Herzberg M C, Meyer M W
Department of Preventive Sciences, School of Dentistry, University of Minnesota, Minneapolis, USA.
J Periodontol. 1996 Oct;67(10 Suppl):1138-42. doi: 10.1902/jop.1996.67.10s.1138.
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 ischemic 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 x 10(9) 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.
在牙源性菌血症发作期间，草绿色链球菌会接触血小板。在这些微生物中，某些血链球菌可在体外诱导人和兔血小板聚集。在实验兔中，循环中的链球菌会诱导血小板聚集，促使血小板和纤维蛋白在感染性心内膜炎的心脏瓣膜赘生物中蓄积。尸检时，受影响的兔心脏显示出缺血区域。因此，我们推测循环中的血链球菌可能会导致冠状动脉血栓形成和心肌梗死（MI）的体征。在给兔输注4至40×10⁹个血链球菌133 - 79细胞的血小板聚集剂量后，监测其MI体征。输注导致心电图、血压、心率和心脏收缩力出现剂量依赖性变化。这些变化与MI的发生一致。从高脂血症兔分离出的血小板对133 - 79菌株表现出体外聚集反应加速。从患有感染性休克和弥散性血管内凝血体征的免疫抑制儿童中培养出的草绿色链球菌分离株，超过60%在体外测试时可诱导血小板聚集。这些数据与血链球菌在人类疾病中的促血栓形成作用一致，有助于感染性心内膜炎中赘生物病变的发展，并为牙周炎导致MI额外风险提供一种血栓形成机制的解释。
