Investigating Potential Correlations between Endodontic Pathology and Cardiovascular Diseases Using Epidemiological and Genetic Approaches

Introduction

Apical periodontitis (AP) and cardiovascular diseases (CVDs) are chronic conditions triggered by an inflammatory process and sharing similar pathogeneses and molecular players. Previous studies have suggested that AP may perpetuate a systemic inflammation state and, in turn, contribute to CVD. In this study, we investigated the potential association between endodontic pathology and CVD using epidemiological and genetic approaches.

Methods

Epidemiologic analysis was performed by querying the medical and dental records of >2 million patients. We retrieved information on positive/negative history for endodontic pathologies and CVDs using diagnostic and treatment codes from a dental school–based and a hospital-based patient electronic health record system. A case-control genetic association study was also performed; 10 single nucleotide polymorphisms in genes identified as strongly associated with CVDs were genotyped in 195 cases with AP and 189 control individuals without AP. Data analyses were performed using the chi-square and Fisher exact tests. P ≤.05 indicates significant difference between groups.

Results

Significant associations were found between the presence of endodontic pathology and a history of hypertension, myocardial infarction, cerebrovascular accident, pacemaker, congestive heart failure, heart block, deep vein thrombosis, and cardiac surgery (0.0001 ≤ P ≤ .008). A modest association was found for heart murmur and atrial fibrillation (P = .04). A trend toward positive association (P = .05) was also found between AP and a single nucleotide polymorphism in KCNK3, a gene known to be involved in increased susceptibility to hypertension.

Conclusions

Significant associations were found between endodontic pathology and various CVDs and CVD-related risk factors, particularly hypertension. A trend toward a positive association was also found between AP and KCNK3, suggesting that common genetic variations may underlie different diseases. Additional studies with larger sample sizes have the potential to elucidate common mechanisms underlying AP and CVD.