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Article: Healing of autogenous intramembranous bone in the presence and absence of homologous demineralized intramembranous bone.

TitleHealing of autogenous intramembranous bone in the presence and absence of homologous demineralized intramembranous bone.
Authors
Issue Date2000
PublisherMosby, Inc. The Journal's web site is located at http://www.elsevier.com/locate/ajodo
Citation
American Journal Of Orthodontics And Dentofacial Orthopedics : Official Publication Of The American Association Of Orthodontists, Its Constituent Societies, And The American Board Of Orthodontics, 2000, v. 117 n. 3, p. 288-297 How to Cite?
AbstractThis study was designed to examine the osteogenecity of demineralized bone matrix (DBM) prepared from intramembranous (IM) bone and to quantitatively assess the amount of new bone formed by IM autogenous bone grafts with or without DBM(IM). Forty-two defects were created in 42 New Zealand White rabbits. Twenty-one defects were grafted with IM bone alone, and the other 21 defects were grafted with composite IM-DBM(IM). Eleven rabbits, 22 defects were used as controls, where 11 defects were left empty (passive control) and the other 11 defects were filled with rabbit skin collagen (active control). Tissues were retrieved on days 1, 2, 3, 4, 5, 6, 7, and 14 for qualitative and quantitative analysis. Cells involved in the healing of composite IM and IM-DBM(IM) bone grafts were identified. No cartilage cells were detected during the healing of either grafts. Appearance of small blood vessels into the newly formed matrix was seen on day 5 in IM bone grafts and on day 4 in composite IM-DBM(IM) bone graft. Quantitative analysis was performed by means of image analysis on 100 sections of tissues retrieved after 14 days. Approximately 204% more new bone was formed in defects grafted with composite IM-DBM(IM) than in those grafted with IM bone alone (P <.0001). No bone was formed across the defects in either active or passive controls. In conclusion, DBM(IM) significantly increases the osteogenicity of IM bone grafts.
Persistent Identifierhttp://hdl.handle.net/10722/154098
ISSN
2023 Impact Factor: 2.7
2023 SCImago Journal Rankings: 1.283
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRabie, ABen_HK
dc.contributor.authorChay, SHen_HK
dc.contributor.authorWong, AMen_HK
dc.date.accessioned2012-08-08T08:23:15Z-
dc.date.available2012-08-08T08:23:15Z-
dc.date.issued2000en_HK
dc.identifier.citationAmerican Journal Of Orthodontics And Dentofacial Orthopedics : Official Publication Of The American Association Of Orthodontists, Its Constituent Societies, And The American Board Of Orthodontics, 2000, v. 117 n. 3, p. 288-297en_HK
dc.identifier.issn0889-5406en_HK
dc.identifier.urihttp://hdl.handle.net/10722/154098-
dc.description.abstractThis study was designed to examine the osteogenecity of demineralized bone matrix (DBM) prepared from intramembranous (IM) bone and to quantitatively assess the amount of new bone formed by IM autogenous bone grafts with or without DBM(IM). Forty-two defects were created in 42 New Zealand White rabbits. Twenty-one defects were grafted with IM bone alone, and the other 21 defects were grafted with composite IM-DBM(IM). Eleven rabbits, 22 defects were used as controls, where 11 defects were left empty (passive control) and the other 11 defects were filled with rabbit skin collagen (active control). Tissues were retrieved on days 1, 2, 3, 4, 5, 6, 7, and 14 for qualitative and quantitative analysis. Cells involved in the healing of composite IM and IM-DBM(IM) bone grafts were identified. No cartilage cells were detected during the healing of either grafts. Appearance of small blood vessels into the newly formed matrix was seen on day 5 in IM bone grafts and on day 4 in composite IM-DBM(IM) bone graft. Quantitative analysis was performed by means of image analysis on 100 sections of tissues retrieved after 14 days. Approximately 204% more new bone was formed in defects grafted with composite IM-DBM(IM) than in those grafted with IM bone alone (P <.0001). No bone was formed across the defects in either active or passive controls. In conclusion, DBM(IM) significantly increases the osteogenicity of IM bone grafts.en_HK
dc.languageengen_US
dc.publisherMosby, Inc. The Journal's web site is located at http://www.elsevier.com/locate/ajodoen_HK
dc.relation.ispartofAmerican journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodonticsen_HK
dc.subject.meshAnalysis Of Varianceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBone Matrix - Blood Supply - Pathologyen_US
dc.subject.meshBone Substitutes - Therapeutic Useen_US
dc.subject.meshBone Transplantation - Methods - Pathologyen_US
dc.subject.meshBone And Bones - Blood Supply - Pathology - Physiopathology - Surgeryen_US
dc.subject.meshChondrocytes - Pathologyen_US
dc.subject.meshCollagen - Therapeutic Useen_US
dc.subject.meshConfidence Intervalsen_US
dc.subject.meshDecalcification Techniqueen_US
dc.subject.meshImage Processing, Computer-Assisteden_US
dc.subject.meshMicroscopy, Electronen_US
dc.subject.meshNeovascularization, Physiologicen_US
dc.subject.meshOsteoblasts - Pathologyen_US
dc.subject.meshOsteocytes - Pathologyen_US
dc.subject.meshOsteogenesis - Physiologyen_US
dc.subject.meshRabbitsen_US
dc.subject.meshTransplantation, Autologousen_US
dc.subject.meshTransplantation, Homologousen_US
dc.subject.meshWound Healingen_US
dc.titleHealing of autogenous intramembranous bone in the presence and absence of homologous demineralized intramembranous bone.en_HK
dc.typeArticleen_HK
dc.identifier.emailRabie, AB: rabie@hku.hken_HK
dc.identifier.authorityRabie, AB=rp00029en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0889-5406(00)70233-2-
dc.identifier.pmid10715088-
dc.identifier.scopuseid_2-s2.0-0034146563en_HK
dc.identifier.volume117en_HK
dc.identifier.issue3en_HK
dc.identifier.spage288en_HK
dc.identifier.epage297en_HK
dc.identifier.isiWOS:000085919700007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridRabie, AB=7007172734en_HK
dc.identifier.scopusauthoridChay, SH=7003856668en_HK
dc.identifier.scopusauthoridWong, AM=7403147117en_HK
dc.identifier.issnl0889-5406-

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