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Article: Influence of nicotine on the biological activity of rabbit osteoblasts

TitleInfluence of nicotine on the biological activity of rabbit osteoblasts
Authors
KeywordsAngiogenic mediator
Nicotine
Osteoblast
Osteogenic mediator
Proliferation
Issue Date2011
PublisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CLR
Citation
Clinical Oral Implants Research, 2011, v. 22 n. 3, p. 338-342 How to Cite?
AbstractObjectives: To assess the influence of nicotine on the proliferation and gene expression of osteogenic and angiogenic mediators of osteoblasts. Material and methods: Rabbit primary osteoblasts were exposed to various concentrations of nicotine (0.001, 0.1 and 10μmol/l). The cell proliferation was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide. The gene expression of transforming growth factor (TGF)-β1, bone morphogenetic protein (BMP)-2, platelet-derived growth factor (PDGF)-AA and vascular endothelial growth factor (VEGF) was evaluated using real-time reverse transcription - polymerase chain reaction. Results: The osteoblast proliferation was inhibited by nicotine at the concentration of 0.001-10μM at 48 and 72h of culture, but with no significant effect at 24h. The expression of TGF-β1, BMP-2, PDGF-AA and VEGF was inhibited by nicotine at the concentrations of 0.1 and 10μM, but with no significant difference at the low concentration of 0.001μM. Conclusions: Nicotine suppresses osteoblast proliferation and inhibits the expression of some key osteogenic and angiogenic mediators in the in vitro experimental model. These inhibitory effects of nicotine on the osteoblast activity may reflect, to a certain degree, the overall detrimental effects of tobacco use on the survival rate of dental implants. © 2011 John Wiley & Sons A/S.
Persistent Identifierhttp://hdl.handle.net/10722/134982
ISSN
2015 Impact Factor: 3.464
2015 SCImago Journal Rankings: 1.427
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong KongHKU200507176219
Funding Information:

This study was supported by the Small Project Funding Programme (Reference code: HKU200507176219) from the University of Hong Kong. We appreciate the valuable 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.authorMa, Len_HK
dc.contributor.authorZwahlen, RAen_HK
dc.contributor.authorZheng, LWen_HK
dc.contributor.authorSham, MHen_HK
dc.date.accessioned2011-07-27T01:25:19Z-
dc.date.available2011-07-27T01:25:19Z-
dc.date.issued2011en_HK
dc.identifier.citationClinical Oral Implants Research, 2011, v. 22 n. 3, p. 338-342en_HK
dc.identifier.issn0905-7161en_HK
dc.identifier.urihttp://hdl.handle.net/10722/134982-
dc.description.abstractObjectives: To assess the influence of nicotine on the proliferation and gene expression of osteogenic and angiogenic mediators of osteoblasts. Material and methods: Rabbit primary osteoblasts were exposed to various concentrations of nicotine (0.001, 0.1 and 10μmol/l). The cell proliferation was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide. The gene expression of transforming growth factor (TGF)-β1, bone morphogenetic protein (BMP)-2, platelet-derived growth factor (PDGF)-AA and vascular endothelial growth factor (VEGF) was evaluated using real-time reverse transcription - polymerase chain reaction. Results: The osteoblast proliferation was inhibited by nicotine at the concentration of 0.001-10μM at 48 and 72h of culture, but with no significant effect at 24h. The expression of TGF-β1, BMP-2, PDGF-AA and VEGF was inhibited by nicotine at the concentrations of 0.1 and 10μM, but with no significant difference at the low concentration of 0.001μM. Conclusions: Nicotine suppresses osteoblast proliferation and inhibits the expression of some key osteogenic and angiogenic mediators in the in vitro experimental model. These inhibitory effects of nicotine on the osteoblast activity may reflect, to a certain degree, the overall detrimental effects of tobacco use on the survival rate of dental implants. © 2011 John Wiley & Sons A/S.en_HK
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CLRen_HK
dc.relation.ispartofClinical Oral Implants Researchen_HK
dc.rightsThe definitive version is available at www3.interscience.wiley.com-
dc.subjectAngiogenic mediatoren_HK
dc.subjectNicotineen_HK
dc.subjectOsteoblasten_HK
dc.subjectOsteogenic mediatoren_HK
dc.subjectProliferationen_HK
dc.titleInfluence of nicotine on the biological activity of rabbit osteoblastsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0905-7161&volume=22&issue=3&spage=338&epage=342&date=2011&atitle=Influence+of+nicotine+on+the+biological+activity+of+rabbit+osteoblasts-
dc.identifier.emailZwahlen, RA:zwahlen@hku.hken_HK
dc.identifier.emailZheng, LW:lwzheng@hku.hken_HK
dc.identifier.emailSham, MH:mhsham@hkucc.hku.hken_HK
dc.identifier.authorityZwahlen, RA=rp00055en_HK
dc.identifier.authorityZheng, LW=rp01411en_HK
dc.identifier.authoritySham, MH=rp00380en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1600-0501.2010.02088.xen_HK
dc.identifier.pmid21561475-
dc.identifier.scopuseid_2-s2.0-79551573134en_HK
dc.identifier.hkuros188010en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79551573134&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume22en_HK
dc.identifier.issue3en_HK
dc.identifier.spage338en_HK
dc.identifier.epage342en_HK
dc.identifier.isiWOS:000286891100015-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridMa, L=36918802900en_HK
dc.identifier.scopusauthoridZwahlen, RA=7004217269en_HK
dc.identifier.scopusauthoridZheng, LW=11241247300en_HK
dc.identifier.scopusauthoridSham, MH=7003729109en_HK
dc.identifier.citeulike8799298-

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