A discussion of epiphysitis is anything but simple, straightforward, or lacking in complexity. To begin with, there is confusion and debate over the term itself. Then there is the matter of whether it is part of the osteochondrosis syndrome. There also is debate as to cause. Is diet alone implicated, or do genetics play a role? There is general agreement on treatment, but even there, practitioners will differ.
There are other questions for discussion. Is epiphysitis involved in physeal fractures? Is it implicated in angular and flexural limb deformities?
There are a few known factors. It is a problem that occurs at the growth plates of young horses that can make them sore and lame, and it is part of the developmental orthopedic disease (DOD) complex.
That being said, let’s take a look at some of the confusion, especially for the layman, that surrounds this troublesome condition.
First, the term itself. Thomas Bohanon, DVM, MS, Diplomate ACVS, of Centennial Valley Equine Hospital in Broomfield, Colo., is one of several authorities on the condition whom we will call upon in an attempt to describe what occurs. He is the author of a chapter on "Developmental Musculoskeletal Disease" in the book, The Horse, Diseases and Clinical Management, and also has dealt with the problem at the clinical level.
"The nomenclature of this disease process varies in the literature because of different interpretations of the disease process," he writes. "Commonly used terminology includes physitis and epiphysitis, but the condition does not necessarily include an inflammatory process and is therefore more accurately described as physeal dysplasia. Furthermore, epiphysitis is inaccurate because the disease process involves the growth plate and metaphysis rather than epiphyseal bone."
While we do not take issue with Bohanon that epiphysitis might not be the basically correct term, we will continue to use it here because it is a term with which most laymen are familiar. However, when quoting Bohanon, we will use the term that he uses—physeal dysplasia.
Another key issue involves the relationship between epiphysitis and osteochondrosis. Are they one and the same? Bohanon describes epiphysitis as "probably an expression of osteochondrosis."
Wayne McIlwraith, BVSc, PhD, Diplomate ACVS, Colorado State University, another researcher who will help guide us through this discussion, has this to say on the relationship between epiphysitis and osteochondrosis—although he uses the term physitis: "Physitis has also been described as epiphysitis and physeal dysplasia. It has even been suggested earlier that epiphysitis was the same as osteochondrosis, but this is incorrect. In many instances, we have pain and swelling at the growth plate without any evidence of retained cartilage. Most cases of physitis do not have any radiographic lesions that are particularly significant and they resolve with time."
So, we might interpret from the two above statements that the researchers aren’t necessarily in disagreement. Epiphysitis might not be the "same as osteochondrosis," but it may be an "expression of osteochondrosis."
Unfortunately, there hasn’t been a great deal of research on epiphysitis.
"Objective data on physeal dysplasia are extremely limited even though the disease process is very common," Bohanon notes. "Reasons for this lack of information probably stem from the fact that physeal dysplasia is not life-threatening, so no large groups of horses have been available for histologic or gross postmortem examination, and biopsy of affected tissue is unnecessary for diagnostic purposes."
Time now to make an attempt at understanding exactly what it is we are talking about.
We mentioned that epiphysitis is a part of the DOD or developmental orthopedic disease process. This term was coined in 1986 to encompass all orthopedic problems seen in the growing foal. The term came out of a blue ribbon panel sponsored by the American Quarter Horse Association.
"It is a term that encompasses all general growth disturbances of horses and is therefore nonspecific," says McIlwraith. "It is felt that one has to be nonspecific when talking about the various limb anomalies of young horses because previous terms such as metabolic bone disease and osteochondrosis implied that they all had a common cause and pathogenesis (mechanism of disease development). It is still to be determined how closely related the various forms of DOD may be, but it is important that the term not be used synonymously with osteochondrosis."
So much for terminology. What we are dealing with here is development and growth of a horse’s long bones, such as the cannon bones, radius, and tibia. These long bones develop from cartilage by a process known as endochondral (within the bone) ossification. Ossification means formation of bone. The centers of ossification develop in the center of the long bone and also at the ends of these long bones. The area at the end of the long bones where growth occurs is the growth plate. The growth plates at the end of the long bones produce longitudinal growth of the metaphyses of the bones—the wide part at the extremity of the shaft of a long bone.
The growth plate consists of the cartilaginous portion (the physis), the bony portion (metaphysis), and the fibrous component surrounding the periphery of the plate. The physis consists of zones comprised in sequence of layers of resting cartilage cells, proliferating cells, hypertrophic (enlarging) cells, and a zone of calcified cartilage.
