I have often debated with myself on how to write an article on OCD and present it in a form which will be readily understood by the readers of The Draft Horse Journal. In the past two years I have received a large volume of inquiries by phone and mail as to the nature of this condition by owners of horses which have been diagnosed with OCD. These people want to know what this condition really is, what to do about it, and how to possibly prevent it in their young animals in the future. This problem is definitely on the increase in the young stock of our various draft breeds so I will try to explain the condition as simply as I can.

Osteochondrosis, of which OCD is a part, is one of the most commonly recognized orthopedic diseases which a veterinarian encounters in an equine practice. It is probably far more common and occurs more often in young horses than is diagnosed by clinicians. It is thought that many cases in these young animals are never diagnosed and go on to resolve themselves with little detrimental effect on the victims. Osteochondrosis is the term applied to the condition whereby cartilage that is destined to become bone is prevented from doing so since the process is arrested or delayed from taking place. Any area in the body where cartilage is changed over to bone, in the developing animal, can be involved. However the most commonly affected sites are the stifles, hocks, fetlocks, shoulders, elbows and knees. The hip joint and cervical spine sites may also be involved.

This disease, osteochondrosis, manifests itself in two forms. One is when pieces of cartilage may be detached or pieces may simply be retained and never process into true bone. This condition is known as OCD. The second manifestation is the formation of cysts in the subchondral bone, which is scientifically termed (SBC).

OCD actually occurs because the articular cartilage affected by osteochondrosis becomes thickened due to inhibited nutrient diffusions and it begins to degenerate with necrosis of the layers making up its base structure. It is believed that ongoing physical stress then causes cracking of the cartilage along its periphery with possible separation of a portion of the damaged cartilage.

Subchondral bone cysts (SBC) are formed when the degenerative cartilage cracks in the center of the joint leaving a fissure for the entrance of synovial fluid.

OCD is an abbreviation for the medical term Osteochondritis Dissecans. This term is used medically to describe the condition which exists in a joint when avulsion of a piece of damaged cartilage occurs.

This piece of damaged cartilage may become entirely detached and be known as a “floater” or be broken into small pieces known as “joint mice.” On the other hand, it could remain attached to other cartilage or bone. The damaged cartilage and the loose piece of cartilage may in time become calcified.

Now you begin to see the problem. This calcified cartilage, either loose or attached, will cause damage to the apposing cartilage of the joint. This in turn is called osteoarthrosis (juvenile arthritis) or secondary degenerative joint disease (DJD). This loose piece of calcified cartilage is the cause of most cases of (DJD) in the horse, which eventually manifests itself by chronic lameness of the affected animal.

As a result of osteochondrosis we can have the actual OCD appearing as well as cyst formation in areas of the subchondral bone. The term “subchondral” refers to that area of the bone beneath the cartilage layer.

Now I hope I have explained that OCD and cyst formation in subchondral bone can occur when osteochondrosis is present in any articular cartilage. In other words osteochondrosis is actually the cause of OCD. This is very important for people to understand since one must eliminate osteochondrosis in order to prevent OCD and cyst formations in subchondral bone.

The places where OCD occurs most commonly are those sites in which the articular cartilage is the “thickest” or heaviest. These areas, in order of their occurrence, are the stifle, hock, fetlock, and shoulder joints. More than one joint may be affected in varying degrees.

OCD of the stifle joint generally will appear in animals 6 months to 2 years of age. In young horses with the problems, 60% are under 1 year of age and these younger horses seem to have more severe lesions than older counterparts. Young foals may have trouble getting up while older horses may exhibit a mild to severe lameness which becomes worse with exercise. There may or may not be some swelling of the affected joint. Both joints, especially in the older horse, are often involved. In these older horses the lameness will rapidly become worse when they are exercised, or they will very quickly develop a stilted gait. As the disease progresses, especially if it involves both stifles, a young stallion will refuse to mount and actually many of these horses will “go down” on the rear legs and have difficulty in getting up. A number of these afflicted horses will reach the point whereby they cannot get onto their feet.

