Christiane Vasconcellos Cruz1, Claudia Trindade Mattos2, José Calasans Maia3, José Mauro Granjeiro4, Maria Fernanda Reis5, José Nelson Mucha2, Beatriz Vilella2, Antonio Carlos Ruellas1, Ronir Raggio Luiz6, Marcelo Castro Costa1, Alexandre Rezende Vieira7. 1. Department of Pediatric Dentistry and Orthodontics, School of Dentistry, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil. 2. Department of Orthodontics, Fluminense Federal University, Niterói, Rio de Janeiro, Brazil. 3. Department of Orthodontics, Fluminense Federal University, Nova Friburgo, Rio de Janeiro, Brazil. 4. National Institute of Metrology, Quality and Technology, Duque de Caxias, Rio de Janeiro, Brazil. 5. Department of Oral Biology, School of Dental Medicine, University of Pittsburgh, Pittsburgh, Pa. 6. Institute for Studies in Public Health, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil. 7. Department of Oral Biology, School of Dental Medicine, University of Pittsburgh, Pittsburgh, Pa. Electronic address: arv11@pitt.edu.
Abstract
INTRODUCTION: Our goal was to verify the association between candidate polymorphisms and skeletal Class III malocclusion in a well-characterized homogeneous sample set. METHODS: Thirty-five single-nucleotide polymorphisms were studied from 10 candidate loci in 54 Class III subjects and 120 controls. Skeletal Class III characteristics included ANB angle less than 0°, SNB angle greater than 83° (mandibular prognathism), SNA angle less than 79° (maxillary deficiency), Class III molar relationship, and negative overjet. Inclusion criteria for the controls were ANB angle between 0° and 4°, Class I molar relationship, and normal overjet. Chi-square and Fisher exact tests and principal component (PC) analysis were used to determine overrepresentation of marker alleles with alpha of 0.05. Odds ratios and 95% confidence intervals were calculated. RESULTS: MYO1H (rs10850110 A<G) (P <0.01; odds ratio, 7.44 [4.02-13.77]) was associated with an increased risk for the mandibular prognathism phenotype. These results were confirmed by PC analysis, which showed 4 PCs representing the sample variations (PC1, 37.24%; PC2, 20.02%; PC3, 12.18%; and PC4, 11.40%), and PC1 was associated with MYO1H (P <0.001). We also found by PC analysis associations between MYO1H (P <0.001) and GHR (rs2973015 A>G) (P = 0.001) with PC2 and between FGF10 (rs593307 A<G) (P = 0.001) with PC4. CONCLUSIONS: Polymorphism in MYO1H could be used as a marker for genetic susceptibility to Class III malocclusion with mandibular prognathism, and polymorphisms in GHR and FGF were associated with maxillomandibular discrepancies. This study may contribute to improved diagnosis and further research assessing possible differences in treatment responses based on genetic polymorphisms.
INTRODUCTION: Our goal was to verify the association between candidate polymorphisms and skeletal Class III malocclusion in a well-characterized homogeneous sample set. METHODS: Thirty-five single-nucleotide polymorphisms were studied from 10 candidate loci in 54 Class III subjects and 120 controls. Skeletal Class III characteristics included ANB angle less than 0°, SNB angle greater than 83° (mandibular prognathism), SNA angle less than 79° (maxillary deficiency), Class III molar relationship, and negative overjet. Inclusion criteria for the controls were ANB angle between 0° and 4°, Class I molar relationship, and normal overjet. Chi-square and Fisher exact tests and principal component (PC) analysis were used to determine overrepresentation of marker alleles with alpha of 0.05. Odds ratios and 95% confidence intervals were calculated. RESULTS:MYO1H (rs10850110 A<G) (P <0.01; odds ratio, 7.44 [4.02-13.77]) was associated with an increased risk for the mandibular prognathism phenotype. These results were confirmed by PC analysis, which showed 4 PCs representing the sample variations (PC1, 37.24%; PC2, 20.02%; PC3, 12.18%; and PC4, 11.40%), and PC1 was associated with MYO1H (P <0.001). We also found by PC analysis associations between MYO1H (P <0.001) and GHR (rs2973015 A>G) (P = 0.001) with PC2 and between FGF10 (rs593307 A<G) (P = 0.001) with PC4. CONCLUSIONS: Polymorphism in MYO1H could be used as a marker for genetic susceptibility to Class III malocclusion with mandibular prognathism, and polymorphisms in GHR and FGF were associated with maxillomandibular discrepancies. This study may contribute to improved diagnosis and further research assessing possible differences in treatment responses based on genetic polymorphisms.
Authors: Antonio Jiménez-Silva; Romano Carnevali-Arellano; Sheilah Vivanco-Coke; Julio Tobar-Reyes; Pamela Araya-Díaz; Hernán Palomino-Montenegro Journal: Clin Exp Dent Res Date: 2020-12-04
Authors: L de Frutos-Valle; C Martin; J A Alarcón; J C Palma-Fernández; R Ortega; A Iglesias-Linares Journal: Sci Rep Date: 2020-10-21 Impact factor: 4.379