This report describes our findings regarding the potential contribution of periodontitis to atherosclerotic processes using a nonhuman primate model. The goal of the investigations was to target general mechanisms which could describe the association of these disease processes, including: (i) systemic translocation of bacteria/products during periodontitis; (ii) alterations in systemic inflammatory biomarkers during periodontitis; and (iii) the relationship of periodontitis to serum lipids /lipoproteins. Increases in serum endotoxin (e.g. LPS) during ligature‐induced periodontitis were observed in these animals. We determined serum levels of various acute phase reactants and chemokines (e.g. CRP. α1‐antitrypsin, haptogiobin, fibrinogen, IL‐8). A number of these host factors were significantly increased during gingivitis and/or periodontitis. Finally, we observed specific changes in serum lipid levels (cholesterol, triglycerides, HDL, LDL) and lipoproteins (apoA‐I) during periodontitis, which were exacerbated by exposure of the animals to a diet with elevated fat content. Thus, we have described systemic manifestations of periodontitis that include detection of bacterial products, inflammatory biomarkers, and dyslipoproteinemia consistent with an increased atherogenic risk.
Journal of Periodontal Research – Wiley
Published: Jan 1, 1999
Keywords: ; ; ; ;
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