By Sarah Ralston, VMD, PhD, with Christine Barakat

Helping a horse grow from a wobbly legged newborn to a strong, athletic adult is a challenging and rewarding experience.

Whether you're raising a pedigreed foal with promise of showring glory or you're bringing up a homebred baby destined for recreational trail riding, developmental orthopedic disease (DOD) can put your dreams in jeopardy. A collection of bone and joint abnormalities that arise in young, rapidly growing horses, DOD can lead to lifelong soundness issues, ranging from mild to crippling.

Therefore, it's no wonder that DOD has been a topic of ongoing research for decades, with breeders closely following any resulting recommendations for preventing the condition. Trouble was, early studies were far from conclusive or even consistent, and the subsequent advice given to horse owners based on these studies has been contradictory or even outright wrong. To further complicate matters, recent advances in our understanding of factors contributing to the problem have not yet reached many veterinarians, who continue to give the outdated advice they were taught years ago.

A case in point is the protein mantra that has dominated discussions of DOD since the 1970s. In the 15 years I've spent investigating dietary causes of DOD, I, along with other researchers, have found that the evidence points to an interplay of the young horse's intake of minerals and metabolic responses to carbohydrates in the ration.

We don't have all the answers yet--exactly how these metabolic processes affect bone growth and mineralization is still not clear--but I can say with confidence that if you want to prevent DOD in a young horse, stop obsessing about restricting protein (which can actually be detrimental!) and pay attention to the carbohydrates and minerals.

Defining DOD
In utero, equine bone begins as cartilage. In the three or four months prior to birth, the rubbery cartilage starts to be converted into hard bone through a process called ossification, in which the cartilage cells are mineralized with calcium, phosphorus and magnesium compounds. The trace minerals copper and zinc also play a key role in this process. By the time a foal is born, 80 percent of his bone is ossified.

Thereafter, cartilage ossification remains critical to normal bone growth. Bones become longer by increasing the number of cartilage cells at either end. These new cartilage cells are laid down in an organized, ladderlike formation, surrounded by supporting material, referred to as the matrix, at the edge of the growth plates located near the ends of the long bones of the legs. At the same time, the oldest cartilage cells, farthest from the bone shaft, become ossified as the capillaries within the matrix carry in the minerals and proteins needed to form new bone. Through this process, a newborn youngster's legs can grow as much as an inch a week.

DOD occurs when the formation of cartilage is overstimulated or the conversion of cartilage to bone is somehow disrupted or inhibited, whether by overly rapid growth or inadequate nutrient intake. When a youngster cannot produce uniform new, strong bone, the result can be orthopedic disease.

In some instances, the cartilage layer becomes too thick for nutrients to diffuse from the blood vessels to the cells at the outer surface. The cartilage then dies, leaving an empty, weak "lesion" in the bone, a condition called osteochondrosis or osteochondritis dissecans (OCD). In other cases, the areas of actively growing cartilage at either end of the bone shaft become too wide to support the weight borne by the bone; mechanical distortion can result as the area is literally crushed under the growing horse's weight, resulting in visible "swellings" at the growth plates, a situation referred to as epiphysitis or physitis.

Epiphysitis is often accompanied by pain and flexure deformities, formerly known as "contracted tendons." Any sort of deviation in the distribution of weight on the growing surfaces can result in uneven growth, which causes angular deformities. All of these problems fall under the collective name of developmental orthopedic disease.

Whatever the specific form of DOD, the first clinical signs are typically mild lameness associated with a visible deviation in the angles of the lower limb and/or epiphysitis. Usually both front legs or all four legs are affected and problems may be seen in one or more areas, though the fetlocks, knees and hocks are the most common sites.

When DOD is recognized and prompt action is taken to address the underlying issues, the condition can be halted and normal bone development can resume--but the areas of incomplete ossification can remain, along with any resulting OCD lesions. A foal with DOD may not be obviously lame, or--as frequently happens with OCD--lameness may emerge only when training begins. Some DODs may never cause lameness: How debilitating a problem will be seems to depend on the severity, location and, to some degree, the individual.

Beyond Protein
In the search for the causes of DOD, researchers have looked at nearly every facet of the management of young horses. It has become clear that many variables are involved in the development of the disorder, ranging from genetics to joint trauma from forced exercise. Mineral imbalances are a well-documented cause of DOD, which is not surprising given that minerals provide the building materials for new bone. Specifically, deficiencies or excesses of copper, zinc, calcium and phosphorus have all been shown to result in abnormal bone maturation. When considering other dietary factors, however, old beliefs are being replaced with findings from new research.

Back in the 1970s, the idea was brought forward that feeding excess protein--more than 16 percent of the total diet--led to the development of DOD. And although the studies were very limited, the notion caught on that protein was the culprit. It seemed like everyone became obsessed with how much protein to feed--or not feed--growing horses. Several well-controlled studies published in the 1980s disproved the protein link, but it remained a key consideration in the minds of many veterinarians and horse owners.

Then, in the early 1990s, I was conducting a series of studies comparing the effect of high and low grain diets on growth and DOD in Standardbred weanlings. In addition to taking radiographs to detect the presence or absence of OCD lesions, we were looking at a number of blood parameters, including glucose/insulin responses to meals of the sweet feed being used.

I'd been looking at glucose/insulin metabolism in horses since my PhD thesis work in the '80s on the control of appetite in horses and have been fascinated by the factors that influence the insulin response to glucose challenges. Insulin is released by the pancreas in response to glucose in the blood and facilitates the movement of glucose into the cells. However, it also affects other hormonal systems, including the release of growth hormone and thyroid hormones. As a result, I usually run glucose/insulin trials in most of the studies I conduct, whether or not it is the primary focus of the research.

When I looked at the insulin results of the weanling Standardbred study, I saw some numbers that seemed to be hugely out of the normal range. When fed grain, certain horses produced dramatically higher levels of insulin than did others receiving the same ration under the same conditions. On any predominantly hay diet, however, their responses were normal. Initially, I thought my laboratory assistant, Anthony Calo, (who is now himself a veterinarian) was making an error in his assays.

Tony, however, knew his techniques were good and began looking for another potential cause of the abnormally high values--searching for any similarities in the horses with the high insulin responses. It was Tony who made what would turn out to be a critical observation: Every horse that had the abnormal insulin response to the grain diet also had had radiographic evidence of OCD lesions in the hocks.