The proliferating chondrocytes (mature cartilage cells) divide rapidly, produce matrix, then mature in the hypertrophic layer. Penetrating blood vessels from the bottom (epiphyseal) side of the growth plate sustain the dividing cells. Penetrating blood vessels from the upper (metaphyseal) side of the growth plate initiate and sustain calcification, the final step in the formation of bone.
Eventually, the growth plate closes as the long bones reach their maximum length. Generally speaking, the growth plates at the lower extremities, such as the cannon bone, will close first, while those at the knee and hock—radius and tibia, respectively—will close later in the young horse’s development.
There is a second growth plate (called the epiphyseal growth plate) that forms as the epiphyseal bone-forming center advances toward the ends of the bone and what is destined to be the articular surface of the joints.
Some people have suggested that epiphysitis is an expression of osteochondrosis. So, what is osteochondrosis?
Basically, osteochondrosis occurs at the end of long bones when there is a defect in the formation of bone from cartilage.
McIlwraith sums it up best: "Osteochondrosis is a defect in endochondral ossification (bone formation) that can result in a number of different manifestations, depending on the site of the endochondral ossification defect. These manifestations include osteochondritis dissecans, which is a disease process of the articular surface of joints. The epiphyseal ossification center advances out until ossification ceases, leaving a layer of cartilage. This layer of cartilage becomes the articular cartilage. If there is a disturbance in endochondral ossification, an area of retained cartilage can be formed with a consequent defect in the bone. Cracking can then proceed in this retained cartilage to give a flap or fragment of cartilage that may contain bone. These flaps and fragments on the surface of the joint result in osteochondritis dissecans."
McIlwraith has much more to say on osteochondrosis, as do other researchers, but the above will suffice because we are primarily concerned with epiphysitis.
Some of the same words as the above can be used in a description of epiphysitis—problems in the process of turning cartilage into bone. However, there are also the factors of tension and compression. In other words, weight bearing can be an integral part of the problem with epiphysitis because it can compromise the flow of blood feeding the growth plate.
One theory concerning the cause of epiphysitis involves undue pressure on, or compression of, the metaphyseal blood vessels on the upper side of the growth plate. What can then occur is a curtailment of the blood flow needed in the calcification process. However, because the epiphyseal blood vessels are better protected on the bottom side of the growth plate, they might continue to bring in nutrients, unhampered and unrestricted.
Because of the damage to the metaphyseal vessels, a decrease in calcification occurs. If the blood flow at the epiphyseal area is unimpeded, the physis will widen as cartilage cells continue to be nourished and proliferate, but no longer are being formed into bone (ossification) at the appropriate rate.
Eventually, the growth plate might become too thick to be sustained by epiphyseal vessels. When that occurs, there is necrosis (cell death) at the cartilage-bone surface. Ultimately, if no steps toward treatment are undertaken, there is continued compression, the entire physis collapses, and there is premature closure of the growth plate.
Along the way, a variety of other problems can arise, such as physeal fractures and angular and flexural limb deformities. More about those conditions later.
When It Strikes
Epiphysitis seems to attack at two levels of equine development. If the condition afflicts the ends of the cannon bones, it normally will be manifested when the weanling is four to six months of age, although there are exceptions.
It also can strike at 12 to 20 months of age. When horses are afflicted at that age, the problem area normally is at the end of the radius or tibia—above the knee or hock. It is at these ages that physeal closure of the respective long bone growth plates occur—four to six months for closure at the distal surface of the cannon bones and 12 to 20 months at the distal surface of the radius and tibia.
And how does the average horseman recognize the condition when it crops up?
Sign number one will be swelling at knee, ankle, or hock in the area of the physis where the problem has occurred. The swelling likely will be warm and the area will be sensitive to touch. Putting pressure on the area with one’s fingers might cause the horse to move away. The horse could very well be lame as a result of the pain. The joint affected often takes on a box-like appearance.
A diagnosis usually is based on clinical signs and radiographs. The X rays might show widened irregular physis and a bony flaring of the metaphysis, as well as other manifestations.
Fodder For Thought
And what, the horseman might ask, can bring on a bout of epiphysitis?
Often, it begins with diet, although other factors can be involved. In many cases, the afflicted horses are fast-growing youngsters on a high-energy diet. Immediately, that brings on visions of a diet heavily laden with grain. In many instances, that is true, but less ambitious diets also can be implicated.
