Human Atherosclerotic Plaque Contains Viable Invasive Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis

Immunoglobulin G antibodies againstPorphyromonas gingivalisorAggregatibacter actinomycetemcomitansin cardiovascular disease and periodontitis

“…Another potential pathogenic pathway is spillover of inflammatory mediators from periodontal tissues to the circulation during such everyday oral procedures [40]. Notably, both viable oral bacteria and DNA from oral bacteria have been isolated in atheromatous plaques distant from the oral cavity [44–46]. Concomitant changes in endothelial permeability promote the entry and retention of cholesterol-containing low-density lipoprotein particles in the artery wall, which may aggravate atherosclerotic lesions and thus the risk of cardiovascular events [47].…”

Subversion of Innate Immunity by Periodontopathic Bacteria via Exploitation of Complement Receptor-3

“…However, since the adhesion of monocytes to the arterial endothelium and their subsequent migration into the subendothelial area is a hallmark of early atherogenesis (Libby, 2002), P. gingivalis-induced CR3 activation may constitute a mechanistic basis linking this pathogen to inflammatory atherosclerotic processes. In this regard, viable P. gingivalis has been found in atherosclerotic plaques (Kozarov et al, 2005), although it is uncertain how the pathogen resists immune elimination and relocates there from the oral environment. An interesting hypothesis is that P. gingivalis not only stimulates the transmigratory activity of monocytes/macrophages but also exploits them as "Trojan horses" for disseminating to systemic tissues.…”

“…The latter is due to the significant instructive role of the innate response in the development of adaptive immunity (Pasare and Medzhitov, 2005). Although P. gingivalis is a successful pathogen that can also be found in systemic tissues (Kozarov et al, 2005), the mechanism(s) whereby P. gingivalis resists immune elimination are poorly understood. In this regard, the pathogen's in vitro ability to inhibit production of the IL-8 chemokine by gingival epithelial cells (Darveau et al, 1998) or to degrade secreted cytokines (Calkins et al, 1998) is thought to suppress host defenses.…”

Human oral, gut, and plaque microbiota in patients with atherosclerosis

“…Furthermore, in a study where bacterial DNA was identified in atherosclerotic plaques, 51.5% of the patients tested positive for Chlamydia in their atheromas (17). Several studies suggest an oral source for atherosclerotic plaque-associated bacteria (18)(19)(20)(21). However, to date, no single study has directly compared the microbial diversity of oral, gut, and atherosclerotic plaque microbiotas within individuals.…”