Ask six veterinarians what causes developmental orthopedic disorders in foals and you might get six different answers. According to Tina Kemper, DVM, there could very well be six causes, and possibly more. Kemper specializes in equine internal medicine and recently shared her knowledge, research, and experiences during the bi-annual meeting of the San Diego-based Piedra Foundation.

The Piedra Foundation is a non-profit humanitarian group that provides veterinary services to horse owners who are financially unable to provide veterinary care in life-threatening situations. The foundation is also dedicated to improving equine health through continuing education and research.

"When we talk about development disorders in young horses, we are basically talking about orthopedic diseases," Kemper told an audience of 150 horse owners and veterinarians. "A lot more horses suffer from developmental orthopedic disease than most people realize."

Kemper said the incidence of developmental orthopedic disorders (DOD) in horses ranges anywhere from 10% to 50%, depending on whose research you accept. The opinion of whether developmental disorders are preventable will again depend on whose research you accept.

Developmental diseases are non-infectious and range from angular deformities in foals that might be remedied by age to crippling cervical vertebral malformations (also known as wobblers). Although there can be any of a number of reasons, or combination of reasons, why a horse develops orthopedic disease, the results are generally the same.

Often there is an error or alteration in endochondral ossification--a disruption in the physiological process that initiates the development of cartilage into bone. The most common developmental diseases found in foals today are: osteochondrosis (OCD), physitis, cervical vertebral malformation, angular limb deformities, flexural limb deformities, and club feet. Clinical signs of DOD might include pain, stiffness, joint effusion, awkward gait, lameness, and/or decreased activity.

"There is so much research going on in the area of developmental disorders that you could spend more than a year reading it all," Kemper said. "What I have found is that there is a lot of conflicting research and information as to what causes DOD and how to treat it. One study claims exercise is good for preventing developmental orthopedic disorders, and another says exercise contributes to developmental disorders. Another says stall confinement is good in some cases and bad in other cases. Zinc is good; zinc is bad. I even found an article that stated that the time of year the horse is born can affect the incidences of developmental diseases."

A limb evaluation is often the first step in determining if a foal suffers from DOD. While angular or flexural deformities might be evident to the eye, less subtle signs, such as incomplete ossification, should be confirmed through X rays.

Following is a definition of each of these deformities.

Osteochondrosis (OCD) is the result of defective maturation of cartilage into bone during growth--cartilage that does not ossify properly and does not reach optimum maturation or strength. A foal can suffer from OCD, but it might not show clinical signs because OCD has no specific clinical signs or symptoms. A horse may or may not suffer pain, joint effusion, or lameness. X rays are the best way to determine if a horse is suffering from OCD. However, even then, more subtle OCD lesions might not be apparent. In less severe cases, OCD can heal itself over time.

Physitis is inflammation of the growth plate. Like OCD, a foal can suffer from minor physitis without any obvious clinical signs. Apparent clinical signs might include an hourglass appearance of the fetlock joint or a bony ridge above the carpus. Once these clinical signs exist, X rays will be needed to determine the severity of the physitis.

Cervical compressive myelopathy is compression of the spinal cord due to either an instability of the vertebral column or narrowing of the spinal canal. Horses with this condition are more commonly referred to as wobblers. A horse, however, might also become a wobbler from a variety of non-developmental disorders.

Angular limb deformities (ALD) are fairly obvious because the limb, or limbs, deviate from the normal weight-bearing axis. The angulation might deviate toward the body or away from the body. ALD can be congenital or developmental. Congenital limb deformities might be a result of a foal's malposition in the uterus and are present at birth. Developmental angular limb deformities occur as an animal ages and might be due to excessive weight placed over unossified carpel or tarsal bones. This excessive weight on the immature bones can cause the bones to become malformed, or in severe cases, cause the joint to collapse completely.

Uneven growth rates across the growth plate also can cause limb deformities in older foals.

For foals born with obvious ALD, Kemper said confinement and regulated exercise are a must. In many cases, congenital angular limb deformities will straighten out as the foal grows older and stronger. In severe cases, balancing the foot through corrective trimming or special glue-on shoes might be beneficial. Surgical intervention might be needed for foals which do not respond to conservative therapy.

"Abnormal bone angulation can be caused by the disparity of growth in the growth plates from side to side," Kemper explained. "If a foal with this type of disparity and deformity is made to chase its dam around the paddock, it is more likely to damage the growth plate. Also, premature or dismature foals that have unossified tarsal or carpal bones may develop ALD if the soft cubodial bones become crushed or misshapen due to excessive weight bearing."

Flexural limb deformities (FLD) are also obvious because the foal will stand with its legs partially flexed. Flexural deformities occur when the functional length of the tendon is not sufficient to maintain the limb in its normal extension. FLD generally involves the superficial digital flexor tendon or the deep digital flexor tendon. In the case of a superficial or deep digital flexure deformity, the clinical signs would be an abnormal upright stance and a knuckling at the fetlock.

