There is hope for horses affected by osteoarthritis as researchers continue to explore and develop disease-modifying techniques.

Most horse owners are already aware that osteoarthritis (OA) is one of the most important health-related problems for horses. The condition limits a horse’s athleticism and can, like any chronically painful condition, negatively impact a horse’s quality of life. Researchers estimate that this disease is the single most important cause of lameness in horses and that 60% of lameness problems are related to OA. Millions of horses are affected by OA, and costs associated with diagnosing and treating it can be as high as $15,000 per horse per year (TheHorse.com/14841).

While there is no cure for OA, treatment options abound. Two types or classes of medical treatments for OA-affected horses exist. One is called "symptomatic" and the other type is "disease-modifying." Symptomatic treatments for OA reduce clinical signs (e.g., heat, pain, lameness, swelling), helping the horse feel more comfortable and move easier. These symptomatic treatments, such as the anti-inflammatory drug phenylbutazone (Bute), however, do not stop the disease from progressing.

How Osteoarthritis Develops

Osteoarthritis (OA) is a painful condition primarily characterized by the progressive destruction of articular cartilage. Articular cartilage lines the ends of long bones where they joint together and transfer load during weight bearing. Without the cartilage, the bones are not "cushioned" during weight bearing, resulting in pain and inflammation during locomotion. A number of factors can cause or contribute to the degradation and destruction of articular cartilage. These include fracture within the joint (e.g., chip fracture); subchondral bone disease (e.g., osteochondritis dissecans); or inflammatory conditions such as synovitis or capsulitis, which are inflammation of the inner lining of the joint (the synovium) or the joint capsule, respectively. Regardless of the inciting factor, once the joint becomes inflamed, the articular cartilage is at risk. Various pro-inflammatory molecules (cytokines) are released into the joint, including interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFα). Metalloproteinases, enzymes that breakdown articular cartilage, are also produced and released in the joint. Together, these molecules cause the progressive deterioration of the articular cartilage and subchondral bone (the bone lying directly under the articular cartilage)

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