Attachment level changes in destructive periodontal diseases

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Abstract
The present communication attempts to summarize some of the features of attachment loss which are of interest to the clinician and the statistician analyzing data from clinical trials. These include the measurements employed to detect changes in attachment level, the nature of the destructive disease process and the effects of therapy on the attachment level measurements. Although there are several difficulties associated with the attachment level measurement, at the present time it appears to be the best estimator of periodontal attachment available. The overall standard deviation of this measurement in >46,000 replicate measurements at periodontal sites in 58 subjects was 0.78 mm (range 0.4 to 1.2 mm). In the periodontally healthy subject, the length of the attachment measured around 28 teeth is approximately 700 mm. Therefore, there are approximately 1400 adjacent points along the periodontal attachment where a measurement could be made using a periodontal probe with a 0.5 mm diameter tip. If 6 measurements were recorded per tooth, then approximately 12% of the possible probeable points would be evaluated.Recent data indicate that destructive periodontal diseases progress with acute bursts of activity rather than as slowly progressive, continual processes. Such findings suggest new models of attachment loss progression. In one likely model, destructive periodontal diseases would progess by asynchronous bursts of activity at individual sites which occur with greater frequency during a finite period of time in an individual's life.3 major patterns of attachment loss could be distinguished when frequency distributions of attachment level measurements were constructed for 61 destructive periodontal disease subjects. Pattern I (30 subjects) exhibited a bimodal distribution with localized destruction occurring at 33% of sites affected) with a trimodal frequency distribution. Pattern III (17 subjects) exhibited a unimodal distribution in which virtually all sites were affected. The proportions ofFusobacterium nucleatum, Streptococcus intermediusandEikenella corrodensin subgingival plaque samples were significantly elevated in sites of subjects with patterns II and III (the widespread disease groups).Bacteroides intermedius, Streptococcus uberisandActinobacillus actinomycetemcomitanswere elevated in sampled sites of localized disease subjects (pattern I).The effects of therapy by Widman flap surgery and systemic tetracycline were examined by several statistical analyses. Mean changes in attachment level did not show major changes at individual sites. Frequency distributions were effective in indicating the number of sites with major losses or gains in attachment and were particularly informative when sites were segregated on the basis of initial pocket depth. Survival analysis was useful in demonstrating the effect of therapy on the future bursts of activity at individual sites.Our biological concepts of periodontal diseases are rapidly changing and design and analysis of data from clinical trials must take these changes into account. It is important to recognize that periodontal diseases are infections and that these infections have different etiologic agents. Further, the diseases are site specific. Different sites within an individual may be infected with different numbers and species of pathogens as well as different protective species. These microbial differences along with the local host response lead to differences in activity of disease at individual sites and account for differences in efficacy of a given therapy. Data analyses should be designed to provide the clinician with knowledge of the effect of the tested therapy at sites with differing clinical, microbiological and immunological features.