Treatment of periodontitis and endothelial function

Abstract

Conclusion: Acute short-term systemic inflammation and endothelial dysfunction results from intensive periodontal treatment. Six months after this treatment, there is improvement in endothelial function. Summary: Atherosclerosis is an inflammatory disease. Some believe periodontitis can be a source of chronic systemic inflammation underlying atherosclerosis. Periodontitis is associated with elevated C-reactive protein and other inflammatory biomarkers (Arch Intern Med 2003;163:1172-9). Endothelial dysfunction may serve as a common pathway through which inflammation mediates atherogenesis. The authors sought to evaluate the treatment of periodontitis on endothelial function. Of 120 patients with severe periodontitis, 59 were assigned randomly to community-based periodontal care and 61 to intensive periodontal treatment. Endothelial function was assessed by brachial artery flow–mediated dilatation. Markers of coagulation and endothelial activation and inflammatory biomarkers were evaluated before treatment and at 1, 7, 30, 60, and 180 days after treatment. Flow-mediated dilatation was significantly lower 24 hours after treatment in the intensive treatment group compared with the control treatment group (absolute difference, 1.4%; 95% confidence interval [CI], 0.5 to 2.3; P = .002). Higher levels of C-reactive protein, endothelial-activation markers, and inflammatory markers were found in the intensive treatment group at 24 hours (P < .05 for all comparisons). At 60 days after therapy, however, flow-mediated brachial artery dilatation was greater in the intensive treatment group. The plasma levels of soluble E-selectin were lower at 60 days in the intensive treatment group than in the control group (absolute difference in brachial artery flow-mediated dilatation 0.9%; 95% CI, 0.1 to 1.7; P = .02) and also at 180 days after therapy (difference 2.0%; 95% CI, 1.2 to 2.8; P < .001). Improvement in brachial artery dilatation and inflammatory markers was associated with improvement in measures of periodontal disease (r = 0.29 by Spearman rank correlation; P = .003). Comment: The severity of periodontitis present in the subjects of this study is likely present in no more than 0.5% to 1% of the adult United States population. Atherosclerosis is obviously considerably more common. It would be interesting to see if future studies can demonstrate improvement in endothelial function with periodontal treatment in patients with lesser degrees of periodontitis.