A new approach to the treatment of mandibular prognathism

Gold, Joseph K.

doi:10.1016/0002-9416(49)90085-8

Cited by 22 publications

(6 citation statements)

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“…MP is important to the understanding of the molecular pathogenesis of skeletal Class III malocclusion. In particular, etiological factors of MP described in the literature [5][6][7][8][9] and genetic susceptibilities on mandible growth have been defined in recent studies. 3,[20][21][22][23][27][28][29][30][31] Although none of the genomewide …”

Section: Discussionmentioning

confidence: 99%

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Relationship between P561T and C422F polymorphisms in growth hormone receptor gene and mandibular prognathism

Bayram

Başçiftçi

Kurar

2014

The Angle Orthodontist

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Objective: To evaluate the allele and genotype frequencies of the P561T and C422F polymorphic sites of the growth hormone receptor (GHR) gene and the relationship between mandibular prognathism (MP) and these two single-nucleotide polymorphisms (SNPs). Materials and Methods: A total of 99 subjects with severe skeletal Class III MP who planned to undergo orthognathic surgery and 99 subjects with Class I occlusion were examined in this study to evaluate the relationship between MP and two SNPs in exon 10 of the GHR gene. GHR was chosen as a candidate gene because growth hormone plays an important role in cartilage growth. A blood sample was used to extract genomic DNA, and the polymerase chain reaction-restriction fragment length polymorphism method was used to determine genotypes of P561T and C422F. The Minitab 14.0 packet program was used to perform statistical analysis. Results: Allele frequencies of the C422F and P561T variants were determined. Because of the low allele frequency of the control group, statistical analysis could not be performed to test the difference between MP and control groups. Therefore, the data were combined to determine the association between the P561T polymorphism and craniofacial measurements. Effective mandibular length (condylion-gnathion) and lower face height (anterior nasal spina-menton) were associated with the P561T variant. Conclusion: This finding supports that the GHR might be a candidate gene for mandibular morphogenesis in this population. (Angle Orthod. 2014;84:803-809.)

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Section: Discussionmentioning

confidence: 99%

“…[6][7][8][9][10] Craniofacial growth in patients who show more pronounced characteristics of mandibular development is difficult to predict. 11 Growth hormone (GH) is a peptide hormone produced in the anterior pituitary gland that plays a major role in regulating the growth and development of the craniofacial complex.…”

Section: Introductionmentioning

confidence: 99%

Relationship between P561T and C422F polymorphisms in growth hormone receptor gene and mandibular prognathism

Bayram

Başçiftçi

Kurar

2014

The Angle Orthodontist

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“…In addition to the strong role of heredity there has been evidence suggesting the contribution of certain environmental factors to mandibular prognathism such as enlarged tonsils 13 , endocrine imbalances 14 , posture, trauma, and disease. 15 …”

Section: Introductionmentioning

confidence: 99%

Genetic variation in Myosin 1H contributes to mandibular prognathism

Tassopoulou-Fishell

Deeley

Harvey

et al. 2012

American Journal of Orthodontics and Dentofacial Orthopedics

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Introduction Several candidate loci have been suggested as influencing mandibular prognathism (1p22.1, 1p22.2, 1p36, 3q26.2, 5p13-p12, 6q25, 11q22.2-q22.3, 12q23, 12q13.13, and 19p13.2). The goal of this study was to replicate these results in a well-characterized homogeneous sample set. Methods Thirty-three single nucleotide polymorphisms spanning all candidate regions were studied in 44 prognathic and 35 Class I subjects from the University of Pittsburgh School of Dental Medicine Dental Registry and DNA Repository. The 44 mandibular prognathism subjects had an average age of 18.4 years, 31 were females and 13 males, and 24 were White, 15 African American, two Hispanic, and three Asian. The 35 Class I subjects had an average age of 17.6 years, 27 were females and 9 males, and 27 were White, six African Americans, one Hispanic, and two Asian. Skeletal mandibular prognathism diagnosis included cephalometric values indicative of Class III such as ANB smaller than two degrees, negative Witts appraisal, and positive A–B plane. Additional mandibular prognathism criteria included negative OJ and visually prognathic (concave) profile as determined by the subject's clinical evaluation. Orthognathic subjects without jaw deformations were used as a comparison group. Mandibular prognathism and orthognathic subjects were matched based on race, sex and age. Genetic markers were tested by polymerase chain reaction using TaqMan chemistry. Chi-square and Fisher exact tests were used to determine overrepresentation of marker allele with alpha of 0.05. Results An association was unveiled between a marker in MYO1H (rs10850110) and the mandibular prognathism phenotype (p=0.03). MYO1H is a Class-I myosin that is in a different protein group than the myosin isoforms of muscle sarcomeres, which are the basis of skeletal muscle fiber typing. Class I myosins are necessary for cell motility, phagocytosis and vesicle transport. Conclusions More strict clinical definitions may increase homogeneity and aid the studies of genetic susceptibility to malocclusions. We provide evidence that MYO1H may contribute to mandibular prognathism.

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“…In the second half of the last century heritage took over the role of the causal factor [19][20][21][22] .…”

Section: Introductionmentioning

confidence: 99%