When OCD is present in the hock of a horse, from 6 months to 3 years of age, hock joint distention or bog spavin as it is called, with or without accompanying lameness, is a very common symptom. An interesting study was done on Standardbreds where twice as many males as females were found to be involved. Of these horses numbering 114 cases, 62% were found with bog spavins and 43% of the affected horses demonstrated some degree of lameness.

Horses showing OCD of the fetlock and shoulder joints are usually younger than 12 months of age. They may have intermittent foreleg lameness. They often develop a so-called “swinging leg” lameness with stumbling. Sometimes the young horse will exhibit muscle atrophy over the shoulder region and definitely have a smaller foot on the affected limb.

Subchondral bone cysts can affect horses from 3 months to 5 years of age but most cases of lameness from these cysts will appear at 5 to 24 months of age. Usually the onset of the lameness will be associated with increased exercise or some traumatic event. Lameness may often be brought on by the start of training.

The diagnosis of OCD and SBC is primarily made by radiographs of the suspected joints. The diseases can be suspected but good radiographic procedures will diagnose the condition.

Treatment will depend upon the severity of the condition, age of the horse and projected uses of the animal. The value of the patient is another factor. Drugs to be used are nonsteroidal anti-inflammatory drugs and articular medications. Arthroscopic surgery is often necessary. However in the case of foals, surgery should be postponed until the animal is a yearling. Often, in the case of foals, a proper diet and suspension of training activities with rest will be sufficient to halt the progress of the disease and restore the diseased areas of the joints.

I believe it is far better to try and prevent osteochondrosis than attempt to treat the OCD and SBC lesions that occur in the aftermath of the disease. Some factors which have been purported to play a part in the onset of the disease are heredity, exercise, trauma, use of corticosteroids and diet. Dietary factors are, vitamins A, D & E, trace minerals and protein.

At one time when this condition was first being studied, hereditary factors were deemed to be a big predisposing cause of so called OCD. I personally do not believe there is a very great hereditary predisposition to the disease, except for one possible inherited trait. It has been my observation that osteochondrosis with OCD and SBC almost always occurs in very fast growing and rapidly developing foals and young horses. These animals that have OCD are always “fast growers.” This may be a hereditary factor.

I can point my finger at the use of corticosteroids as a causative factor of OCD. Don’t kid yourself that a lot of these drugs have not been poured into foals and young horses so they can reach that magic 18 h.h. in record time. One of the costs in using these drugs in this way is the onset of OCD and subchondral bone cysts. I might also add to that list the fact that many of these foals treated with these drugs, male and female alike, will be sterile when they reach sexual maturity.

In my experience, diet plays the greatest role of all in causing or preventing OCD and subchondral cyst formation in the joints of fast growing foals. I can tell you that trace minerals, selenium, copper, zinc and molybdenum plus calcium and phosphorus in the proper concentrations and availability to the growing animal, play a huge role in prevention of these conditions. Equally as important is the overall percentage of protein and carbohydrate in the young animal’s ration. With the correct diet and exercise program in place one can prevent OCDs and even successfully treat them if caught early when they occur in the fast growing young horse.

An example of this is a friend and client of mine who has been raising some fast developing growthy Percheron foals for a few years. He became plagued with a number of OCD cases in his foals. He came to one of my schools, with this problem foremost on his mind. I gave him a proper nutrition program, which he has been following, involving the foals up through 3 years of age or older if the animal stays on the farm. Since the start of the program to date, he has had no more cases of OCD in his stock even though the hereditary factors still are the same.

The prevention of most cases of osteochondrosis in these fast growing young horses involves feeding an adequate amount of what I refer to as a “balanced mineral” plus adjusting the carbohydrate and protein percentages in the diet. Do not push these young animals. A growing foal, through 2 years of age, requires only a 14% protein diet plus 1 ounce of a balanced mineral and 1/2 ounce of salt per 1000 lbs. of weight per day, to develop properly.

An ounce of prevention is often worth a pound of cure and translated into dollars it’s a great savings when it comes to preventing OCD.