Developmental orthopedic disease (DOD) remains one of the top concerns of breeders worldwide. Not one condition, but rather a series of related syndromes, DOD encompasses anything that contributes to poor skeletal development in foals: angular limb deformities, osteochondrosis, osteochondritis dessicans (OCD), contracted tendons, cervical malformations, subchondral bone cysts, club foot, and physitis among them.
C. Wayne McIlwraith, BVSc, PhD, Diplomate ACVS, of Colorado State University, one of the United States' leading orthopedic researchers, notes that there is a great deal of confusion in this area of study over terminology.
"Osteochondrosis, OCD, metabolic bone disease...all of these are terms, like DOD, that have been used to describe the overall syndrome," said McIlwraith. "And all cases of DOD are not the same. We need to get more specific. It's important to differentiate between clinical signs (like filling of the joints) and radiographic signs.
"A single cause for all types of DOD is unlikely, however much we'd like it to be there. As we continue to study these problems, it becomes more clear that some of our initial conceptions were incorrect."
Physitis, or physeal dysplasia, is one of the many manifestations of DOD--essentially, it's an inflammation of the growth plates in long bones of a growing foal. Physitis was formerly known as epiphysitis--which most horsemen had just learned to pronounce when the terminology was changed! McIlwraith explains: "(Epiphysitis) was not an accurate description of where the problem was--the epiphysis is the site of secondary ossification in a bone, while the physis is the actual growth plate."
When we focus in on physitis, it's helpful first of all to understand how bones grow and develop in a foal.
Normal Bone Development
Development of the skeleton of a foal begins in the first month of gestation. A miniature "framework" of cartilage is formed initially, and as the fetus grows, the cartilage undergoes a gradual and progressive change into bone--a process called endochondral ossification.
"Long bones," such as those in the limbs, are the typical model to consider when examining the developmental process in the womb. The first area of the fetal cartilage to ossify (be replaced by bone) is the central shaft, or diaphysis. Secondary ossification follows at the epiphyseal ossification centers, or epiphyses, at each end of the bone. By the time the foal is born, almost all of the original cartilage has been transformed into bone, leaving "growth cartilage" at only two sites: the transverse cartilaginous zone, near the ends of the bone, which separates the diaphyseal and epiphyseal ossification centers (otherwise known as the "growth plate" or physis); and a layer between the articular (joint) cartilage and the bone of the epiphysis. It's from the first of these two sites, the growth plate, that the bone grows in length as the foal matures--and it's from here that growth plate abnormalities, or physitis, arise.
After birth, the foal's bones continue to lengthen and develop for at least another 18 months. The growth plates, which can be divided into a series of layers, produce chondrocytes (cartilage cells) in the layer nearest the epiphysis. As they multiply, these cells are pushed toward the main shaft of the bone by the next generation of dividing cells, and they gradually assemble into columns, enlarge (a process called hypertrophy), and change. As the cells reach the end of the hypertrophic layer, complexes of calcium and phosphate (and a few other trace minerals) are deposited in the matrix between the cell columns, and the cell columns that remain between the lines of newly calcified cartilage matrix are then invaded by blood vessels. Over time, the mixture of calcified cartilage and immature bone is replaced by mature bone, and the limb lengthens as the foal grows.
The growth process is such that the rate of production of cartilage cells at the epiphyseal end of the growth plate is almost exactly matched by the rate at which cartilage is replaced by bone at the shaft end. Or, at least, that's how it works when everything goes according to plan. (This same process of endochondral ossification happens as well at the end of each bone, in the growth cartilage between the articular cartilage and the epiphysis.) At the end of the process, skeletal maturity is reached and bone growth ceases, leaving the horse with cartilage only at the articular surfaces of the joints, and in a few select areas such as the muzzle and ears.
Where It Goes Awry
Osteochondrosis is a process in which the growing cartilage is not replaced by bone in the normal manner (sometimes called dyschondroplasia). The cartilage progresses through all the normal stages to begin with, then becomes abnormal in the hypertrophic zone, when calcification doesn't occur and blood vessels fail to invade. In affected areas, the normal columnar bone structure fails to organize, and the hypertrophic cartilage might instead thicken and project into the bone of the epiphysis or the diaphysis.
When osteochondrosis affects the growth of the articular (joint surface) cartilage at the ends of the bones, osteochondritis dessicans, or OCD, can result. This is a situation where, usually as a result of biomechanical stresses, a piece of the thickened, abnormal cartilage separates from the bone. It might remain loosely attached to the articular surface, or it might break away completely and float freely in the joint capsule. Either way, it causes intense irritation to the joint, pain, and lameness.
