Horse breeders have long known that problems can develop in the bones of young horses as they grow. The term developmental orthopedic disease (DOD) was coined in 1986 to encompass all orthopedic problems seen in the growing foal and has become a generally accepted term, says Wayne McIlwraith, BVSc, PhD, DSc, FRCVS, Dipl. ACVS, director of orthopedic research at Colorado State University. Developmental orthopedic disease is a blanket term for various manifestations of limb abnormalities in young horses, but they all don't have the same cause(s), and they might involve joints or growth plates rather than just bone, notes McIlwraith.
In this article, we will discuss some of the common developmental ailments of young horses, including osteochondrosis, bone cysts, and physitis. We will explain what these conditions are, what is thought to cause them, and what to do about them.
There are basically four causes of osteochondrosis, and affected horses usually have a combination of these:
1. Genetic predisposition;
2. Rapid growth (which includes growth spurts that can occur when foals "catch up" after the stress of weaning, illness, or some other factor when growth was temporarily slowed);
3. Nutrition (high energy intake, mineral shortage, or imbalances); and
4. Trauma and the role of exercise and overload.
"The latest information is that it's better to provide foals with free turnout than to confine them completely or to confine them and give them short bouts of high-speed activity," says Michael Schramme, DrMedVet, CertEO, PhD, Dipl. ECVS, clinical associate professor of equine surgery at North Carolina State University. "Joint cartilage of foals that have not had free turnout loses the ability to adapt functionally to the load placed on it by the time the foals reach five months of age. Once cartilage loses this ability, it is more apt to become injured and degenerate more quickly."
Osteochondritis dissecans (OCD) and subchondral bone cysts are manifestations of osteochondrosis, according to McIlwraith. Let's look at one way OCD can develop.
At the ends of long bones are areas where the bone elongates called growth plates or physes. The normal epiphyseal ossification center advances out until ossification (conversion of cartilage into hard bone) ceases, leaving a layer of cartilage. This layer of cartilage becomes the articular (joint surface) cartilage. A disturbance in endochondral ossification can result in an area of retained cartilage, with a consequent defect in the bone. Subsequent cracking or separation in this retained cartilage can result in a flap or fragment of cartilage that might contain bone. These flaps and fragments on the surface of the joint result in the clinical entity of OCD.
Clinical OCD can also develop without a defect in the bone and therefore, presumably, no defect of endochondral ossification, says McIlwraith. He says that during arthroscopic surgery, it is becoming increasingly common to find elevated (separated from the bone) articular cartilage that is of normal thickness and unassociated with a clear defect in the subchondral bone.
"In addition to being a diagnostic challenge (because of the absence of a defect in the subchondral bone), there is obvious implication of different pathways because there seems to be a specific structural breakdown between the articular cartilage and bone," McIlwraith says. "Recent work with biomarkers provides evidence for a collagen defect in the pathogenesis of OCD and this could feasibly cause separation of cartilage of normal thickness from the bone because of loss of integrity of the collagen framework."
OCD in Stifles, Hocks, Fetlocks
The joints most commonly affected with OCD are the stifle, hock, and fetlock. "Although other joints can be involved concurrently, this is uncommon," McIlwraith says. "In one study of 161 horses with stifle OCD, five also had OCD affecting the rear fetlocks, four had hock OCD, and one had OCD of a shoulder joint."
However, he adds that bilateral involvement (i.e., both stifle joints or both hock joints) is sufficiently common that the opposite joint should always be radiographed when lesions are found.
"In one study, 57% of affected animals had bilateral (stifle) involvement," reports McIlwraith.
Although stifle OCD can be diagnosed in almost any breed, it seems to be more common in Thoroughbreds than in other breeds, McIlwraith notes. Affected horses usually present with a sudden onset of joint swelling and lameness, he says. Lameness sometimes is very mild, with a stiff action and shortened stride being observed, rather than the horse having a prominent
lameness. "Some more severely affected horses will have a 'bunny hop' action behind that can initially be confused with a neurologic problem," notes McIlwraith. He adds that joint distention is the most consistent sign seen with OCD of the stifle.
