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Article: Changes in blood perfusion and bone healing induced by nicotine during distraction osteogenesis

TitleChanges in blood perfusion and bone healing induced by nicotine during distraction osteogenesis
Authors
Issue Date2008
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/bone
Citation
Bone, 2008, v. 43 n. 2, p. 355-361 How to Cite?
AbstractNicotine is the main chemical in cigarettes responsible for the tobacco's pathological effects. The influence of nicotine on bone healing remains controversial. Distraction osteogenesis provides an ideal model to study bone healing and regeneration. The present study aims to evaluate the effects of nicotine on blood perfusion, angiogenesis and bone formation using a rabbit model of mandibular lengthening. Twenty adult New Zealand white rabbits were randomly assigned to the control group and nicotine group. The total nicotine or placebo exposure time for all animals was 7 weeks. After 2- or 4-week of consolidation following osteotomy, 3-day of latency and 11-day of active distraction, the animals were sacrificed and the mandibles were harvested. Blood perfusion and vascularization were evaluated by Laser Doppler monitoring and Collagen IV immunohistochemistry staining respectively. Bone formation was assessed by radiological, histological and immunohistochemical examination. Results showed that nicotine exposure increased microvessel density, whereas inhibited blood flow and bone formation. The expression of bone morphogenetic protein (BMP)-2 in osteoblasts was also decreased. Frequent appearance of cartilage islands suggested ischemia and low oxygen tension in the distraction regenerate. We concluded that nicotine compromises bone regeneration possibly by causing ischemia and directly inhibitory effect on osteoblastic cells. Nicotine exposure enhances angiogenesis but cannot compensate for the adverse effect of vasoconstriction. © 2008 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/66679
ISSN
2015 Impact Factor: 3.736
2015 SCImago Journal Rankings: 1.752
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, WZen_HK
dc.contributor.authorMa, Len_HK
dc.contributor.authorCheung, LKen_HK
dc.date.accessioned2010-09-06T05:48:24Z-
dc.date.available2010-09-06T05:48:24Z-
dc.date.issued2008en_HK
dc.identifier.citationBone, 2008, v. 43 n. 2, p. 355-361en_HK
dc.identifier.issn8756-3282en_HK
dc.identifier.urihttp://hdl.handle.net/10722/66679-
dc.description.abstractNicotine is the main chemical in cigarettes responsible for the tobacco's pathological effects. The influence of nicotine on bone healing remains controversial. Distraction osteogenesis provides an ideal model to study bone healing and regeneration. The present study aims to evaluate the effects of nicotine on blood perfusion, angiogenesis and bone formation using a rabbit model of mandibular lengthening. Twenty adult New Zealand white rabbits were randomly assigned to the control group and nicotine group. The total nicotine or placebo exposure time for all animals was 7 weeks. After 2- or 4-week of consolidation following osteotomy, 3-day of latency and 11-day of active distraction, the animals were sacrificed and the mandibles were harvested. Blood perfusion and vascularization were evaluated by Laser Doppler monitoring and Collagen IV immunohistochemistry staining respectively. Bone formation was assessed by radiological, histological and immunohistochemical examination. Results showed that nicotine exposure increased microvessel density, whereas inhibited blood flow and bone formation. The expression of bone morphogenetic protein (BMP)-2 in osteoblasts was also decreased. Frequent appearance of cartilage islands suggested ischemia and low oxygen tension in the distraction regenerate. We concluded that nicotine compromises bone regeneration possibly by causing ischemia and directly inhibitory effect on osteoblastic cells. Nicotine exposure enhances angiogenesis but cannot compensate for the adverse effect of vasoconstriction. © 2008 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/boneen_HK
dc.relation.ispartofBoneen_HK
dc.rightsBone. Copyright © Elsevier Inc.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBlood Vessels - drug effectsen_HK
dc.subject.meshBone Morphogenetic Protein 2en_HK
dc.subject.meshBone Morphogenetic Proteins - genetics - metabolismen_HK
dc.subject.meshBone Regeneration - drug effectsen_HK
dc.subject.meshCollagen Type IV - metabolismen_HK
dc.subject.meshFracture Healing - drug effectsen_HK
dc.subject.meshGene Expression Regulation - drug effectsen_HK
dc.subject.meshMandible - blood supply - drug effects - pathology - radiographyen_HK
dc.subject.meshNicotine - pharmacologyen_HK
dc.subject.meshOsteogenesis, Distractionen_HK
dc.subject.meshPerfusionen_HK
dc.subject.meshRabbitsen_HK
dc.subject.meshTomography, X-Ray Computeden_HK
dc.subject.meshTransforming Growth Factor beta - genetics - metabolismen_HK
dc.titleChanges in blood perfusion and bone healing induced by nicotine during distraction osteogenesisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=8756-3282&volume=43&spage=p. 355&epage=361&date=2008&atitle=Changes+in+blood+perfusion+and+bone+healing+induced+by+nicotine+during+distraction+osteogenesis.+en_HK
dc.identifier.emailLi, WZ:lwzheng@hku.hken_HK
dc.identifier.authorityLi, WZ=rp01411en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.bone.2008.04.002en_HK
dc.identifier.pmid18538646-
dc.identifier.scopuseid_2-s2.0-52449131092en_HK
dc.identifier.hkuros171261en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-52449131092&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume43en_HK
dc.identifier.issue2en_HK
dc.identifier.spage355en_HK
dc.identifier.epage361en_HK
dc.identifier.isiWOS:000257928300018-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, WZ=11241247300en_HK
dc.identifier.scopusauthoridMa, L=36071946000en_HK
dc.identifier.scopusauthoridLim, KC=15119192900en_HK

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