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Article: Neovascularization and mandibular condylar bone remodeling in adult rats under mechanical strain

TitleNeovascularization and mandibular condylar bone remodeling in adult rats under mechanical strain
Authors
KeywordsAdult
Condylar growth
Mechanical strain
Micro-CT
Type X collagen
VEGF
Issue Date2005
PublisherFrontiers in Bioscience. The Journal's web site is located at http://www.frontbiosci.org/
Citation
Frontiers In Bioscience, 2005, v. 10 n. 1, p. 74-82 How to Cite?
AbstractThe present study was designed to explore the relationship between neovascularization, hypertrophic cartilage and the microstructural properties of cancellous bone in adult rat's condyle in response to mechanical strain produced by mandibular advancement. Seventy-eight 120-day-old female Sprague-Dawley rats were randomly allotted to six groups, nine animals in each experimental group according to different time points. Mandibular advancement appliances were used to produce mechanical strain onto to the mandibular condyles of rats. Immunostaining of VEGF and type X collagen were carried out. Tartrate-Resistant Acid Phosphatase (TRAP) reaction was used to assess the activity of chondroclasts. Direct three-dimensional morphometric analysis was carried out with microcomputed tomography (Micro-CT) scanning to evaluate the properties of microstructure of cancellous bone in the mandibular condyles. Results showed that mechanical strain produced by mandibular advancement induced neovascularization in the posterior condyle marked by the increased expression of VEGF. Neovascularization coupled the remodeling of calcified cartilage as marked by the expression of type X collagen and new bone formation. The new bone formed in the adult condyle was characterized by thinner trabecular thickness, more trabecular number and increased trabecular space. In conclusion, mechanical strain produced by mandibular advancement induces neovascularization and osteogenesis leading to adaptive growth of condyle in adult rats.
Persistent Identifierhttp://hdl.handle.net/10722/65917
ISSN
2020 Impact Factor: 4.009
2020 SCImago Journal Rankings: 1.117
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXiong, Hen_HK
dc.contributor.authorRabie, ABMen_HK
dc.contributor.authorHagg, Uen_HK
dc.date.accessioned2010-09-06T05:42:05Z-
dc.date.available2010-09-06T05:42:05Z-
dc.date.issued2005en_HK
dc.identifier.citationFrontiers In Bioscience, 2005, v. 10 n. 1, p. 74-82en_HK
dc.identifier.issn1093-9946en_HK
dc.identifier.urihttp://hdl.handle.net/10722/65917-
dc.description.abstractThe present study was designed to explore the relationship between neovascularization, hypertrophic cartilage and the microstructural properties of cancellous bone in adult rat's condyle in response to mechanical strain produced by mandibular advancement. Seventy-eight 120-day-old female Sprague-Dawley rats were randomly allotted to six groups, nine animals in each experimental group according to different time points. Mandibular advancement appliances were used to produce mechanical strain onto to the mandibular condyles of rats. Immunostaining of VEGF and type X collagen were carried out. Tartrate-Resistant Acid Phosphatase (TRAP) reaction was used to assess the activity of chondroclasts. Direct three-dimensional morphometric analysis was carried out with microcomputed tomography (Micro-CT) scanning to evaluate the properties of microstructure of cancellous bone in the mandibular condyles. Results showed that mechanical strain produced by mandibular advancement induced neovascularization in the posterior condyle marked by the increased expression of VEGF. Neovascularization coupled the remodeling of calcified cartilage as marked by the expression of type X collagen and new bone formation. The new bone formed in the adult condyle was characterized by thinner trabecular thickness, more trabecular number and increased trabecular space. In conclusion, mechanical strain produced by mandibular advancement induces neovascularization and osteogenesis leading to adaptive growth of condyle in adult rats.en_HK
dc.languageengen_HK
dc.publisherFrontiers in Bioscience. The Journal's web site is located at http://www.frontbiosci.org/en_HK
dc.relation.ispartofFrontiers in Bioscienceen_HK
dc.subjectAdulten_HK
dc.subjectCondylar growthen_HK
dc.subjectMechanical strainen_HK
dc.subjectMicro-CTen_HK
dc.subjectType X collagenen_HK
dc.subjectVEGFen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBone Remodelingen_HK
dc.subject.meshCollagen Type X - chemistryen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshMandibular Condyle - metabolism - pathologyen_HK
dc.subject.meshNeovascularization, Physiologicen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshStress, Mechanicalen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshTomography, X-Ray Computeden_HK
dc.subject.meshVascular Endothelial Growth Factor A - metabolismen_HK
dc.titleNeovascularization and mandibular condylar bone remodeling in adult rats under mechanical strainen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1093-9946&volume=10&spage=74&epage=82&date=2005&atitle=Neovascularization+and+mandibular+condylar+bone+remodeling+in+adult+rats+under+mechanical+strainen_HK
dc.identifier.emailRabie, ABM: rabie@hku.hken_HK
dc.identifier.emailHagg, U: euohagg@hkusua.hku.hken_HK
dc.identifier.authorityRabie, ABM=rp00029en_HK
dc.identifier.authorityHagg, U=rp00020en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2741/1508-
dc.identifier.pmid15574349-
dc.identifier.scopuseid_2-s2.0-17444362627en_HK
dc.identifier.hkuros98729en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-17444362627&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume10en_HK
dc.identifier.issue1en_HK
dc.identifier.spage74en_HK
dc.identifier.epage82en_HK
dc.identifier.isiWOS:000232319300009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXiong, H=36852325600en_HK
dc.identifier.scopusauthoridRabie, ABM=7007172734en_HK
dc.identifier.scopusauthoridHagg, U=7006790279en_HK
dc.identifier.issnl1093-4715-

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