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Rheumatology Advance Access originally published online on November 15, 2005
Rheumatology 2006 45(4):405-413; doi:10.1093/rheumatology/kei187
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Inhibition of COX-2 by celecoxib in the canine groove model of osteoarthritis

S. C. Mastbergen, A. C. Marijnissen, M. E. Vianen, B. Zoer, P. M. van Roermund1, J. W. Bijlsma and F. P. Lafeber

Rheumatology and Clinical Immunology, 1 Department of Orthopaedics, University Medical Center Utrecht, The Netherlands.

Correspondence to: S. Mastbergen, University Medical Center Utrecht, PO Box 85500 (F02.127), 3508 GA Utrecht, The Netherlands. E-mail: S.Mastbergen{at}azu.nl

Objective. In vitro studies showed a beneficial effect of celecoxib on proteoglycan turnover and content of osteoarthritic cartilage. In the present study we evaluated whether these favourable effects of celecoxib could also be demonstrated in vivo.

Methods. In 24 Beagle dogs, osteoarthritis (OA) was induced in one knee according to the groove model. The animals were divided into three groups and received oral placebo or 100 or 200 mg celecoxib daily, starting directly after surgery. After 15 weeks joint tissue from all dogs was analysed.

Results. Induction of OA resulted in macroscopic and histological damage of cartilage, changes in cartilage proteoglycan turnover, loss of cartilage matrix proteoglycans and slight synovial inflammation, all characteristic of early OA. Surprisingly, none of the parameters was significantly changed upon celecoxib treatment. Synovial fluid prostaglandin E2 levels were dose-dependently diminished by celecoxib, demonstrating that the celecoxib had reached the joint in sufficient amounts. Using an in vitro setup, canine cartilage under degenerative conditions was favourably influenced by celecoxib, demonstrating that canine cartilage is sensitive to celecoxib.

Conclusion. The present study showed a chondroneutral effect of celecoxib on the characteristics of experimentally induced OA in vivo, in contrast to the observed beneficial effect in vitro. It could be that celecoxib had been beneficial to degenerated cartilage in vivo but that these effects were counteracted by increased loading of the affected joint and the associated progression of OA, occurring because of the well-known analgesic effects of celecoxib.


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