"Gum bug, leave my heart alone!"--epidemiologic and mechanistic evidence linking periodontal infections and atherosclerosis.
Evidence from epidemiologic studies suggests that periodontal infections are independently associated with subclinical and clinical atherosclerotic vascular disease. Although the strength of the reported associations is modest, the consistency of the data across diverse populations and a variety of exposure and outcome variables suggests that the findings are not spurious or attributable only to the effects of confounders. Analysis of limited data from interventional studies suggests that periodontal treatment generally results in favorable effects on subclinical markers of atherosclerosis, although such analysis also indicates considerable heterogeneity in responses. Experimental mechanistic in vitro and in vivo studies have established the plausibility of a link between periodontal infections and atherogenesis, and have identified biological pathways by which these effects may be mediated. However, the utilized models are mostly mono-infections of host cells by a limited number of 'model' periodontal pathogens, and therefore may not adequately portray human periodontitis as a polymicrobial, biofilm-mediated disease. Future research must identify in vivo pathways in humans that may (i) lead to periodontitis-induced atherogenesis, or (ii) result in treatment-induced reduction of atherosclerosis risk. Data from these studies will be essential for determining whether periodontal interventions have a role in the primary or secondary prevention of atherosclerosis.
Kebschull
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Division of Periodontics, Section of Oral and Diagnostic Sciences, College of Dental Medicine, 630 W 168th Street, PH-7-E-110, New York, NY 10032, USA.
Demmer
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Papapanou
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D000818:Animals; D050197:Atherosclerosis / Q000453:epidemiology / Q000209:etiology* / Q000382:microbiology / Q000517:prevention & control; D015551:Autoimmunity; D016470:Bacteremia / Q000150:complications / Q000382:microbiology; D002545:Brain Ischemia / Q000209:etiology / Q000517:prevention & control; D015986:Confounding Factors, Epidemiologic; D003327:Coronary Disease / Q000209:etiology* / Q000517:prevention & control; D004195:Disease Models, Animal; D015987:Effect Modifier, Epidemiologic; D004730:Endothelium, Vascular / Q000382:microbiology; D006801:Humans; D015227:Lipid Peroxidation; D009000:Monocytes / Q000276:immunology; D018384:Oxidative Stress; D010518:Periodontitis / Q000150:complications* / Q000453:epidemiology / Q000382:microbiology / Q000628:therapy; D010974:Platelet Aggregation; D012907:Smoking / Q000009:adverse effects; D020521:Stroke / Q000209:etiology* / Q000517:prevention & control; D051193:Toll-Like Receptors / Q000276:immunology
D051193:Toll-Like Receptors