Osteochondrosis is one of the most important and prevalent developmental orthopedic diseases of horses. Although its specific etiology is not known, it is considered to arise from a focal disturbance in endochondral ossification. The term osteochondrosis is currently used to describe the clinical manifestation of the disorder; however, the term dyschondroplasia is preferred when referring to early lesions because primary lesions are seen in cartilage.
Osteochondrosis has a multifactorial etiology that includes rapid growth, overnutrition, mineral imbalance, and biomechanics (ie, trauma to cartilage). Genetics has been implicated in some breeds (eg, Standardbred and Swedish Warmblood). The condition mainly affects articular growth cartilage, but the metaphysis may also be involved. If the physeal metaphyseal cartilage is affected, bone contours and longitudinal growth are disturbed (see physitis, Physitis). Involvement of articular cartilage at the periphery of joint surfaces leads to regressive changes at the joint margins, dissecting lesions, and the formation of flaps (osteochondrosis). Central articular lesions, because of weight-bearing effects, involve focal retention of cartilage within the subchondral bone. Axial skeletal involvement includes vertebral articular facets, and this may lead to stenosis of the vertebral canal and, ultimately, ataxia and proprioceptive deficits (ie, wobbler syndrome).
The clinical signs of equine osteochondrosis are difficult to characterize specifically because of the wide range of lesions and sites involved. In severe cases, other signs of developmental orthopedic disease also may be apparent. Furthermore, lesions of dyschondroplasia do not always progress to osteochondrosis and produce clinical signs. These signs may begin with mild stiffness or lameness, but if there is superimposed biomechanical trauma, the joint damage progresses to pain and lameness or loss of performance.
The most common sign of osteochondrosis is a nonpainful distention of an affected joint (eg, gonitis, bog spavin). Clinical signs may be divided broadly into two categories; those seen in foals <6 mo old and those seen in older animals. Often the first sign noted in foals is a tendency to spend more time lying down. This is accompanied frequently by joint swelling, stiffness, and difficulty keeping up with other animals in the paddock. An accompanying sign may be the development of upright conformation of the limbs, presumably as a result of rapid growth. Fetlock osteochondrosis is particularly seen in younger foals (<6 mo old).
Marked lameness is not usually a feature of equine osteochondrosis, although it is seen with damage in some sites. For example, lesions in the shoulder frequently result in moderate to severe lameness, muscle atrophy, and pain on joint flexion. In the stifle, some horses with subchondral bone cysts in the medial femoral condyle present with lameness severe enough that a fracture may be suspected but without a discernible site of pain or any joint swelling. The true origin of pain in osteochondrosis is unknown. Horses often exhibit severe pathologic changes without showing much pain or distress in contrast to some situations seen in some other species and sites (eg, canine elbow).
The main signs in yearlings or older horses are stiffness of joints, flexion responses, and varying degrees of lameness. These signs are usually associated with the onset of training and, therefore, suggest a biomechanical influence and an activation of subclinical or “silent” lesions.
Clinical diagnosis can often be made on the basis of signalment and signs. More definitive diagnosis requires the use of some specific clinical aids. Radiographic examination has been the traditional method of confirming diagnosis; however, early lesions involving cartilage without significant subchondral bone damage will not be visualized. In the distal limb, oblique views may be helpful; in the hock, because the most common site of a lesion is the distal intermediate ridge of the tibia, the best view is a plantarolateral/dorsomedial oblique. Ultrasonographic examination of the swollen joints can also be helpful and can delineate articular damage and “joint mice.” The most accurate way to confirm diagnosis is by arthroscopy, and most of the predilection sites are accessible except for the cervical articulations.
Other aids include nuclear imaging (scintigraphy), which usually has negative results unless there is active secondary bone damage. Magnetic resonance imaging is ideal for diagnosis of both early and late lesions but is not widely available. Clinical pathology and the evaluation of synovial fluid may be helpful but is used largely to eliminate inflammatory causes of swollen joints.
Management of osteochondrosis depends on the site and severity of signs. Mild cases recover spontaneously, and a conservative approach may be appropriate. In young animals (<12 mo old), this involves restricted exercise for some weeks combined with a reduction in feed intake to slow the growth rate. Particular care should be taken to ensure appropriate mineral supplementation (eg, suspected copper deficiency). It is controversial whether correcting the diet, once signs have developed, will actually assist resolution, but it may help limit or prevent further cases on stud farms. Intra-articular medication with hyaluronic acid may be beneficial, and injection of long-acting corticosteroids may help reduce swelling and improve any associated synovitis.
Those cases considered for surgery are mainly treated arthroscopically. This technique has been successful in most affected sites, particularly the hock, stifle, and fetlock. In addition to removing damaged cartilage and loose pieces of subchondral bone (ie, “joint mice”), the bone overlying the lesion is curetted and the joint flushed extensively. Prognosis should be good in all but those cases with severe joint disruption or secondary arthrosis (degenerative joint disease).
Treatment of osteochondrotic lesions in the shoulder are often more problematic to treat surgically because arthroscopic access is more difficult, and there is usually more extensive subchondral bone damage, often with formation of multiple cysts. Therefore, the prognosis is always rather guarded.