Abstract
Atherosclerotic vascular disease is a leading cause of myocardial infarction and cerebrovascular accident, and independent associations with periodontal disease (PD) are reported. PD is caused by polymicrobial infections and aggressive immune responses. Genomic DNA of Porphyromonas gingivalis, the best-studied bacterial pathogen associated with severe PD, is detected within atherosclerotic plaque. We examined causal relationships between chronic P. gingivalis oral infection, PD, and atherosclerosis in hyperlipidemic ApoEnull mice. ApoEnull mice (n = 24) were orally infected with P. gingivalis for 12 and 24 weeks. PD was assessed by standard clinical measurements while the aorta was examined for atherosclerotic lesions and inflammatory markers by array. Systemic inflammatory markers serum amyloid A, nitric oxide, and oxidized low-density lipoprotein were analyzed. P. gingivalis infection elicited specific antibodies and alveolar bone loss. Fluorescent in situ hybridization detected viable P. gingivalis within oral epithelium and aorta, and genomic DNA was detected within systemic organs. Aortic plaque area was significantly increased in P. gingivalis-infected mice at 24 weeks (P<0.01). Aortic RNA and protein arrays indicated a strong Th2 response. Chronic oral infection with P. gingivalis results in a specific immune response, significant increases in oral bone resorption, aortic inflammation, viable bacteria in oral epithelium and aorta, and plaque development.
Highlights
Atherosclerotic vascular disease (ASVD) is the leading cause of death in the U.S, and one third of Americans have some form of the disease, which includes coronary disease with myocardial ischemia, cerebrovascular disease with strokes, and peripheral arterial disease with gangrene [1]
A recent statement by the American Heart Association supports an association between periodontal disease (PD) and ASVD that is independent of known confounders, but this report has stated that current data are insufficient to support a causal relationship [1]
With these studies we examine a potential correlation between chronic infection with a known predominant oral pathogen seen in PD and accelerated atherosclerotic plaque growth using a mouse model for PD and ASVD
Summary
Atherosclerotic vascular disease (ASVD) is the leading cause of death in the U.S, and one third of Americans have some form of the disease, which includes coronary disease with myocardial ischemia, cerebrovascular disease with strokes, and peripheral arterial disease with gangrene [1] Half of those with the disease do not have traditional disease risk factors such as obesity, hypercholesterolemia, hypertension, history of smoking, or genetic background [2,3,4], and the cause(s) of rapid atherosclerotic plaque progression and disease is unknown in many patients. A recent statement by the American Heart Association supports an association between PD and ASVD that is independent of known confounders, but this report has stated that current data are insufficient to support a causal relationship [1] With these studies we examine a potential correlation between chronic infection with a known predominant oral pathogen seen in PD and accelerated atherosclerotic plaque growth using a mouse model for PD and ASVD. Live P. gingivalis bacteria have been detected in human atherosclerotic plaque by fluorescence in situ hybridization (FISH) [13], invasion assays [14], and culture [15], indicating metabolically active organisms, which are able to invade, survive, and replicate within atheromatous plaques
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