Oral P. gingivalis infection alters the vascular reactivity in healthy and spontaneously atherosclerotic mice

Abstract

BackgroundConsidering that recent studies have demonstrated endothelial dysfunction in subjects with periodontitis and that there is no information about vascular function in coexistence of periodontitis and atherosclerosis, we assessed the impact of oral inoculation with the periodontal pathogen Porphyromonas gingivalis on vascular reactivity in healthy and hypercholesterolemic apolipoprotein E-deficient (ApoE) mice. In vitro preparations of mesenteric arteriolar bed were used to determine the vascular responses to acetylcholine, sodium nitroprusside and phenylephrine (PE).ResultsAlveolar bone resorption, an evidence of periodontitis, was assessed and confirmed in all infected mice. Acetylcholine- and sodium nitroprusside-induced vasorelaxations were similar among all groups. Non-infected ApoE mice were hyperreactive to PE when compared to non-infected healthy mice. P gingivalis infection significantly enhanced the vasoconstriction to PE in both healthy and spontaneous atherosclerotic mice, when compared to their respective controls.ConclusionsThis study demonstrates that oral P gingivalis affects the alpha-adrenoceptor-mediated vascular responsiveness in both healthy and spontaneous atherosclerotic mice, reinforcing the association between periodontitis and cardiovascular diseases.

Porphyromonas gingivalis Strain Specific Interactions with Human Coronary Artery Endothelial Cells: A Comparative Study

“…Moreover, several independent studies have detected P. gingivalis DNA or retrieved live bacteria from human aortic aneurysms, aortic thrombi, atheromas, and atherosclerotic plaque specimens [1], [2], [7]–[15]. Experimental infection with different strains of P. gingivalis have shown that the bacterium can promote varying degrees of cardiovascular disease including endothelial dysfunction [16], vascular smooth muscle proliferation [17], [18], aortic aneurysm [19]–[21], and atherosclerosis [22]–[27]. Although not specific to P. gingivalis , intensive periodontal therapy has been shown to improve endothelial function in the long-term in patients with periodontal disease [28].…”

“…More recent work suggests that other virulence factors of P. gingivalis may be equally important for the progression of atherosclerosis since the fimbriae-deficient strain W83 [41] also promotes atherosclerosis in ApoE deficient mice [26]. In contrast, strain 33277, which is closely related to strain 381 [42] does not accelerate atherosclerosis in ApoE deficient mice [16].…”

“…Our objective for this study was to perform a comparative study between P. gingivalis strains W83, A7436, 381, and 33277 since these strains produce varying disease outcomes in ApoE deficient mice (Table 1) [16], [26], [27], [50]. Moreover, these strains also express a different array of virulence factors that may impact microbial/endothelial cell interactions such as fimbriae type (Figure S1) [51], fimbriae expression [52], [53], and polysaccharide capsule type [54] (Table 1).…”

Porphyromonas gingivalis and its lipopolysaccharide differentially regulate the expression of cathepsin B in endothelial cells

“…, 2003; Amar et al. , 2009; Pereira et al , 2011). Various theories have been proposed to explain this link.…”

Porphyromonas gingivalisin periodontal pockets and heart valves

“…4 It was also demonstrated that a P. gingivalis infection causes an increased vasoconstrictor response to phenylephrine both in mice with spontaneous atherosclerosis and in healthy mice. 35 However, the virulence mechanisms are different for various P. gingivalis strains and a detailed examination of these processes needs to be performed. 32 In this study, the assessment of the presence of P. gingivalis DNA in cardiac valves in relation to its presence in periodontal pockets was performed.…”