Intra-articular dexamethasone to inhibit the development of post-traumatic osteoarthritis.

ABSTRACT: Injury to the joint provokes a number of local pathophysiological changes, including synthesis of inflammatory cytokines, death of chondrocytes, breakdown of the extra-cellular matrix of cartilage, and reduced synthesis of matrix macromolecules. These processes combine to engender the subsequent development of post-traumatic osteoarthritis (PTOA). To prevent this from happening, it is necessary to inhibit these disparate responses to injury; given their heterogeneity, this is challenging. However, dexamethasone has the necessary pleiotropic properties required of a drug for this purpose. Using in vitro models, we have shown that low doses of dexamethasone sustain the synthesis of cartilage proteoglycans while inhibiting their breakdown after injurious compression in the presence or absence

SUBMITTER: Grodzinsky AJ 

PROVIDER: S-EPMC5604325 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature