Monocytes play crucial role in the initiation and progression of periodontal disease. Monocyte activity is, in part, characterized and mediated by the production of various cytokines. These molecules can be used as markers of periodontal disease activity and indicators of the outcome of treatment. OBJECTIVE: To measure cytokine (TNF-a, IL-1b, and MMP-1) secretion by peripheral blood monocytes from periodontal patients before and after periodontal treatment METHODS: 91 subjects diagnosed with chronic adult periodontitis were evaluated in this study. The patients were randomly assigned to one of 8 different treatment groups comprising scaling with all possible combinations of surgery, local antibiotics (ActisiteŽ) and systemic antibiotics (metronidazole + amoxicillin). Blood samples were collected at baseline, at the completion of scaling and root planing and surgery, and 2 years post-baseline. Monocytes were isolated by discontinuous Ficoll-Hypaque gradient centrifugation and cultured in RPMI 1640 supplemented with 5% human AB serum for 18 hours. Cytokines secreted into the culture medium after stimulation were measured by ELISA. RESULTS: Subjects with severe periodontitis exhibited significantly elevated cytokine responses at baseline. All 8 combinations of therapy caused a transient reduction in the monocyte response. However, treatment by surgery or scaling alone did not sustain the reduced response. In these subjects, monocyte-mediated cytokine production returned to high levels equivalent to baseline at the end of 2 years. Systemic and local antibiotic therapy in conjunction with surgical treatment resulted in a long-term (2 year) maintenance of the reduction in cytokine production (p<0.05). Furthermore, local antibiotic administration was significantly more effective (p<0.05) in sustaining the monocytic cytokine reduction in cytokine release compared to systemic antibiotics as an adjunct to mechanical therapy. CONCLUSION: These findings suggest that antibiotic support of mechanical periodontal therapy provides long-term inflammatory reduction that could better stabilize periodontal therapy. Supported by NIDCR grants DE11814 and DE12861.

Back to the Periodontal Research - Therapy Program
Back to the 81st General Session of the International Association for Dental Research (June 25-28, 2003)

Top Level Search