Oral infection-inflammatory pathway, periodontitis, is a risk factor for endothelial dysfunction in patients with coronary artery disease.

OBJECTIVE Several studies have shown that periodontitis is a risk factor for cardiovascular diseases. There is an association between inflammation and endothelial dysfunction. The purpose of this study was to evaluate endothelial function in patients with coronary artery disease (CAD) who had periodontitis. METHODS AND RESULTS We evaluated forearm blood flow (FBF) responses to acetylcholine (ACh), an endothelium-dependent vasodilator, and to sodium nitroprusside (SNP), an endothelium-independent vasodilator, in 101 CAD patients with periodontitis (37 men and 11 women, 63+/-12 yr) and without periodontitis (36 men and 17 women, 62+/-13 yr). FBF was measured by using strain-gauge plethysmography. Circulating levels of C-reactive protein and interleukin-6 were significantly higher in the periodontitis group than in the non-periodontitis group. FBF response to ACh was significantly smaller in the periodontitis group than in the non-periodontitis group. SNP-stimulated vasodilation was similar in the two groups. Periodontal therapy reduced serum concentrations of C-reactive protein from 2.7+/-1.9 to 1.8+/-0.9mg/L (P<0.05) and interleukin-6 from 2.6+/-3.4 to 1.6+/-2.6ng/L (P<0.05) and augmented ACh-induced vasodilation from 14.7+/-5.2 to 20.1+/-6.1mL/(min100mL) tissue (P<0.05) in patients with periodontitis. The SNP-stimulated vasodilation was similar before and after treatment. After administration of N(G)-monomethyl-l-arginine, a nitric oxide synthase inhibitor, FBF response to ACh was similar before and after treatment. CONCLUSION These findings suggest that periodontitis is associated with endothelial dysfunction in patients with CAD through a decrease in nitric oxide bioavailability. Systemic inflammation may be, at least in part, a cause and predictor of progression of endothelial dysfunction.