Jadwiga Banach

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

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 multivariate 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.

Are KIR genes associated with clinical parameters in the course of periodontitis

INTRODUCTION Periodontitis is a common chronic inflammatory disease. It seems that natural killer (NK) cells play a role in the pathogenesis of periodontitis. KIRs are a family of inhibitory or activating receptors expressed on the surfaces of NK cells and some subpopulations of T lymphocytes. The aim of this study was to evaluate the impact of KIR genes on the pocket depth (PD) and clinical attachment loss (CAL) parameter values as markers of disease clinical course. MATERIALS AND METHODS The patients in the study were submitted to anamnesis and to clinical and periodontal examination. The subjects (400) were categorized into two groups: periodontitis (250 including 100 with moderate and 140 with severe periodontitis) and controls (150). Both groups were divided into two subgroups: KIR gene positive (presence of KIR gene in the genome) and KIR gene negative (lack of the KIR gene in the genome). RESULTS The mean value for CAL was more than 5 mm, and the mean value for PD was more than 4 mm in the periodontitis group. The ANOVA test performed for the control group showed that neither PD nor CAL parameters differed between particular KIR-positive and KIR-negative healthy individuals. Similar results were obtained for all subgroups of chronic periodontitis patients and periodontitis patients (moderate as well as severe): no association between KIR genes and PD or CAL parameters was found. DISCUSSIONS The activated immune system is important in pathogenesis of periodontal disease. On the other hand, tissue damage as a response to infection could be due to activation mediated by KIR. In our study no association between either KIR genes presence or absence and PD and CAL parameters was found. Nevertheless, the impact of KIR genes on the clinical course of periodontal disease requires further investigations.