Like ALD, FLD can be either congenital (present at birth) or can be acquired as a developmental disorder. Congenital flexural abnormalities are usually caused by the foal being malpositioned in the uterus or decreased fetal movement in utero. If a foal is born with FLD and the degree of flexion is severe, the foal might not be able to stand. If the foal does not stand so that it can receive colostrum immediately following birth, the foal will be prone to infection. It also may become hypoglycemic, hypothermic, and dehydrated.

"If the foal has a mild flexural deformity, sometimes stall confinement is all that is needed," Kemper said. "If the degree of flexion is severe, then the foal should be placed in leg wraps and splints that go from the coronary band up to the elbow. This will help support the limbs, relax the tendons, and prevent rupture of the common digital extensor tendon. Intravenous administration of oxytetracycline has also been successful in relaxing tendons. Lastly, surgery may be necessary for severe cases that are not resolved with medical treatment."

Club feet can be inherited, the result of injury and decreased weight bearing, or the result of flexural deformities involving the deep digital flexor tendon. A club foot is generally smaller and steeper in angle than a normal hoof. The foot is often contracted and might have a dish in the dorsal hoof wall. When a club foot is deformed unilaterally, it is possible that the foal suffered an earlier injury that prevented proper use of the hoof. A club foot is generally treated with corrective trimming and shoeing.

Causes of DOD

Any one of several factors, or a combination of factors, can predispose a foal to developmental orthopedic disorders or diseases--nutrition, rapid growth, genetics, or trauma to the metaphyseal growth plate or articular cartilage.

Of all of the factors that might predispose a foal to DOD, Kemper believes the most manageable factor is nutrition. Fortunately, the development of balanced feeds take much of the mystery out of feeding the average, healthy, mature horse. Feed companies, however, are only now developing complete feeds that meet the nutritional needs of growing foals.

"Purina appears to be the winner in this race, having just recently released Purina Junior for weanlings," noted Kemper.

Nutritional areas under scrutiny in relation to DOD are dietary energy, micro- and macro-nutrients, and protein imbalances. Of these, excess dietary energy appears to create the most problems by stimulating rapid growth. Overfeeding a weanling which was not allowed to creep feed while nursing can cause a compensatory growth spurt that might predispose the foal to alterations in endochondral ossification. Excessive dietary energy becomes an even greater problem when certain nutrients are lacking while others are excessive.

"This excess dietary energy leads to rapid bone growth, and rapid growth tends to be one of the major factors for the development of orthopedic disease," Kemper explained.

Nutrient imbalances of calcium, phosphorous, zinc, iodine, and copper can become more problematic if the foal experiences a rapid growth phase. If a foal experiences slow to normal growth, nutrient imbalances might not be significant in contributing to developmental disease. If, however, the bone growth is rapid, the imbalances might predispose the foal to DOD.

Not only must the foal receive adequate amounts of each nutrient, it must also receive the proper ratios between nutrients to ensure bone development. A foal should receive a ratio of two parts calcium to one part phosphorus. Calcium should make up .8% of a weanling's dry matter intake, and .5% of a yearling's dry matter intake. Phosphorus should make up .5% of a weanling's dry matter and .3% of a yearling's dry matter.

While calcium is imperative to bone growth, excess calcium in the diet can inhibit the absorption of phosphorus. So, while a diet might appear to have an adequate amount of phosphorus, it might actually be lacking because the body tends to absorb calcium over phosphorus. A phosphorous imbalance, either excessive or deficient amounts, can lead to osteochondrosis.

Inadequate or excessive amounts of copper or zinc can also be problematic for a growing foal. Copper is needed for bone collagen and elastin synthesis, which make up the lattice-work of bone formation. Inadequate dietary copper can lead to osteochondrosis.

Horses are fairly resistant to copper toxicosis, but excessive copper can cause liver damage. Kemper recommends supplementing foals with calcium and phosphorous. When it comes to copper, she believes it is also important to supplement the mare with copper while the foal is in utero. During gestation, a foal's liver accumulates copper and stores it for use after foaling. Nutritionally, a foal needs about 8-10 milligrams of copper a day. However, it receives only 3-6 milligrams through a mare's milk. The rest is extracted from its liver stores.

"I would make sure the mare has adequate copper throughout gestation," Kemper said. "If you follow the National Research Council's or Dr. Lon Lewis' recommendations for copper for mature animals, and the copper is not being antagonized by another nutrient like zinc, the foal should have all the copper it needs by the time it is born."

Kemper added that she believes Lon Lewis, DVM, PhD, Diplomate of the College of Veterinary Nutrition, is one of the leading equine nutritionists in the country, and she agrees with most of his nutritional guidelines and recommendations.

