title: Are KIR genes associated with clinical parameters in the course of periodontitis?
abstract: BACKGROUND
  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.
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Periodontology, Pomeranian Medical University, Szczecin, Poland.
authors.forename: Małgorzata
authors.initials: M
authors.lastname: Mazurek-Mochol
authors.affiliation: Laboratory of Immunogenetics and Tissue Immunology, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences Wrocław, Poland.
authors.forename: Edyta
authors.initials: E
authors.lastname: Majorczyk
authors.affiliation: Department of Periodontology, Pomeranian Medical University, Szczecin, Poland.
authors.forename: Jadwiga
authors.initials: J
authors.lastname: Banach
authors.affiliation: Department of Periodontology, Pomeranian Medical University, Szczecin, Poland.
authors.forename: Elżbieta
authors.initials: E
authors.lastname: Dembowska
authors.affiliation: Department of Pharmacology, Pomeranian Medical University, Szczecin, Poland.
authors.forename: Andrzej
authors.initials: A
authors.lastname: Pawlik
authors.affiliation: Laboratory of Immunogenetics and Tissue Immunology, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences Wrocław, Poland.
authors.forename: Piotr
authors.initials: P
authors.lastname: Kuśnierczyk
mesh_terms: D000328:Adult; D002908:Chronic Disease; D018450:Disease Progression; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010518:Periodontitis / Q000235:genetics*; D054340:Receptors, KIR / Q000235:genetics*
chemical_list: D054340:Receptors, KIR