4.0 Article

The influence of KIR gene presence/absence polymorphisms on the development of periodontal disease in smokers and non-smokers

Journal

CENTRAL EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 42, Issue 4, Pages 347-353

Publisher

TERMEDIA PUBLISHING HOUSE LTD
DOI: 10.5114/ceji.2017.72796

Keywords

killer immunoglobulin-like receptors (KIRs); natural killer cells; inhibitory/activating receptors

Categories

Funding

  1. Ministry of Science and Higher Education [9/09/PB, MNiSW N N403 416736]

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Introduction: Periodontal diseases are highly prevalent inflammatory, multifactorial diseases. Smoking is one of the most important environmental risk factors for the development and severity of periodontal disease. Killer cell immunoglobulin-like receptors (KIRs) are members of the immunoglobulin (Ig) superfamily and play an essential role in the regulation of NK cell activity, allowing natural killer (NK) cells to sense and respond to human leukocyte antigen (HLA) class I. The aim of this study was to evaluate the influence of KIR gene presence/absence polymorphisms on the development of periodontal disease in smokers and non-smokers. Material and methods: This study enrolled 400 Caucasian subjects (age range 25-69 years) from the West Pomeranian region of Poland. The subjects were categorized into four subgroups (smoking and non-smoking patients with periodontal disease; smoking and non-smoking subjects without periodontal disease-control subjects). Results: The differences of KIR gene frequencies between non-smoking patients and non-smoking control subjects as well as smoking patients and control subjects were not statistically significant. In multi-variate regression analysis advanced age of patients and smoking were independent factors associated with increased frequency of periodontal disease. Conclusions: The results of this study suggest that the main factor associated with increased risk of periodontal disease is smoking, whereas KIR presence/absence polymorphism is not a significant factor involved in the pathogenesis of periodontal disease.

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