1. Introduction
Degenerative joint disease (DJD) or osteoarthritis in the equine athlete is a major cause of economic loss to the
equine industry through loss of revenue from an inability to perform and expense of treatment. Biomechanical stress
either as a major event or multiple low-grade events is a common etiology of DJD and results in a synovial inflammation,
degradation of cartilage, and changes of the subchondral bone. Development and propagation of changes
within the joint as a result of DJD is a consequence of the combination of a release of proinflammatory cytokines
(interleukin-1 and tumor necrosis factor alpha [TNF-a]),extracellular matrix degrading enzymes, arachidonic acid
metabolites, and oxygen free radicals [1–3]. These substances in turn cause synovial inflammation, cartilagedegradation, and subchondral bone remodeling creating a vicious cycle. Joint pain, which is commonly manifested
as lameness, is a result of exposure of sensory nerves of the synovial capsule, synovium, and subchondral bone to
a combination of mechanical stimuli, such as joint effusion, and chemical mediators, such as those involved in inflammation.
1. Introduction
Degenerative joint disease (DJD) or osteoarthritis in the equine athlete is a major cause of economic loss to the
equine industry through loss of revenue from an inability to perform and expense of treatment. Biomechanical stress
either as a major event or multiple low-grade events is a common etiology of DJD and results in a synovial inflammation,
degradation of cartilage, and changes of the subchondral bone. Development and propagation of changes
within the joint as a result of DJD is a consequence of the combination of a release of proinflammatory cytokines
(interleukin-1 and tumor necrosis factor alpha [TNF-a]),extracellular matrix degrading enzymes, arachidonic acid
metabolites, and oxygen free radicals [1–3]. These substances in turn cause synovial inflammation, cartilagedegradation, and subchondral bone remodeling creating a vicious cycle. Joint pain, which is commonly manifested
as lameness, is a result of exposure of sensory nerves of the synovial capsule, synovium, and subchondral bone to
a combination of mechanical stimuli, such as joint effusion, and chemical mediators, such as those involved in inflammation.
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