Periodontal disease results in increased local gingival bleeding, larger areas of ulcerated sulcular epithelium, and a larger number of oral bacteria within the gingival crevice.82 Patients with periodontitis have also been shown to experience high levels of bacteremia and endotoxemia with innocuous stimuli such as chewing.83 This dissemination of bacteria associated with periodontitis may play a role in the influence of periodontal disease on CVD. Many species of periodontal and oral pathogens have been shown to invade endothelial cells, including P. gingivalis,84,85 P. endodontalis,84 S. mutans,86 S. gordonii,87 S. mitis,87 and S. oralis.87 Furthermore, invasion of endothelial cells by P. gingivalis has been shown to upregulate a host of pro-inflammatory and pro-coagulation genes.88,89 Periodontal pathogens have also been identified in atherosclerotic plaques in vivo and may be associated with an increase in coagulation at those sites.78,90
The transport of these bacteria to the endothelium may occur through bacteremias or transport within phagocytic cells, which then enter the media as a part of atherogenesis.91 Bacterial invasion at the site of the atheroma is associated with an increase in acute inflammation and an increase in proinflammatory mediators, thus creating a feedback loop for atheroma formation.92
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