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Pathogenesis of Gingivitis and Periodontal Disease in Children and Young Adults Dr PEDIATRIC DENTISTRY/Copyright ° 1981 by The American Academy of Pedodontics Vol. 3, Special Issue Pathogenesis of gingivitis and periodontal disease in children and young adults Dr. Ranney Richard R. Ranney, DOS, MS Bernard F. Debski, DMD, MS John G. Tew, PhD Abstract Introduction In adults and animal models, gingivitis consistently The most common forms of human periodontal dis- develops when bacterial plaque accumulates, and progresses ease are gingivitis and periodontitis. Gingivitis is sequentially through neutrophil, T-lymphocyte and B- defined as an inflammation of the gingiva. The gingiva lymphocyte/plasma cell dominated stages in a reproducible is all soft tissue surrounding the tooth coronal to the time frame. Periodontitis, also plasma cell dominated, crest of alveolar bone and to a varying extent lateral develops at a later time on the same regime, but with time- variability and less than 100% consistency. Gingivitis rarely to the bone, extending to the mucogingival junction. progresses to periodontitis in pre-pubertal children and On the other hand, the definition of periodontium in- seems to remain lymphocyte- rather than plasma cell- cludes cementum, periodontal ligament, alveolar bone, dominated. Bacteria are the accepted etiologic agents, with and the gingiva; and periodontitis includes loss of some particular species being associated with specific attachment of periodontal tissues from the tooth and clinical features; however, definitive correlations have not net loss of alveolar bone height.1 Gingivitis is reversi- been shown and a number of different species may be of ble, while regeneration after the destruction during etiologic significance in given cases. The signs of disease are periodontitis is not predictably achievable. Periodon- more easily explained on the basis of activities of host titis in healthy children is not an extremely frequent response rather than solely to effects of bacterial enzymes or occurrence. The most frequent periodontal disease in cytotoxins. Immunological responses have been implicated children, by far, is gingivitis. in this regard. Polyclonal, as well as antigen-specific, stimulation may be important. In studies of severe Until quite recently, there was no information dis- periodontal destruction in adolescents and young adults, tinguishing gingivitis in children from gingivitis in dysfunctional PMN-chemotaxis has been associated with adults, either clinically or histopathologically. It was many cases, and B-cell hyperresponsiveness to polyclonal perceived as a lesion confined to the marginal gingiva activation (which may be attributed to a T-cell regulatory that might slow progress with age, although virtually defect), with some cases. Three working hypotheses are no detailed study of the "juvenile marginal lesion" suggested: 1) periodontal disease presents as a well had been done.2 Consequently, hypotheses of patho- contained and regulated inflammation in children until genesis have arisen almost exclusively from study of around puberty, after which the usual, relative slow- adult humans and animals. Therefore, concepts of progression of a B-cell mediated adult lesion is the rule; pathogenesis related to these studies will be reviewed 2) exceptions to the self-containment in pre-puberty would be found in systemic disease states; and 3) exceptions briefly while considering emerging information related beginning in young adulthood (rapid progression) would be to children and young adults. Hypotheses of patho- found additionally in rather subtle functional aberrations of genesis in children and young adults will be devel- host defense. oped; however, definitive proof of disease mechan- ism^) is lacking. Acknowledgments Clinical Studies of Disease Progression Work at Virginia Commonwealth University, referred to The foundation for current concepts of pathogen- in this review has been supported by grants DE-05139, DE esis of gingivitis lies in the now classic experimental 05054 and DE 04397 from the National Institute for Dental 34 Research. gingivitis studies of Loe and coworkers. The central observations that cessation of oral hygiene results in PEDIATRIC DENTISTRY 89 Volume 3, Special Issue gingivitis, and that resumption of oral hygiene reverts in contrast to rapid development in the young adults gingivitis to health, are critical indictments of the was documented by the relatively objective measures causative relationship of dental plaque to gingivitis. of gingival exudate and bleeding units. In a cross- These observations have been confirmed repeatedly. sectional investigation, young children exhibited a The production of gingivitis in this model is universal higher proportion of non-inflamed gingival units and among