Equine Developmental Orthopedic Disease

Tracy A. Turner, DVM, MS, Dipl. ACVS
St. Paul, Minnesota 55108

Developmental orthopedic disease (D.O.D.) can be loosely defined as any musculoskeletal disorder that occurs in the young animal as a result of growth and maturation. Invariably, it is related to the process of endochondral ossification and the maturation of cartilage to bone in the developing skeletal system. In the horse there are four clinical manifestations; physitis, osteochondrosis, angular limb deformity, and flexural limb deformity. Etiological factors involved include trauma, excessive concussion, illness, conformation, genetic predisposition, and nutrition.

Nutritional factors related to D.O.D. in animals less than eight weeks of age include; unbalanced mineral intake of either major or trace minerals, excessive quantities of mare's milk or unbalanced minerals in the milk. D.O.D. in animals under 4 months of age is due to inadequate intake of a balanced ration, over production of milk by the mare, or the foal is experiencing a rapid growth rate. D.O.D. in weanlings and yearlings is usually due to a ration incorrectly balanced, or rapid growth rate and/or excess body weight.

An unbalanced diet would be a mature horse ration fed to any horse less than 2 years of age. Feeding 128% or more of energy requirements will produce developmental orthopedic disease. Diets with excessive protein are usually NOT a problem. Horses should be fed as a percentage of body weight:

Horse Type Work Type
Expected Feed Consumption
Mature horse Maintenance
Mature horse Late Gestation
Mature horse Early Lactation
Mature horse Late Lactation
Working horse Light
Working horse Moderate
Working horse Intense
Young horse Weanling
Young horse Yearling
Young horse Long Yearling
Young horse Two Year Old


D.O.D. can be caused by feeding growing horses less than 0.5% phosphorus, or less than 10 ppm copper (best to feed 30 ppm), or less than 100 ppm zinc, (Zn:Cu ratio = 4:1). Calcium phosphorus ratios can also be critical. In the suckling foal Ca: P > 1.5:1 or <1:1, in the weanling >3.0:1 or <1:1, in the yearling >3.0:1 or <1:1, and in the broodmare >6.0:1 or <1:1.

Management factors that effect D.O.D. are ignoring the pregnant mare, feeding fast growers the same as the slow growers, and feeding an unbalanced ration. If you ignore nutrients in forage or limit the forage and feed greater than 10 lbs of grain/day, you may cause D.O.D. Confining the growing horse and allow it access to free choice grain or feeding adequate protein and energy with inadequate mineral are other methods of causing D.O.D. If the developing bones are traumatized due to overweight or due to excessive work, such as longeing a young horse more than 10 min/day, this can also result in D.O.D. D.O.D. can be prevented if growth rates are monitored and feed intake is adjusted to growth rate. "At risk" individuals should be treated as individuals.

Osteochondrosis is a local or generalized failure of endochondral ossification affecting epiphyseal and/or metaphyseal cartilage. In the horse there are two clinical syndromes: osteochondrosis dessicans (OCD) and subchondral cyst-like lesions (bone cysts). Normal endochondral ossification occurs in the bones of the extremities, vertebral column, pelvis, and base of the skull. The bone is formed from a hyaline cartilage matrix, which is replaced by bone. There are several steps in normal endochondral ossification. Chondrocytes mature and enlarge. The intracellular matrix thins and the mature chondrocyte produces alkaline phosphatase, which causes calcification of the intercellular matrix. Calcification of the matrix causes chondrocytes to die due to lack of adequate nutrition. Capillaries invade the region bringing osteoblasts and the osteoblasts produce bone, which matures to lamellar bone.

Osteochondrosis occurs when cartilage cells proliferate normally but maturation and differentiation is abnormal. Failure of cartilage matrix to calcify or failure of vascular penetration and osseous replacement results in thickened cartilage. Cartilage necrosis develops in deeper layer fissures due to lack of nutrition and a cartilage flap (OCD) formation occurs. Another scenario is the thickened cartilage persists without fissuring and becomes surrounded by subchondral bone as adjacent cartilage continues endochondral ossification; the retained cartilage dies resulting in a subchondral cyst-like lesion.

