Osteochondritis dissecans (OCD) is an affliction, if left untreated, that can have long-term harmful effects on the young, growing horse as well as the performing or racing horse. OCD actually is a disease subset of osteochondrosis and is classified under the umbrella term of developmental orthopedic disease.

Osteochondrosis affects the joint cartilage and also involves the subchondral bone just beneath the cartilage surface. Thus, we are, in a sense, faced with discussion of osteochondrosis, osteochondritis dissecans, and subchondral bone cysts.

To do this, one must find a way through a labyrinth of knowledge and speculation. This requires the services of sophisticated guides. To help show the way through the maze, we call on three experts from Colorado State University who have carried out a great deal of research and have written and spoken extensively on the subject. They are C. Wayne McIlwraith, BVSc, PhD, Dipl. ACVS; Gayle W. Trotter, DVM, MS, Dipl. ACVS; and Gary Baxter, VMD, MS, Dipl. ACVS.

Much of the information they proffer was set forth in proceedings from a seminar conducted at CSU entitled, "Lameness in the Horse: An In-Depth Short Course for the Horseman."

We also will interject along the way a variety of other information that research has brought to light. First, let’s allow our guides to start at the beginning with an explanation of the term developmental orthopedic disease that carries the acronym DOD.

McIlwraith tells us that the term developmental orthopedic disease was coined in 1986 to encompass all orthopedic problems seen in the growing foal. It came out of a blue ribbon panel sponsored by the American Quarter Horse Association. It is a term that encompasses all general growth disturbances of horses and is, therefore, non-specific.

Before getting into specifics about certain forms of DOD, we will briefly review what happens when bones grow.

Long bones develop from cartilage by a process of endochondral (within cartilage) ossification. The centers of ossification or bone formation develop in the center of the future long bone (diaphysis) and also at the ends of these long bones (epiphyses). As bone formation proceeds, both a bony epiphysis and diaphysis develop. Between those two centers of bone formation is a metaphyseal growth plate. It is this growth plate that enables the limb to lengthen after birth as the foal grows.

There is a second growth plate—called the ephyseal growth plate—that forms as the ephyseal bone formation center advances toward the ends of the bone and what is destined to be the articular surfaces of the joints.

It is during this time of bone formation in the young horse that osteochondrosis, osteochondritis dissecans, and subchondral bone cysts can develop.

The McIlwraith statement that follows offers some clarification on osteochondrosis, OCD, and subchondral bone cysts, but it also points to the complexities and the need for additional research:

"Osteochondrosis was initially defined as a disturbance of cellular differentiation in the growing cartilage. It is considered to be a result of the failure of endochondral ossification (bone formation) and may affect either the articular epiphyseal cartilage complex or the metaphyseal growth plate.

"It was considered that the loss of normal differentiation of the cartilage cells means the transitional calcification of the matrix, which is important for bone formation, did not take place. Therefore, ossification ceases and cartilage is retained. This retained cartilage then undergoes cellular death (necrosis) in the basal layers, and it is proposed that subsequent stresses give rise to fissures in the damaged cartilage and that progressive breakdown of the cartilage can then lead to the syndrome designated as osteochondritis dissecans or subchondral bone cysts."

That much of the statement is pretty straightforward and explanatory. However, McIlwraith continues with an explanation of some findings that add enough confusion to keep researchers busy for years to come:

"That these entities are part of the generalized condition of osteochondrosis have resulted from studies in other species and extrapolation to the condition in the horse. There is still considerable argument about the exact association, and with more experience, one comes up with more cases that don’t quite fit the pattern.

"For example, we see cases of osteochondritis dissecans in the stifle that do not have thickened cartilage or a defect in the bone and that do not quite fit with the retained cartilage phenomenon. However, they could still fit with some developmental abnormality.

