Systemic manifestations of periodontitis in the non-human primate

This report describes our Endings regarding the potential contribution of p eriodontitis to atherosclerotic processes using a nonhuman primate model. T he goal of the investigations was to target general mechanisms which could describe the association of these disease processes, including: (i) systemi c translocation of bacteria/products during periodontitis; (ii) alterations in systemic inflammatory biomarkers during periodontitis; and (iii) the re lationship of periodontitis to serum lipids/lipoproteins. Increases in seru m endotoxin (e.g. LPS) during ligature-induced periodontitis were observed in these animals. We determined serum levels of various acute phase reactan ts and chemokines (e.g. CRP, alpha(1)-antitrypsin, haptoglobin, fibrinogen, IL-8). A number of these host factors were significantly increased during gingivitis and:or periodontitis. Finally, we observed specific changes in s erum lipid levels (cholesterol, triglycerides, HDL, LDL) and lipoproteins ( apoA-I) juring periodontitis. which were exacerbated by exposure of the ani mals to a diet with elevated fat content. Thus. we have described systemic manifestations of periodontitis that include detection of bacterial product s, inflammatory biomarkers, and dyslipoproteinemia consistent with an incre ased atherogenic risk.