Since most horses are used for recreational or performance activities, soundness is understandably of vital importance to horse owners. A 2003 study suggested that 60% of lameness problems in horses are related to osteoarthritis, thus stressing the importance of advancements in treating this disease. In humans, osteoarthritis is the most common type of arthritis and in the U.S. alone afflicts more than 20 million people.

A horse’s joints give its skeleton flexibility and allow walking, trotting, running, jumping and moving its neck and head. The primary factors limiting these activities in the horse are pain and lameness that accompany joint disease. While it may develop in any joint, it is most common in weight-bearing joints, such as the hock, fetlock, pastern and coffin. Other joints may also be affected as the result of previous injury or from repetitive or abnormal stress.

Osteoarthritis may be considered as a group of disorders marked by progressive deterioration of the articular cartilage (cartilage that covers the surfaces of bones connected at a joint) accompanied by changes in the bone and soft tissues of the joint. This cartilage, which is critical for joints to function normally and alleviates the stress placed on a horse's joints during exercise, coats the ends of the articulating bones and contributes to friction-free motion.

The earliest stage of osteoarthritis (OA), or degenerative joint disease (DJD), occurs when the biochemical components of the articular cartilage (collagen and proteoglycans) start degenerating and the cartilage commences to break down. As the cartilage deteriorates, the body attempts to repair it but is unsuccessful, in part because of the loss of specialized cells called chondrocytes. Because the remaining cells are damaged, they prove unable to produce new cartilage of sufficient quality for effective repair.

Among the contributors to OA are synovitis (inflammation of the soft, pliable membrane lining a joint) and capsulitis (inflammation and thickening of the fibrous tissue enveloping the joint). Other contributors are bone fractures and injury to the bone just beneath the cartilage (subchondral bone). Damage to the subchondral bone not only contributes to degraded articular cartilage and the osteoarthritic process but is also the first stage in the development of fractures. Soft tissue injuries, including disruption of an intraarticular ligament or a meniscus, can also lead to OA.

The principal methods for treating OA revolve around the cause of the cartilage breakdown. Treatments for synovitis and capsulitis include physical therapy, intraarticular corticosteroids, intraarticular and intravenous hyaluronan, polysulfated glycosaminoglycans (PSGAG) and new biological therapies, such as gene therapy with interleukin one-receptor antagonist (this protocol has been shown to effectively combat OA but is not yet commercially available) and or autologous conditioned serum (IRAP™).

All are used to try and decrease the inflammation in joints to relieve pain and decrease the cartilage breakdown. All have been shown to be beneficial through research.

Fractures and subchondral bone disease are addressed by arthroscopic surgery, as are meniscal and some ligamentous injuries, while more severe fractures require internal fixation to stabilize the joint. Immediate and correct treatment of these injuries is important to prevent progressive loss of articular cartilage and OA.

Once articular cartilage is lost, restoration of repair tissue is challenging. It is possible that modern medicine in conjunction with a judicious balance between exercise and rest might enable a horse to return to some level of activity, usually at a lower level than before the onset of the disease. On the other hand, OA can end a horse’s competitive career. Though advances are being made in treatments, such as