Osteoarthritis in the horse

In vivoeffects of meloxicam on inflammatory mediators, MMP activity and cartilage biomarkers in equine joints with acute synovitis

“…For this reason, anti-inflammatory therapy is still a mainstay in the treatment of equine joint disease (Goodrich and Nixon 2006). Nonsteroidal anti-inflammatory drugs (NSAIDs) are a common first line treatment in joint disorders that require alleviation of pain and control of inflammation (Kidd et al 2001). However, our knowledge of the in vivo effects of NSAIDs on joint homeostasis is limited.…”

Survey of the therapeutic approach and efficacy of pentosan polysulfate for the prevention and treatment of equine osteoarthritis in veterinary practice inAustralia

“…Osteoarthritis (OA) is an important cause of lameness and poor performance in horses and has a significant economic impact on the equine industry . OA is characterised by degeneration of the synovial joint and involves varying degrees of articular cartilage loss, abnormal bone proliferation, subchondral sclerosis and synovial membrane dysfunction . Corticosteroids and non‐steroidal anti‐inflammatory drugs are commonly used to reduce joint inflammation and pain.…”

“…[2][3][4] OA is characterised by degeneration of the synovial joint and involves varying degrees of articular cartilage loss, abnormal bone proliferation, subchondral sclerosis and synovial membrane dysfunction. 5,6 Corticosteroids and nonsteroidal anti-inflammatory drugs are commonly used to reduce joint inflammation and pain. However, these agents have limited capacity to slow the pathological processes of OA or to promote healing of diseased cartilage.…”

Antioxidant capacity and oxidative damage determination in synovial fluid of chronically damaged equine metacarpophalangeal joint

“…We suggest that this increase is a consequence of an accelerated turnover rate of matrix biocomponents with antioxidant properties (i.e., glycosaminoglycans, hyaluronic acid and proteoglycans) due to a higher activity of matrix degradative enzymes (metalloproteinases and aggrecanases) that has been described in osteoarthritic joints (Dimock et al 2000;Sandell and Aigner 2001;Campo et al 2003). The increased activity of theses enzymes is triggered by proinflamatory cytokines such as IL-1, 17, 18 and TNFα which inhibit the synthesis of tissue inhibitor of metalloproteinases (TIMPs) (Caron 1992;Sandell and Aigner 2001;Kidd et al 2001;Goodrich and Nixon 2006;Grishko et al 2009). …”

“…Within the joint, trauma can cause an increase in prooxidants production, cited as the main osteoarthritic etiological factor (Kehrer 1993;Kidd et al 2001). The post traumatic inflammatory episode leads to the activation of phagocytes by proimflammatory cytokines (IL-1, IL-6 and TNFα).…”