Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases.
Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases.
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DOI：
10.1111/jcpe.12060
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发表时间：
2013-04
影响因子：
6.7
通讯作者：
Loos BG
中科院分区：
文献类型：
--
作者：
Schenkein HA;Loos BG
本文就牙周病与心血管疾病的炎症机制进行综述。本文是一篇文献综述。文献中的研究暗示了许多可能的机制，这些机制可能是牙周感染导致动脉粥样硬化病变中炎症反应增加的原因。这些包括在远离口腔的部位处由细菌及其产物刺激的炎性介质的全身水平增加，促进血栓前状态和炎症的血栓形成和止血标志物升高，促进炎症并与动脉粥样化相互作用的交叉反应性全身抗体，促进血脂异常并随之增加促炎脂质类和亚类，以及两种疾病中存在的共同遗传易感性因子，导致炎症反应增加。这些机制可能被认为是协同作用，以增加牙周病的全身炎症，并促进或加剧动脉粥样硬化。然而，缺乏证据表明牙周炎引起的全身炎症增加会影响动脉粥样硬化发展、血栓形成事件或心肌梗死或中风期间的炎症反应。
In this paper, inflammatory mechanisms that link periodontal diseases to cardiovascular diseases (CVD) are reviewed. This paper is a literature review. Studies in the literature implicate a number of possible mechanisms that could be responsible for increased inflammatory responses in atheromatous lesions due to periodontal infections. These include increased systemic levels of inflammatory mediators stimulated by bacteria and their products at sites distant from the oral cavity, elevated thrombotic and hemostatic markers that promote a prothrombotic state and inflammation, cross-reactive systemic antibodies that promote inflammation and interact with the atheroma, promotion of dyslipidemia with consequent increases in proinflammatory lipid classes and subclasses, and common genetic susceptibility factors present in both disease leading to increased inflammatory responses. Such mechanisms may be thought to act in concert to increase systemic inflammation in periodontal disease and to promote or exacerbate atherogenesis. However, proof that the increase in systemic inflammation attributable to periodontitis impacts inflammatory responses during atheroma development, thrombotic events, or myocardial infarction or stroke is lacking.