alexa Mechanisms of Osteoarthritis from Animal Models

Journal of Osteoarthritis
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Considering the opinion of the Editorial Board Members, the publisher has decided to merge Journal of Osteoarthritis to International Journal of Clinical Rheumatology. Therefore, all the existing and future readers, authors are hereby requested to visit the International Journal of Clinical Rheumatology now onwards.
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Research Article

Mechanisms of Osteoarthritis from Animal Models

Hiroshi Kawaguchi*

Spine Center, Japan Community Health Care Organization (JCHO), Japan

*Corresponding Author:
Hiroshi Kawaguchi
Spine Center
Japan Community Health Care Organization (JCHO), Japan
Tel: 03-3269-8111
Fax: 03-3260-7840
Email: [email protected]

Received date: November 17, 2015; Accepted date: December 21, 2015; Published date: January 19, 2016

Citation: Hiroshi Kawaguchi (2016) Mechanisms of Osteoarthritis from Animal Models. J Ost Arth 1:101. doi: 10.4172/joas.1000101

Copyright: © 2016 Kawaguchi H. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Osteoarthritis (OA), one of the most common skeletal disorders characterized by cartilage degradation and osteophyte formation in joints, is induced by accumulated mechanical stress; however, little is known about the underlying molecular mechanism. Several experimental OA models in mice by producing instability in the knee joints have been developed to apply approaches from mouse genetics. Although proteinases like matrix metalloproteases and aggrecanases have now been proven to be the principal initiators of OA progression, clinical trials of proteinase inhibitors have not been successful for the treatment, turning the interest of researchers to the upstream signals of proteinase induction. These signals include undegraded and fragmented matrix proteins like type II collagen or fibronection that affects chondrocytes through distinct receptors. Another signal is pro-inflammatory factors that are produced by chondrocytes and synovial cells; however, recent studies that used mouse OA models in knockout mice did not support that these factors have a role in the central contribution to OA development. Our mouse genetic approaches found that the induction of a transcriptional activator Runx2 in chondrocytes under mechanical stress contributes to the pathogenesis of OA through chondrocyte hypertrophy. In addition, chondrocyte apoptosis has recently been identified as being involved in OA progression. We hereby propose that these endochondral ossification signals may be important for the OA progression, suggesting that the related molecules can clinically be therapeutic targets of this disease

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