title: NADPH oxidase (CYBA) and FcgammaR polymorphisms as risk factors for aggressive periodontitis: a case-control association study.
abstract: BACKGROUND
  Neutrophils (PMN) in aggressive periodontitis (AgP) patients have been reported to be hyperactive especially with regards to superoxide production. Polymorphisms in genes influencing PMN function have been proposed as candidate risk factors for AgP. The aim of this study was to test the association of specific gene polymorphisms affecting PMN functions with AgP.
  
  
  METHODS
  Two hundred and twenty-four patients with confirmed diagnosis of AgP and 231 subjects with healthy periodontium took part in the study. A blood sample was collected from subjects and genotypes for p22phox (CYBA) NADPH oxidase, FP, Fcalpha and Fcgamma receptors were analysed in a blind fashion.
  
  
  RESULTS
  The C242T p22phox NADPH oxidase T allele was significantly associated with AgP in a multiple logistic regression model adjusting for confounders, and this was observed for all subjects [p = 0.002, odds ratio (OR) = 1.87, 95% confidence interval (CI) = 1.27-2.83] and Caucasians (p = 0.009, OR=2.07, 95% CI = 1.20-3.59). Concomitant presence of C242T p22phox NADPH oxidase T allele and FcgammaRIIIb NA1 homozygosity was associated with the generalized AgP phenotype in Caucasians (p = 0.001, OR = 30.35, 95% CI = 3.81-241.97).
  
  
  CONCLUSIONS
  C242T p22phox NADPH oxidase and FcgammaR polymorphisms may predispose to AgP through a modulation of neutrophil superoxide production.
authors.affiliation: Periodontology Unit, University College London (UCL), London, UK.
authors.forename: L
authors.initials: L
authors.lastname: Nibali
authors.forename: M
authors.initials: M
authors.lastname: Parkar
authors.forename: P
authors.initials: P
authors.lastname: Brett
authors.forename: J
authors.initials: J
authors.lastname: Knight
authors.forename: M S
authors.initials: MS
authors.lastname: Tonetti
authors.forename: G S
authors.initials: GS
authors.lastname: Griffiths
mesh_terms: D000328:Adult; D000483:Alleles; D015703:Antigens, CD / Q000235:genetics; D016022:Case-Control Studies; D005260:Female; D058851:GPI-Linked Proteins; D006239:Haplotypes / Q000235:genetics; D006801:Humans; D007070:Immunoglobulin A / Q000235:genetics; D008297:Male; D019255:NADPH Oxidases / Q000502:physiology*; D018375:Neutrophil Activation / Q000235:genetics / Q000502:physiology; D010518:Periodontitis / Q000201:enzymology / Q000209:etiology* / Q000276:immunology; D011110:Polymorphism, Genetic / Q000235:genetics*; D011961:Receptors, Fc / Q000235:genetics; D044042:Receptors, Formyl Peptide / Q000235:genetics; D017452:Receptors, IgG / Q000235:genetics*; D012307:Risk Factors; D012737:Sex Factors; D016037:Single-Blind Method; D012907:Smoking
chemical_list: D015703:Antigens, CD; C499173:FCGR2B protein, human; C428200:FCGR3B protein, human; C080568:Fc gamma receptor IIA; C036832:Fc(alpha) receptor; D058851:GPI-Linked Proteins; D007070:Immunoglobulin A; D011961:Receptors, Fc; D044042:Receptors, Formyl Peptide; D017452:Receptors, IgG; D019255:NADPH Oxidases; C086986:CYBA protein, human