Periodontal Disease and Atherosclerotic Cardiovascular Disease: Confounding Effects or Epiphenomenon?

and Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago; and the Department of Pharmacy, Cook County Hospital, Chicago, Illinois.

Pharmacotherapy. 2000;20(7) 

In This Article

Abstract and Introduction


Recent evidence suggests that periodontal disease may predispose to atherosclerotic cardiovascular disease. Data support mechanisms of host-derived local and systemic proinflammatory responses similar to atherosclerosis, consisting of monocytic-derived cytokines and other inflammatory mediators, which are induced by periodontal pathogens and its endotoxin, lipopolysaccharide. These mechanisms may contribute to the start of vascular endothelial dysfunction and further sequelae leading to atherosclerosis. Experimental evidence and biologic plausibility appear to support this proposal. However, clinical evidence from a MEDLINE search from January 1966-December 1999 proposed a weak or no correlation primarily due to confounding factors. The aim of care is to reduce vulnerable pathogens from the infected periodontium by standard treatment; however, new approaches appear promising. Increased awareness of a potential link among infective agents, immunoinflammatory processes, and atherosclerosis may clarify clinical implications.


Atherosclerotic cardiovascular diseases (ACVD) such as myocardial infarction and stroke are a major health problem, causing nearly 50% of deaths in the American population and other developed countries.[1] Reducing conventional modifiable risk factors (e.g., smoking, systemic hypertension, diabetes mellitus, hyperlipidemia) is effective in preventing ACVD. However, these strategies, together with interventions to reduce nonmodifiable risk factors (e.g., age, gender, family history), do not explain why the frequency of ACVD has not decreased as much as would be expected on epidemiologic grounds. Thus, it is likely that other, unrecognized factors contribute to the pathogenesis of atherosclerosis. This led many to speculate that ACVD may have an infectious etiology.[2]

Local dental infections, specifically periodontal disease, may increase the risk for ACVD. Periodontal disease is an inflammatory response to predominately gram-negative anaerobic bacterial infections of tissues surrounding the tooth, including periodontal ligament, cementum, and alveolar bone.[3] A chronic inflammatory burden ensues in the absence of treatment. Periodontitis refers to actual loss of periodontal ligament around the tooth resulting from gram-negative, anaerobic bacteria and the host response to these pathogens. Moderate to severe forms of disease affect approximately 15% of Americans over age 18 years and perhaps more in other countries.[4]

Both periodontal disease and atherosclerosis have numerous characteristics in common. They are most likely to occur in individuals who are elderly, male, of low economic and education status; who smoke; have diabetes, elevated cholesterol, and systemic hypertension; and are stressed.[3] These commonalties indicate that the diseases may share similar etiologic pathways.


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