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Issue 1088 coverNeuroendocrine and Immune Crosstalk Volume 1088 published November 2006
Ann. N.Y. Acad. Sci. 1088: 251–264 (2006). doi: 10.1196/annals.1366.032
Copyright © 2006 by the New York Academy of Sciences
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Articles by MOUTSOPOULOS, N. M
Articles by MADIANOS, P. N
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Articles by MADIANOS, P. N

Part VI. Neuroimmunomodulation in Chronic Infectious and Inflammatory Diseases

Low-Grade Inflammation in Chronic Infectious Diseases

Paradigm of Periodontal Infections

NIKI M MOUTSOPOULOSa AND PHOEBUS N MADIANOSb

a Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland USA b Department of Periodontology, School of Dentistry, University of Athens, Athens, Greece

Key Words: periodontitis • acute myocardial infarction (AMI)

Address for correspondence: Phoebus N. Madianos, Department of Periodontology, School of Dentistry, University of Athens, Thivon 2, 115 27 Athens, Greece. Voice: +30-210-7461181; fax: +30-210-7461202.  e-mail: pmadian{at}dent.uoa.gr

Increasing evidence implicates periodontitis, a chronic inflammatory disease of the tooth-supporting structures, as a potential risk factor for increased morbidity or mortality for several systemic conditions including cardiovascular disease (atherosclerosis, heart attack, and stroke), pregnancy complications (spontaneous preterm birth [SPB]), and diabetes mellitus. Cross-sectional, case–control, and cohort studies indicate that periodontitis may confer two- and up to sevenfold increase in the risk for cardiovascular disease and premature birth, respectively. Given the recently acquired knowledge that systemic inflammation may contribute in the pathogenesis of atherosclerosis and may predispose to premature birth, research in the field of periodontics has focused on the potential of this chronic low-grade inflammatory condition to contribute to the generation of a systemic inflammatory phenotype. Consistent with this hypothesis clinical studies demonstrate that periodontitis patients have elevated markers of systemic inflammation, such as C-reactive protein (CRP), interleukin 6 (IL-6), haptoglobin, and fibrinogen. These are higher in periodontal patients with acute myocardial infarction (AMI) than in patients with AMI alone, supporting the notion that periodontal disease is an independent contributor to systemic inflammation. In the case of adverse pregnancy outcomes, studies on fetal cord blood from SBP babies indicate a strong in utero IgM antibody response specific to several oral periodontal pathogens, which induces an inflammatory response at the fetal–placental unit, leading to prematurity. The importance of periodontal infections to systemic health is further strengthened by pilot intervention trials indicating that periodontal therapy may improve surrogate cardiovascular outcomes, such as endothelial function, and may reduce four- to fivefold the incidence of premature birth. Nevertheless, further research is needed to fully discern the underlying mechanisms by which local chronic infections can have an impact on systemic health, and in this endeavor periodontal disease may serve as an ideal disease model.




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