Physitis, on the other hand, is generally more subtle because it occurs in the growth plate or physis, and the resulting thickened cartilage projects into the epiphysis rather than the end surfaces of the bone. Clinically, foals with physitis present with unusually "knobby" joints (particularly the knees and/or fetlocks); enlarged radial growth plates give the knee a characteristic "dished-in" appearance, while affected fetlocks might acquire an hourglass shape. Radiographically, the growth plates might appear widened, asymmetric, flaring, irregular in width, or sclerotic. The sites most often affected are the lower growth plates of the cannon bone, the radius, and the tibia.
Different sites can be affected at different ages. Growth plate abnormalities in the cannon bone usually surface between four and nine months of age, while abnormalities in the radius and tibia are more likely to appear between one and two years of age. There might or might not be lameness, depending on the severity of the condition, and there is often detectable heat in the area, with the foal resisting palpation. Sometimes, though, the only detectable sign is that the foal does not play actively with the herd.
It's estimated that between 73% and 88% of developmental bone disorders of growing horses are flexural deformities (such as contracted tendons) and physitis. Researchers know now that no one factor--nutrition, genetics, environment, or bad karma--can create DOD on its own, and that prevention is considerably more complicated than originally had been hoped. Still, significant progress is being made in understanding the "multifactorial etiology" of DOD.
Cause and Effect
Most studies of developmental orthopedic disorders in foals have looked either at the overall syndrome, or have focused on OCD. The findings of these studies, however, do have important implications for physitis as well. Researchers have identified several predisposing factors in DOD, including nutritional excesses or imbalances, rapid growth, genetic predisposition, and trauma to the cartilage.
Genetic Predisposition: Radiographic studies of warmbloods and Swedish trotters have demonstrated that certain stallions produced foals with a significantly higher frequency of OCD, compared with other stallions of the same breed. A similar study in Denmark showed that the progeny of one stallion (out of eight studied) had an unusually high incidence of osteochondrosis even though the stallion himself showed no radiographic signs of the condition. Anecdotal evidence in North America does seem to indicate a higher incidence of physitis, particularly in heavy-bodied breeds such as Quarter Horses and Paints. While it seems probable that heredity plays a role in DOD, it's not likely that anyone will be able to develop a screening program for stallions or mares to prevent the condition from showing up in foals.
Mechanical Stress And Trauma: Injuries to the growth plates and/or articular cartilage can result from the sort of rough play in which foals frequently engage, and many researchers believe that clinical signs of OCD (when flaps or fragments of cartilage separate from the bone) can arise from these injuries. Shear forces, it is hypothesized, might disrupt capillaries in the subchondral bone and give rise to cartilage cell damage. How common this is, however, is still under investigation.
Growth And Body Size: Rapid growth has been implicated in osteochondrosis in dogs, chickens, and pigs, and numerous anecdotal studies of Standardbred and Thoroughbred racehorses (breeds in which quick maturity is an advantage, and to some extent has been selected for in breeding programs) have suggested that major growth spurts have been associated with a high incidence of OCD lesions. In a Swedish study, a higher incidence of osteochondrosis of the hock joint was found to be linked with foals which had a larger than average birth weight, large skeletal frame, and demonstrated a higher average daily weight gain.
Other studies, however, have called the significance of growth rates into question. Differences in the criteria used by various researchers are part of the problem. Nonetheless, many researchers do recommend close monitoring of the growth rates of foals (weekly measurements of height and weight, for example) as part of routine management.
Growth rate can be greatly modified by feed intake. A horse with a genetic capacity for rapid growth can be forced to grow more slowly by restricting its feed intake, and a horse can also be induced to grow more quickly by overfeeding.
Sudden growth spurts, which can occur when a foal is weaned and placed on a grain ration, are suspected of having a large role to play in the development of physitis. Many researchers recommend feeding a creep ration before the foal is weaned, so as to accustom him to carbohydrate intake (as well as compensate for the declining quality of his dam's milk as he ages) and avoid a sudden growth spurt at weaning time.
Excess Energy: Overnutrition as a cause of OCD and physitis was originally extrapolated from work in dogs and pigs. An Australian study demonstrated that high energy diets (120% of National Research Council, NRC, recommendations) consistently produced osteochondrosis lesions in weanlings. Although excesses of protein often have been blamed for high incidences of DOD, the more likely culprit appears to be excesses of digestible energy (DE). High energy intake can be particularly damaging when coupled with restricted exercise.
Excess digestible energy almost invariably comes from the feeding of grains and concentrates, rather than hay. Nutritionist Sarah Ralston, VMD, PhD, of Rutgers University, notes that when hay is digested, it is broken down into fatty acids, while grain is broken down to its component sugars. Both of these can yield energy, but sugars influence the balance of insulin and thyroxin in the body; and excess thyroxin production is thought to increase the risk of OCD. Thus, the more energy provided by grain and the less provided by forage, the more likely it is that OCD will result. Ralston is currently investigating the possibility that glucose-intolerant and/or insulin-resistant foals can be identified at an early age as being at risk, allowing owners to tailor the horses' diets to avoid the formation of OCD lesions.
