By Debbie Brooks DVM – Sept/Oct 2001 Borderlines
When talking about orthopedic problems with Border Collie owners, one problem that repeatedly comes up is that of osteochondrosis. This topic is the subject of much debate in both veterinary and human orthopedics. Osteochondrosis is often called OCD, which is an abbreviation for osteochondritis dessicans. Technically, osteochondritis dessicans involves a flap. For the sake of brevity, I will use the abbreviation OCD throughout the remainder of this discussion although the term may not always be correct. It is quite common in people, horses, pigs, poultry, and large breed dogs and the pathophysiology of the disease appears to be the same in all species.
In the fetus, long bone is formed from a cartilage precursor. The growth cartilage is found in the growth plate of long bones and allows for longitudinal growth. It also ultimately covers the articular ends of long bones and becomes part of a joint surface. The growth cartilage is converted to bone through a process called endochondral ossification. The cartilage is invaded by blood vessels and differentiates into four histologically distinct zones – resting, proliferative, hypertrophic, and calcifying. Bone producing cells produce osteoid (a bone precursor) on the calcified cartilage layer so it acts as a scaffold for bone formation. Since growth cartilage is not present in adults, OCD is a disease of the young and growing animal. However, it may not appear clinically until that animal is an adult.
The articular cartilage is an avascular structure in adults but growth cartilage does have a blood supply that gradually disappears with increasing age and body weight in a normal situation. It is this blood supply that provides nutrition to the growing and maturing joint while the adult articular cartilage derives its nutrition from the joint fluid. Studies in pigs suggest that during growth, the viability of the growing and differentiating cartilage is highly dependent on the blood supply located in the growth cartilage. In chickens, surgical destruction of the blood supply has produced lesions like OCD.
In OCD, there is a failure of the process of endochondral ossification leading to retention of cartilage rather than conversion to bone as well as death of the cartilage cells. It is the bone underneath the articular cartilage (subchondral bone) that supports the cartilage surface of the joint. The result is that the dead cartilage site collapses and creates a defect in the articular surface of the joint. The cause of this is not clearly understood although several factors are suggested. Trauma is one hypothesis but has never been definitively determined to be a cause. Genetic factors appear to play a clear role. In humans, there are both familial and racial tendencies. OCD is very common in domestic pigs of all breeds but nonexistent in wild or miniature pigs. This is presumably due to human selection of pigs with certain physical traits. In dogs, predisposition of certain breeds has been well documented. In humans, dogs, and horses the male is predisposed which is probably related to their growth rate being more rapid than females. Ischemia, or loss of blood supply, will produce OCD lesions but the cause of ischemia remains unknown. Trauma is suggested as a cause of ischemia as well.
OCD lesions tend to occur in specific locations – the caudal humeral head in the shoulder, the trochlea of the distal humerus in the elbow, the medial condyle of the distal femur, and either trochlear ridge of the talus in the hock are the most commonly described sites. In recent years, OCD has been reported in the joints of the spine. The site and size of the lesions will determine the signs the dog shows, indeed some dogs never show problems. The cartilage defect in the joint causes effusion and synovitis that is painful. Remember that in the adult, nutrition of the articular cartilage comes from the joint fluid, so unhealthy joint fluid will produce an unhealthy joint. OCD ultimately leads to degenerative joint disease. In some cases, most notably in the caudal humeral head of the shoulder, the cartilage flap may break free and cause pain as it moves in the joint (joint mouse). Since cartilage derives its nutrition from the joint fluid, this flap can continue to grow.
The big question is how to prevent or avoid OCD. Studies are underway which are mapping the canine genome with the intent of being able to map an individual to determine what disorders that dog may carry. This will be great information in the future, but is not very helpful now. We do know that there is a genetic link. This appears to be a multifocal recessive trait. Whether this is a true inherited defect or the tendency toward very rapid growth is the heritable link we do not yet know. We do know that breeding dogs that are determined to be free of elbow dysplasia and hip dysplasia will reduce the frequency and severity of the diseases. Growing dogs on high-energy diets and/or being free fed results in an increased frequency in OCD (and hip dysplasia) in controlled studies. It is my observation after 11+ years of surgical referral practice that the pups most likely to be seen for OCD, elbow dysplasia, or hip dysplasia are very heavy. Excess dietary calcium has been linked to an increase in OCD (and other musculoskeletal problems in horses). With commercially available diets, true dietary deficiencies are extremely rare but oversupplementation is not unusual.
Guidelines for decreasing the frequency of OCD would be:
1) Identify affected animals and exclude them from a breeding program.
2) Identify dams and sires that produce the defect and use caution in future breedings. Evaluation of siblings and other offspring may be helpful in determining whether or not these individuals should be bred and what crosses are not advisable.
3) Limit energy intake and supplementation or individuals at risk.
4) Screening of asymptomatic dogs prior to breeding if a history of OCD exists within their families.