Abstract

ObjectivesOne of the plausible mechanisms in the relationship between periodontitis and coronary artery disease (CAD) is the systemic inflammatory burden comprised of circulating cytokines/mediators related to periodontitis. This study aims to test the hypothesis that periodontal inflamed surface area (PISA) is correlated with higher circulating levels of acute phase reactants (APR) and pro-inflammatory cytokines/mediators and lower anti-inflammatory cytokines/mediators in CAD patients.Material and MethodsPatients aged from 30 to 75 years who underwent coronary angiography with CAD suspicion were included. Clinical periodontal parameters (probing depth - PD, clinical attachment loss, and bleeding on probing - BOP) were previously recorded and participants were divided into four groups after coronary angiography: Group 1: CAD (+) with periodontitis (n=20); Group 2: CAD (+) without periodontitis (n=20); Group 3: CAD (-) with periodontitis (n=21); Group 4: CAD (-) without periodontitis (n = 16). Serum interleukin (IL) −1, −6, −10, tumor necrosis factor (TNF)-α, serum amyloid A (SAA), pentraxin (PTX) 3, and high-sensitivity C-reactive protein (hs-CRP) levels were measured with ELISA.ResultsGroups 1 and 3 showed periodontal parameter values higher than Groups 2 and 4 (p<0.0125). None of the investigated serum parameters were statistically significantly different between the study groups (p>0.0125). In CAD (-) groups (Groups 3 and 4), PISA has shown positive correlations with PTX3 and SAA (p<0.05). Age was found to predict CAD significantly according to the results of the multivariate regression analysis (Odds Ratio: 1.17; 95% Confidence Interval: 1.08-1.27; p<0.001).ConclusionsAlthough age was found to predict CAD significantly, the positive correlations between PISA and APR in CAD (-) groups deserve further attention, which might depend on the higher PISA values of periodontitis patients. In further studies conducted in a larger population, the stratification of age groups would provide us more accurate results.

Highlights

  • Periodontitis and atherosclerotic cardiovascular diseases, coronary artery diseases (CAD), comprise a major health problem with their high prevalence and mortality rates for the latter6

  • One of the plausible mechanisms in the relationship between periodontitis and coronary artery disease (CAD) is the systemic inflammatory burden comprised of circulating cytokines/mediators related to periodontitis

  • This study aims to test the hypothesis that periodontal inflamed surface area (PISA) is correlated with higher circulating levels of acute phase reactants (APR) and pro-inflammatory cytokines/mediators and lower anti-inflammatory cytokines/mediators in CAD patients

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Summary

Introduction

Periodontitis and atherosclerotic cardiovascular diseases, coronary artery diseases (CAD), comprise a major health problem with their high prevalence and mortality rates for the latter. The most biologically plausible mechanism in the relationship between periodontitis and CAD was suggested to be the entry of oral bacteria into the circulation, resulting in activation of the host inflammatory response in favor of atheroma formation. The inflammatory nature of atherosclerosis has led to attention the focus on acute host inflammatory markers regarding their increase in circulation to predict and/or reflect the intensity of cardiovascular diseases. APR, such as the Pentraxin (PTX) family, were suggested as sensitive biomarkers to predict the development and progression of atherosclerosis. Short PTX (25 kDa), such as C-reactive protein (CRP) and serum amyloid P (SAP), are mainly produced in the liver by IL-6 stimulation in response to the inflammatory stimuli; and the long PTX3 (40-40 kDa), is produced by IL-1 stimulation, tumor necrosis factor (TNF)-α or oxidized low-density lipoprotein (OxLDL). Serum amyloid A (SAA) was suggested to enhance the local effect and to be a more valuable biomolecular diagnosis for acute myocardial infarctions than the other APR18

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