| Chondrocyte apoptosis: a cause or consequence of osteoarthritis? | |
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MedLine Citation:
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PMID: 21518315 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Osteoarthritis (OA) is a degenerative joint disease characterized by articular cartilage degradation and changes in the subchondral bone. Over the last two decades, there has been increasing evidence showing association between cartilage degradation and chondrocyte death, and different types of cell death in cartilage have been reported, including apoptosis and chondroptosis as well as necrosis, but which of these types of cell death predominate in OA is debatable. There are also some methodological difficulties in detecting the specific form of cell death in articular cartilage. Current 'gold standard' for detecting chondrocyte death is electron microscopy which suggests that the morphological changes of chondrocytes in OA cartilage are attributed to apoptosis and/or chondroptosis. However, the current literature appears to suggest that classic apoptosis plays an important role in OA; but whether chondrocyte apoptosis is a cause or a result of cartilage degeneration in OA is hotly contested. Studies of suitable animal models, especially longitudinal studies, are needed to address the cause-and-effect relationship. |
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Authors:
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Zaitunnatakhin Zamli; Mohammed Sharif |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: International journal of rheumatic diseases Volume: 14 ISSN: 1756-185X ISO Abbreviation: Int J Rheum Dis Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-04-26 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101474930 Medline TA: Int J Rheum Dis Country: England |
Other Details:
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Languages: eng Pagination: 159-66 Citation Subset: IM |
Copyright Information:
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© 2011 The Authors. International Journal of Rheumatic Diseases © 2011 Asia Pacific League of Associations for Rheumatology and Blackwell Publishing Asia Pty Ltd. |
Affiliation:
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Department of Anatomy, University of Bristol, Bristol, UK. |
Export Citation:
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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