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Article: Uncoupled angiogenesis and osteogenesis in nicotine-compromised bone healing

TitleUncoupled angiogenesis and osteogenesis in nicotine-compromised bone healing
Authors
KeywordsAngiogenesis
Bone healing
Bone morphogenetic protein 2
Hypoxia inducible factor 1α
Nicotine
Osteogenesis
Vascular endothelial growth factor
Issue Date2010
PublisherAmerican Society for Bone and Mineral Research. The Journal's web site is located at http://www.jbmr.org/view/0/index.html
Citation
Journal Of Bone And Mineral Research, 2010, v. 25 n. 6, p. 1305-1313 How to Cite?
AbstractNicotine is the main chemical component responsible for tobacco addiction. This study aimed to evaluate the influence of nicotine on angiogenesis and osteogenesis and the associated expression of angiogenic and osteogenic mediators during bone healing. Forty-eight adult New Zealand White rabbits were randomly assigned to a nicotine group and a control group. Nicotine pellets (1.5 g, 60-day time release) or placebo pellets were implanted in the neck subcutaneous tissue. The nicotine or placebo exposure time for all the animals was 7 weeks. Unilateral mandibular distraction osteogenesis was performed. Eight animals in each group were euthanized on day 5, day 11 of active distraction, and week 1 of consolidation, respectively. The mandibular samples were subjected to radiographic, histologic, immunohistochemical, and real-time reverse-transcriptase polymerase chain reaction examinations. Nicotine exposure upregulated the expression of hypoxia inducible factor 1α and vascular endothelial growth factor and enhanced angiogenesis but inhibited the expression of bone morphogenetic protein 2 and impaired bone healing. The results indicate that nicotine decouples angiogenesis and osteogenesis in this rabbit model of distraction osteogenesis, and the enhanced angiogenesis cannot compensate for the adverse effects of nicotine on bone healing. © 2010 American Society for Bone and Mineral Research.
Persistent Identifierhttp://hdl.handle.net/10722/147620
ISSN
2015 Impact Factor: 5.622
2015 SCImago Journal Rankings: 2.773
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong KongHKU200507176099
Funding Information:

This study was supported by the Small Project Funding Programme (Reference code HKU200507176099) from the University of Hong Kong. We appreciate the valuable advice given by Professor J Glowacki from the Harvard School of Dental Medicine. We also appreciate the technical assistance provided by the Laboratory Animal Unit of the Li Ka Shing Faculty of Medicine and the Centralized Research Laboratories of the Faculty of Dentistry.

References

 

DC FieldValueLanguage
dc.contributor.authorLi, Men_HK
dc.contributor.authorLi, WZen_HK
dc.contributor.authorMai, HSen_HK
dc.contributor.authorLim, KCen_HK
dc.date.accessioned2012-05-29T06:05:01Z-
dc.date.available2012-05-29T06:05:01Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Bone And Mineral Research, 2010, v. 25 n. 6, p. 1305-1313en_HK
dc.identifier.issn0884-0431en_HK
dc.identifier.urihttp://hdl.handle.net/10722/147620-
dc.description.abstractNicotine is the main chemical component responsible for tobacco addiction. This study aimed to evaluate the influence of nicotine on angiogenesis and osteogenesis and the associated expression of angiogenic and osteogenic mediators during bone healing. Forty-eight adult New Zealand White rabbits were randomly assigned to a nicotine group and a control group. Nicotine pellets (1.5 g, 60-day time release) or placebo pellets were implanted in the neck subcutaneous tissue. The nicotine or placebo exposure time for all the animals was 7 weeks. Unilateral mandibular distraction osteogenesis was performed. Eight animals in each group were euthanized on day 5, day 11 of active distraction, and week 1 of consolidation, respectively. The mandibular samples were subjected to radiographic, histologic, immunohistochemical, and real-time reverse-transcriptase polymerase chain reaction examinations. Nicotine exposure upregulated the expression of hypoxia inducible factor 1α and vascular endothelial growth factor and enhanced angiogenesis but inhibited the expression of bone morphogenetic protein 2 and impaired bone healing. The results indicate that nicotine decouples angiogenesis and osteogenesis in this rabbit model of distraction osteogenesis, and the enhanced angiogenesis cannot compensate for the adverse effects of nicotine on bone healing. © 2010 American Society for Bone and Mineral Research.en_HK
dc.languageengen_US
dc.publisherAmerican Society for Bone and Mineral Research. The Journal's web site is located at http://www.jbmr.org/view/0/index.htmlen_HK
dc.relation.ispartofJournal of Bone and Mineral Researchen_HK
dc.subjectAngiogenesisen_HK
dc.subjectBone healingen_HK
dc.subjectBone morphogenetic protein 2en_HK
dc.subjectHypoxia inducible factor 1αen_HK
dc.subjectNicotineen_HK
dc.subjectOsteogenesisen_HK
dc.subjectVascular endothelial growth factoren_HK
dc.subject.meshAnimalsen_US
dc.subject.meshAntigens, Cd31 - Metabolismen_US
dc.subject.meshBone Morphogenetic Protein 2 - Genetics - Metabolismen_US
dc.subject.meshBone Regeneration - Drug Effectsen_US
dc.subject.meshBone And Bones - Blood Supply - Drug Effects - Pathology - Radiographyen_US
dc.subject.meshCollagen Type Iv - Metabolismen_US
dc.subject.meshGene Expression Regulation - Drug Effectsen_US
dc.subject.meshHypoxia-Inducible Factor 1, Alpha Subunit - Genetics - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshModels, Biologicalen_US
dc.subject.meshNeovascularization, Physiologic - Drug Effects - Geneticsen_US
dc.subject.meshNicotine - Pharmacologyen_US
dc.subject.meshOsteogenesis, Distractionen_US
dc.subject.meshRna, Messenger - Genetics - Metabolismen_US
dc.subject.meshRabbitsen_US
dc.subject.meshVascular Endothelial Growth Factor A - Genetics - Metabolismen_US
dc.subject.meshWound Healing - Drug Effects - Geneticsen_US
dc.titleUncoupled angiogenesis and osteogenesis in nicotine-compromised bone healingen_HK
dc.typeArticleen_HK
dc.identifier.emailLi, WZ:lwzheng@hku.hken_HK
dc.identifier.emailMai, HS:mhsham@hkucc.hku.hken_HK
dc.identifier.authorityLi, WZ=rp01411en_HK
dc.identifier.authorityMai, HS=rp00380en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/jbmr.19en_HK
dc.identifier.pmid20200934-
dc.identifier.scopuseid_2-s2.0-77953529300en_HK
dc.identifier.hkuros170977-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77953529300&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume25en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1305en_HK
dc.identifier.epage1313en_HK
dc.identifier.eissn1523-4681-
dc.identifier.isiWOS:000279441300011-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, M=36480313400en_HK
dc.identifier.scopusauthoridLi, WZ=11241247300en_HK
dc.identifier.scopusauthoridMai, HS=7003729109en_HK
dc.identifier.scopusauthoridLim, KC=15119192900en_HK

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