There is some evidence that feeding large grain meals (which dumps large quantities of sugars into the system at once) also can be detrimental to cartilage development. Feeding small amounts, often, which of course has been recommended for horses for decades, is the preferable method for many reasons.
Mineral Imbalances: Calcium and phosphorus are integral to bone development, as nearly every horseman knows. Both the levels of these two minerals in the diet, and the ratio of one to the other, are important. Current NRC recommendations for growing horses are a Ca:P ratio of 1.8:1--although anywhere between 1.2:1 and 2.5:1 is considered acceptable. High phosphorus levels (where there is more phosphorus than calcium) have been implicated in OCD lesions, and one study did consistently produce lesions in young foals fed five times the NRC level. Foals fed three times the recommended levels of calcium, however, failed to develop lesions.
Mineral intake is an area where over-supplementation is common. Many horse owners operate under the assumption that "if some is good, more is better." Calcium is commonly over-supplemented in horses, and while by itself it might not produce DOD, it can interfere with the absorption of zinc, copper, manganese, and iron--all trace minerals that have been suspected of having a role to play in DOD. Calcium and phosphorus also are closely linked, and feeding too much calcium interferes directly with phosphorus absorption.
Copper, a component of normal bone collagen and elastin synthesis (the latticework of bone formation), is a mineral that has gotten a lot of attention in the study of DOD. In one epidemiologic study of clinical cases in foals, low copper levels seemed to be the most consistent factor. An artificially induced copper-deficient diet (1.7 parts per million) did produce OCD-like lesions and flexural deformities in foals. Other studies also have produced a higher incidence of lesions in foals with low-copper diets--but it should be noted that the majority of those lesions turned up in the cervical vertebrae, not in the limbs. Unfortunately, higher levels of copper intake have not been shown to completely prevent the development of OCD. Copper supplementation might help (most researchers now recommend an intake of 25 mg/kg or higher), but it will not, by itself, eliminate the problem.
Zinc, a mineral which competes for the same transport mechanisms as copper, has also been implicated in DOD. Excessive zinc intake, as was noted in one study where foals were raised near a zinc smelter, can cause DOD lesions. Currently, the NRC recommends a copper to zinc ratio of about 1:4, so if copper levels are raised in the diet, zinc levels should be raised as well. Since cartilage development in utero is influenced directly by the nutrition of the mare, the diet of broodmares should be assessed for mineral imbalances or deficiencies. Many nutritionists now recommend feeding mares 25-30 mg/kg of copper and 65 mg/kg of zinc during late gestation and lactation.
Endocrine Factors: Stressed foals which have consistently high levels of cortisol in their systems also might be at higher risk for DOD. McIlwraith notes that cortisol inhibits endochondral ossification, and that long-term use of corticosteroids can have a similar effect.
Prognosis of Physitis
Most researchers agree that physitis, by itself, tends to resolve on its own. Unless there are complicating factors, such as cystic lesions in the bone, it should gradually disappear as growth slows and the physes close.
"Physitis is definitely one of the less severe forms of DOD," says McIlwraith. "It can sometimes be a warning sign of other, more serious manifestations of DOD cropping up, but it's not necessarily tied in with other DOD problems."
What to do when a foal develops physitis? In most cases, says McIlwraith, nothing.
"It all depends on how bad it is, of course. If there's swelling at the growth plates, but no detectable lameness, it will resolve on its own as the foal grows. If the problem is more severe, and the horse is lame, then you have to consider restricting exercise somewhat. But because too much confinement can predispose the horse to more severe problems, such as contracted tendons or flexural limb deformities, you have to balance confinement with controlled exercise--sometimes alternating stall rest with exercise in a small paddock. The use of non-steroidal anti-inflammatory drugs to control pain can also be considered if the foal is lame."
McIlwraith points out that if a foal is sore, then physitis is probably not the only problem he has. At that point, a veterinarian should examine the animal for evidence of OCD and subchondral bone cysts.
In any case where physitis is diagnosed, radiographic monitoring is a good idea--both to determine how well the physeal abnormalities are resolving, and to detect any other DOD conditions that might be associated with it. Some forms of DOD can, if necessary, be treated surgically, but physitis by itself is best treated by a correctly balanced diet, good management, and time.
About the Author
Karen Briggs is the author of six books, including the recently updated Understanding Equine Nutrition as well as Understanding The Pony, both published by Eclipse Press. She's written a few thousand articles on subjects ranging from guttural pouch infections to how to compost your manure. She is also a Canadian certified riding coach, an equine nutritionist, and works in media relations for the harness racing industry. She lives with her band of off-the-track Thoroughbreds on a farm near Guelph, Ontario, and dabbles in eventing.
POLL: Managing Working Horses