A case in point involves a weanling six months of age which recently was treated by Glen and Gunda Gamble, DVM, of Riverton, Wyo. The weanling was being fed exceptionally lush, green alfalfa hay as the main ingredient in its diet, and it was growing rapidly. The horse developed a severe case of epiphysitis at the distal surface of the radius. Also involved was a physeal fracture.
A radical change in diet, treatment of the fracture, plus rest, brought about a pronounced improvement in three weeks.
"The treatment for physeal dysplasia," Bohanon tells us, "is usually conservative and begins with assessment of the foal’s diet and correction of any nutritional errors. Clinicians have traditionally recommended assessment of calcium and phosphorus and a 25% reduction in caloric intake, but it is more appropriate to perform a complete evaluation of the feeding program, including laboratory analysis of the animal’s hay, grain, supplements, and pasture grass. One investigation demonstrated a significant decrease in the incidence of physeal dysplasia when food intake was decreased by 7.4% to 7.5 kilograms per day and copper consumption was increased by 41.5% to 200 milligrams per day."
It is important to know a few basics about feeding programs. Horses require feed to supply energy, protein, minerals, and vitamins for maintenance and, in the case of young horses, growth. Energy sources must be digestible and provide fuel efficiently in the form of carbohydrates and fats.
Researchers figure the amount of energy needed by a horse in megacalories (Mcal). One Mcal is equal to 1,000 calories referred to in human diets. Energy intake above the amount needed for maintenance and growth will be deposited as fat. Thus, a young horse which is ingesting far more energy than required might wind up carrying too much weight for its rather fragile growth centers, especially if it also is genetically predisposed to rapid growth.
The National Research Council has made use of years of research at universities around the world in compiling recommended nutrient levels for horses at various stages of growth and development as well as various stages of work or performance.
There are specific recommendations for nutrient concentrations in rations for growing horses. The recommendations that follow are made by the National Research Council based on the assumption that the grain mix being fed provides 1.5 Mcal per pound and that the hay being fed provides 1 Mcal per pound of dry matter.
1. Weanling, four months of age—1.25 Mcal per pound of animal weight in the form of digestible energy. Diet proportion—70% grain and 30% hay. Crude protein—13.1%. Calcium—0.62%. Phosphorous—0.34%. Vitamin A—650 international units (IU) per pound.
2. Weanling, six months of age being fed for moderate growth—1.25 Mcal per pound of animal weight in the form of digestible energy. Diet proportion—70% grain and 30% hay. Crude protein—13.1%. Calcium—0.50%. Phosphorous—0.28%. Vitamin A—760 IU per pound.
3. Yearling, 12 months of age being fed for moderate growth—1.15 Mcal per pound of animal weight in the form of digestible energy. Diet proportion—60% grain and 40% hay. Crude protein—11.3%. Calcium—0.39%. Phosphorous—0.21%. Vitamin A—890 IU per pound.
4. Yearling, 18 months of age and not in training—1.05 Mcal per pound of digestible energy. Diet proportion—45% grain and 55% hay. Crude protein—10.1%. Calcium—0.31%. Phosphorous—0.17%. Vitamin A—903 IU per pound.
5. Two-year-old not in training—1.00 Mcal per pound of animal weight in the form of digestible energy. Diet proportion—35% grain and 65% hay. Crude protein—9.4%. Calcium—0.28%. Phosphorous—0.15%. Vitamin A—1,080 IU per pound.
Horses of all ages also need trace minerals. Copper has already been mentioned, but also needed are appropriate amounts of magnesium, potassium, iron, manganese, zinc, iodine, and selenium.
Highly important in balancing the nutritional needs of the young, growing horse is knowledge about the calcium and phosphorous content, as well as the protein content, of hay being fed. This is because not all hay is created equal. Even within a particular type of hay, such as alfalfa, there are variations depending on the state of maturity when the hay was harvested. Without testing the hay, we can wind up with an out-of-balance ration.
For example, alfalfa that was harvested in mid-bloom normally has 1.04 Mcal per pound of digestible energy and the crude protein level will run about 18%. In mid-bloom alfalfa, calcium will run up to 1.37% while phosphorous will be only 0.24%. This means that if only mid-bloom alfalfa hay is being fed, the calcium-phosphorous ratio would be out of balance. Remember, the NRC guidelines called for 0.62% calcium and 0.34% phosphorous for the four-month-old weanling foal.
Mature alfalfa hay closes the gap somewhat, but there still is an imbalance. The percent for calcium is 1.19% while the number for phosphorous is still only 0.27%.
