Department of Periodontology, The Forsyth Institute, Cambridge, MA 02142, USA.
Oral Dis. 2011 Jul;17(5):450-61. doi: 10.1111/j.1601-0825.2010.01784.x. Epub 2011 Jan 11.
It is now well accepted that besides the cholesterol associated mechanisms of atherogenesis, inflammation plays a crucial role in all stages of the development of the atherosclerotic lesion. This 'inflammation hypothesis' raises the possibility that through systemic elevations of pro-inflammatory cytokines, periodontal diseases might also contribute to systemic inflammation and, therefore, to atherogenesis. In fact, there is evidence that periodontal diseases are associated with higher systemic levels of high-sensitivity C-reactive protein and a low grade systemic inflammation. This phenomenon has been explained based on mechanisms associated with either the infectious or the inflammatory nature of periodontal diseases. The purposes of this article were to review (1) the evidence suggesting a role for oral bacterial species, particularly periodontal pathogens, in atherogenesis; (2) the potential mechanisms explaining an etiological role for oral bacteria in atherosclerosis; (3) the evidence suggesting that periodontal infections are accompanied by a heightened state of systemic inflammation; (4) the potential sources of systemic inflammatory biomarkers associated with periodontal diseases; and (5) the effects of periodontal therapy on systemic inflammatory biomarkers and cardiovascular risk.
现在人们普遍认为,除了与胆固醇相关的动脉粥样硬化形成机制外,炎症在动脉粥样硬化病变的所有阶段都起着至关重要的作用。这种“炎症假说”提出了一种可能性,即通过全身炎症细胞因子的升高,牙周病也可能导致全身炎症,并因此导致动脉粥样硬化形成。事实上,有证据表明牙周病与更高的全身高敏 C 反应蛋白水平和低度全身炎症有关。这种现象可以用与牙周病的感染或炎症性质相关的机制来解释。本文的目的是综述(1)提示口腔细菌,特别是牙周致病菌在动脉粥样硬化形成中起作用的证据;(2)解释口腔细菌在动脉粥样硬化中具有病因作用的潜在机制;(3)提示牙周感染伴有全身性炎症状态升高的证据;(4)与牙周病相关的全身性炎症生物标志物的潜在来源;以及(5)牙周治疗对全身炎症生物标志物和心血管风险的影响。