Osteochondrosis is a complex disease involving interactions of inherited genetic and external environmental risk factors.
Environmental factors thought to play a role in disease development include nutrition, exercise, conformation and other biomechanical
factors, trauma, stress response, the in utero environment, toxins, hormonal interactions and iatrogenic factors.2,5,6 It has been suggested that osteochondrosis could be caused by either abnormal forces on normal cartilage or by normal forces
on abnormal cartilage.6 In either case, the pathologic insult to a susceptible bone was likely of short duration, during a window of susceptibility
of joint vulnerability.6 While osteochondral abnormalities may be observed early in life (as early as a few days to weeks of age), many lesions go
on to heal spontaneously and do not require treatment.7
Nutritional factors have been found to produce cartilage and bone abnormalities, including osteochondrosis, in young horses.
These include consumption of high-energy diets or diets with a high glycemic index, an imbalance of calcium and phosphorus
or excessive phosphorus with low calcium. Decreased copper and increased concentrations of zinc also are thought to be associated
with an increased incidence of various developmental orthopaedic disorders.7
A documented predisposition to osteochondrosis or OCD is noted in several equine breeds, including Warmbloods, Standardbreds,
Thoroughbreds, Quarter horses, Arabians and Paints. In fact, in Standardbreds, up to 50 percent of disease risk is thought
to be inheritance.8 A specific genetic defect leading to this predisposition has not yet been identified.
Exercise regimen is also suggested as a potential factor in the etiology or progression of various developmental orthopaedic
diseases. As opposed to confinement, voluntary exercise may be beneficial to reduced incidence of disease.7 However, the exact role of exercise in osteochondrosis is far from clear-cut. In one large study, forced exercise was found
to affect the distribution of osteochondrosis lesions within joints, but not the total number of lesions.9 Another study found that regular but limited exercise seemed to reduce the risk of osteochondrosis development.10
Elucidation of specific risk factors underlying the development of osteochondrosis or OCD is of current interest to researchers
in several veterinary laboratories within the United States. Among these are:
- Sarah Ralston, VMD, PhD, DACVN, associate professor at Rutgers University Equine Science Center, who studies management and
nutrition factors and metabolic profiles of horses that develop osteochondrosis.
- Molly McCue, DVM, PhD, DACVIM, assistant professor, and Annette McCoy, DVM, DACVS, postdoctoral fellow, both at the University
of Minnesota College of Veterinary Medicine, Veterinary Population Medicine Department, who are studying genetic risk factors
Management: Growth and nutrition
Seasonal growth spurts are associated with an increased occurrence of bone abnormalities in young horses. Sustained modest
growth rates are preferred to minimize some developmental orthopedic disease conditions, especially before the earliest window
of susceptibility for specific joints.
"Foal growth is not even from birth to 1 year of age," says Ralston. "One week they'll gain weight—the next gain in height.
And, especially in the first six months, the rates of gain can be very rapid— over 2 pounds a day for foals that will mature
at 1,200 pounds.
"A high incidence of osteochondrosis has been correlated with rapid growth, but not all foals that are growing rapidly will
develop lesions," Ralston continues. "And in predisposed foals, cartilage defects can appear even during moderate growth.
The key is to feed for optimum nutrition to maintain steady growth. If you try to slow growth by depriving the foal of protein
or energy, when it is refed, there will be a rapid compensatory growth spurt that can lead to problems, though not necessarily
Ralston says that the biggest concern for osteochondrosis is now thought to be associated with excessive caloric intake, or
getting foals too fat and pushing their growth with excessively high-energy-type rations. "The concern about excess protein
is no longer valid," say Ralston. "We've repeatedly documented that high protein is not a major concern. It's more important
to feed adequate protein for growth and good bone deposition."
She notes a strong genetic component to osteochondrosis development in Standardbreds. "There's a large, distinct metabolic
profile of horses that get osteochondrosis when others do not, even when they're on the same rations," she says. "Once we
discover the details of the metabolic profile, we can hopefully identify the horses that are predisposed and determine the
metabolic defect that's the cause."
She says researchers are close to being able to identify affected foals even before they get the lesion. "We're also in the
process of developing targeted supplements that potentially will circumvent what the defect is and allow foals to develop
normally," says Ralston.
The glucose-insulin responses are not as important of an issue as once thought, Ralston says. But she does recommend avoiding
large amounts of high-starch feeds. However, if a young horse is receiving a sweet feed in its ration, it doesn't necessarily
mean that the horse is going to develop osteochondrosis. The total ration's mineral content is what is critical, according
"If you're feeding concentrates, they need to be balanced for calcium and phosphorus and have adequate copper and zinc. Oversupplementation
is probably just as bad as under-supplementation," says Ralston.
According to the National Research Council, sufficient copper has been shown to be necessary for formation and repair of collagen,
the main component of bone matrix.7 It was reported that rations deficient in copper resulted in clinically diagnosed bone disorders in foals. And foals whose
dams were given supplemental copper in the latter stages of pregnancy had a lower incidence of osteochondrosis.