Effects of Oral Flora on Platelets: Possible Consequences in Cardiovascular Disease

Abstract

During episodes of dental bacteremia, viridans group streptococci encounter platelets. Among these microorganisms, certain _{Streptococcus sanguis} induce human and rabbit platelets to aggregate in vitro. In experimental rabbits, circulating streptococci induced platelets to aggregate, triggering the accumulation of platelets and fibrin into the heart valve vegetations of endocarditis. At necropsy, affected rabbit hearts showed ischemie areas. We therefore hypothesized that circulating _{S. sanguis} might cause coronary thrombosis and signs of myocardial infarction (MI). Signs of MI were monitored in rabbits after infusion with platelet-aggregating doses of 4 to 40 × 10₉ cells of _{S. sanguis} 133-79. Infusion resulted in dose-dependent changes in electrocardiograms, blood pressure, heart rate, and cardiac contractility. These changes were consistent with the occurrence of MI. Platelets isolated from hyperlipidemic rabbits showed an accelerated in vitro aggregation response to strain 133-79. Cultured from immunosuppressed children with septic shock and signs of disseminated intravascular coagulation, more than 60% of isolates of viridans streptococci induced platelet aggregation when tested in vitro. The data are consistent with a thrombogenic role for _{S. sanguis} in human disease, contributing to the development of the vegetative lesion in infective endocarditis and a thrombotic mechanism to explain the additional contributed risk of periodontitis to MI. J Periodontol 1996;67:1138-1142.

Keywords: Coronary thrombosis/etiology; Streptococcus sanguis; myocardial infarction/etiology; platelet aggregation.