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 composition of the tissue lesions at sites with progressive attachment loss in periodontitis susceptible subjects. 300 subjects with periodontal disease 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 first and the second 12 month interval. These 8 subjects (progressive disease group; PD) were recalled for a microbiological and histopathological examination. A group of age- and sex-matched subjects were identified who during the 2 years of monitoring exhibited gingivitis and deep pockets, but no further attachment loss. This group of 11 subjects (non-progressive disease group; NPD) served as controls. From the 8 active disease subjects, greater than or equal to 1 interproximal site which had displayed disease activity (progressive disease active; PDA) and greater than or equal to 1 contralateral site without disease progression (progressive disease inactive; PDI) were sampled. From the 11 control subjects, 1 site/subject was sampled (NPD). The total number of viable micro-organisms (TVC) in the subgingival microbiota was estimated and a series of bacterial species were identified and enumerated. The gingival tissue of the sampling site was excised and the soft tissue prepared for morphometrical and immunohistochemical analyses. No differences were observed in the subgingival microbiota of the sample sites in the subjects who exhibited disease progression (PD) when compared with the subjects with periodontally diseased but stable conditions (NPD). Furthermore, no marked difference could be noted between progressive (PDA) and non-progressive (PDI) sites in the PD group of subjects. The results from the morphometric determinations revealed that the 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/macrophages and a lower numerical density of lymphocytes than the corresponding sites in the NPD group. Both T cell markers (CD3 and CD4) and B cell markers (CD22) examined were significantly elevated in the PDA compared 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 corresponding ratios for PDA and PDI lesions were 3 and 2.1 (p<0.05) respectively. The present data indicate that differences exist between disease 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.