Lesions of Endodontic Origin and Risk of Coronary Heart Disease
Howard E. Strassler
Caplan DJ, Chasen JB, Krall EA, et al. J Dent Res. 2006;85:996-1000.
A paucity of epidemiologic research exists regarding systemic health consequences of endodontic disease. This study evaluated whether incident radiographically evident lesions of endodontic origin were related to development of coronary heart disease (CHD) among 708 male participants in the VA Dental Longitudinal Study. At baseline and every three years for up to 32 years, participants (who were not VA patients) received complete medical and dental examinations, including full-mouth radiographs. Cox regression models estimated the relationship between incident lesions of endodontic origin and time to CHD diagnosis. Among those < 40 years old, incident lesions of endodontic origin were significantly associated with time to CHD diagnosis (P < .05), after adjustment for covariates of interest, with hazard ratios decreasing as age increased. Among those > 40 years old, no statistically significant association was observed. These findings are consistent with research that suggests relationships between chronic periodontal inflammation and the development of CHD, especially among younger men.
Well-established risk factors for atherosclerosis and its complications include dyslipidemia, obesity, hypercholesterolemia, hypertension, diabetes mellitus, and smoking. In recent years a number of studies have demonstrated the association between periodontal conditions and coronary heart disease (CHD). While the pathways by which a chronic oral infection can lead to cardiovascular disease remain controversial, it has been hypothesized that there can be two different courses: 1) direct invasion of the arterial wall by periodontal pathogens, and 2) the release of systemic inflammatory mediators with atherogenic effects in response to infection.
Acute or chronic inflammatory lesions around the apex of a tooth caused by bacterial infection usually occur due to bacterial infection of the root canal system. This apical periodontitis may present itself as an acute, painful lesion or a chronic, asymptomatic condition. While there are differences between chronic inflammatory periodontal disease and endodontic derivation, there are also some similarities, including the presence of gram-negative anaerobic organisms and elevated systemic cytokine levels.
The role of chronic endodontic disease and its effects on systemic disease has not been well explored. With the increased interest in the risk factors for chronic systemic diseases, the authors of this paper have investigated the relationship between the presence of radiographically evident endodontic lesions and CHD.
This study was conducted over a period of 32 years. The participants in the study were enrolled in the Veteran’s Administration Dental Longitudinal Study (Boston area) with baseline established in the 1960s. Acute endodontic inflammation is usually not evident radiographically. This study looked at only chronic endodontic inflammation as evidenced by radiographic films.
While this study did not account for a number of important variables—HDL cholesterol, inflammatory mediators, no collection of bacterial samples, and inadequate values for past smoking history—it did establish that lesions of endodontic origin may be a contributor to risk of CHD for younger patients (< 40 years). From the evidence of this report, there is reason to pursue the development of a well-designed prospective study on the elimination of lesions of endodontic origin through successful endodontic treatment or extraction and its effects on CHD risk.
The author has received honorarium or grant/research support from 3M ESPE, Den-Mat, and Ultradent.
Howard E. Strassler, DMD