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Return to Home Page Return to Recent Articles Page Gingivitis in the Genesis of Heart Attack and Other Arteriosclerotic Diseases "Dentistry Today", November 2001 by: William H. Wehracher, MD, FACP. FACC

    New evidence of microbial aggravation and its mechanisms in coronary disease and other atherosclerotic disorders appeared during the 50th annual session of the American College of Cardiology in Orlando, Florida (2001). This worsening of underlying atherosclerosis and its mechanisms, in the perspective of classical concepts, deserves attention among today's practicing dentists and physicians. Few patients recognize how much infection and inflammation are present in their mouths. Their risk should be identified for them by a dentist.

    As part of an entire session devoted to "Infection, Inflammation and Atherosclerosis," on March 20th, Salomon Amar and coworkers from the Boston University Medical Center demonstrated that Porphyromonas gingivalis would accelerate atherogenic plaque progression in the aorta of a particularly susceptible mouse model, and concluded that dental infections affecting tooth supporting tissues (periodontal disease) could serve as the portal of entry for such acceleration. Knockout Mice were selected for their study, and have become a worthwhile model for other studies of atherogenesis. Challenge by p gingivalis produced two-fold greater area and extent of the atherosclerotic lesions than was present in the unchallenged controls.

    Louis F. Rose, DDS, MD, University of Pennsylvania, Hahnemann, and New York Univeristy said "There is sufficient evidence to conclude that oral lesions, especially advanced periodontopathies, place certain patients at risk for cardiovascular disease and stroke."

    Atherosclerosis is the leading cause of death in the world today. Today one recognizes the fatty streak as the incipient lesions, developing into a complex inflammatory- fibroproliferative response to plasma-derived lipoproteins invading and retained within the arterial intima, smooth muscle proliferation, and immune activation. Plaques of these materials exist, where monocytes adhere to the endothelial surface and migrate into it, here there is foam-cell formation, lipid-core formation, smooth muscle proliferation, and cap formation that also includes T -lumphocytes and response to immune mechanisms. Plaques become disrupted with the breaking of the fibrous cap, and attract platelets, leading to thrombosis and vascular occlusion, partial (as in unstable angina) or complete (myocardial infarction).