Degenerative joint diseases, such as osteoarthritis, adversely impact the health of the equine athlete as well as the economics of the equine industry. Our understanding of the aetiology of osteoarthritis, although not nearly exhaustive, has increased substantially in recent years. Molecules, including cytokines, inflammatory mediators, and metalloproteinases, have been identified and associated with the progression of joint disease. Several factors, including trauma to the joint, immobilization, conformation, shoeing, and ageing, have been linked with osteoarthritis. Our continued efforts into elucidating critical biological mediators and risk factors, coupled with better chondroprotective therapies and diagnostic tools, should facilitate our ability to maintain the skeletal health of the equine athlete

Traumatic injury to a joint can initiate cartilage degradation. Blunt trauma increases matrix damage and decreases proteoglycan synthesis in in vitro models. Few studies have investigated gene expression of articular cartilage (AC) following mechanical loading. Recent advances in microarray technology allow analysis of a number of genes, and may elucidate pathways of AC degradation. In the present study, we used a bovine cDNA microarray to determine how acute trauma of cartilage explants in the absence of underlying bone alters gene expression. Results indicate that at least 19 genes were differentially expressed at 3 h after trauma. Fourteen genes were up-regulated and five genes were down-regulated relative to control explants. The up-regulated genes included cytokine and chemokine receptors, enzymes, and molecules involved in signal transduction. Genes of adhesion molecules and apoptosis were down-regulated. The results of this study highlight the potential benefits of using a bovine cDNA microarray to study cartilage metabolism.

No abstract