Selected gingival bacteria and cytokine profiles associated with patients who did not respond to conventional periodontal therapy (refractory) were evaluated. 10 subjects with a high incidence of post-active treatment clinical attachment loss (> 2% sites/year lost > or = 3 mm) were compared to 10 age-, race-, and supragingival plaque-matched patients with low post-treatment clinical attachment loss (< 0.5% sites/year) relative to the following parameters at 2 sites/patient with the deepest probing depths: (1) presence of 3 selected periodontal pathogens (Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Eikenella corrodens) in subgingival plaque as determined by selective culturing, and (2) gingival crevicular fluid (GCF) levels of 3 cytokines associated with bone resorption (IL-1 alpha, IL-1 beta, IL-6) as determined by two-site ELISA. Results indicated no significant differences in any clinical measurement (except incidence of clinical attachment loss), in the presence of any bacterial pathogen, or in GCF cytokine levels between refractory subject sites versus stable subject sites. However, when sites producing the greatest total GCF cytokine/patient were compared, sites from refractory patient produced significantly more IL-6 (30.1 +/- 4.0 versus 15.4 +/- 2.8 nM, p < 0.01). The subgingival presence of each of the 3 bacterial pathogens was associated with elevated GCF IL-1 concentrations. These data suggest that gingival IL-1 and IL-6 production is different in response to local and systemic factors associated with periodontitis, and that IL-6 may play a role in the identification and mechanisms of refractory periodontitis.
The purpose of this study was to evaluate lymphocyte subset densities and distributions within gingival biopsies from active sites (>2 mm clinical attachment loss within three months of biopsy) versus clinically similar but stable or healthy sites. Small interproximal gingival biopsies representing at least one of each of the above categories were obtained from each of 20 periodontal maintenance patients. Serial cryostat sections displaying a cross section of the gingiva were labeled with monoclonal antibodies for (1) pan T cells, (2) T cytotoxic/suppressor cells, (3) T helper/inducer cells and (4) pan B cells and were developed using an avidin‐biotin‐peroxidase system. Lymphocyte populations were enumerated in repeatable fields from the sulcular, middle and oral one‐third of each section. Relative proportions of the same lymphocyte subsets were analyzed in peripheral blood samples from the same patients using direct immunofluorescence.
Pan B cells were significantly more prevalent in infiltrates from active sites than in stable (P < 0.05) or healthy (P < 0.01) sites. The T/B cell ratio was also significantly lower in active than stable biopsies (P < 0.05), and in active biopsies versus blood (P < 0.05). The T helper/T suppressor cell ratio did not vary significantly between blood and any gingival tissue disease group or location, but a trend toward lower relative numbers of T helper cells in the sulcular infiltrates of active sites was noted. These results support the premise that active periodontal sites display elevated B cell populations and abnormal immune regulation possibly involving the T helper cell subset.
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