"At this stage, we, therefore, like to say that osteochondrosis may lead to osteochondritis dissecans or subchondral cystic lesions. It may also occur in the physis and lead to retained cartilage in that area. It is currently presumed that many instances of subchondral bone cysts result from osteochondrosis.

"On the other hand, we have demonstrated the development of bone cysts secondary to a defect. In early work, osteochondrosis was suggested to be a generalized condition and, therefore, occurred in multiple sites. However, based on our clinical material, it was found that osteochondritis dissecans will be found in a particular joint and a lesion will commonly occur in the same joint, but will not occur elsewhere."

That last sentence carries with it a good deal of mystery that awaits resolution. Why does OCD normally show up in one joint rather than multiple joints? It would seem logical to assume that if the horse is predisposed to the condition for one reason or another, that the affliction would be found in multiple joints.

We will discuss in detail what happens in specific joints when OCD strikes, but first we will look at why the condition occurs in the first place. Unfortunately, in this area there is more conjecture than solid answers.

How It Starts

There are those who believe that genetics are involved. Others maintain that a rapid growth rate is the culprit. Still others maintain that diets that are too high in protein are causative. Yet others believe that mineral imbalances might be implicated. Then, of course, there is the matter of mechanical stress when the horse runs at speed. This can cause an OCD flap or fragment to separate from the bone and bring on a bout of lameness.

Time to take a closer look at these theories.

Genetic Predisposition: Radiographic studies in Swedish trotters and Warmbloods have shown progeny of one stallion from each breed having a significantly high frequency of OCD when compared to progeny from other stallions. In another study in Denmark, it was shown that there was a significantly high proportion of osteochondrosis in the progeny of one of eight stallions, even though the stallion himself did not show radiographic signs of osteochondrosis.

"There has been little work done in the United States with regard to heredity," says McIlwraith, "and we certainly haven’t been able to develop any type of screening program for osteochondrosis in stallions and mares that will ensure freedom from that condition. However, it would appear very likely that there are genetic components to the disease. Individual instances of certain stallions and mares producing these individuals have been seen."

Growth and Body Size: Rapid growth was found by early researchers to result in osteochondrosis in dogs and pigs, so it naturally followed that the same might be true for the horse. Yet, there has been no substantial evidence to prove that this is true.

"It has been pointed out," McIlwraith states, "that the most intense phase of growth occurs in the first three months of life and if growth was a big factor, we expect this would be the time that most lesions would occur, but this is not when we see them clinically. At this stage, the evidence implicating growth rate and body size in the pathogenesis is largely unsubstantiated. In one study done at Ohio (The Ohio State University), foals with a higher number of lesions had similar growth rates to those with fewer or no lesions, suggesting that rapid growth may not be a necessary predisposing factor in the development of cartilage lesions. Growth was based on measurements of body weight with a height in cannon bone circumference, and it was part of a study on the effect of dietary copper." Recent work by Joe Pagan, PhD, and Steve Jackson, PhD, in Kentucky has shown the foals developing OCD had a significantly higher weight at a specified time, implying increased growth rate might be a factor.

Mineral Imbalances: Eighteen mineral elements are known to be required by many animal species. They are divided into two groups, with one group under the umbrella of macrominerals and the other group under the umbrella of trace or microminerals.

The macrominerals include calcium, phosphorus, sodium, chlorine, potassium, magnesium, and sulfur. The microminerals include iodine, manganese, iron, zinc, copper, molybdenum, fluorine, chromium, selenium, silicon, and cobalt.

Approximately 70% of the mineral content of a horse’s body consists of calcium and phosphorus. About 99% of the calcium and more than 80% of the phosphorus are found in the bones and teeth. Obviously, a deficiency or imbalance involving these major minerals would be significant in proper bone development, but the question then surfaces: Can a deficiency or imbalance involving a single micromineral have a harmful effect on growing young bones? Research indicates that this is a strong probability.

As mentioned above, research was conducted at The Ohio State University to determine if an imbalance in copper intake could be a causative factor in osteochondrosis.

