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j.joca.2011.04.007.pdf | 16.3 MB | Adobe PDF | 見る/開く |
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dc.contributor.author | Kudo, Satoshi | en |
dc.contributor.author | Mizuta, Hiroshi | en |
dc.contributor.author | Takagi, Katsumasa | en |
dc.contributor.author | Hiraki, Yuji | en |
dc.contributor.alternative | 開, 祐司 | ja |
dc.date.accessioned | 2011-08-09T03:04:10Z | - |
dc.date.available | 2011-08-09T03:04:10Z | - |
dc.date.issued | 2011-07 | - |
dc.identifier.issn | 1063-4584 | - |
dc.identifier.uri | http://hdl.handle.net/2433/143679 | - |
dc.description.abstract | Objective:We studied the effects of the transient activation of parathyroid hormone (PTH)/PTH-related peptide (PTHrP) signaling during the repair of 5-mm-diameter full-thickness defects of articular cartilage in the rabbit. Materials and methods:Cylindrical full-thickness articular cartilage defects of 5 mm in diameter were artificially created in the femoral trochlea of male adolescent Japanese white rabbits using a hand-drill. Recombinant human PTH(1-84) was then administered into the joint cavity continuously or intermittently for 2 weeks post-injury. The reparative tissues were histologically examined at 2, 4, and 8 weeks, and were also immunohistochemically examined for type II collagen. Double immunostaining analysis was also performed for the PTH/PTHrP receptor and proliferating cell nuclear antigen (PCNA) in the regenerating tissues. Results:No evidence of cartilage formation was evident throughout the period of the experiments in injured animals administered saline alone. In contrast, cartilage formation occurred at 4 weeks in both the continuous and intermittent PTH-treated defects. At 8 weeks post-injury, for the intermittently treated defects, the regenerated cartilage successfully resurfaced the defects and the original bone-articular cartilage junction was recovered. In contrast, the defects were covered with fibrous or fibrocartilaginous tissues in the continuously administered group. PCNA and PTH/PTHrP receptor-double positive mesenchymal cells were significantly increased in both the continuous and intermittent PTH-treated defects at 2 weeks post-injury. Conclusions:The present results suggest that the transient activation and release from PTH/PTHrP signaling during the early stages of the cartilage repair process facilitates the induction of regenerative chondrogenesis in full-thickness articular cartilage defects. | en |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Elsevier Ltd. | en |
dc.rights | Copyright © 2011 Osteoarthritis Research Society International Published by Elsevier Ltd. | en |
dc.rights | この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。 | ja |
dc.rights | This is not the published version. Please cite only the published version. | en |
dc.subject | PTH/PTHrP signaling | en |
dc.subject | Chondrogenesis | en |
dc.subject | Tissue repair | en |
dc.subject | Articular cartilage | en |
dc.subject | Osteochondral defects | en |
dc.title | Cartilaginous repair of full-thickness articular cartilage defects is induced by the intermittent activation of PTH/PTHrP signaling. | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.ncid | AA10998176 | - |
dc.identifier.jtitle | Osteoarthritis and cartilage | en |
dc.identifier.volume | 19 | - |
dc.identifier.issue | 7 | - |
dc.identifier.spage | 886 | - |
dc.identifier.epage | 894 | - |
dc.relation.doi | 10.1016/j.joca.2011.04.007 | - |
dc.textversion | author | - |
dc.identifier.pmid | 21571083 | - |
dcterms.accessRights | open access | - |
出現コレクション: | 学術雑誌掲載論文等 |
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