Treatment principles for conservative therapy for osteochondrosis consist of rest and limited exercise. The horse's feed intake should be decreased in an attempt to decrease total energy in the diet. The diet should be analyzed for mineral imbalances. Articular medications such as hyaluronic acid or polysulfated glycosaminoglycans (PSGAGs), given IM or IA are useful adjunctive therapy. Surgical therapy requires either arthroscopy or arthrotomy to debride the lesion. Arthroscopy allows better inspection of the joint. The objective of surgery is to remove cartilage flaps and osteochondral fragments, leave sharp edges around cartilage defects, and debride the lesion down to bleeding bone. Curettage (forage) of cystic lesions and leaving sharp cartilage edges, removing all debris within the cyst and exposing bleeding bone is the treatment for cyst-like lesions. Frequently surgery needs to be combined with conservative therapy. In many cases, surgery will significantly increase the prognosis for an athletic animal.

Flexural deformities are developmental problems affecting tendons and ligaments. Flaccidity or weakness of the flexor tendons in newborn foals is not uncommon. It is due to musculotendinous weakness, which can result from systemic illness, lack of exercise or excessively long toes. Clinically, the foal walks on the caudal aspect of the foot and the toe of the hoof "rocks-up". Generally the condition occurs in rear feet or all four legs. Treatment is to trim the hooves so that the foal has a flat weight-bearing surface. Exercise is to be encouraged (swimming is excellent). A more severe expression is digital hyperextension deformity in foals. The etiology is unknown but the clinical signs of the condition are apparent immediately after birth. It is characterized by extreme dorsiflexion of the phalangeal joints. Severely affected animals will bear weight on the ventral surface of the proximal sesamoid bones. Treatment consists of supporting the hoof with heel extensions. Bandaging methods (bandaging, etc) are not satisfactory as they cause further weakness. Lightweight fetlock supporting braces may be of some benefit. There is a report of surgical shortening of the flexor tendons; however, the results are poor. The prognosis for these animals is poor to guarded.

Congenital flexural deformities are usually due to uterine malpositioning, genetic defects (such as trisomy), toxic or infectious insults during pregnancy, and recently congenital hypothyroidism has been identified as a cause. Clinical signs consist of either fetlock flexion deformity (fetlock knuckling), which is the most common or DDF contraction (club foot). Generally the deep and superficial flexor tendons are involved. Congenital flexion deformities of the carpus also occur. Individual tendon involvement is difficult to define in these cases. Contraction of the carpal fascia is an important component and may prevent any correction. Correction in some foals is spontaneous. Others may need treatment, oxytetracycline, 3 gms IV, up to 2 injections 48 hrs apart has been used very effectively to relax the deformity. In addition, splints and casts can be used for fetlock and coffin joint deformities. Splints and casts need careful and close management. If the limb cannot be straightened in extension with splints, the prognosis is poor. Surgery may help in some cases, either inferior and/or superior check desmotomy or superficial flexor tenotomy may be required to straighten the limbs(s).

Acquired flexural deformities are frequently related to pain. Any pain in the limb will initiate the flexor withdrawal reflex and this in turn may lead to a flexural deformity. Faulty nutritional management constitutes the most important cause of this flexure deformity. Overfeeding and excess energy / protein in the diet leads to epiphysitis or osteochondrosis. Imbalanced feeding such as calcium/phosphorus imbalances or deficiencies in copper, vitamin E etc., have resulted in flexural deformities. These imbalances may induce tendon a shortening of the musculotendonous unit directly or indirectly via epiphysitis and osteochondrosis. Anatomical changes that occur are ill defined. Some researchers think that bone growth exceeds tendon lengthening but this has NOT been proven to occur.

