the population samples was based on the conventional division of the development of the dentition into three distinct stages, each occurring during a certain age period. These three developmental stages are: (1) the deciduous dentition, (2) the mixed or transitional dentition, and (3) the permanent dentition. The eruption of the deciduous teeth starts at the age of about six months and continues for some two years. At the age of two to three years all 20 deciduous teeth have erupted and the child has entered the deciduous dentition stage. This stage lasts until the age of 6 to 7, or when the first permanent molars erupt. The mixed dentition stage is that during which both deciduous and permanent teeth are present in the mouth. This stage spans the period between 6 to 7 and 12 to 13 years of age, or until all deciduous teeth have been exfoliated and the permanent dentition stage has started. The findings of selected clinical surveys pertaining to the prevalence of malocclusion are summarized in Tables 4.1 and 4.2. Even though considerable variation exists it is unlikely, although possible, that all the differences in the prevalence of malocclusion are real. Some variation, no doubt, is due to examiner differences, both in methodology and in the application of Angle's classification. Nonetheless, Table 4.1 lists the findings of seven surveys of the prevalence of malocclusion in the deciduous dentition. F o u r of these surveys were done in the United States, and the other three originated in Germany, England, and C a n a d a . The four United States reports vary greatly in their total prevalence of malocclusion: the lowest reported is 17 percent 9 and the highest is 60 percent. 6 These two studies, however, may not be fully representative of the age group studied. The low prevalence report was based on the findings of orthodontists " a n d individuals familiar with the service" who took part in a survey of oral condi-

MALOCCLUSION | 79

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