McIlwraith has this to say: "Low copper has been implicated as a cause (of DOD). An epidemiologic study on clinical cases of developmental orthopedic disease implicated low copper levels as the most consistent factor. In experimental studies, it has been noted that a marked copper deficiency (1.7 parts per million—a very artificially low level) produced OCD-like lesions and flexural deformities.

"In another study in Thoroughbred foals in which osteochondrosis developed before weaning, seven had serum copper and ceruloplasmin concentrations below normal.

"In a third controlled experiment in Canada with high (30 parts per million) and low (seven parts per million) copper diets, there was a much higher incidence of lesions seen in the foals fed the low copper diet. However, it is to be noted that most of the changes were present in the cervical vertebrae rather than the limbs, where we commonly see clinical problems."

Excessive levels of calcium and phosphorus also have been suspects in causing osteochondrosis. Experiments with excessive calcium did not result in lesions, McIlwraith says, but diets that were five times higher in phosphorus than recommended by the National Research Council did produce OCD lesions in young foals.

In one of the studies conducted by The Ohio State University involving 384 yearlings raised on 19 breeding farms in Ohio and Kentucky, it was found that the average calcium content of the rations on farms with the fewest skeletal problems was 1.16% and the phosphorus content was 0.72%. Involved in the study were Thoroughbreds, Standardbreds, Arabians, and Quarter Horses.

Two researchers at Cornell University—Lennart Krook, PhD, and George Maylin, DVM—are convinced that overfeeding of calcium to the growing horse can be a cause of osteochondrosis, and the same overfeeding of calcium to the pregnant mare can result in future osteochondrosis in her fetus. An overfeeding of alfalfa hay, they believe, is the underlying villain. The publication of their original findings and conclusions stirred up a hornets’ nest of controversy that continues today in the scientific world.

Krook and Maylin maintain in their findings that a dietary calcium overload causes excessive secretion of the hormone calcitonin, which acts directly on the bone of growing horses in a negative way. Calcitonin can inhibit the conversion of cartilage to bone, and it also can inhibit the resorption of calcium from bone.

In the pregnant mare, calcitonin can be transferred through the placenta to the fetus and this, they maintain, can result in a foal’s being born with osteochondrosis. Alfalfa hay, they contend, should not be fed to pregnant mares or young, growing horses.

Excessive zinc in the diet also has been suspected as being a villain. In one anecdotal instance, it was found that a number of individuals in a group of foals raised near a zinc smelter suffered from osteochondrosis. There is some suspicion that high zinc might suppress copper levels.

Until science comes up with some definitive answers concerning the effects of imbalances of the various minerals, horse owners can only practice moderation in their feeding regimens and seek to provide an appropriate balance.

Many of the macrominerals and microminerals are included in hay and grain that are involved in a normal diet. However, in some areas of the country, the soil might be deficient in a specific mineral and, as a result, the plants grown thereon also will be deficient. When that is the case, the deficient mineral should be supplemented. However, it is important to know which minerals are in the deficient category and only supplement those. Oversupplementing can be as dangerous as deficiencies.

An interesting study at Washington State University involved rabbits and alfalfa. The study used generation after generation of rabbits fed on alfalfa, with one group receiving hay produced on low-phosphorous soils and the other group eating alfalfa grown on high-phosphorous soils. The rabbits in the low-phosphorous soil alfalfa group were retarded in growth, required 12% more matings per conception, and had 47% lower breaking strength of bones than the rabbits that received an appropriate amount of phosphorus in their diet. The point is that nutrients within the soil affect the plants grown thereon as well as the animals that consume those plants.

Again, the key word is balance. It long has been known that an excess of phosphorus in a diet in relation to calcium can be harmful, but the Washington State study indicates that too little phosphorus can be just as harmful.

(For more on the importance of mineral balance in the young, growing horse for building healthy, strong bone and the potential problems with OCD that an imbalance can cause, see sidebar on page 28.)


