Common Pathways of Immune Response and Inflammatory State

The role of inflammation in the pathogenesis of atherosclerosis is highlighted by the associations between systemic pro-inflammatory biomarkers and measurements of CVD and its outcomes.80 While atherosclerosis contributes to the elevation of systemic inflammatory biomarkers, population studies have found that smoking, age, and adiposity are more highly associated with pro-inflammatory mediators than atherosclerotic plaque thickness.41 Adiposity, in particular, has been shown to be associated with up to 30% of the systemic inflammation in large-scale population studies.41,67 Many of these pro-inflammatory risk factors are associated with increased risk of both periodontal disease and CVD.3-7,41 The action of these risk factors on CVD demonstrates that inflammation from a distant site, such as the periodontium, can increase systemic levels to a point that conveys increased cardiovascular risk.

Periodontal disease involves an inflammatory-mediated resorption of the supporting tissues around the teeth, it is also associated with an increase in systemic levels of inflammation. A meta-analysis of the effect of periodontal disease on CRP, a potent marker of inflammation, concluded that “there is strong evidence…that plasma CRP in periodontitis is elevated compared with controls.”81 The mean CRP levels reported in the studies reviewed were 3.41 mg 1-1 for subjects with periodontal disease and 1.72 mg 1-1 for periodontally healthy subjects.81 Since elevated risk for atherosclerosis has been associated with CRP levels ≥ 3 mg 1-1, these data may indicate a rationale for the association seen between these two diseases.

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