Maria Messing1, Letícia Chaves de Souza2, Franco Cavalla3, Krishna Kumar Kookal4, Gabriella Rizzo1, Muhammad Walji5, Renato Silva2, Ariadne Letra6. 1. Department of Endodontics, University of Texas Health Science Center at Houston School of Dentistry, Houston, Texas. 2. Department of Endodontics, University of Texas Health Science Center at Houston School of Dentistry, Houston, Texas; Center for Craniofacial Research, University of Texas Health Science Center School of Dentistry at Houston, Houston, Texas. 3. Center for Craniofacial Research, University of Texas Health Science Center School of Dentistry at Houston, Houston, Texas; Department of Conservative Dentistry, School of Dentistry, University of Chile, Santiago, Chile; Department of Biological Sciences, School of Dentistry of Bauru, University of São Paulo, Bauru, São Paulo, Brazil. 4. Office of Technology Services and Informatics, University of Texas Health Science Center at Houston School of Dentistry, Houston, Texas. 5. Office of Technology Services and Informatics, University of Texas Health Science Center at Houston School of Dentistry, Houston, Texas; Department of Diagnostic and Biomedical Sciences, University of Texas Health Science Center at Houston School of Dentistry, Houston, Texas. 6. Department of Endodontics, University of Texas Health Science Center at Houston School of Dentistry, Houston, Texas; Center for Craniofacial Research, University of Texas Health Science Center School of Dentistry at Houston, Houston, Texas; Department of Diagnostic and Biomedical Sciences, University of Texas Health Science Center at Houston School of Dentistry, Houston, Texas. Electronic address: Ariadne.M.Letra@uth.tmc.edu.
Abstract
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.
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.
Authors: P J Pussinen; S Paju; J Viikari; A Salminen; L Taittonen; T Laitinen; D Burgner; M Kähönen; T Lehtimäki; N Hutri-Kähönen; O Raitakari; M Juonala Journal: J Dent Res Date: 2020-06-01 Impact factor: 6.116
Authors: Muhammad F Walji; Heiko Spallek; Krishna Kumar Kookal; Jane Barrow; Britta Magnuson; Tamanna Tiwari; Udochukwu Oyoyo; Michael Brandt; Brian J Howe; Gary C Anderson; Joel M White; Elsbeth Kalenderian Journal: J Am Med Inform Assoc Date: 2022-03-15 Impact factor: 4.497