Question: What do we know about environmental factors that could make a horse more or less likely to get OCD?
Answer: Osteochondrosis (OC) is widely understood to be a disturbance of endochondral ossification (the formation of bone from cartilage) and is arguably one of the most clinically relevant developmental orthopedic diseases in the equine patient. Although it was once thought that OC lesions were static, sequential radiographic studies on foals, weanlings, and yearlings revealed that the characteristic lesions of OC could increase in size or completely regress (“heal”) up to 12 months of age. The timeline of this lesion formation and regression is different for each joint, and has supported the idea that there are number of environmental factors, in addition to genetics, that play a role in the progression of osteochondrosis.
Although no definitive cause of osteochondrosis has been determined, factors such as nutrition and exercise have been shown to play a role in the development and progression of OC lesions. Of these possible etiologies, the role of nutrition has been most closely investigated. Initial research into the effect of diet on OC focused largely on dietary energy level, usually in relation to a high growth rate. Although the results of many of these studies seem to be conflicting, many support the conclusion that high growth rate (a combination of genetics and diet) is associated with an increase in the severity of OC lesions. It is important to note, however, that this is a combined effect: decreasing nutritional plane below maintenance levels will not decrease the incidence or severity of OC lesions and can lead to other dietary imbalances.
Studies investigating the role of trace elements (copper, zinc, calcium, and phosphorus) have determined that low copper levels (which can be induced by increased zinc) are linked to decreased resolution of OC lesions, and copper supplementation, to a certain extent, was able to reduce the severity of cartilage lesions. Investigations into the role of calcium and phosphorus in OC have determined that high calcium diets failed to produce OC lesions, whereas high phosphorus diets (five times NRC) reliably produced lesions in foals.
The role of exercise in the formation of OC lesions seems intuitive; it is well known that exercise is vital to the formation of a functional articular cartilage surface and OC is a developmental defect in articular cartilage. Investigations into the exact role of exercise in OC however, have yielded conflicting results. In some studies, increased exercise was correlated with decreased incidence in OC, whereas other research was unable to find decreased incidence in OC lesions with exercised horses but did notice a decrease in severity of existing lesions. As with nutrition, it is clear that although exercise can play a supporting role in decreasing the incidence or severity of OC, no single factor is responsible for the course of the disease.
Since the process of cartilage metabolism and bone formation is highly dynamic, especially during the first year of age, it is widely thought that there are certain periods of times (“windows of susceptibility”) during which environmental factors can play a pivotal role in the severity of OC lesions. Research investigating these developmental periods, as well as the exact pathogenesis of osteochondrosis, will yield more answers and recommendations in the future.
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