While rapid growth itself might not bring on osteochondrosis, there is evidence that an overly high energy diet could be a causative factor.

McIlwraith says: "There has been an increased incidence of OCD lesions noted in horses fed 130% of what the National Research Council recommends for carbohydrate and protein. A second study in Australia by Dr. Kate Savage, which was very well controlled, showed that high energy diets (120% National Research Council requirements) consistently produced lesions of osteochondrosis in weanling foals compared to a control diet based on 100% NRC requirements. Some people have focused on ‘high protein’ being a problem, but this has not been demonstrated."

Again, the horse owner must approach feeding with moderation, seeking to provide a balanced diet without excesses in any department.

Mechanical Stress And Trauma

As mentioned earlier, it has been recognized that mechanical stresses often result in clinical signs of OCD, such as lameness. It is presumed that this occurs when the OCD flap or fragment separates from the parent bone. However, the question is something in the nature of which came first, the chicken or the egg?

McIlwraith says: "Whether trauma or physical stress is involved in the primary induction of an OCD lesion is controversial. However, some people do tend to feel this is the case, and we do recognize there are certain predisposing sites for the occurrence of OCD, suggesting possible mechanical factors. A notable veterinary bone and joint pathologist, Roy Pool, DVM (a researcher of long standing at the University of California, Davis), feels that shear forces may disrupt capillaries in the subchondral bone (bone under the cartilage) and give rise to chondrocyte or cartilage cell damage."

Once again, the above information reveals, when looking at a particular equine affliction, that there is no single known cause and no clear-cut understanding of all aspects of the problem. A variety of factors appears to be involved.

One thing that researchers think might help in the prevention of osteochondrosis is exercise.

"There is some data suggesting a ‘protective’ effect of exercise," says McIlwraith. "This particular study was done on early-weaned Warmblood foals, and there was a dramatic reduction in the incidence of OCD in foals subjected to forced exercise and a high energy diet compared to foals fed the same diet, but with limited exercise."

Where OCD Occurs

Let’s take a look at the various sites that OCD strikes and what practitioners and researchers have learned concerning treatment. Time also to follow a new guide. This time we look to Gayle Trotter as our information source. He underlines the point made earlier about isolation of the condition with this statement:

"Although multiple joints can be affected, this is unusual, and commonly only one joint is involved. However, bilateral involvement (both stifle joints or both hock joints, etc.) is sufficiently common that the opposite joint should always be radiographed. Nonetheless, 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.

"It is theorized that clinical signs develop when the joint surface is breached by the dissecting lesion. Sometimes the OCD fragment will completely detach and become a free body or ‘joint mouse.’ In most cases, however, the fragments will remain loosely attached in their bone of origin. The debris that is released into the joint from beneath the flap results in synovitis or joint inflammation, and the clinical signs of pain and lameness are seen.

"OCD can affect many joints, but the most common joints involved are the hock and stifle. The fetlock and shoulder joints also get OCD, but are less frequently affected."

With that information as a base, we will take a look at just how OCD affects each of the four joints listed.

OCD Of The Stifle Joint

As Trotter states, this is one of the principal joints where OCD occurs. Although OCD can be found in the stifle joint in almost any breed, it seems to be most common in the Thoroughbred. Approximately 60% of affected horses will be one year of age or less at the time symptoms are obvious. It also appears that the younger the animal is when afflicted, the more serious the joint damage will be, although there are exceptions to the rule.

The observable symptoms generally involve joint swelling and lameness. This often will occur in the afflicted horse in the wake of an increase in the exercise regimen. Sometimes the lameness is very mild, with a stiff action and shortened stride being observed, rather than prominent lameness. Some more severely affected horses, says Trotter, will have a "bunny hop" action behind that initially can be confused with a neurologic problem.

