Department of Prosthetic Dentistry, Center for Dental and Oral Medicine, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany.
Int J Mol Sci. 2018 Jul 6;19(7):1978. doi: 10.3390/ijms19071978.
Oral infections occur frequently in humans and often lead to chronic inflammations affecting the teeth (i.e., caries), the gingival tissues surrounding the teeth (i.e., gingivitis and endodontic lesions), and the tooth-supporting structures (i.e., periodontitis). At least four basic pathogenic mechanisms have been proposed that involve oral inflammations in the pathogenesis of atherosclerosis: (1) low level bacteremia by which oral bacteria enter the blood stream and invade the arterial wall; (2) systemic inflammation induced by inflammatory mediators released from the sites of the oral inflammation into the blood stream; (3) autoimmunity to host proteins caused by the host immune response to specific components of oral pathogens; (4) pro-atherogenic effects resulting from specific bacterial toxins that are produced by oral pathogenic bacteria. In this narrative review, we summarize published experimental evidence related to these four mechanisms and discuss their impact on the pathogenesis of atherosclerosis.
口腔感染在人类中很常见，常导致慢性炎症，影响牙齿（如龋齿）、牙齿周围的牙龈组织（如牙龈炎和牙髓病变）以及牙齿支持组织（如牙周炎）。至少有四个基本的发病机制被提出，涉及口腔炎症在动脉粥样硬化发病机制中的作用：（1）低水平菌血症，即口腔细菌进入血液并侵入动脉壁；（2）炎症介质从口腔炎症部位释放到血液中引起的全身炎症；（3）宿主对口腔病原体特定成分的免疫反应引起的自身免疫；（4）特定细菌毒素产生的促动脉粥样硬化作用，这些毒素由口腔致病菌产生。在本综述中，我们总结了与这四个机制相关的已发表的实验证据，并讨论了它们对动脉粥样硬化发病机制的影响。
