Endothelial dysfunction is one component of the pathogenesis of arterial disease, occurring in response to risk factors that predict cardiovascular events. Recent studies have demonstrated that the presence of periodontal bacteria has been associated with increased thickness of the carotid intima media. Other studies have suggested a link may exist between the effects of periodontal disease and cardiovascular disease. The actual mechanism by which periodontitis affects endothelial function is not known. The periodontal pathogens or their products could affect endothelial function directly, or act as a trigger for a systemic inflammatory response that may have deleterious effects on the vascular wall, leading to platelet aggregation, foam-cell formation, and the development of atheromas, fatty deposits in the innermost lining of an artery which can affect blood flow.

This study confirms previous findings demonstrating that periodontitis increases the risk for systemic inflammation, supported by high CRP levels in subjects with severe periodontitis, and consequently the risk for endothelial dysfunction. Since endothelial dysfunction occurs early in the pathogenesis of arterial disease, and the clinical phase of atherosclerosis is associated with an adverse prognosis, improving endothelial function is important for both the prevention of arterial disease and for an improved prognosis in people with atherosclerosis. The clinical implications of this study, therefore, are that intensive non-surgical therapy of severe periodontitis may be an important risk reduction strategy for patients at risk for cardiovascular disease, and may improve the prognosis for those with existing atherosclerosis.