CHAPTER 18 Nutritional Factors in Developmental Orthopedic Disease
Developmental orthopedic disease (DOD) is a term used to encompass many orthopedic problems in the growing horse. It includes physitis, osteochondrosis, subchondral bone cysts, cervical vertebral malformation, flexural limb deformities, and angular limb deformities. Clinical signs include lameness, joint effusion, change in posture or limb positioning, and crooked limbs, depending on the disorder. Many of these disorders affect bone and joint formation and sometimes result in abnormal or defective cartilage development, particularly at the metaphyseal or epiphyseal growth plates. Even when this is not the case, such as in horses with acquired flexural deformities, the pain associated with other DODs, such as physitis, may result in less weight-bearing in the limb and shortening of the suspensory ligament or flexor tendons as ground force decreases in response to pain. Although many DODs have no relationship to each other and share no commonality other than affecting growing horses, in instances such as this, a relationship seems to exist. Additionally, it is not uncommon for a horse to have several DODs at the same time.
One difficulty associated with use of the term DOD is that the included disorders vary substantially. Causative factors can be numerous and may include such factors as nutrition, genetic predisposition, growth rate, conformation, traumatic injury, improper exercise, or even in utero malposition. Often these factors are interrelated. When attempting to determine a cause of DOD or to take a prophylactic approach to reducing the incidence rate, the veterinarian should focus attention on the horse’s nutrition; this seems to be especially warranted for horses with physitis and osteochondrosis. Certainly many nutritional factors affect skeletal development and have been implicated in DODs. These factors include the trace minerals copper, zinc, manganese, and silicon and dietary energy and protein as they relate to growth rate and the macrominerals calcium and phosphorus.
Copper is critical for the formation and repair of collagen, the major component of bone matrix. Copper is required for activity of lysyl oxidase, the enzyme needed to form crosslinks in collagen. Thus, copper deficiency could impair the strength of collagen and, in turn, bone. Insufficient copper in the diet has been implicated in osteochondrosis and flexural deformities. Some studies have strongly suggested that low copper concentrations are associated with the development of osteochondrosis. In one of these studies, an epidemiologic study, a greater perceived prevalence of DOD was found on farms that fed lower amounts of dietary copper compared with farms that fed higher copper concentrations. However, results from that study appear to be strongly influenced by data from 2 of the 19 farms surveyed. Furthermore, farms with a higher incidence of DOD also tended to feed diets low in calcium and high in phosphorus. In a controlled study in which foals were sacrificed so that joints could be examined for lesions, more lesions were detected in control foals than in copper-supplemented foals. Similar to findings in the epidemiologic study, the results of this controlled study were influenced by a single foal in the control group that had a disproportionately high number of lesions.
When dealing with small numbers, as is often the case in research involving horses, 1 or 2 subjects can heavily influence the results, and this effect must be considered in evaluation of results from any study (see Chapter 9, Reading and Interpreting Scientific Literature). Hence, although these studies provide some evidence of copper’s role in prevention of DOD, they do not provide proof. In a series of published papers from work conducted in New Zealand, no substantial differences were seen between supplemented and nonsupplemented foals. It should be noted that the incidence rate and severity of lesions were relatively low in this group of foals, so the ability to detect treatment differences may have been impaired.
Insufficient copper in the diet of broodmares has also been implicated as a cause of DOD. The series of papers from New Zealand mentioned previously suggested that supplementation of mares grazing low-copper pasture (containing 4.4 to 8.6 ppm copper) had a greater effect on reducing the severity of physitis scores in their foals at 150 days of age and the prevalence of articular cartilage lesions than did supplementation of the foals themselves, suggesting an in utero role for copper in skeletal development. However, supplementation of copper in mares did not eliminate DOD in their foals. In another study conducted in Germany, no relationship was found between copper intake by pregnant mares and development of osteochondrosis in 629 foals from 83 farms.
Although copper deficiency may play a role in causing DOD, and ensuring that dietary concentrations of copper are sufficient in foals that have osteochondrosis may help promote repair of osteochondrotic lesions as they develop, the overemphasis on supplemental copper to prevent osteochondrosis is likely unwarranted. Since the mid-1980s, with the first reports implicating low dietary copper in the development of osteochondrosis and physitis, it has been common for commercial concentrates to contain much higher amounts of copper than the recommended minimum. Despite this practice, the incidence rate for DOD remains high in certain populations of horses, suggesting that the problem is multifactorial and not simply a result of insufficient dietary copper.
The other concern regarding the evaluation of dietary copper is the question concerning the minimum acceptable amount. The 2007 NRC guidelines suggest that the daily copper requirement for growing horses is 0.25 mg copper per kilogram of body weight. This value is intended to meet endogenous losses plus an additional requirement for growth of 0.017 mg copper/kg of body weight while maintaining a minimum of 10 ppm concentration with an overall feed intake of 2.5% of body weight. The copper requirement for mares in the last 3 months of gestation and during lactation was also set at 0.25 mg copper per kilogram of body weight. Therefore, in a pregnant mare consuming 2% of her body weight, 12.5 ppm would be needed to accommodate any additional needs by the foal in utero. However, many of the studies implicating low copper concentrations in the development of DOD evaluated dietary copper levels below these amounts. Hence, if one is feeding at or above the amount required by the growing horse or the pregnant or lactating broodmare, and if there are no excesses of other minerals that act as a copper antagonist, there is little reason to suspect low copper as a primary cause of DOD.