Conversely, if hay that is low in calcium is fed, along with corn, oats, or barley, it could be that the phosphorous content will be higher than calcium, something that is fraught with potential for DOD problems. According to the NRC guidelines, there always should be somewhere between 1.5 and 2.5 times more calcium than phosphorous in diets of horses.
If one were to seek out a hay that had a more appropriate calcium-phosphorous ratio than alfalfa, timothy or Bermuda grass might be the choice. Mid-bloom timothy hay runs about 0.48% calcium and 0.23% phosphorous. Bermuda grass is similar with 0.40% calcium and 0.23% phosphorous.
While most hay will always have more calcium than phosphorous, that is not the case with grains. Following are the nutrient contents of three grains that often are fed to horses—oats, corn, and barley:
Barley—1.65 Mcal per pound; 13% crude protein; 0.05% calcium and 0.38% phosphorous.
Corn—1.7 Mcal per pound; 10% crude protein; 0.04% calcium and 0.53% phosphorous.
Heavy oats—1.54 Mcal per pound; 13% crude protein; 0.06% calcium and 0.33% phosphorous.
The important thing is that we take a scientific approach when designing a diet for the young, growing horse. The NRC guidelines are a good place to start, but the growth and development of individual young horses must be monitored closely in order to prevent problems.
Above all, an appropriate balance of nutrients, vitamins, and minerals is a must.
Let’s turn now to treatment of the horse which has developed epiphysitis. We are going to assume that at least part of the problem involves overfeeding. However, it should be noted that malnutrition also can be a cause, along with an out-of-balance diet.
Step number one, in most cases, involves cutting back on the amount of food energy the horse is ingesting. Just how much of a cutback is involved will depend on the individual and the amount being fed. In some cases, it might involve the elimination of all grain, with the horse being put on a grass hay or alfalfa/grass hay diet. If it hasn’t already been done, this is the time for a complete analysis of the horse’s ration along with consultation with a veterinarian.
Early treatment of the condition is a must so that permanent damage is prevented.
Stall rest might be recommended, but here, too, there must be a proper balance. Vigorous exercise can exacerbate the condition, but no exercise at all can be harmful. It can result in flexural limb deformities if flexor muscles contract through lack of use.
The problem with vigorous exercise, even of a short duration, is that it can result in continued trauma to the growth plate and lead to permanent damage. The exercise, as recommended by a veterinarian, should be on a soft surface.
Phenylbutazone has been advocated by some researchers and practitioners as a way in which to help alleviate pain and inflammation, but, again, there must be a proper balance. High doses of bute over a relatively long period heighten the risk of the horse’s developing gastric ulcers.
Changing the diet of a young horse afflicted with epiphysitis should bring about a positive response in six to eight weeks or less. The weanling discussed above showed improvement in as little as three weeks.
Once the horse is no longer sore and the swelling has disappeared, it is time again to involve the animal in light exercise and, over time, gradually to increase its diet, again following the recommendations of a veterinarian.
Radiographs taken four months or so after treatment will do much to let one know how successful the recovery process has been.
"The prognosis for physeal dysplasia," reports Bohanon, "is generally considered good because the disease is usually self-limiting, unless cystlike lesions are present in the bone. However, any delay in treatment can result in serious angular and flexural limb deformities that may require surgical intervention and diminish the overall prognosis for the horse."
As was the case with the aforementioned Wyoming weanling, physeal fractures can occur in conjunction with epiphysitis. Almost always, the fractures will affect the cartilaginous area of the growth plate—the physis.
A system, known as the Salter-Harris classification system, has been developed for identifying physeal injuries based on the fracture configuration and the relationship of the fracture plane to the growing cells of the metaphyseal growth plate.
Following is the classification for pressure physeal fractures:
Type 1—The fractures occur through the zone of hypertrophied chondrocytes only, without involvement of the adjacent epiphysis or metaphysis.
Type 2—The fracture occurs through the physis across part of the width of the bone and through the metaphysis, leaving a segment of metaphysis attached to the epiphysis.
Type 3—Fractures extend through the physis across part of the width of the bone and traverse through the epiphysis, entering the joint.
Type 4—The fracture extends across the epiphysis, growth plate, and a portion of the metaphysis perpendicular to the plane of the physis.
Type 5—This is a compression fracture of the growth plate with little or no displacement.
Type 6—These fractures are similar to Type 5, but involve a crushing injury to part of the growth plate and result in a deviation of the limb toward the side of injury and could be the start of an angular limb deformity.
Generally speaking, physeal fractures are treated surgically with the use of screws and other fixation devices.
