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(Circulation. 2004;109:1095-1100.)
© 2004 American Heart Association, Inc.

Clinical Investigation and Reports

Asymptotic Dental Score and Prevalent Coronary Heart Disease

Sok-Ja Janket, DMD, MPH; Markku Qvarnström, DDS, MS; Jukka H. Meurman, DDS, MD; Alison E. Baird, MD, PhD; Pekka Nuutinen, MD, PhD; Judith A. Jones, DDS, MPH, DScD

From Boston University Goldman School of Dental Medicine (S.-J.J., J.A.J.), Boston, Mass; Department of Otorhinolaryngology/Oral Surgery (M.Q.) and Department of Cardiothoracic Surgery (P.N.), Kuopio University Hospital, Kuopio, Finland; Institute of Dentistry (J.H.M.), University of Helsinki, Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital, Helsinki, Finland; National Institute of Neurological Disorders and Stroke (A.E.B.), National Institutes of Health, Bethesda, Md; Harvard School of Public Health (S.-J.J.), Harvard University, Boston, Mass; and VA Center for Health Quality, Outcomes and Economic Research (J.A.J.), Bedford, Mass.

Correspondence to Sok-Ja Janket, DMD, MPH, Department of General Dentistry, Boston University Goldman School of Dental Medicine, 100 E. Newton St, Boston, MA 02118. E-mail sjanket{at}hsph.harvard.edu

Received August 12, 2003; revision received October 31, 2003; accepted November 13, 2003.

Background— Oral infections have been postulated to produce cytokines that may contribute to the pathogenesis of coronary heart disease (CHD). We hypothesized that by estimating the combined production of inflammatory mediators attributable to several oral pathologies, we might be able to explain CHD with better precision.

Methods and Results— A total of 256 consecutive Finnish cardiac patients from Kuopio University Hospital with angiographically confirmed CHD and 250 age-, gender-, and residence-matched noncardiac patients (controls) were recruited. All dental factors expected to generate inflammatory mediators, including pericoronitis, dental caries, dentate status, root remnants, and gingivitis, were examined, and an asymptotic dental score (ADS) was developed by logistic regression analyses with an appropriate weighting scheme according to the likelihood ratio. We validated the explanatory ability of ADS by comparing it to that of the Total Dental Index and examining whether the ADS was associated with known predictors of CHD. A model that included ADS, C-reactive protein, HDL, and fibrinogen offered an explanatory ability that equaled or exceeded that of the Framingham heart score (C statistic=0.82 versus 0.80). When ADS was removed from this model, the C-statistic decreased to 0.77, which indicates that the ADS was a significant contributor to the explanatory ability of a logistic model.

Conclusions— ADS may be useful as a prescreening tool to promote proactive cardiac evaluation among individuals without overt symptoms of CHD. However, additional prospective study is needed to validate the use of an oral health score as a predictor of incident CHD.

Key Words: oral health • heart diseases • lipoproteins • interleukins • fibrinogen

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