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Equine Osteochondrosis Dissecans

August 26, 2020

Equine Osteochondrosis Dissecans – September 2020

B Hunter DVM MS MANZCVS DACVS-LA

Osteochondrosis dissecans (OCD) is a disease affecting joint cartilage and bone in juvenile horses that has a serious economic impact on the equine industry. The disease has been heavily researched for decades. Despite this, a clear understanding of the underlying causes still eludes experts. The following is an explanation of the basic underlying events, clinical signs, diagnosis and treatment of the disease, as well as discussion of the most important factors currently thought to influence the development of this multifactorial disease.

The traditional definition of OCD is that it is a failure in a process called endochondral ossification in the neonate. While more current research shows that that is not precisely true, understanding this relatively straightforward process in normal development does give one a base upon which to build more complex ideas.

When a foal is formed in utero, its bones start out as a cartilage template. This template then ossifies or mineralizes into bone in the process known as endochondral ossification.  The mineralization process starts from specific centers, known as ossification centers, within the bone and these centers are in predictable locations. In long bones, the main part of the bone (diaphysis) has an ossification center in the middle and mineralization moves toward both ends of the bone. At the end of each bone are separate centers of ossification known as epiphyses (Figure 1). These epiphyses are important as they are the part of the bone that enter joints and are affected by OCD. When a foal is born, endochondral ossification is complete within the long part of the bone, but not at the epiphyses. These areas still have thick layers of cartilage that need to develop into bone. That is why the boney aspect of long bone ends is rounder and smaller in neonates than adults. Disruption to this cartilage as it ossifies is what leads to OCD lesions. The tricky part is understanding that disruption is instigated by a combination of factors. The most influential of these factors varies by breed, environment and the joint affected.

The primary clinical sign of OCD is effusion or extra fluid within a joint in a juvenile horse. Most commonly this effusion develops when a horse is first started into work, thus the age at which clinical signs are seen varies between breeds. Thoroughbreds and Standardbreds typically show signs as yearlings, while Warmbloods often do not show signs until 2-3 years of age as they are generally started into work later. Although joint effusion can be dramatic, lameness associated with the effusion will depend on the severity of the lesion and the joint affected. Lesions within the fetlock and hock very rarely are associated with lameness. Extremely large stifle lesions can be associated with lameness of varying degrees. Lesions within the shoulder and elbow are almost always associated with lameness.

Diagnosis of OCD is made on radiographs. There are two basic types of lesions that occur: fragments (Figure 2) and bone cysts (Figure 3). The treatment for fragments is relatively straight forward regardless of what joint they are in. With a few minor exceptions, fragments should be surgically removed. The age at which removal should be done varies by joint. Fetlock and hock fragments should be removed as soon as possible as leaving them only gives the joint time to develop secondary arthritic changes. Stifle fragments should be left until the horse is 14 months of age. This joint develops later than other joints and some lesions can heal, or at least improve if left until 14 months of age. Surgical treatment for most fragments, provided surgery is done in a timely fashion and the fragment is mild to moderate, carries an excellent prognosis for future athletic function and a cosmetic result.

Bone cyst lesions are more difficult to treat. There are often limited surgical options for these lesions. In many cases, horses need to be given time to grow, have their plane of nutrition lowered, and if lame, be confined. In some cases, bone cysts will heal of their own accord. In other cases, bone cysts remain, however the lameness resolves and the horse can go on to a successful athletic career despite the lesion.

Several factors have been shown to influence the development of OCD. Among these biomechanical stress, disruption in vascular supply to the ossifying cartilage, exercise, nutrition and genetics are the most heavily researched factors. Biomechanical stress is thought to be the reason why OCD occurs at highly predictable locations within affected joints. Current research suggests that while biomechanical stress is not a sole cause of OCD, it is an additive factor needed during the age of critical development for a joint for OCD to result. A complicating factor to this is that different joints develop at different ages (eg: hocks and fetlocks reach maturity far earlier than stifles). Thus, the critical age where a joint is susceptible to biomechanical stress varies by joint. Disruption in vascular supply at the bone-cartilage interface is a process that occurs as part of natural development. The disruption occurs, presumably as a slight ‘error’, and then the body repairs the error before a lesion can result. Unfortunately, the body does not always recognize the error or correct it in a timely fashion, and OCD lesions then result. The underlying mechanism for this is complex and currently an area of significant research. Factors that seem to play a role include nutrition, genetics and exercise.

The overall role of exercise in the development of OCD is not as straightforward as initially thought. Some research suggests that too much controlled exercise pre-disposes to OCD, while other research suggests that confinement predisposes. Essentially, best practice seems to be to allow foals and weanlings to ‘live naturally’ with adequate pasture turnout and limited controlled exercise. Nutrition has long been earmarked as a primary culprit in causing OCD. While feeding foals and weanlings a high energy diet has been reliably shown to result in an increased incidence of OCD, many of the earlier theories on trace mineral influence have been set aside. Trace minerals have now been shown to have little impact on OCD development so long as the mare and foal are both fed a balanced diet with adequate mineral. Genetics is perhaps the most complex factor to assess in OCD development. The fact that different breeds have different incidences of OCD indicates that genetics is certainly an important factor. What becomes confusing however is that the heritability of OCD in specific joints also varies by breed. Essentially, multiple genes control inheritance of OCD. There is increasing evidence that different genes control heritability in different joints. Because of the complex nature of OCD inheritance, it is difficult to suggest that affected horses should not be part of the breeding pool. In fact, the Royal Dutch Warmblood Studbook has shown that eliminating all stallions from their registry with hock and stifle OCD over a 25-year period has not significantly diminished the incidence of OCD in this breed. A more conservative approach is now taken whereby stallions with a history of mild OCD are provisionally accepted into the studbook and the incidence and severity of OCD in their progeny is monitored for some years prior to full acceptance.  Given the complex interaction of genetic and environmental influences on OCD incidence and severity, this is a considerably more reasonable approach.

Ultimately OCD is a disease with complex origins that are likely several years of research away from being understood. In the mean time, awareness of clinical signs, timely diagnosis and treatment, and allowing foals to live their first year in a natural environment without overdoing supplemental feeding are the best tools horse owners have in limiting long term effects of this disease.