"Joint distention," he states, "is the most consistent sign seen with OCD of the stifle. Careful palpation of the joint may identify free bodies, or the surface irregularity associated with the damage within the joint. Bilateral involvement is common in the stifle, so careful examination of both stifles should be completed. In one study, 57% of affected animals had bilateral involvement. Flexing of the limb will usually exacerbate the lameness, and anesthetic (nerve block) placed into the joint will improve or eliminate the lameness. However, intra-articular anesthesia is usually not necessary to confirm a diagnosis.

"Lateral to medial radiographs provide the most useful information regarding specific lesion location and size. The most common defect identified is a variably sized irregularity or flattening of the lateral trochlear ridge of the femur. The area of the ridge that comes in contact with the bottom portion of the patella (in a human, this would be the kneecap) is most commonly involved. Partial calcification of the tissue within the defect is sometimes seen, and free bodies are occasionally identified. It is rare to see OCD primarily affecting the patella, but secondary radiographic change in the patella resulting from the trochlear ridge damage can be seen. The medial ridge of the femur is much less commonly involved."

Generally, Trotter adds, it is found during surgery that damage to the joint is more severe than what could be detected by X ray.

While other joints can be involved at the same time as the stifle, he reiterates it is uncommon. 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. All of the rest had OCD in the stifle only.

When a horse is diagnosed with stifle OCD, surgery generally is the treatment of choice. However, Trotter says, smaller lesions identified in younger horses might respond to rest. Generally speaking, these would be lesions that are not causing severe clinical signs. If lameness and swelling are prominent, Trotter says, arthroscopic surgery is indicated.

"As with all joint surgery," he states, "the joint is thoroughly explored, and suspicious lesions are probed. Loose or detached tissue is elevated and removed. Loose bodies are also removed. The defect site is debrided down to healthy tissue. Care must be taken not to be overly aggressive with bone debridement in young animals having soft subchondral bone.

"Animals (which undergo surgery) are usually stall rested for two weeks after surgery, at which time walking is started. Restricted exercise is usually continued for two to three months after surgery, at which time training is started or the horse is turned out."

There is a fairly positive success ratio for surgical cases of OCD of the stifle joint. In one study from Colorado State University involving 161 horses, follow-up information was available on 134. Of those 134 horses, 64% returned to their previous use; 7% were in training; 16% were unsuccessful; and 13% were unsuccessful due to reasons not related to the stifle.

"The success rate was higher in horses having smaller lesions," Trotter says, "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."

OCD Of The Hock Joint

The most common clinical sign of hock OCD is effusion (swelling) of the joint. While OCD of the stifle seems to be more prevalent among Thoroughbreds, hock OCD seems to show up most often in Standardbreds.

The effusion of the hock joint, says Trotter, "is manifested clinically as ‘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."

Racing horses which develop the problem, he said, normally do it as two-year-olds, while non-racehorses usually develop the problem as yearlings prior to going into training.

"Although lameness is usually minimal with hock OCD," Trotter says, "surgery is the recommended treatment. Lameness may only be a problem at racing speeds, or at upper levels of performance, that cannot be determined during a clinical examination. Resolution of the effusion (swelling) cannot be expected without removal of the abnormal tissue. This is not to say, however, that all horses having hock OCD need to have surgery. Horses with small lesions, minimal effusion, no lameness, and a potential career as a pleasure horse or light use horse may not require surgery. Surgery should be considered early enough in the course of the disease so that the joint capsule is not unduly stretched, making resolution of the effusion less likely.

"Arthroscopic identification and removal of fragments are recommended, although an arthrotomy (surgical incision into the joint) can be used successfully and is preferred by some for certain OCD lesions in the joint. Postoperative management is similar to that for OCD of the stifle, although for small lesions the time period for restricted exercise may be decreased. Maintenance of good bandages is more difficult for the hocks, and care must be taken in the early postoperative period to avoid bandage slippage and subsequent infection into the joint through the small surgical incisions."

