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*Compound via MeSH
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*Joint Disorders
The Journal of Immunology, 2002, 169: 507-514.
Copyright © 2002 by The American Association of Immunologists

Inhibition of Endogenous TGF-{beta} During Experimental Osteoarthritis Prevents Osteophyte Formation and Impairs Cartilage Repair

Alwin Scharstuhl1, Harrie L. Glansbeek, Henk M. van Beuningen, Elly L. Vitters, Peter M. van der Kraan and Wim B. van den Berg

Rheumatology Research Laboratory, Department of Rheumatology, University Medical Center, Nijmegen, The Netherlands

Osteoarthritis has as main characteristics the degradation of articular cartilage and the formation of new bone at the joint edges, so-called osteophytes. In this study enhanced expression of TGF-{beta}1 and -{beta}3 was detected in developing osteophytes and articular cartilage during murine experimental osteoarthritis. To determine the role of endogenous TGF-{beta} on osteophyte formation and articular cartilage, TGF-{beta} activity was blocked via a scavenging soluble TGF-{beta}-RII. Our results clearly show that inhibition of endogenous TGF-{beta} nearly completely prevented osteophyte formation. In contrast, treatment with recombinant soluble TGF-{beta}-RII markedly enhanced articular cartilage proteoglycan loss and reduced the thickness of articular cartilage. In conclusion, we show for the first time that endogenous TGF-{beta} is a crucial factor in the process of osteophyte formation and has an important function in protection against cartilage loss.




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