Degenerative joint disease is a common malady of the horse. It most frequently strikes the hocks, front fetlocks, and front navicular bones, and its consequences can be severe. In fact, degeneration of the joints is the most common reason for retirement of a horse from athletic use. What mechanisms underlie this joint erosion, and what can be done to stop it?

In the limbs of a healthy horse, bone meets bone within the specialized confines of a fluid-filled structure termed the synovial joint. The synovial joint is designed to allow free movement between the ends of the bones, which are encased by a sack-like joint capsule. The capsule’s outer layer is tough and fibrous, and along with additional ligaments, it connects the bones and restricts their relative movement to the desired directions. Inside the joint capsule, the bones are coated with thin layers of smooth cartilage, while the capsule itself is coated with a delicate connective tissue termed the synovial membrane. This membrane is responsible for producing the lubricant component of the synovial fluid that fills the joint cavity. With a cushion of lubricant interposed, the opposing surfaces of cartilage can slide easily against one another.

With disease, however, the structure of the joint is affected such that this smooth, low-friction movement is no longer possible. The term degenerative joint disease, or DJD, refers to a group of disorders resulting in a common outcome: progressive deterioration of the health of the joint cartilage, along with destructive changes to the associated bone and soft tissues. The surface of the joint cartilage becomes split and fragmented, and the synovial lining of the joint capsule may become inflamed, causing the joint to swell with abnormal, excessive fluid. The affected horse shows pain, lameness, and loss of normal joint function.

The health of the joint cartilage depends on a delicate and complex balance between the formation and the degradation of its components. Because cartilage does not receive its vital nutrients directly from blood vessels, supplies are limited and may be inadequate in times of increased cartilage cell turnover. Virtually any insult to the cartilage may affect its nutritional state and result in tissue damage, including such common events as traumatic injury to the joint, mechanical misalignment, vascular disease, use of some non-steroidal anti-inflammatory drugs, and either total immobilization or excessive activity