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STR/ORT mice exhibit an inherent endochondral growth defect and redeploy transient chondrocyte behaviours prior to osteoarthritis onset

DOI: 10.1016/j.joca.2014.02.659 DOI Help

Authors: Katherine Staines (Royal Veterinary College, U.K.) , S Parker (Royal Veterinary College, U.K.) , Blandine Poulet (University College London, U.K.) , Sam Mirczuk (Royal Veterinary College, U.K.) , Rob Fowkes (Royal Veterinary College, U.K.) , Mark Hopkinson (Royal Veterinary College, U.K.) , Kamel Madi (University of Manchester, U.K.) , Peter Lee (University of Manchester, U.K.) , Andrew Pitsillides (Royal Veterinary College, U.K.)
Co-authored by industrial partner: No

Type: Conference Paper
Conference: Osteoarthritis Research Society International, World Congress on Osteoarthritis, 2014
Peer Reviewed: Yes

State: Published (Approved)
Published: April 2014
Diamond Proposal Number(s): 5972 , 8665

Abstract: Increasing evidence implicates the re-initiation of embryonic processes, responsible for long bone development and growth, in osteoarthritic pathology. We aimed to establish whether an aberrant redeployment of the transient chondrocyte phenotype is observed in the STR/Ort mouse (spontaneous osteoarthritis), and whether this can be attributed to an inherent endochondral growth defect in these mice. Furthermore, we aimed to establish the role of the Wnt inhibitor sclerostin and its downstream target matrix extracellular phosphoglycoprotein (MEPE), a mineralisation inhibitor, in the maintenance of the healthy joint, and in the regulation of these endochondral processes in osteoarthritic joints.

Subject Areas: Biology and Bio-materials, Medicine, Technique Development

Instruments: I13-2-Diamond Manchester Imaging

Added On: 27/10/2014 13:28

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