NADPH oxidase (CYBA) and FcγR polymorphisms as risk factors for aggressive periodontitis: A case–control association study
Article first published online: 17 JUL 2006
Journal of Clinical Periodontology
Volume 33, Issue 8, pages 529–539, August 2006
How to Cite
Nibali, L., Parkar, M., Brett, P., Knight, J., Tonetti, M. S. and Griffiths, G. S. (2006), NADPH oxidase (CYBA) and FcγR polymorphisms as risk factors for aggressive periodontitis: A case–control association study. Journal of Clinical Periodontology, 33: 529–539. doi: 10.1111/j.1600-051X.2006.00952.x
- Issue published online: 17 JUL 2006
- Article first published online: 17 JUL 2006
- Accepted for publication 28 April 2006
- aggressive periodontitis;
- genetic polymorphisms;
- NADPH oxidase;
- risk factors
Introduction: 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.
Material and 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, Fcα and Fcγ 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 FcγRIIIb 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 FcγR polymorphisms may predispose to AgP through a modulation of neutrophil superoxide production.