Role of Gingivalis in atherosclerosis progression in apolipoprotein-e knockout mice

Abstract

Recent studies have demonstrated an association between the periodontal-periapical pathogen and atherosclerosis and cardiovascular disease in humans. We have established that the periapical pathogen Porphyromonas gingivalis can invade aortic endothelial cells and that fimbria is required for invasion and the expression of chemokine and cell adhesion molecules. The strength of the epidemiological associations of P. gingivalis with atherosclerosis can be increased by the demonstration that oral challenge with P. gingivitalis will stimulate atherosclerotic plaque accumulation in an appropriate animal model. In this study ApoE-/-mice were orally challenged with wild type P. gingivalis strain 381, or with non-invasive P. gingivalis filmA mutant (DPG3) and atherosclerotic plaque accumulation measured 17 weeks after challenge. Mice orally challenged with strain 381 exhibited oral bone loss, while mice challenged with DPG3 had only slight levels of oral bone loss. Sudan IV staining and morphometric analysis of the intimal surface of the aorta, demonstrated that only the ApoE -/- mice challenged with wild type P. gingivalis exhibited significant levels of atherosclerotic plaque accumulation. Both P. gingivalis strains elicited a potent P. gingivalis-specific IgG response. Mice challenged with P. gingivalis 381 or DPG3 presented with transient bacteria as detected by PCR 2hr post-challenge. Likewise, P. gingivalis 381 and DPG3 were detected in the aortic arch tissues 2hr post-challenge. These results demonstrate that oral infection with invasive P. gingivalis exacerbates atherosclerotic plaque accumulation in the aorta.