Degenerative joint disease (DJD), also commonly referred to as osteoarthritis (OA), may be considered a group of disorders characterized by a common end stage, progressive deterioration of the articular cartilage, accompanied by changes in the bone and soft tissues of the joint. Synovitis and joint effusion are often associated with the disease. Clinically, the disease is characterized by pain and dysfunction of the affected joint. Human DJD has been classified conventionally into primary and secondary varieties. The term "primary" is used when the causes are unidentified and is typified by the insidiously developing disease of old people. The term "secondary" is used when an etiologic factor can be demonstrated. The term degenerative joint disease (DJD) has been used as a synonym for primary OA. However as more etiologic factors become identified, the distinction between primary and secondary lessens and osteoarthritis is more commonly used than DJD.
Photo 1: Diagnosis is an important component of managing osteoarthritis in the horse. A thorough examination of the horse is the first step to a meaningful diagnosis, and treatment, if necessary.
OA or DJD has a number of entities.
1. Acute is associated with synovitis and high motion joints and typically affecting the athlete on the high motion joints such as the carpal metacarpophalangeal joint.
2. Insidious involves the high load/low motion joints such as the interphalangeal and intertarsal joints. This type was initially classified as a disease that predominates in mature and aged horses, but is also a major problem in young, competitive horses and overlaps considerably with the acute category.
3. Incidental (non-progressive) articular cartilage erosion is recognized at arthroscopy or during necropsy and is of questionable significance.
4. Secondary to other identified problems such as intra-articular fractures, ligamentous tears and dislocations, wounds, septic arthritis and OCD. If the latter conditions are not treated effectively, secondary OA develops and leads to functional limitations.
Understanding the disease
The most common scenario facing the equine clinician is the DJD entity associated with synovitis, that, if treated ineffectively, leads to progressive degeneration of the articular cartilage. The pathobiologic pathways have been identified over recent years and are depicted in Figure 1, p. 6. Much of the early suggestions on pathogenesis and factors involved came from mediators identified in other species. However, all the mediators depicted have been identified as elevated and involved in equine joint disease. Most of the final definitive degradation comes from the action of neutral metalloproteinases and aggrecanase. Proteoglycans and their component glycosaminoglycans are degraded early in the osteoarthritic process. While stromeolysin (MMP3) was considered the main agent responsible, more recently it appears that aggrecanase causes most of the proteoglycan degradation in OA. Degradation of collagen results in the physical lesions we recognize histologically, arthroscopically and later, grossly. Most of the collagen degradation is effected by neutral metalloproteinases 1 and 13 (collagenase 1 and 3). The neutral proteinases can be produced by inflamed synoviocytes directly, but also by both synoviocytes and chondrocytes in response to stimulation from interleukin-1. IL-1 can be considered at the top of the osteoarthritic cascade. Low quantities are present in normal joints to allow for regular turnover of components, but in the osteoarthritic process, their levels are elevated. By stimulating cell surface receptors, IL-1 upregulates the production of neutral metalloproteinases, aggrecanase as well as prostaglandin E2 (PGE2). PGE2 is released from cells on stimulation by IL-1, but also can be produced directly. PGE2 not only increases pain sensitivity, but also can promote the degradation of proteoglycans and collagen as well as inhibit proteoglycan synthesis. Free radicals are also present in increased amounts in inflamed equine joints and seem to be the way the hyaluronin (HA) gets degraded in the joint fluid. Effective inhibition of these mediators is key to effective treatment of inflammatory joint disease in the horse and prevention of the osteoarthritic process.
Photo 2: Arthroscopic examination is considered a gold standard for evaluating early articular disease.
Diagnosis is a key part of the management of OA. Clinical examination is still critical with lameness being localized to a particular joint or joints, synovial effusion in the acute stage and capsular fibrosis developing in the more chronic stage (Photo 1, p. 4). Radiographs are important to eliminate the presence of fractures and other bony problems, but are very limited in identifying the early osteoarthritic process. A number of advances have been made in recent years with diagnosis. Nuclear imaging can localize a process to an area or joint and is quite sensitive. However, it has poor specificity. Computed tomography (CT) is very useful for showing early subchondral bone change (microdamage in the subchondral bone is an early component of the osteoarthritic process and contributes to disease in the athlete). The usefulness of MRI in diagnosing early joint disease in the phalanges has been documented recently and the equipment is becoming available whereby more proximal joints can be imaged. This will provide a significant improvement in our ability to diagnose early disease in the articular cartilage, subchondral bone, menisci ligaments and joint capsule. Until that is achieved, arthroscopic examination is still the gold standard for evaluating early articular disease (Photo 2). Synovial fluid analysis has always been useful in defining the amount of inflammation in the joint. More recently, the development of biomarkers that can detect early degradation in proteoglycans and collagen has improved our ability to diagnose early articular disease. The accuracy for defining early osteoarthritis with biomarkers is now up to 90 percent, based on recent studies done at Colorado State University.