The prognosis usually is positive with surgery. In a study involving 183 horses with OCD of the hock, Trotter says, 76% raced successfully or performed at their intended use after surgery.

"If degenerative changes were identified at surgery in the cartilage surrounding the OCD lesion," he says, "the prognosis was less favorable."

OCD Of The Fetlock Joint

The most common clinical sign of OCD of the fetlock joint is the same as for the hock joint—swelling. If the problem is severe, the horse will be lame. It is not unusual, Trotter says, for all four fetlocks to be involved. However, it is most common for both front fetlocks or both rear fetlocks to be afflicted.

"The diagnosis," Trotter reports, "is confirmed on radiographs, and clinically silent lesions (no swelling or baseline lameness) are often identified along with the lesions causing clinical signs. Lameness can sometimes be induced by flexion in these clinically silent joints.

"A variety of radiographic presentations are seen with a fetlock OCD. Some joints will show only flattening of the sagittal ridge (Type 1 OCD), others will have a fragment in place within the area of flattening (Type 2 OCD), and others have a flattening with or without a fragment in place, but also have free or loose bodies within the joint (Type 3 OCD).

"A conservative approach (to treatment) is initially recommended where only flattening without fragmentation is identified. Many of these cases will have resolution of clinical signs, as well as improvement or disappearance of radiographic signs; however, surgery will eventually be necessary in some of these cases.

"Surgical debridement is recommended for lesions where fragmentation or loose bodies are present."

The prognosis is quite favorable for Type 1 lesions, Trotter feels, but is more guarded for Types 2 and 3. In one study involving 42 horses, the success rate was approximately 60% overall.

"Horses having other signs of articular cartilage erosion or wear lines within the joint had a less favorable prognosis," Trotter says. "If the lesion extended out into the condyle of the metacarpus/metatarsus (cannon bone) from the sagittal ridge, the prognosis was also less favorable. It was determined that clinical signs would persist in approximately 25% of the cases."

Another way in which OCD of the fetlock might be manifested is in the form of fragments within the joint at the upper end of the long pastern bone. Two types of fragments have been identified at this location. Type 1 fragments are most often found in the hind fetlock joints and are located between the midline of the bone and its caudomedial (to the rear and inside) borders. Type 2 fragments almost always are found in the hind fetlock joints. The Type 2 fragments generally are located at the most lateral (outside) borders of the bone.

"With Type 1 fragments," Trotter says, "effusion is uncommon, and, typically, lameness is identified only as a somewhat vague problem at racing speeds or at the upper levels of performance. Flexion tests often are positive and anesthetic (nerve blocks) placed within the joint will usually eliminate any clinical signs that may be present. Regular oblique radiographs will usually demonstrate the lesions, although a special view is often used to highlight their location. Most fragments are present medially (to the inside aspect of the joint). Lameness and effusion are rare with Type 2 fragments.

"Arthroscopic surgery is recommended for Type 1 fragments where clinical signs are present. If these lesions are identified incidentally on fetlock radiographs, treatment is based on what the intended use is for the horse.

If vigorous athletic activity is planned, prophylactic surgery is justified. If less rigorous pursuits are planned, most horses will not require surgery and the fragment will not lead to further arthritic change within the joint."

Normally, Trotter says, surgery is not performed with Type 2 fragments as they eventually will unite with the parent bone, although it takes months to do so. The problem becomes a bit more complicated when both Type 1 and Type 2 fragments appear in the same joint, because the Type 1 fragments generally require surgery.

OCD Of The Shoulder Joint

OCD of the shoulder joint is the most serious type of OCD that can afflict the horse. The good news is that it also is the least common. When it does strike, large areas of the joint surfaces usually are involved and secondary joint disease is common. However, says Trotter, it is unusual to have free or loose bodies develop.

As breeds go, OCD of the shoulder seems to affect Quarter Horses and Thoroughbreds most frequently.

