Oral Infection With a Periodontal Pathogen Accelerates Early Atherosclerosis in Apolipoprotein E–Null Mice

Abstract

Objective-Because recent epidemiologic evidence suggests that periodontal infections may increase the risk of atherosclerosis and related events in humans, we assessed the impact of oral inoculation with the periodontal pathogen Porphyromonas gingivalis on atherogenesis in hypercholesterolemic apolipoprotein E-null mice. Methods and Results-In the absence of alterations in distinct risk factors, P gingivalis infection exacerbated the early stages of atherogenesis in this model. Infected animals displayed evidence of local periodontal infection, as the severity of alveolar bone loss, the hallmark of periodontitis, was increased.

Interleukin-1 Receptor Signaling Mediates Atherosclerosis Associated With Bacterial Exposure and/or a High-Fat Diet in a Murine Apolipoprotein E Heterozygote Model

“…3 This view is strengthened by evidence that exposure to microbial pathogens can potentiate atherosclerosis and its associated inflammatory changes. 7,18 Studies have attempted to reduce the level or action of cytokines such as IL-1, which has been shown to recruit and stimulate cells into the inflammatory process. 27 Recently, Kirii et al 41 recently showed that, in ApoE Ϫ/Ϫ mice, genetic ablation of IL-1␤ reduced atherosclerosis by only 30%, perhaps because of persistent IL-1␣ stimulation of the IL-1R or because of alternative pathways.…”

“…We and others have described a model in which systemic exposure to an oral pathogen, Porphyromonas gingivalis (P gingivalis), potentiates the development of atherosclerosis in mice with genetic and dietary susceptibility. 7,18 In both models, progressive atherosclerosis was associated with activation of the inflammatory process, as evidenced by increases in molecules such as serum amyloid-associated protein (SAA) and interleukin-1 (IL-1). 7 The question remains, however, whether the inflammatory changes play a causal role in the atherosclerotic process or are only secondarily involved.…”

Porphyromonas gingivalisin periodontal pockets and heart valves

“…What is more, treatment of periodontal diseases, including a control of periodontal infections, results in improved levels of markers of systemic inflammation and endothelial dysfunction. [22][23][24] The ability of oral pathogens to colonize coronary atheromatous plaque has already been confirmed by studies showing the 27 It has been reported that P. gingivalis accelerated atheroma formation, [28][29][30] caused an increase in systemic inflammatory marker levels, 20,21 invaded endothelium and vascular smooth muscle cells, 31,32 and appeared to alter endothelial function. 33,34 P. gingivalis activates endothelial cells and upregulates various adhesion molecules, and thus, increases the likelihood of macrophage diapedesis and subsequent conversion to foam cells.…”

Periodontitis as a risk factor of stroke: a review of literature

“…Gingivitis is primarily caused by dental plaque, and affects gingival tissue only, while connective tissue attachment and alveolar bone remain intact. Conversely, periodontitis is a disease of multifactorial etiology with a complex clinical picture, manifested by the gradual, irreversible destruction of tooth-supporting tissues (gingiva, periodontal ligament, bone) which leads to the loss of teeth [2,3]. Periodontitis disease is a common condition that affects about 90% of the world›s population [4].…”