Kemper recommends copper levels in the feed be 50 parts per million dry matter for nursing foals and 25 parts per million dry matter for weanlings. To combat zinc deficiencies, Kemper recommends supplementing a weanling with 60 parts per million dry matter of zinc per day and yearlings with 40 parts per million dry matter daily.

"Zinc is very important for the different enzyme systems, and supplementing zinc may decrease the severity of osteochondrosis," Kemper explained. "I don't know exactly how zinc works, but it does seem to play a part in preventing developmental disease."

Like copper, excess zinc has its complications. Because zinc and copper compete for the same transport mechanism, zinc can interfere with the absorption of copper
in the foal's gastrointestinal tract. Insufficient copper might contribute to osteochondrosis.

Protein is another nutrient horse owners must monitor. A foal's diet should consist of 14% protein. While excessive amounts of protein alone will not increase a foal's growth rate, combining excessive protein with an excess of other nutrients can cause rapid bone growth and predispose a foal to DOD. Insufficient protein can decrease bone growth and decrease bone mass, and can lead to DOD.

Controlling Diet

With such complex needs, how does the average horse owner mix and match nutrients to meet a horse's nutritional needs?

"The average horse owner would have to look at the feed bag to determine the nutrient ratios," Kemper said. "Most of your better feeds are balanced for the average adult horse, but we are seeing more and more feeds that base the nutrient levels to the age of the horse. Of course, horse owners can always consult their veterinarian."

While a high-energy diet often can result in a rapid growth rate, rapid bone growth also can be genetically based. Kemper advises her clients to start creep feeding foals around the second or third month of age. This will lessen the chance of a compensatory growth rate when the foal is weaned and fed high-energy grains.

Kemper also believes that some developmental orthopedic diseases might be inheritable under certain conditions. She also has noted that certain breeds suffer a greater incidence of DOD.

"Incidents of cervical vertebral compression are much greater in Thoroughbreds than Arabians," she noted. "Heavier bodied breeds like Quarter Horses and Paints seem to attract more than their share of physitis problems. Standardbreds tend to have more osteochondrosis lesions of the hocks. It appears big-bodied colts suffer a greater incidence of cervical vertebral compression than fillies.

"I don't think anyone really knows how much the manisfestation of osteochondrosis sites has to do with genetics, and how much has to do with a function of what the animal does for a living," Kemper added. "Genetically we may not be selecting for DOD, but we are selecting for rapid growth and increased body weight in a lot of our performance horses. By doing this, we may very well, unconsciously, be breeding horses which may be predisposed to developing DOD."

The question many researchers are trying to answer is whether DOD is a result of rapid growth, or if the breeds themselves actually harbor a genetic code that predisposes them to the disorders.

DOD And Injuries

Traumatic incidences that might lead to DOD include poor conformation, lameness, lack of exercise, or excessive exercise. Subclinical DOD might become apparent and create clinical signs of lameness with excessive trauma to the joint. The most common DOD injuries resulting from trauma are OCD lesions and flap lesions. These problems might be minimal, but continued trauma on the limb might result in the problem becoming clinical, i.e., an injured foal is forced to bear an excessive amount of weight on one limb while trying to protect an injury. The increased weight bearing inflicted upon the healthy limb can cause alterations in bone development or endochondral ossification and result in developmental problems.

Poor conformation can lead to uneven concussion across growth plates, resulting in metaphyseal osteochondrosis. Horses with club feet or short, upright pasterns suffer from increased concussion and trauma to the fetlock and foot resulting in lameness or unsoundness.

Lameness, for whatever reason, can result in increased weight bearing on one limb while the foal tries to protect the injured limb. Lameness also might lead to uneven concussion across growth plates. Increased or uneven weight bearing on young, soft bones can cause inflammation of the physis and predispose the foal to physitis and pain-induced flexural deformities. Excessive exercise, or lack of exercise, can result in physitis or possibly micro fractures.

"Most researchers agree that exercise is a good thing," Kemper said. "I don't mean lunging a weanling in a small circle for a half-hour each day. What I mean is that a foal should be allowed to move around a good portion of the day. Allowing the foal to remain active may lower its chances of contracting DOD. However, once the foal develops an orthopedic lesion, exercise should be restricted."

During the course of Kemper's four-hour presentation, she reiterated several times that although many different factors might predispose a foal to DOD, most of the factors are intertwined with the complex physiology of the foal.

"As you can see, everything is interconnected," Kemper said in closing. "Physitis may lead to flexural deformities or angular limb deformities. Osteochondrosis can create physeal problems or articular problems. Rapid growth is related to genetics and nutrition."

Because everything is interrelated, Kemper believes it will be difficult to pinpoint specific causes that predispose foals to DOD.

"And because DOD is so multifactorial," she added, "there is not going to be one single injection or magic pill that is going to cure developmental orthopedic diseases."

About the Author

Aleta Walther

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