Periodontitis, endothelial dysfunction and atherosclerosis

During periodontitis, dental plaque microorganisms may disseminate through the blood to infect the vascular endothelium and contribute to the occurrence of atherosclerosis and risk of myocardial ischemia and infarction. Aggregation of platelets is induced by the platelet aggregation-associated protein (PAAP) expressed on plaque bacteria, including Streptococcus sanguis and Porphyromonas gingivalis. Findings from the Dental Atherosclerosis Risk in Communities study also indicate that periodontal disease is associated with carotid intima media wall thickness, a measure of subclinical atherosclerosis. Inflammation is increasingly recognized as a major component of atherosclerosis, especially in plaques associated with acute coronary syndromes, as often demonstrated at necropsy. Chronic infection is now recognized as one of the possible causes of chronic inflammation that could lead to atherogenesis and plaque instability. Periodontitis is an inflammatory reaction (to Gram-negative, anaerobic bacterial infections) of the surrounding tooth, including the periodontal ligament, cementum, and alveolar and supporting bone. The next step will be to determine whether periodontitis could be an inflammatory-infectious trigger to endothelial dysfunction and vascular inflammation (leading to atherosclerosis), and whether proper management would improve endothelial dysfunction and vascular inflammation and thus, prevent atherogenesis.