Analysis of genetic polymorphisms in skeletal Class I crowding

Am J Orthod Dentofacial Orthop. 2011 Jul;140(1):e9-15. doi: 10.1016/j.ajodo.2010.12.015.

Abstract

Introduction: Dental crowding is a problem for both adolescents and adults in modern society. The purpose of this research was to identify single nucleotide polymorphisms (SNPs) responsible for crowding in subjects with skeletal Class I relationships.

Methods: The case subjects consisted of healthy Chinese people living in Hong Kong with skeletal Class I relationships and at least 5 mm of crowding in either arch. The control subjects met the same requirements but lacked crowding or spacing. SNP genotyping was performed on the MassARRAY platform. The chi-square test was used to compare genotype and allele type distributions between the case and the control groups. Logistic regression was used to calculate odds ratios with 95% confidence intervals, and the effects of age and sex for each SNP. Analyses of linkage disequilibrium and haplotype associations between SNPs were performed with software.

Results: Five SNPs were found to be significantly different in genotype or allele type distributions. SNP rs372024 was significantly associated with crowding (P = 0.004). Two SNPs, rs3764746 and rs3795170, on the EDA gene were found to be associated marginally. SNPs rs1005464 and rs15705 also exhibited marginal association with crowding. The effects of associated SNPs remained significant after adjustments for age and sex factors.

Conclusions: This study suggests an association for the genes EDA and XEDAR in dental crowding in the Hong Kong Chinese population.

MeSH terms

  • Adolescent
  • Asian People / genetics
  • Case-Control Studies
  • Chi-Square Distribution
  • DNA Mutational Analysis / methods
  • Ectodysplasins / genetics*
  • Female
  • Gene Frequency
  • Hong Kong
  • Humans
  • Linkage Disequilibrium
  • Logistic Models
  • Male
  • Malocclusion, Angle Class I / genetics*
  • Mass Spectrometry / methods
  • Oligonucleotide Array Sequence Analysis / methods
  • Polymorphism, Single Nucleotide*
  • Xedar Receptor / genetics*

Substances

  • EDA protein, human
  • EDA2R protein, human
  • Ectodysplasins
  • Xedar Receptor