IADR Abstract Archives
Genetic Polymorphisms Associated with Mandibular Prognathism
Objectives: To verify the association between polymorphisms in ten candidate loci with skeletal Class III malocclusion with mandibular prognathism in a well characterized homogeneous sample set.
Methods: From a cohort of 652 individuals, we genotyped 35 single nucleotide polymorphisms in ten candidate loci (1p22.1, 1p22.2, 1p36, 3q26.2, 5p13-p12, 6q25, 11q22.2-q22.3, 12q24.11, 12q13.13, and 19p13.2) in 174 selected patients, distributed as following, 54 Class III subjects (27 males and 27 females, mean age 19.7± 8.5 years) and 120 Class I subjects (53 males and 67 females, mean age 20.48 ± 11.1 years). The diagnostic criteria to skeletal Class III malocclusion with mandibular prognathism included ANB<0o, SNB>83o, molar Class III, and negative overjet. Inclusion criteria for skeletal Class I were 0oo, molar Class I and normal overjet. Genetic markers were tested by polymerase chain reaction using TaqMan chemistry. Chi-square and Fisher’s exact tests were used to determine overrepresentation of marker alleles with alpha of 0.05. Odds ratios (OR) and respective 95% confidence intervals were calculated.
Results: The MYO1H (rs10850110, A>G) [p<0.01; OR=7.44 (4.02 -13.77)] G allele was more commonly found in the mandibular prognathism phenotype. The FBN3 (rs7351083, A>G) [p=0.05; OR=1.77 (1.0 – 3.13)] G allele was borderline significantly over-represented in mandibular prognathism.
Conclusions: We provide evidence that polymorphisms in MYO1H (locus 12q24.11) and FBN3 (locus 19p13.2) are associated with mandibular prognathism underlying skeletal Class III malocclusion. This study will delineate future research assessing possible differences in treatment responses based on genetic polymorphisms.
Methods: From a cohort of 652 individuals, we genotyped 35 single nucleotide polymorphisms in ten candidate loci (1p22.1, 1p22.2, 1p36, 3q26.2, 5p13-p12, 6q25, 11q22.2-q22.3, 12q24.11, 12q13.13, and 19p13.2) in 174 selected patients, distributed as following, 54 Class III subjects (27 males and 27 females, mean age 19.7± 8.5 years) and 120 Class I subjects (53 males and 67 females, mean age 20.48 ± 11.1 years). The diagnostic criteria to skeletal Class III malocclusion with mandibular prognathism included ANB<0o, SNB>83o, molar Class III, and negative overjet. Inclusion criteria for skeletal Class I were 0o
Results: The MYO1H (rs10850110, A>G) [p<0.01; OR=7.44 (4.02 -13.77)] G allele was more commonly found in the mandibular prognathism phenotype. The FBN3 (rs7351083, A>G) [p=0.05; OR=1.77 (1.0 – 3.13)] G allele was borderline significantly over-represented in mandibular prognathism.
Conclusions: We provide evidence that polymorphisms in MYO1H (locus 12q24.11) and FBN3 (locus 19p13.2) are associated with mandibular prognathism underlying skeletal Class III malocclusion. This study will delineate future research assessing possible differences in treatment responses based on genetic polymorphisms.