Journal of clinical periodontology · 2003
Gm (23) allotypes and Fcgamma receptor genotypes as risk factors for various forms of periodontitis.
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Chung Hsien-Yang, Lu Hsi-chi, Chen Woan-Ling, Lu Chun-Tai, Yang Yi-Hsin, Tsai Chi-Cheng
Аннотация
OBJECTIVES: Given the diversity of the distribution of the Gm (23) allotypes and FcgammaR genotypes in different ethnic groups, it was our purpose to examine their clinical significance in periodontitis in Taiwan.
MATERIAL & METHODS: Genomic DNA of 50 patients with chronic periodontitis (CP), 30 patients with generalized aggressive periodontitis (G-AP) and 74 healthy controls were harvested. The Gm (23) allotypes were determined by radial immunodiffusion test, and the FcgammaR IIa (CD32) and IlIb (CD16) genotypes were determined by polymerase chain reaction-based allele-specific oligonucleotide hybridization.
RESULTS: The overall carrier rate of the Gm (23+) allotype was higher than 85%, and the Gm (23-) allotype was statistically over-represented in patients with CP compared to the controls. There were no differences in the distributions of the three genotypes of FcgammaR IIa and IIIb among the three tested groups. The frequency of the R131 allele of the FcgammaR IIa polymorphisms was higher in G-AP than in CP when R/H allelic frequencies (p = 0.01) were examined by the chi2 test.
CONCLUSION: The Gm (23-) allotype might be a potential risk factor for CP. Although the R131 allele of FcgammaR IIa occurred more frequently in G-AP than in CP, its clinical significance could not be justified in this study.
MATERIAL & METHODS: Genomic DNA of 50 patients with chronic periodontitis (CP), 30 patients with generalized aggressive periodontitis (G-AP) and 74 healthy controls were harvested. The Gm (23) allotypes were determined by radial immunodiffusion test, and the FcgammaR IIa (CD32) and IlIb (CD16) genotypes were determined by polymerase chain reaction-based allele-specific oligonucleotide hybridization.
RESULTS: The overall carrier rate of the Gm (23+) allotype was higher than 85%, and the Gm (23-) allotype was statistically over-represented in patients with CP compared to the controls. There were no differences in the distributions of the three genotypes of FcgammaR IIa and IIIb among the three tested groups. The frequency of the R131 allele of the FcgammaR IIa polymorphisms was higher in G-AP than in CP when R/H allelic frequencies (p = 0.01) were examined by the chi2 test.
CONCLUSION: The Gm (23-) allotype might be a potential risk factor for CP. Although the R131 allele of FcgammaR IIa occurred more frequently in G-AP than in CP, its clinical significance could not be justified in this study.