Endodontic inflammatory disease and myocardial infarction

Abstract

Atherosclerosis is the underlying cause to suffering an acute myocardial infarction. Disruption of atherosclerotic plaques lead to thrombus formation and occlusion of the coronary arteries which impedes blood supply to the heart. Inflammation plays a role in the pathogenesis. Through spread of pro-inflammatory mediators, oral inflammatory diseases may contribute to the risk of acute coronary events. The PAROKRANK study reported an independent association between marginal periodontitis and the risk of acute myocardial infarction. The main objective of this thesis was to explore if a similar association exists between endodontic inflammatory disease and acute myocardial infarction. Study I addressed observer reliability in assessment of endodontic variables in panoramic radiographs. Calibration improved agreement between three observers and a reference standard in assessment of periapical lesions (from weighted  0.22, 0.30 and 0.60 to 0.59, 0.64 and 0.80 respectively). In Study II, endodontic variables in PAROKRANK patients and controls were compared. Following adjustment for confounders, more missing teeth increased the risk (OR 1.04; 95% CI 1.02-1.06), whilst number of filled teeth reduced the risk (OR 0.98; 95% CI 0.96-1.00), of myocardial infarction. Decayed teeth (OR 1.18; 95% CI 1.02-1.37) and primary apical periodontitis (OR 1.57; 95% CI 1.08-2.29) increased the risk in younger age-groups while root filled teeth (OR 1.18; 95% CI 1.03-1.36) increased risk in older age groups. Study III explored a composite of endodontic inflammatory disease as an indicator of acute myocardial infarction. In a multivariable logistics regression model, the composite, calculated as the sum of seven weighted endodontic variables, best predicted the risk of myocardial infarction (OR 1.97; 95% CI 1.23-3.17). Study IV analysed correlations between endodontic variables and systemic levels of pro-inflammatory markers in blood. In adjusted analyses, presenting ≥1 root filled tooth related to lower levels of several cytokines (IL-1, IL-2, IL-6, and IL-12p70), whilst ≥1 primary apical periodontitis related to higher levels of interleukin-8 (=0.06). In Study V, national registries were assessed for mortality and morbidity data of the PAROKRANK cohort during a follow-up of eight years. Following adjustment for confounders, remaining teeth and non-root filled teeth decreased the risk of future events, whilst higher DMFT-score increased the risk and ≥1 primary apical periodontitis decreased the risk of suffering cardiovascular events. Higher DMFT-score and decayed teeth increased the risk of all-cause mortality.