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Article: Genes, genetics, and Class III malocclusion

TitleGenes, genetics, and Class III malocclusion
Authors
KeywordsAssociation study
Class III malocclusion
Condylar growth
Linkage analysis
Single nucleotide polymorphisms
Issue Date2010
PublisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1601-6335&site=1
Citation
Orthodontics And Craniofacial Research, 2010, v. 13 n. 2, p. 69-74 How to Cite?
AbstractTo present current views that are pertinent to the investigation of the genetic etiology of Class III malocclusion. Class III malocclusion is thought to be a polygenic disorder that results from an interaction between susceptibility genes and environmental factors. However, research on family pedigrees has indicated that Class III malocclusion might also be a monogenic dominant phenotype. Recent studies have reported that genes that encode specific growth factors or other signaling molecules are involved in condylar growth under mechanical strain. These genes, which include Indian hedgehog homolog (IHH), parathyroid-hormone like hormone (PTHLH), insulin-like growth factor-1 (IGF-1), and vascular endothelial growth factor (VEGF), and variations in their levels of expression play an important role in the etiology of Class III malocclusion. In addition, genome-wide scans have revealed chromosomal loci that are associated with Class III malocclusion. It is likely that chromosomal loci 1p36, 12q23, and 12q13 harbor genes that confer susceptibility to Class III malocclusion. In a case-control association study, we identified erythrocyte membrane protein band 4.1 (EPB41) to be a new positional candidate gene that might be involved in susceptibility to mandibular prognathism. Most of the earlier studies on the genetic etiology of Class III malocclusion have focused on the patterns of inheritance of this phenotype. Recent investigations have focused on understanding the genetic variables that affect Class III malocclusion and might provide new approaches to uncovering the genetic etiology of this phenotype. © 2010 John Wiley & Sons A/S.
Persistent Identifierhttp://hdl.handle.net/10722/124416
ISSN
2015 Impact Factor: 1.64
2015 SCImago Journal Rankings: 0.881
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXue, Fen_HK
dc.contributor.authorWong, RWKen_HK
dc.contributor.authorRabie, ABMen_HK
dc.date.accessioned2010-10-31T10:33:10Z-
dc.date.available2010-10-31T10:33:10Z-
dc.date.issued2010en_HK
dc.identifier.citationOrthodontics And Craniofacial Research, 2010, v. 13 n. 2, p. 69-74en_HK
dc.identifier.issn1601-6335en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124416-
dc.description.abstractTo present current views that are pertinent to the investigation of the genetic etiology of Class III malocclusion. Class III malocclusion is thought to be a polygenic disorder that results from an interaction between susceptibility genes and environmental factors. However, research on family pedigrees has indicated that Class III malocclusion might also be a monogenic dominant phenotype. Recent studies have reported that genes that encode specific growth factors or other signaling molecules are involved in condylar growth under mechanical strain. These genes, which include Indian hedgehog homolog (IHH), parathyroid-hormone like hormone (PTHLH), insulin-like growth factor-1 (IGF-1), and vascular endothelial growth factor (VEGF), and variations in their levels of expression play an important role in the etiology of Class III malocclusion. In addition, genome-wide scans have revealed chromosomal loci that are associated with Class III malocclusion. It is likely that chromosomal loci 1p36, 12q23, and 12q13 harbor genes that confer susceptibility to Class III malocclusion. In a case-control association study, we identified erythrocyte membrane protein band 4.1 (EPB41) to be a new positional candidate gene that might be involved in susceptibility to mandibular prognathism. Most of the earlier studies on the genetic etiology of Class III malocclusion have focused on the patterns of inheritance of this phenotype. Recent investigations have focused on understanding the genetic variables that affect Class III malocclusion and might provide new approaches to uncovering the genetic etiology of this phenotype. © 2010 John Wiley & Sons A/S.en_HK
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1601-6335&site=1en_HK
dc.relation.ispartofOrthodontics and Craniofacial Researchen_HK
dc.rightsThe definitive version is available at www3.interscience.wiley.com-
dc.subjectAssociation studyen_HK
dc.subjectClass III malocclusionen_HK
dc.subjectCondylar growthen_HK
dc.subjectLinkage analysisen_HK
dc.subjectSingle nucleotide polymorphismsen_HK
dc.subject.meshChondrogenesis - genetics-
dc.subject.meshChromosomes, Human, Pair 1-
dc.subject.meshChromosomes, Human, Pair 12-
dc.subject.meshGenetic Linkage-
dc.subject.meshMalocclusion, Angle Class III - genetics-
dc.titleGenes, genetics, and Class III malocclusionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1601-6335&volume=13&issue=2&spage=69&epage=74&date=2010&atitle=Genes,+genetics,+and+Class+III+malocclusion-
dc.identifier.emailWong, RWK: fyoung@hku.hken_HK
dc.identifier.emailRabie, ABM: rabie@hku.hken_HK
dc.identifier.authorityWong, RWK=rp00038en_HK
dc.identifier.authorityRabie, ABM=rp00029en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1601-6343.2010.01485.xen_HK
dc.identifier.pmid20477965-
dc.identifier.scopuseid_2-s2.0-77954375263en_HK
dc.identifier.hkuros175619en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77954375263&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume13en_HK
dc.identifier.issue2en_HK
dc.identifier.spage69en_HK
dc.identifier.epage74en_HK
dc.identifier.isiWOS:000276863700001-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXue, F=8373582400en_HK
dc.identifier.scopusauthoridWong, RWK=7402127170en_HK
dc.identifier.scopusauthoridRabie, ABM=7007172734en_HK

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