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Conference Paper: Biology of statin-induced osteogenesis

TitleBiology of statin-induced osteogenesis
Authors
Issue Date2004
PublisherOxford University Press
Citation
The 80th Congress of the European Orthodontic Society, Aarhus, Denmark, 7-11 June 2004. In The European Journal of Orthodontics, 2004, v. 26 n. 5, p. e83 Abstract no.167 How to Cite?
AbstractAIMS: To study histologically, ultrastructurally, quantitatively, and immunologically the biology of statin-induced osteogenesis. MATERIAL AND METHOD: Forty-five bone defects were created on the parietal bone of 24 New Zealand White rabbits. In the quantitative study, five defects were grafted with statin together with the carrier, five defects were left empty (passive control) and five defects were grafted with the carrier alone (active control). After 14 days, all rabbits were sacrificed and serial sections were histologically analysed. The passive control group showed no bone formation across the defects. Quantitative analysis on area of new bone formation was performed on 100 sections of the experimental and positive control groups using an image analyser. RESULTS: In the experimental group new bone could be seen spanning across the defect. Three hundred and eighty per cent more new bone was formed in defects grafted with statin than those grafted with the carrier alone (P < 0.001). Immunolocalization studies on the early healing of the defects grafted with statin, showed that growth factor expression occurred one day earlier than those grafted with the carrier alone. Ultrastructurally, bone cells were identified in the newly formed bone. CONCLUSIONS: Statin induces and accelerates bone formation locally. It triggers the early expression of growth factors that regulate osteogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/94697
ISSN
2015 Impact Factor: 1.44
2015 SCImago Journal Rankings: 1.090

 

DC FieldValueLanguage
dc.contributor.authorWong, RWKen_HK
dc.contributor.authorRabie, ABMen_HK
dc.date.accessioned2010-09-25T15:39:11Z-
dc.date.available2010-09-25T15:39:11Z-
dc.date.issued2004en_HK
dc.identifier.citationThe 80th Congress of the European Orthodontic Society, Aarhus, Denmark, 7-11 June 2004. In The European Journal of Orthodontics, 2004, v. 26 n. 5, p. e83 Abstract no.167en_HK
dc.identifier.issn0141-5387-
dc.identifier.urihttp://hdl.handle.net/10722/94697-
dc.description.abstractAIMS: To study histologically, ultrastructurally, quantitatively, and immunologically the biology of statin-induced osteogenesis. MATERIAL AND METHOD: Forty-five bone defects were created on the parietal bone of 24 New Zealand White rabbits. In the quantitative study, five defects were grafted with statin together with the carrier, five defects were left empty (passive control) and five defects were grafted with the carrier alone (active control). After 14 days, all rabbits were sacrificed and serial sections were histologically analysed. The passive control group showed no bone formation across the defects. Quantitative analysis on area of new bone formation was performed on 100 sections of the experimental and positive control groups using an image analyser. RESULTS: In the experimental group new bone could be seen spanning across the defect. Three hundred and eighty per cent more new bone was formed in defects grafted with statin than those grafted with the carrier alone (P < 0.001). Immunolocalization studies on the early healing of the defects grafted with statin, showed that growth factor expression occurred one day earlier than those grafted with the carrier alone. Ultrastructurally, bone cells were identified in the newly formed bone. CONCLUSIONS: Statin induces and accelerates bone formation locally. It triggers the early expression of growth factors that regulate osteogenesis.-
dc.languageengen_HK
dc.publisherOxford University Press-
dc.relation.ispartofThe European Journal of Orthodonticsen_HK
dc.titleBiology of statin-induced osteogenesisen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailWong, RWK: fyoung@hkucc.hku.hken_HK
dc.identifier.emailRabie, ABM: rabie@hkusua.hku.hken_HK
dc.identifier.authorityWong, RWK=rp00038en_HK
dc.identifier.authorityRabie, ABM=rp00029en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/ejo/26.5.e1-
dc.identifier.hkuros110887en_HK

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