3.8 Article

Oral infection, hyperglycemia, and endothelial dysfunction

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MOSBY-ELSEVIER
DOI: 10.1016/j.tripleo.2007.06.027

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  1. Intramural NIH HHS Funding Source: Medline
  2. NIDCR NIH HHS [R01 DE015566, P01 DE013191, R01 DE015566-01A1] Funding Source: Medline

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Metabolic syndrome and type 2 diabetes ( T2DM) resulting from sustained hyperglycemia are considered as risk factors for cardiovascular disease ( CVD) but the mechanism for their contribution to cardiopathogenesis is not well understood. Hyperglycemia induces nonenzymatic glycation of protein-yielding advanced glycation end products ( AGE), which are postulated to stimulate interleukin-6 ( IL-6) expression, triggering the liver to secrete tissue necrosis factor alpha ( TNF-alpha) and C-reactive protein ( CRP) that contribute to CVD pathogenesis. Although the high prevalence of periodontitis among individuals with diabetes is well known by dental researchers, it is relatively unrecognized in the medical community. The expression of the same proinflammatory mediators implicated in hyperglycemia ( i.e., IL-6, TNF-alpha, and CRP) have been reported to be associated with periodontal disease and increased risk for CVD. We will review published evidence related to these 2 pathways and offer a consensus.

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