Periodontal therapy alters systemic inflammatory mediator levels

Title: Periodontal therapy alters systemic inflammatory mediator levels

Objectives: We investigated prospectively the effect of periodontal therapy on levels of several systemic biomarkers potentially relevant to cardiovascular disease risk.

Methods: Patients (n=29) with advanced periodontal disease and non-contributory medical history were comprehensively treated with non-surgical and surgical periodontal therapy within a 6-week time period. Clinical parameters were obtained at enrollment and 4 weeks after completion of therapy. Blood samples were obtained at 4 time points: one week prior to therapy (T1), at start of therapy (T2), immediately after completion (T3) and 4 weeks after therapy (T4). Assessments of serum concentrations of 19 biomarkers were performed using multiplex assays and of IgG antibodies against 11 periodontal bacteria by checkerboard immunoblotting. At T2 and T4, dental plaque samples were obtained from 6-8 interproximal sites/person and analyzed with respect to 11 species using checkerboard DNA-DNA hybridizations.

Results: At T3, CRP was elevated while soluble E-selectin, PAI-1, MMP-9, myeloperoxidase (MPO), sVCAM and a composite inflammatory score including all analyzed mediators (SIS) were reduced (p<0.05). At T4, sE-selectin, sICAM, and serum amyloid P were reduced (p<0.05). Greater probing depth reductions were associated with an increase in adiponectin (p=0.05), MMP-9 (p=0.01) and MPO (p=0.003) at T4. There were no significant associations between changes in bacterial levels and serum mediator levels. Relatively low baseline values of a combined IgG antibody titer against A. actinomycetemcomitans, P. gingivalis, T. denticola, and T. forsythia predicted larger decreases in sE-selectin, sICAM and sVCAM at T3.

Conclusions: Periodontal therapy altered the levels of circulating inflammatory mediators, but the responses were complex, inconsistent across subjects, and more pronounced immediately after completion of therapy.

Supported by NIH DE015649 and Colgate-Palmolive, NJ, USA