Bone Formation Problems in Young Horses

The normal development of equine bone is a multiphase process occurring as a continuum of activity resulting in calcification of degenerating physeal cartilage, reabsorption, and redeposition as trabecular bone. The process takes place at the metaphyseal side of the physis and circumferentially around the ossification fronts of all epiphyses and cuboidal bones simultaneously.

The growth process requires the formation of cartilage, which causes the increase in size or length. The cartilage degenerates in an orderly fashion as its intercellular matrix is calcified. This calcified cartilage must be reabsorbed and bone must be redeposited as trabeculae, oriented against the lines of stress and deposited in sufficient numbers and size, to handle the load applied to the bone. It is not until trabeculae are deposited that ossification has occurred. If this process is disturbed or interrupted, the result is some type of developmental orthopedic disease.

The conditions referred to as developmental orthopedic disease are those that result from a disturbance in the change from the cartilage precursor of the skeleton into functional bone. Clinical manifestations include, but are not limited to, physitis, osteochondritis dissecans (OCD), and some angular limb deformities. Because acquired contracted flexor tendons can develop as a sequela to the pain resulting from these diseases, they are generally included as a part of the syndrome. Histologic changes in the cervical vertebrae of horses diagnosed as having cervical vertebral malformation have been reported and recently incriminated as a form of developmental orthopedic disease. Articular bone cysts and juvenile arthritis due to malformation of articular surfaces and cuboidal bones, especially of the distal tarsal joints and interphalangeal joints, are manifestations of this same disease complex.

Defective or slowed conversion of the calcified cartilage into mature (trabecular) bone results in a weakened metaphyseal component of the growth plate complex. This weakened bone leads to structural overload, microfracture and inflammation. The response to the microfractures is inflammation and callus formation, leading to the enlargement of the physis. Physitis in the long bones, which results from a disturbance in the ossification of the calcified cartilage on the metaphyseal side of the physis, is largely reversible because the physeal plate is a temporary structure, which is remodeling continuously and disappears at skeletal maturity. A disturbance in ossification of calcified physeal growth cartilage is seen most commonly clinically. A disturbance in the physeal cartilage degeneration and calcification results in retention of cartilage and a much more severe structural deficit, which is more difficult to overcome but is fortunately less frequently seen clinically. The initial clinical signs are similar but the cause is a different process.

When either of these two disturbances involves the subarticular epiphyseal growth surfaces, the articular surface becomes involved and may permanently affect the pain-free function of the joint. In the epiphysis, defective formation of the subchondral bone results in a poorly supported articular surface. Increasing weight and activity levels that result from advancing maturity overload the poorly formed joint surfaces. The articular cartilage, undermined by abnormal bone formation, fractures, becomes detached or loosened (osteochondritis dissecans), and results in signs of arthritis. Osteochondritis dissecans is often the underlying cause of secondary degenerative joint disease (osteoarthritis) in the young horse. Though bone formation problems and their clinical manifestations differ depending on the site of the disturbance, similar types of problems can yield a clue as to where to look in the process of bone formation for the cause of the disturbance.