SOME MICROBIOLOGICAL, HISTOPATHOLOGICAL AND IMMUNOHISTOCHEMICAL CHARACTERISTICS OF PROGRESSIVE PERIODONTAL-DISEASE

The aim of the present investigation was to study the local nature of human periodontal disease by assessing the microbiota and the composit ion of the tissue lesions at sites with progressive attachment loss in periodontitis susceptible subjects. 300 subjects with periodontal dis ease were monitored for 2 years without treatment. 8 subjects lost >2 mm of attachment at greater than or equal to 3 sites during both the f irst and the second 12 month interval. These 8 subjects (progressive d isease group; PD) were recalled for a microbiological and histopatholo gical examination. A group of age- and sex-matched subjects were ident ified who during the 2 years of monitoring exhibited gingivitis and de ep pockets, but no further attachment loss. This group of 11 subjects (non-progressive disease group; NPD) served as controls. From the 8 ac tive disease subjects, greater than or equal to 1 interproximal site w hich had displayed disease activity (progressive disease active; PDA) and greater than or equal to 1 contralateral site without disease prog ression (progressive disease inactive; PDI) were sampled. From the 11 control subjects, 1 site/subject was sampled (NPD). The total number o f viable micro-organisms (TVC) in the subgingival microbiota was estim ated and a series of bacterial species were identified and enumerated. The gingival tissue of the sampling site was excised and the soft tis sue prepared for morphometrical and immunohistochemical analyses. No d ifferences were observed in the subgingival microbiota of the sample s ites in the subjects who exhibited disease progression (PD) when compa red with the subjects with periodontally diseased but stable condition s (NPD). Furthermore, no marked difference could be noted between prog ressive (PDA) and non-progressive (PDI) sites in the PD group of subje cts. The results from the morphometric determinations revealed that th e lesions from the PD and NPD subjects on the average were of similar size, but the PD lesions were comprised of a larger relative volume of plasma cells, a higher % number of plasma cells and monocytes/macroph ages and a lower numerical density of lymphocytes than the correspondi ng sites in the NPD group. Both T cell markers (CD3 and CD4) and B cel l markers (CD22) examined were significantly elevated in the PDA compa red to the PDI lesions. The CD4/CD8 ratios calculated from assessments made in the PD and NPD tissue samples were 2.4 and 2, while the corre sponding ratios for PDA and PDI lesions were 3 and 2.1 (p<0.05) respec tively. The present data indicate that differences exist between disea se active and inactive subjects and sites and it is suggested that the human model described may be used to study disease progression using shorter time intervals between examinations and additional parameters.