| Literature DB >> 10907970 |
Abstract
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.Entities:
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Year: 2000 PMID: 10907970 DOI: 10.1592/phco.20.9.805.35189
Source DB: PubMed Journal: Pharmacotherapy ISSN: 0277-0008 Impact factor: 4.705