The role of inflammatory and immunological mediators in periodontitis and cardiovascular disease.
Epidemiological studies have implicated periodontitis (PD) as a risk factor for development of cardiovascular disease (CVD). Persistent infections such as periodontitis induce inflammatory and immune responses which may contribute to coronary atherogenesis, and, in conjunction with other risk factors, may lead to coronary heart disease (CHD). In this review, mechanisms are described that may help explain the association between periodontal infections and CHD. Periodontal diseases are bacterial infections associated with bacteremia, inflammation, and a strong immune response, all of which may represent significant risk factors for the development of atherogenesis, CHD, and myocardial infarction (MI). Several mechanisms may participate in this association, including those induced by oral organisms, and those associated with host response factors. This review will focus on host factors. Oral pathogens and inflammatory mediators (such as interleukin [IL]-1 and tumor necrosis factor [TNF]-alpha) from periodontal lesions intermittently reach the bloodstream inducing systemic inflammatory reactants such as acute-phase proteins, and immune effectors including systemic antibodies to periodontal bacteria. This review will describe the potential role of various inflammatory as well as immunologic factors that may play a role in periodontitis as a possible risk factor for CHD.
De Nardin
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Department of Oral Biology, School of Dental Medicine, Department of Microbiology, School of Medicine, University at Buffalo, Buffalo, New York, USA.
D000209:Acute-Phase Proteins / Q000276:immunology; D000907:Antibodies, Bacterial / Q000276:immunology; D001161:Arteriosclerosis / Q000276:immunology; D016470:Bacteremia / Q000276:immunology; D001424:Bacterial Infections / Q000276:immunology; D002318:Cardiovascular Diseases / Q000276:immunology*; D015815:Cell Adhesion Molecules / Q000276:immunology; D003324:Coronary Artery Disease / Q000209:etiology / Q000276:immunology; D006801:Humans; D007155:Immunologic Factors / Q000502:physiology*; D007249:Inflammation / Q000276:immunology / Q000382:microbiology; D018836:Inflammation Mediators / Q000502:physiology*; D007375:Interleukin-1 / Q000276:immunology; D009203:Myocardial Infarction / Q000276:immunology; D010518:Periodontitis / Q000276:immunology* / Q000382:microbiology; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
D000209:Acute-Phase Proteins; D000907:Antibodies, Bacterial; D015815:Cell Adhesion Molecules; D007155:Immunologic Factors; D018836:Inflammation Mediators; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha