Possible Causative Factors of Osteochondrosis in Horses

Osteochondrosis is a defect in the process by which cartilage matures into bone in young horses. This process of endochondral ossification can result in a number of different manifestations, depending on the site of the endochondral ossification defect. In many cases, cartilage flaps, cysts, or shreds occur at a joint, usually causing inflammation and lameness. Certain etiologic factors have been recognized that contribute to the development of these osteochondritis dissecans (OCD) lesions.

These factors have been varied, but the idea that there is a multifactorial etiology (a number of contributing causes) has generally been accepted. Much of the information is from clinical and pathologic reports, as well as experimental studies in the horse. The studies have given some answers but have also created confusion. The primary problem has been that the lesions are often somewhat different than what veterinarians most commonly encounter as they look at clinical cases. However, major factors have been identified that seem to predispose the growing animal to osteochondrosis-type problems. These include rapid growth, genetic predisposition, nutritional excesses or imbalances, and superimposed trauma on the cartilage.

Genetic predisposition. Radiographic studies in Swedish Trotters and Warmbloods have shown progeny of one stallion from each breed having a significantly higher frequency of OCD among his progeny, compared with the progeny of the other stallions. In another study in Denmark, radiographic evidence of a significantly higher proportion of osteochondrosis was seen in the progeny of one of eight stallions, even though the stallion himself did not show radiographic signs of osteochondrosis. Since that time, there have been two more studies on the heritability of osteochondrosis in the hocks of Swedish Trotters. There has been little work done in the United States with regard to heredity, and no type of screening program has been developed 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 this disease. Individual instances of certain stallions and mares producing these individuals have been seen.

Growth and body size. In pigs, it has been demonstrated that a rapid growth rate is the main reason for high incidence of osteochondrosis and that the growth rate is the result of both genetic selection and caloric intake. Some genetic predispositions have been demonstrated in the horse and increased energy will increase the incidence of osteochondrosis. However, it is not a simple cause/effect relationship. Fast growth was also implicated with a high incidence of osteochondrosis in dogs. There have been anecdotal reports of this in the horse. However, the controlled studies that have been done in the horse question whether growth rate is indeed a factor. It has been pointed out that the most intense phase of growth occurs in the first three months of life, and if growth was a big factor, this would be the time that most lesions could be expected to occur, but this is not when they are seen clinically. However, growth rate is obviously associated with a number of factors. In one study done at Ohio, 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, height, and cannon bone circumference and it was part of a study on the effect of dietary copper.

Mechanical stress and trauma. It has certainly been recognized that mechanical stresses often precipitate clinical signs with OCD and it is presumed that this is by separating the OCD flap or fragment from the parent bone. Whether trauma or physical stress is involved in the primary induction of an OCD lesion is controversial. There are certain predisposing sites for the occurrence of OCD, suggesting possible mechanical factors. A notable veterinary bone and joint pathologist, Dr. Roy Pool, feels that shear forces may disrupt capillaries in the subchondral bone (bone under the cartilage) and give rise to chondrocyte or cartilage cell damage. This is based on histologic observations of various lesions.

Nutrition. As discussed previously, the idea of overnutrition as a cause of equine OCD has been extrapolated from work in dogs and pigs. There has been an increased incidence of OCD lesions noted in horses fed 130% of accepted recommendations for carbohydrate and protein. A well-controlled study in Australia by Dr. Kate Savage showed that high energy diets (120% NRC 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 levels being a problem, but this has not been demonstrated. Many generalizations have been made about excessive growth causing OCD, and this is based on the early work done in Sweden in 1978 which was primarily extrapolated from pigs. However, even when the pig work is carefully looked at, a direct association is not demonstrated in some studies. Unfortunately, the correlation of growth and OCD has led to the practice of virtually starving horses (grass hay and water) in an attempt to reduce the incidence (which it has not). This creates a whole new malnutrition situation. It may be that lowering energy and protein is a good part of the protocol in some instances to prevent OCD, but the possibility of inducing other nutritional imbalances needs to be carefully considered and compensated for. It has also been pointed out that overfeeding can induce endocrine imbalances.

Mineral imbalances. Various mineral imbalances have been implicated as causative factors with OCD, including high calcium, high phosphorus, low copper, and high zinc. Although high calcium levels have been implicated, experimental research in the horse with three times the NRC level of calcium in the diet failed to produce lesions of osteochondrosis. High phosphorus diets (five times NRC) did produce lesions of OCD in young foals. Low copper has been implicated as a cause. An epidemiologic study on clinical cases of DOD implicated low copper levels as the most consistent factor. In experimental studies, it has been noted that a marked copper deficiency (1.7 ppm – 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 ppm) and low (7 ppm) 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 clinical problems are commonly seen. Excessive zinc intake has been related to equine osteochondrosis. Generalized osteochondrosis has been seen in foals raised near a zinc smelter. The relationship between zinc and copper (it has been suggested that high zinc suppresses copper levels) is still being elucidated.

Endocrine factors. It has been postulated by one investigator that the production of osteochondrosis lesions in association with overfeeding is mediated by the endocrine system. Certainly the long-term administration of dexamethasone has produced osteochondrosis-type lesions, and it is considered that glucocorticoids induced a parathyroid hormone resistance at the level of the osteocyte causing an inhibition of normal remodeling. Glucocorticoids also induced decreased glycosaminoglycans levels and this decrease in turn inhibits capillary penetration of the cartilage which is a very important step in forming bone from cartilage. The failure of ossification could also be mediated through induced defects in vitamin D metabolism. Corticosteroids are also a potent inhibitor of lysyl oxidase which is involved in cross-linking of collagen in cartilage and bone. It is felt this could be a way of inducing lesions.

Site vulnerability. Because the lesions of equine osteochondrosis occur at specific anatomic sites, this obviously suggests site vulnerability. This predilection could be related to an ossification defect or trauma caused by excessive stress in that region. In nearly all instances, the sites of occurrence of OCD are very close to the limits of articulation and it is known from basic research that the makeup of the cartilage between articulating and nonarticulating surfaces is different. OCD lesions are frequently bilateral in the stifle and hock and quadrilateral in the fetlock joint, although they frequently involve different joints in the same animal. It is felt this may suggest a window of vulnerability in the endochondral ossification of that specific joint when an environmental insult may have occurred. If the causative factor was present intermittently or for a transient period during the foal’s growth period, this would explain the development of the disease in only one pair of joints. It is not possible from these data to ascertain different periods of onset of the disease process in different joints.

Exercise. Adequate exercise in foals would logically be important for the maintenance of cartilage and bone quality. There are some data suggesting a protective effect of exercise. 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 with foals fed the same diet but with limited exercise.