Periodontal disease and inflammatory blood cytokines in patients with stable coronary artery disease.

Cassio Kampits,Marlon M Montenegro,Carisi A Polanczyk,Cassiano K Rösing,Ingrid W J Ribeiro,Mariana V Furtado,Alex N Haas

doi:10.1590/1678-775720160082

Cassio Kampits, Marlon M Montenegro + Show 5 more

Open Access

https://doi.org/10.1590/1678-775720160082

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Abstract

ABSTRACTPeriodontal disease has been associated with elevations of blood cytokines involved in atherosclerosis in systemically healthy individuals, but little is known about this association in stable cardiovascular patients. The aim of this study was to assess the association between periodontal disease (exposure) and blood cytokine levels (outcomes) in a target population of patients with stable coronary artery disease (CAD). Material and Methods This cross-sectional study included 91 patients with stable CAD who had been under optimized cardiovascular care. Blood levels of IL-1β, IL-6, IL-8, IL-10, IFN-γ, and TNF-α were measured by Luminex technology. A full-mouth periodontal examination was conducted to record probing depth (PD) and clinical attachment (CA) loss. Multiple linear regression models, adjusting for gender, body mass index, oral hypoglycemic drugs, smoking, and occurre:nce of acute myocardial infarction were applied.Results CAD patients that experienced major events had higher concentrations of IFN-γ (median: 5.05 pg/mL vs. 3.01 pg/mL; p=0.01), IL-10 (median: 2.33 pg/mL vs. 1.01 pg/mL; p=0.03), and TNF-α (median: 9.17 pg/mL vs. 7.47 pg/mL; p=0.02). Higher numbers of teeth with at least 6 mm of CA loss (R2=0.07) and PD (R2=0.06) were significantly associated with higher IFN-γ log concentrations. Mean CA loss (R2=0.05) and PD (R2=0.06) were significantly related to IL-10 concentrations. Elevated concentrations of TNF-α were associated with higher mean CA loss (R2=0.07).Conclusion Periodontal disease is associated with increased systemic inflammation in stable cardiovascular patients. These findings provide additional evidence supporting the idea that periodontal disease can be a prognostic factor in cardiovascular patients.

Highlights

QÀDPPDWLRQ SOD\V DQ LPSRUWDQW UROH LQ WKH initiation and development of atherosclerosis19
Atherosclerotic lesions are comprised of various FHOOW\SHVWKDWSURGXFHSURDQGDQWLLQÀDPPDWRU\ cytokines, which participate in the plaque formation cascade in vessel walls12 6SHFL¿FDOO\ LQWHUOHXNLQ (IL)-6, tumor necrosis factor (TNF)-a, and interferon,)1DŽ DUH IRXQG LQ HOHYDWHG FRQFHQWUDWLRQV LQ blood from cardiovascular patients22,29, and the IL
Probing depth and clinical attachment loss are the most frequent SHULRGRQWDOSDUDPHWHUVXVHGWRGH¿QHSHULRGRQWDO health/disease status, and they may be expressed as individual averages or by the number of teeth affected per individual

Summary

Introduction

QÀDPPDWLRQ SOD\V DQ LPSRUWDQW UROH LQ WKH initiation and development of atherosclerosis. Be expressed using various clinical parameters and GH¿QLWLRQV E\ ZKLFK WKH\ DUH DVVRFLDWHG ZLWK ULVN factors and systemic conditions. Studies have demonstrated that periodontitis, which is the destructive form of periodontal disease, increases systemic levels of some of the aforementioned CVD-related cytokines. Studies have demonstrated that periodontitis, which is the destructive form of periodontal disease, increases systemic levels of some of the aforementioned CVD-related cytokines3,15 Most evidence supporting this claim has been provided by studies conducted in otherwise systemically healthy individuals, suggesting that periodontal disease may be a risk factor for CVD. There is little information about the systemic effects of periodontal disease on patients with stable CVD, with few studies evaluating the association between periodontal disease and a small number of V\VWHPLFLQÀDPPDWRU\ELRPDUNHUVLQFDUGLRYDVFXODU patients

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