Current studies suggest that periodontal disease is an important risk factor for heart disease. Other known risk factors include age, smoking, diabetes, hypetension and hypercholestemia.

Chronic, gram negative anaerobic infections may represent a previously unrecognized risk factor for atherosclerosis and thromboembolic events. An underlying inflammatory response trait may place an individual at high risk for both periodontal disease and atherosclerosis. There is a biologic burden of bacterial endotoxins and inflammatory cytokines resulting from established periodontal infections. These may initiate and exacerbate atherosclerosis and thromboembolic events. Additionionally, a known periodontal pathogen, porphyromonas gingivalis has been isolated from arteriosclerotic plaques. A review of several studies indicates that patients with periodontitis have a 1.5 to 2.0 fold greater risk of a fatal cardiovascular disease event than patients without periodontitis.

Thromboembolic events such as myocardial infarction and stroke can occur following bacteremia. Periodontal disease has been shown to induce episodes of significant bacteremias. Streptococcus sanguis and Porphyromonas gingivalis have been demonstrated to cause platelets to aggregate upon contact with bacteria. The resultant bacterially induced platelet aggregates can form the emboli which are responsible for the acute MI or stroke.

Approximately 58 million Americans, or 1 in 5, suffer from cardiovascular disease. According to The American Heart Association, it is the leading cause of death in The United States. In light of this new information, the need to eliminate periodontal infection takes on a heightened role.