Horse Care, July 1991
Reprinted with permission of author, Nancy S. Loving, D.V.M.

COPPER AND DEVELOPMENTAL BONE DISEASE
BY NANCY S. LOVING, D.V.M.

BESIDES LOOKING to be sure your horse's hay and grain are of good quality and free of dust and mold, do you ever consider its nutritive value as you throw it into his manger? If the hay looks palatable and your horse is the picture of health, it's easy to assume his diet is adequate. Yet there is much more to take into consideration...For instance, a pregnant mare's or growing foal's dietary needs differ greatly from an adult, nonbreeding horse's. Research has implicated dietary imbalances during critical stages of gestation and growth as contributing to developmental orthopedic disease (DOD), a syndrome more frequently recognized in the past decade as a cause of seriously debilitating and crippling lameness in horses (for more information, see "Developmental Orthopedic Disease: A Question Of Management," HORSE CARE July/August and September/October '89).

Under normal conditions, cartilage is removed grtadually and continuously replaced with bone cells, as shown below. If this processs doesn't proceed normally, cartilage is retained in areas where it should have mineralized into bone. Defective joint cartilage can separate from underlying bone, forming osteochondritic lesions indicative of DOD.

Photos by Nancy S. Loving, DVM

At the 1990 American Association of Equine Practitioners (AAEP) convention in Lexington, Kentucky, Dr. Mark Hurtig presented new information supporting the role of copper deficiency in DOD. Copper is essential for the synthesis and maintenance of elastic connective tissue, and for copper-related enzyme systems responsible for "digesting" cartilage before its conversion to bone.

Dr. Hurtig explained a study testing the role of copper in bone development in which two groups of three-month-old foals were fed diets containing different quantities of copper, with all other nutritive and environmental considerations kept equal.

Initial blood samples and liver biopsies were obtained for a baseline value of circulating and stored levels of copper and zinc. Also, repeated blood samples were obtained from each foal to measure osteocalcin levels during the two-month study period to determine if this could be as useful an indicator of metabolic bone disease in foals as it is in people. Osteocalcin is a polypeptide that is incorporated into bone and released into the bloodstream during the remodeling and conversion process.

By radiographing major joints in each foal (knees, hocks, fetlocks, shoulders, and neck vertebrae), it was discovered that many of the test foals came into the program with OCD lesions already present.

One group was placed on a low-copper diet of seven parts per million (ppm; or seven milligrams per kilogram of feed), while the other group received a high-copper supplement of 30 ppm. During the two-month test period, foals on the low-copper diet attempted to eat non-feed materials such as dirt or wood, a phenomenon known as pica. It is thought this was an attempt to obtain the deficient mineral. However, despite eating foreign matter, liver biopsies of foals on low-copper diets showed no increase in copper stores.

The low-copper foals displayed dull hair coats and clinical symptoms of DOD, such as physitis (growth plate inflam-mation), intermittent joint effusion (fluid loss) and lameness, and upright patterns indicative of beginning flexural deformities. Foals on the high-copper diet showed no clinical lameness or other DOD symptoms.

At five months of age, all foals were radiographed again, euthanized, and necropsied. Normal growth rates in both copper-deficient and copper-supplemented foals were similar, eliminating rapid growth as an exclusive cause of DOD. After analysis of all data, several startling observations were made. Foals on the high-copper diet that had entered the program with OCD lesions showed a normalization and steady disappearance of those lesions; any remaining lesions were mild and few.

On the other hand, the low-copper foals had profuse, characterestic OCD lesions on postmortem exam. While not all of them had developed signs of OCD, those that had showed a marked reduction in collagen cross-links, a requirement for the mineralization of cartilage into bone. Cartilage retention and thickening were apparent, as were microfractures in many joints.

Examination of cervical vertebrae in the low-copper group showed profound and severe lesions. Microfractures visible in long bones also appeared in vertebral surfaces. If abnormal articular spaces of vertebral joints are accompanied by osteochondrotic lesions and an inherited narrow spinal canal, resultant spinal cord compression will produce the neurological disease known as "wobbler" syndrome. Based on this study, it is possible that cervical radiographs may be a useful diagnostic predictor of animals affected with developmental orthopedic disease.

Interestingly, blood levels of copper, calcium, phosphorus, and zinc did not differ between normal and DOD-affected individuals, making such analysis worthless for diagnostic purposes. However, blood levels of osteocalcin did differ between the groups, with those on the copper-deficient diet showing increased osteocalcin levels relative to the high-copper group.

Continuous microfractures and remodeling of abnormal bone in foals having trouble turning cartilage into bone was responsible for this increase. In time, once normal osteocalcin values have been established in horses, such a simple blood analysis could prove an invaluable diagnostic test for DOD. By comparing subsequent blood samples, it may even be a useful prognostic guide.

An important point was substantiated by this study - clinical signs of DOD are just the tip of the iceberg. If a lesion is found in one joint, there is a high probability that multiple lesions will be found in other joints throughout the body.

Another essential piece of information derived from this and other similar research studies (by Drs. Knight and Gabel) is a need to increase minimum daily copper requirements to at least 30 ppm, for both pregnant mares and growing foals. Although previous studies illustrate 15 ppm support a foal's normal growth rate, it's a marginal level for cartilage development. Growing joints have a higher nutrient threshold, especially between three and six months of age. Therefore, at least 50 to 100 mg of copper fed daily provides adequate, safe amounts.

A predisposition for DOD may begin during a broodmare's last trimester of pregnancy, when trace minerals are transferred through her placenta and deposited in her foal's liver tissues. Because concentrations of copper, zinc, and manganese in a lactating mare's milk are generally quite low, her foal is dependent on his reservoir of micronutrients, along with dietary supplementation once he begins eating solid foodstuffs, to sustain him through a rapid growth phase during the first two to three months of life.

Supplementing your lactating mare with extra quantities of copper, zinc, or manganese will not increase their concentration in her milk. If she doesn't receive a diet containing ample amounts of specific micronutrients during late pregnancy, her in utero foal may not store adequate reserves to sustain healthy bone growth.

Even if you've fed seemingly good-quality hay to a pregnant mare, it's possible that harvesting the same fields year after year may deplete soil of essential minerals, the result being hay deficient in mineral micronutrients. Since copper is transferred from mare to in utero foal, you should supplement your mare with a balanced mineral mix in her last months of pregnancy to compensate for minerals lacking in her forage.

Trace-mineral salt blocks will not supply necessary quantities of minerals, as they are composed of 98-percent regular salt (sodium chloride) and only minute amounts of microminerals. Feed materials vary in nutrient content, so for an accurate assessment of nutrient concentration in your horse's diet, send your feed to a professional laboratory. Discuss the results with your veterinarian or an equine nutritionist so together you can formulate a vitamin/mineral supplement to complement your horse's hay and grain ration.

Once OCD lesions have developed, they may not be entirely reversible. To establish the greatest athletic potential in your horse, it is essential to prevent DOD from occurring in the first place. By carefully managing all aspects of your pregnant mare's diet, and carefully controlling the nutritive values of your foal's rations during growth periods, it's possible to enhance healthy formation of bones, joints, and connective tissue. Structural stability and strength will give your horse the opportunity to display his true genetic potential in athletic performance.