Document Detail


Genetic variation in myosin 1H contributes to mandibular prognathism.
MedLine Citation:
PMID:  22196185     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 subjects with mandibular prognathism had an average age of 18.4 years; 31 were female and 13 male; and 24 were white, 15 African American, 2 Hispanic, and 3 Asian. The 36 Class I subjects had an average age of 17.6 years; 27 were female and 9 male; and 27 were white, 6 African American, 1 Hispanic, and 2 Asian. Skeletal mandibular prognathism diagnosis included cephalometric values indicative of Class III such as an ANB smaller than 2°, a negative Wits appraisal, and a positive A-B plane. Additional mandibular prognathism criteria included negative overjet and visually prognathic (concave) profile as determined by the subject's clinical evaluation. Orthognathic subjects without jaw deformations were used as the comparison group. The mandibular prognathic and orthognathic subjects were matched by race, sex, and age. Genetic markers were tested by polymerase chain reaction with TaqMan chemistry. Chi-square and Fisher exact tests were used to determine overrepresentation of marker allele with an 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 might increase homogeneity and aid the studies of genetic susceptibility to malocclusions. We provide evidence that MYO1H can contribute to mandibular prognathism.
Authors:
Maria Tassopoulou-Fishell; Kathleen Deeley; Erica M Harvey; James Sciote; Alexandre R Vieira
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodontics     Volume:  141     ISSN:  1097-6752     ISO Abbreviation:  Am J Orthod Dentofacial Orthop     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2011-12-26     Completed Date:  2012-02-14     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  8610224     Medline TA:  Am J Orthod Dentofacial Orthop     Country:  United States    
Other Details:
Languages:  eng     Pagination:  51-9     Citation Subset:  D; IM    
Copyright Information:
Copyright © 2012 American Association of Orthodontists. Published by Mosby, Inc. All rights reserved.
Affiliation:
Department of Orthodontics, School of Dental Medicine, University of Pittsburgh, Pittsburgh, PA 15261, USA.
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
African Americans / genetics
Asian Americans / genetics
Case-Control Studies
Chi-Square Distribution
Child
Chromosomes, Human, Pair 12 / genetics*
European Continental Ancestry Group / genetics
Female
Humans
Male
Malocclusion, Angle Class III / genetics*
Mandible / abnormalities*
Middle Aged
Myosin Type I / genetics*
Pilot Projects
Polymorphism, Single Nucleotide
Prognathism / genetics*
Young Adult
Grant Support
ID/Acronym/Agency:
5TL1RR024155-02/RR/NCRR NIH HHS; TL1 RR024155/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/myosin 1H, human; EC 3.6.1.-/Myosin Type I
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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