The prognosis for a young horse being athletically sound after a physeal fracture is guarded, thus lending further weight to the need for preventive measures and for immediate treatment when epiphysitis rears its head.
In the case of angular and flexural limb deformities, it often is unclear whether epiphysitis is the cause of the condition or results from it.
Acquired flexural limb deformities, reports Dean A. Hendrickson, DVM, MS, of Colorado State University, often are thought to be secondary to chronic pain, which initiates a protracted withdrawal reflex. Angular limb deformities might develop secondary to the disturbed bone growth when one side of the growth plate is more or less involved than the other side. (Treatment of flexural and angular limb deformities was dealt with extensively in the March 1999 issue.)
Unfortunately, epiphysitis and other developmental orthopedic diseases are not rare. McIlwraith reported on a study in Canada that underlined this fact and revealed that the affliction struck at a very early age:
"Mild to moderate physitis and flexural deformities (concurrent with physitis in most cases) occurred in 88% of 42 weanlings between weeks six to eight of a study looking at the effect of dietary energy and phosphorous on blood chemistry and development of growing horses."
At that age, he noted, the condition, for the most part, healed quickly on its own with few adverse effects.
Another study defining the incidence of DOD in Thoroughbred horses was conducted in Ireland over a period of 18 months.
"It was found (in that study)," reports McIlwraith, "that angular limb deformities and physitis together constituted 72.9% of the cases treated. The peak incidence of DOD problems occurred between weaning and the end of December. In a retrospective study, 193 of 1,711 (11.3%) were treated for DOD (21 had more than one type), and they are detailed as follows—angular limb deformities, 92; physitis, 64; flexural deformity, 18; wobbler’s syndrome, 7; and osteochondritis dissecans, juvenile arthritis, and other joint problems, 28.
"More than half the animals treated (53.9%) recovered completely, that is, they achieved expected sale value as yearlings; 27.5% showed incomplete recovery and mild to moderate loss of sale value; and 18.7% were either killed or lost much of their sale value.
"It was also noted that 67.7% of the animals showed some evidence of DOD, but only 11.3% were deemed to need treatment.
"This study was a good start and points out the need to have definition of what disease process we have. I think it can be seen from these studies that when ‘developmental orthopedic disease’ occurs, it commonly involves angular limb deformities and physitis problems that spontaneously self-correct."
We have dealt at some length with the role that diet can play in the development of epiphysitis. The next question that rears its head involves genetics. Can a tendency toward the problem be inherited?
McIlwraith reports that radiographic studies in Swedish trotters and Warmbloods have shown one stallion from each of those two breeds to have a significantly higher frequency of osteochondrosis dissecans of the hock among his progeny when compared with other stallions in the respective breeds.
In another study, this one in Denmark, radiographic evidence indicated a significantly high proportion of osteochondrosis in the progeny of one stallion while seven others in the study did not demonstrate the same genetic tendency. Interestingly, the stallion whose progeny had a significantly high proportion of osteochondrosis was not afflicted with the problem himself.
"There has been little work done in the United States with regard to heredity, and we certainly haven’t been able to develop any type of screening program for osteochondrosis in stallions and mares that will ensure freedom from that condition," says McIlwraith. "However, it would appear very likely that there are genetic components to this disease. Individual instances of certain stallions and mares producing a higher incidence of these individuals have been seen."
While the above studies were aimed at learning whether genetics were involved in osteochondrosis, the findings could also apply to epiphysitis, it would seem, because of the relationship between the two afflictions.
As is the case in the area of so many equine disease problems, much more research is needed to provide definitive answers.
When assessing what we know at present, there is a good deal more good news than bad when discussing epiphysitis. First, it can be prevented, in many cases with a well-balanced diet where special attention is paid to the amount of energy the young animal consumes. Second, even if the young horse is afflicted, it often can recover fully if immediate steps for treatment are taken.
That will remain a key—taking steps for treatment immediately. If we don’t, the bad news scenario will set in, and we might be dealing with a horse which also suffers from angular or flexural deformities or physeal fractures.
It’s an area where the old adage of a bit of prevention being worth a ton of cure applies.
About the Author
Les Sellnow is a free-lance writer based near Riverton, Wyo. He specializes in articles on equine research, and operates a ranch where he raises horses and livestock. He has authored several fiction and non-fiction books, including Understanding Equine Lameness and Understanding The Young Horse, published by Eclipse Press and available at www.exclusivelyequine.com or by calling 800/582-5604.
POLL: University Equine Hospitals