Shoulder joint OCD generally shows up when the horse is a yearling or even younger. The clinical signs are forelimb lameness of variable severity. Many of the horses will have prominent lameness, and if lameness has been present for a long period, muscle atrophy will be seen.

"Because of the altered gait and use of the limb," Trotter says, "many cases also develop an upright or club-footed appearance to the foot, and the foot may appear smaller on the affected limb. Deep pressure over the shoulder joint will often cause discomfort, and forced flexion/extension of the limb will sometimes accentuate the lameness that is seen. Intra-articular anesthesia will improve or eliminate the lameness."

The outcome of treatment procedures is still a bit murky because there haven’t been very many surgeries.

Trotter explains: "Conservative treatment is rarely associated with a successful outcome, and sufficient numbers having surgery have not yet been accumulated to identify accurately the prognosis with surgery. However, there is little doubt that surgery dramatically improves the clinical signs in most cases. If extensive degenerative arthritic changes are present on radiographs at the time of initial examination, the prognosis for an athletic career is unfavorable, and surgery should only be considered for relative improvement in the degree of lameness. However, for most localized lesions, the prognosis is favorable for a successful outcome.

"The shoulder is probably the most difficult joint on which to perform arthroscopic surgery, due to the depth of the joint below the muscles in the area. Surgery is easier on young animals due to their relatively small muscle mass."

As stated, because of the small number of surgeries for OCD of the shoulder, it is a bit difficult to arrive at a prognosis. However, Trotter is of the opinion that the success ratio would be about 50%.

Subchondral Cystic Lesions

A discussion involving osteochondrosis and OCD would not be complete without inclusion of comment concerning subchondral cystic lesions, which are bone cysts or bony cyst-like lesions.

For this part of the discussion we turn to a new guide—Gary Baxter.

He tells us that some subchondral cystic lesions involve a joint surface while others do not. However, most lesions that contribute to lameness do involve a joint surface.

The most common age for diagnosis of the affliction through clinical signs is three years or less. However, Baxter says, horses demonstrate clinical signs related to subchondral cystic lesions over a wide age range, and the relationship when the lesion develops and when the horse begins to show clinical signs is not known.

The most common location for subchondral bone cysts is the stifle, although they can appear in the knee, elbow, fetlock, pastern, coffin, shoulder, hock, and hip joints.

"Subchondral cystic lesions can occur in multiple sites in horses," Baxter tells us, "and controversy exists as to whether these lesions are a manifestation of osteochondrosis, secondary to joint trauma, or a combination of both. Subchondral cystic lesions have been described as resulting from an infolding of abnormal cartilage into the underlying bone, and instances of this have been documented. The infolded cartilage becomes necrotic (dies) and its matrix remains non-mineralized (soft) so that osteoclasts (cells that remove damaged bone) and blood vessels do not migrate into the defect to enable repair of the defective cartilage and bone. The cystic lining is made up of fibrous (scar) tissue, and the cyst is sometimes filled with a gelatinous-type material. Subchondral cystic lesions nearly always develop in major weight-bearing sites within joints."

There are two basic approaches to treatment of most subchondral cystic lesions—conservative and surgical. In the conservative approach, rest is advocated with or without joint medications or non-steroidal anti-inflammatory drugs. With the more aggressive approach, Baxter says, surgical debridement is involved.

"The goal of surgery," Baxter says, "is to evacuate the contents and debride the margins that hopefully will permit healing of the lesion."

Much is known, but much is yet to be learned. In the meantime, the horse owner can rest secure in the knowledge that sophisticated arthroscopic surgery can provide a major assist in rectifying the problem when it occurs.

About the Author

Les Sellnow

Les Sellnow is a free-lance writer based near Riverton, Wyo. He specializes in articles on equine research, and operates a ranch where he raises horses and livestock. He has authored several fiction and non-fiction books, including Understanding Equine Lameness and Understanding The Young Horse, published by Eclipse Press and available at www.exclusivelyequine.com or by calling 800/582-5604.

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