Vet Insight: Osteochondrosis & OCD

By Camilla Nock MA(cantab) VetMB MRCVS. Certificate in Equine Sports Medicine

Osteochondrosis

& OCD Genetics Prevalence of osteochondrosis varies, particularly between different breeds. The most commonly affected breed appears to be warmbloods with as many as 67.5 A disease of genetics or management? percent of Dutch Warmbloods yearlings affected in one survey. This is significantly higher than the propotion of Thoroughbreds Osteochondrosis (OC) is a failure in the process OCD can occur in any joint, but is most affected, whilst diagnosis of OC in ponies of bone formation from a cartilage framework. commonly diagnosed in fetlocks, stifles and is rare. This supports the role of genetics in OCD stands for Osteochondritis Dissecans hocks. The facet joints of the vertebrae of the the development of lesions, and has driven and specifically refers to those cases that neck are also commonly affected sites, and selection programs like those implemented develop fragments. Most commonly diagnosed more rarely knees, elbows and shoulders. by the Royal Dutch Warmblood Studbook by X-rays that show areas of flattening or Lameness may be seen in foals with large (KWPN). Candidate sires with evidence of fragmentation of the joint surface, lesions are lesions, usually in association with visible osteochondrosis in the hocks (since 1984) thought to result from damage to the small distension of the joint, but more commonly and stifles (since 1992) were rejected for blood vessels supplying this developing bone lameness first occurs when the horse enters breeding, however this strict program did not in the foetus or foal. Defects may be present training. OCD is however often found on lead to significant reductions in the incidence in new born foals, or may develop in the first routine screening radiographs of older of osteochondrosis in the population so few months of life. It is also possible for lesions horses, for instance during a pre-purchase a grading scale has since been adopted, to repair and resolve without intervention, examination, with no evidence of lameness. including screening of the first crop of however by the time the horse is 12 months Whilst lameness usually occurs on just one leg offspring, alongside DNA testing. old further progression or repair is unlikely to the opposite joint is also affected in more than So why was this selection process occur. 50 percent of horses with stifle or hock OCD. unsuccessful? Firstly the sires were screeened as mature horses, and so those individuals that had lesions as foals that subsequently resolved will not have been detected, but may have carried genes associated with development of osteochondrosis. Secondly, recent genetic studies into osteochondrosis have shown a complex

Photography courtesy of Camilla Nock A severe case of stifle OCD with mutliple fragments

picture of heritability, with a large number of different genes identified as conveying an increased risk. These genes are involved in a number of different processes including collagen formation, hormone regulation, blood vessel formation, and inflammation. Different genes are associated with osteochondrosis of different locations, in different breeds, and between lesions that show fragmentation (OCD) rather than just flattening (OC).

Thirdly, genetic predisposition interacts with complex environmental factors, particularly biomechinaical loading, and nutrition, that all act to determine if a lesion develops.

Biomechanical Loading

Biomechanical loading may be influenced by the exercise regime of foals, roughness of terrain, and conformation. There is significant evidence to show the conditioning effects on cartilage of exercise in the foal, with consequences for injury resistance and susceptibility to degenerative joint disease later in life. An optimum balance exists between sufficient loading to drive cartilage organisation, and excessive exercise leading to overloading. Evidence so far suggests rough and slippery grazing areas carry an increased risk, as does mixed housing (stable overnight, and turnout during the day) when compared to permanent turnout during the first year.

Nutrition

The link between nutrition and osteochondrosis is intricately associated with genetics. For example a high growth rate during certain high risk windows of susceptibility is associated with an increased risk of osteochondrosis, regardless of whether this increased growth rate is driven by nutrition or genetics. Additionally, high levels of insulin have been linked to development of osteochondrisis, and are associated with a diet of easily digestible carbohydrates, but this response varies between horses fed the same diet.

This link between carbohydrates may also lead to a seasonal affect on osteochondrosis. Foals in Kentucky were shown to have different rates of hock vs stifle osteochondrosis depending on what time of year they were born, and how peaks of energy in the Kentucky bluegrass in spring and autumn conincided with different stages of bone development.

Trace elements have also been implicated in the development of osteochondrosis. Copper deficiency, or excessive zinc, may influence either the development of lesions or the repair process, while excess phosphorous may lead to osteoporosis and weakening of subchondral bone.

In summary there is a complex interaction of different factors that combine to cause development of osteochondrosis lesions. A A typical fetlock osteochondrosis

biomechanical consult is required of sufficient magnitude, direction and repetition, and acting on tissues influenced by genetics, nutrition and hormonal imbalances, at a crucial moment in development.

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