McIlwraith says it is uncommon for the hocks and stifles, or the stifles and shoulders, to be involved in the same animal at the same time. It is also uncommon to treat OCD in one joint(s) and have it develop at a later time in other joints.
"Hock OCD is very common in Standardbreds, but can be diagnosed in most breeds," McIlwraith states. "The most common clinical sign of hock OCD is effusion of the tarsocrural joint. This is manifested clinically as a 'bog' spavin, which simply refers to the prominent swelling seen most readily along the medial or inside aspect of the joint. Lameness can also be seen, but it is not common and is rarely prominent. Racehorses usually present as 2-year-olds, but non-racehorses usually present as yearlings prior to going into training."
Horses most often affected by OCD show mild to moderate lameness when first introduced to training or rigorous athletic activity, when the joints become stressed, notes Schramme.
"Approximately 60% of affected horses will be one year of age or less at the time the condition becomes symptomatic, and younger animals that develop clinical signs often have more severe damage within the joint," explains McIlwraith. "However, incidental lesions are sometimes identified in older horses where no clinical signs have ever been observed."
"When you rest these young horses, they get better; when you push them to go harder, they get worse," says Schramme. "In general, the bigger the fragment, the earlier the signs will appear."
Sometimes the OCD fragment will completely detach and become a free body or "joint mouse," he adds. In most cases, fragments remain loosely attached in their bone of origin, but the debris released into the joint from beneath the flap results in synovitis or joint inflammation, which causes the clinical signs of pain and lameness that are seen with the disease.
There is wide variation in looseness of the fragments, which can be seen on radiographs. During surgical removal, some are so firmly attached they must be chiseled off, some are barely hanging on, while others have already come loose and are floating around in the joint. If these "joint mice" catch in the joint, they are very painful and can cause significant damage to joint cartilage, says Schramme. These horses are constantly lame.
Generally, the extent of damage to the joint identified at surgery is more extensive than would be predicted from radiographs, says McIlwraith.
Treatment for OCD will vary, depending on the joint involved and the intended purpose for the horse. The faster the horse is expected to go (such as a racehorse or cross country event horse), the more likely the condition will interfere with its performance. A general purpose riding horse might live with fragments without any problems, says Schramme.
"They can be removed relatively easily through arthroscopic 'keyhole' surgery that usually leaves no significant scar," says Schramme. "It's just two little stabs (one for the arthroscope and one for fragment removal) and two sutures," he says.
It is accepted that surgical debridement of the lesions is the treatment of choice. However, smaller lesions identified in younger horses might respond to rest and no longer be seen on radiographs, says McIlwraith. "These are generally lesions that are not causing severe clinical signs," he says. "If lameness and swelling are prominent, arthroscopic surgery is indicated."
Animals are usually stall rested for two weeks after surgery, at which time hand walking is started, says McIlwraith. Restricted exercise is continued for two to three months after surgery, at which time training is started or the horse is turned out.
McIlwraith published a study in 1992 in Equine Veterinary Journal on 252 cases of stifle OCD in 161 horses; follow-up information was available for 134 horses. Of these 134 horses, 64% returned to their previous use, 7% were in training, 16% were unsuccessful, and 13% were unsuccessful due to reasons unrelated to the stifle. The success rate was higher in horses with smaller lesions, and it was also higher for older horses. However, this age factor was considered to be due to the fact that the most severe lesions were generally
identified in the younger horses.
McIlwraith also reported on a study of hock OCD lesions involving 183 horses, in which 76% raced successfully after surgery. He said if degenerative changes were identified at surgery in the cartilage surrounding the OCD lesion, the prognosis was less favorable. He also noted that while swelling did not resolve fully with some lesion locations, this did not seem to affect performance.
Subchondral Bone Cysts
Unlike OCD, subchondral cystic lesions (simple sac-like cavities in bone beneath the joint surface that are filled with fluid or another soft material) occur in various locations, says McIlwraith. The most common place is in the medial condyle of the femur in the stifle (inner projection of the femur's lower end), followed by the distal metacarpus (lower end of the cannon bone) in the fetlock joint. In Quarter Horses, the pastern joint might be affected.
