Published online before print June 27, 2005, doi: 10.1161/CIRCULATIONAHA.104.511998
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(Circulation. 2005;112:19-24.)
© 2005 American Heart Association, Inc.
Coronary Heart Disease |
Periodontal Disease and Coronary Heart Disease
A Reappraisal of the Exposure
From the Departments of Dental Ecology (J.D.B., K.M., J.E.), Epidemiology (G.H.), Biostatistics (D.C.), and Periodontology (D.L., S.O.), University of North Carolina, Chapel Hill; Centers for Disease Control and Prevention, Division of Oral Health, Atlanta, Ga (P.E.); and University of Athens, Athens, Greece (P.M.).
Correspondence to James D. Beck, PhD, Department of Dental Ecology, CB 7450, University of North Carolina, Chapel Hill, NC 27599. E-mail James_Beck{at}unc.edu
Received November 15, 2004; revision received February 24, 2005; accepted March 28, 2005.
Background— Results from studies relating periodontal disease to cardiovascular disease have been mixed. Residual confounding by smoking and use of clinical measures of periodontal disease rather than measures of infection have been 2 major criticisms. The aims of this study were to investigate relationships between prevalent coronary heart disease (CHD) and 2 exposures, (1) clinical periodontal disease and (2) IgG antibodies to 17 oral organisms, and to evaluate the role of smoking in these relationships.
Methods and Results— Our study is based on a subset of participants in the Atherosclerosis Risk in Communities (ARIC) Study, who received a complete periodontal examination during visit 4 (1996–1998). The exposures were periodontal status and serum IgG antibody levels against 17 periodontal organisms, and the outcome was prevalent CHD at visit 4. Multivariable analyses indicate that periodontal status is not significantly associated with CHD in either ever smokers or never smokers. Similar analyses evaluating antibodies indicate that high antibodies (above the median) to Treponema denticola (odds ratio [OR]=1.7; 95% CI, 1.2 to 2.3), Prevotella intermedia (OR=1.5; 95% CI, 1.1 to 2.0), Capnocytophaga ochracea (OR=1.5; 95% CI, 1.1 to 2.1), and Veillonella parvula (OR=1.7; 95% CI, 1.2 to 2.3) are significantly associated with CHD among ever smokers, whereas Prevotella nigrescens (OR=1.7; 95% CI, 1.1 to 2.6), Actinobacillus actinomycetemcomitans (OR=1.7; 95% CI, 1.2 to 2.7), and Capnocytophaga ochracea (OR=2.0; 95% CI, 1.3 to 3.0) were associated with CHD among never smokers.
Conclusions— Clinical signs of periodontal disease were not associated with CHD, whereas systemic antibody response was associated with CHD in ever smokers and never smokers. These findings indicate that the quality and quantity of the host response to oral bacteria may be an exposure more relevant to systemic atherothrombotic coronary events than clinical measures.
Key Words: antibodies • coronary disease • epidemiology • risk factors • smoking
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Circulation 2005 112: 1.
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