An Hypothesis on the Etio‐Pathogenesis of Equine Inflammatory Joint Disease

The role of oxygen-derived free radicals is considered critical to the etio-pathogenesis of equine inflammatory joint disease. In vivo, the superoxide radical in the joint may be derived either from activated polymorphonuclear leukocytes or from an ischemia/reperfusion cycle. In the presence of ferrous iron, it may generate the highly reactive hydroxyl radical (OH *). Predisposing factors may include synovitis, exercise-induced ischemia and minor traumatic injury to the joints. Unlike other inflammatory mediators, oxygen-derived free radicals may damage tissue directly and these reactive species could account for the tissue injury and insidious onset of equine exercise-induced degenerative joint disease.