Deep digital tendon contracture (coffin joint flexural deformity) presents with the hoof having a raised heel or "club foot" appearance. The deep digital flexor tendon is very tense. Two stages of contracure are documented, Stage 1 is when the dorsal surface of the hoof wall is less than 90o and Stage 2 is when the dorsal surface is greater than 90o. Treatment consists of making necessary dietary changes (grass hay and ration balancing), exercise to stretch the tendon or complete rest to relax the muscle have both been advocated. Likewise, hoof trimming to lower the heel, if possible, is performed but maintenance of comfortable heel contact is imperative. A toe extension is usually helpful. Phenylbutazone or other NSAIDs are used for analgesia. Inferior check desmotomy has shown good results for stage 1 but deep flexor tenotomy is usually necessary for stage 2. Tenotomy may be performed above or below fetlock. Some cases do not respond due to joint capsule contracture.

Superficial Digital Contracture (Fetlock flexural deformity) is seen as knuckling at the fetlock with the hoof in normal alignment. Tendon involvement is complex and variable. In most cases, contraction of both the SDF and DDF tendons is present; the DDF may even be primary. Careful palpation in the flexed and extended positions will help elucidate the relative involvement of the tendons. Treatment consists of dietary changes to decrease the caloric intake. Exercise should be encouraged to stretch the tendons. Raised heel shoes with toe extensions have been shown to be useful. Again NSAIDs are used for analgesia. Surgery is not as successful and the surgery should be determined by carefully assessing the structures involved. Superior check ligament desmotomy lengthens the SDF; inferior check ligament desmotomy lengthens the DDF. Combinations of superior and inferior check desmotomy are usually necessary. Superficial digital flexor tenotomy or suspensory ligament desmotomy may be required to straighten the leg. Combinations of surgery are often necessary.

Rupture of the common digital extensor tendon occurs for no known reason but they rarely cause a problem but contracted tendons may occur secondarily. Clinical signs consist of mild carpal flexion with normally extended fetlocks. The most characteristic feature is swelling over the craniolateral aspect of the carpus. Recovery is spontaneous but casts or splints may be helpful to keep the carpus straight and help prevent tendon contracture. Suturing of the tendon ends is not indicated because the prognosis is good without any treatment.

Angular limb deformities are defined as any medial or lateral deviation of joints from their normal axis. This primarily involves the carpus, tarsus, or fetlocks. There are 4 causes: 1. tendon or ligament laxity (joint instability), 2. compressional physitis, 3. Malformed or displaced carpal or tarsal bones, 4. Fractures of the cuboidal bones. Radiographs are needed to establish the cause and location of the deviation, as well as the prognosis. Conservative treatment and management consists of corrective trimming to keep the hooves level and splinting or casts applied to the concave side of leg. Lateral or medial hoof extensions may be helpful. Surgical techniques include periosteal stripping/release, which is performed above the slow growing physis. The release allows the slow growing side to "catch up". Physeal bridging procedures (staples or screws and wires) are performed across the rapid growing physis to slow growth and allow the opposite to "catch up". Nutritional management to decrease energy and balance the ration is recommended. Exercise should be controlled until the leg straightens.

Compressional Physitis, "epiphysitis" is defined as structural changes in the physis (growth plate) due to compression, which may result in growth defects and/or pain. Different parts of the physis may or may not be growing at different rates. Physitis most commonly involves the distal radius, the distal tibia, distal cannon bones, and proximal first and second phalanges. Two age groups are commonly affected. Foals with pre-existing angular limb deformities and weanlings or yearlings with straight legs. The older animals may be lame. They have "Hour-glass" appearance of the knee and ankle joints and are usually on high caloric or high supplemented diets. The cause of physitis is both nutritional and mechanical. Compression of the growth plate is the final common pathway. Treatment consists of managing the diet (usually seen in animals on high energy diets, may also involve Ca, P, Zn, and/or Cu imbalances) and the judicious use of analgesic/anti-inflammatory.

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