adult subjects, the only significant variable less gingival= fluid than did adolescents. being the time necessary to reach a predetermined Thus, there is definite suggestion at the clinical endpoint of gingivitis severity for each individual sub- level for differences in pathogenesis between pre- ject. This significant relationship of plaque bacteria to pubertal children and older individuals. Differences in gingivitis has been buttressed further by demonstra- histopathology also exist, and will be discussed later in tions that prevention of plaque formation5 or repeti- this review. If we accept dental plaque bacteria as the tive removal6 also prevents gingivitis. Since the latter causative agents, variances in rates of progression and study involved children, the causative relationship of exceptions to progression could be explained either by plaque to gingivitis is affirmed for children as well differences in bacteria present or by differences in host as adults. responsiveness~ to the bacteria. Although the perceived irreversibility prevents ethical extension of this model to periodontitis in Bacteriology 7,8 humans, analogous efforts in animals indicate that In contrast to earlier concepts, there is good continuance of the model for longer times results in evidence that all dental bacterial plaques are not the periodontitis. This tends to reinforce the earlier pre- same. There are qualitative differences between sumptions based on epidemiological surveys which plaques adjacent to healthy sites and those adjacent showed the amount of debris on the teeth to be the to diseased sites, and between supragingival and only significant correlate, other than age, of the sever- subgingival floras; 6 Healthy sites are associated with a ity of periodontal disease.*" More recent longitudinal predominantly gram-positive flora, with major repre- observations in human populations indicate much sentation of Streptococcus and Actinom~vces species.~~ greater severity and rate of progression of periodon- The flora adjacent to diseased sites has a higher repre- titis in human populations with poor oral hygiene, sentation of gram-negative rods and motile forms in- than in populations of the same age with good oral hy- cluding spirochetes, with Fusobactedum nucleatum giene; 2 Clinical studies relating mechanical control of and Bacteroides species being among the most promi- bacteria to successful periodontal therapy and preven- nent representatives; ~-~ There are also suggestions of tion of recurrence~*’5 also support the concept of etiolo- rather specific associations between certain microor- gic significance for oral bacteria in periodontitis as ganisms and specific periodontal conditions; e.g., a rel- well as gingivitis. It is generally conceded that bac- ative dominance of Bacteroides assacharolyticus (pre- teria’*~8 are the etiologic agents. sumably now recognized as B. gingiyalis) in highly inflamed destructive sites, ~ B. melaninogenicus ss. in- There are very important differences, however, termedius and Eikenella corrodens in destructive sites between the results of experimental gingivitis studies with minimal inflammation, ~ and Capnocytophaga and efforts at natural induction of periodontitis. species, Actinobacillus actinomycetemcomitans and Whereas the former are uniformly effective in induc- other unidentified saccharolytic gram-negative rods in ing gingivitis amongadult individuals, only 8070 of the areas of severe destruction in young people. ~ - dogs9 studied for four years developed periodontitis; Recent reviews~-~ have favored this concept of bac- There are other confirmations that gingivitis does not terial specificity in periodontal diseases. However,as invariably progress to periodontitis, and that it can concluded by others, ~ correlation of specific groups of persist for considerable time in some instances with- organisms with certain clinical syndromes is not de- out~ such progression in adults. finitively established. Results of research in this In children, progression to periodontitis is the ex- emerging area of knowledge are highly method-de- ception rather than the rule; There are also notable pendent. Ongoing work in our clinics and laboratories contrasts with respect to clinical development of gin- in association with W. E. C. Moore and L. V. givitis between children and adults documented in Holdeman attempts complete enumeration of the per- recent years. Mackler and Crawford~’ reported that six iodontal flora. ~,~ Results have been in general agree- of eight children 3-5½ years of age failed to develop ment with the previous findings of different flora in gingivitis during 26 days of an experimental gingivitis healthy and diseased states, and gram-negative organ- protocol. Another study of six children, 4-5 years old, isms being more numerous
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