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.
journal_name
Pharmacotherapyjournal_title
Pharmacotherapyauthors
Chong PH,Kezele Bdoi
10.1592/phco.20.9.805.35189subject
Has Abstractpub_date
2000-07-01 00:00:00pages
805-18issue
7eissn
0277-0008issn
1875-9114journal_volume
20pub_type
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