"When we have a yearling with a large subchondral cystic lesion in one medial femoral condyle and a defect in the other, we feel comfortable in assuming that the cause is osteochondrosis," states McIlwraith. "However, we also get subchondral cystic lesions that develop in older horses, and in some instances we have noted them developing after a cartilage surface defect has been recognized."
In McIlwraith's laboratory, it has been demonstrated that subchondral cystic lesions could develop from defects in the joint surface and in mature animals. "In research from our laboratory, examination of the contents of these bone cysts after their removal has shown that the linings have high levels of degradative enzymes and can actively resorb bone (break it down)," says McIlwraith. "The same findings probably explain how cysts expand after endochondral ossification has ceased."
In most cases, the cause of bone cysts is thought to be improper maturation of cartilage to bone. During cartilage maturation in young horses, there might be retention of thick cartilage in certain spots that doesn't turn into bone; subsequently a hollow spot (cyst) forms in the end of a long bone, just below the joint surface. Lameness and joint distension caused by bone cysts can appear from six months to three years of age, or when the horse is put into training, says Schramme.
Treatment for cysts can be more complicated than for fragments and doesn't have a good prognosis.
"The ends of bones in foals have a thick layer of cartilage over them," Schramme says. "During normal growth, cartilage progressively turns to bone, producing bone growth. At maturity there is a thin layer of cartilage with thick, strong bone under it."
Another common developmental problem is physitis or epiphysitis, although the proper term is physeal dysplasia. This condition presents as swelling around the growth plates of the distal radius (lower end of the upper forelimb bone) and distal metacarpus (lower end of the forelimb cannon bone), explains McIlwraith. "It is usually a clinical diagnosis, but sometimes radiographic lesions with spurring and some lysis (bone loss) at the edge of the growth plate will be seen," he says. "In other instances, it may be an area of retained cartilage (osteochondrosis) or pathologic change more consistent with trauma.
"In recent work in New Zealand, it was noted that swelling of the distal metacarpus and distal metatarsus (lower end of the hindlimb cannon bone) previously considered physitis is unassociated with any
problems in the physis," says McIlwraith. "With such a variation of change in this syndrome, any etiologic associations are difficult."
Treatment consists of slowing down the growth of the foal and restricting exercise to reduce stress and pressure on the thickened growth plates, notes Schramme. It might mean weaning a foal or reducing carbohydrate intake if he's already weaned. Diet must be properly balanced in terms of minerals, with supplements given if needed. Especially important are the calcium/phosphorus ratio (there should never be more phosphorus than calcium) and adequate levels of copper, says Schramme. Heather Smith Thomas and Kimberly S. Herbert
Some OCD Lesions Are Normal
There is research evidence that fragmenting lesions on the bone surface of a young horse's joint can keep changing and even repair themselves (in the hock up to five months of age, in the stifle up to eight months). Scientists at the University of Utrecht in the Netherlands followed a number of these foals through the first months of life. They found evidence of lesions at three months in many foals, but by five to six months the lesions were gone. They hypothesized that a repair process exists early in life. The same potential applies to bone cysts, since cartilage can repair itself in animals up to a year old. It has blood supply and a high metabolic rate while the horse is still growing.
Once a horse is a year old, however, this tissue becomes set and is almost inert. "Finding an articular cartilage lesion in an older horse is bad news because it will never repair itself and will only continue to degenerate further," says Michael Schramme, DrMedVet, CertEO, PhD, Dipl. ECVS, clinical associate profeesor of equine surgery at North Carolina State University. "But in foals, there is a repair capacity and a window of opportunity--which according to some authorities goes to eight months--in which cartilage can self-repair some of those lesions."
Consequently, if a young horse has radiographic abnormalities, veterinarians might not rush in with surgery until the self-repair window of cartilage has come to a close at about a year of age. Some lesions might be part of the normal growing process and only become important if the self repair hasn't worked.--Heather Smith Thomas
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