DOD is the acronym for developmental orthopedic disease, a term used to encompass a variety of bone and joint problems in young horses. It’s a complicated disease that requires care based on individuals.
Osteochondrosis dessicans, or “OCD,” involves a disorder of the transitional zone between bone and cartilage. Instead of being firmly bonded to the bone beneath, the cartilage is loose in areas. Cracks or fissures may develop and, in some cases, the cartilage is elevated off the bone in flaps. Flaps may also break off.
Synovitis, or inflammation of the synovial membrane lining the joint, is also usually present, and with this goes the production of increased amounts of joint fluid, sometimes in tremendous amounts. Boggy hocks, or “bog spavin,” frequently are caused by OCD.
Most experts agree that some cases of OCD have a genetic component. There’s also a strong nutritional link. Excesses, deficiencies or imbalances in calcium and phosphorus may be involved, and the trace-mineral intake of zinc and copper is an important factor. The pregnant mare must have adequate major mineral intakes, and her intakes of zinc and copper are between 2.5 and three times the current NRC recommendations.
OCD lesions may also be due to trauma. Rapid growth isn’t proven to be a risk factor, but overfeeding does appear to increase the risk. Whether this is because the foal is fat or related to some imbalance or excess in nutrients hasn’t been determined.
The old standard treatment for young horses in training with nagging joint problems or boggy hocks was to turn them out for a year. This often worked and, while the horse might be left with a chronically distended joint, at least he was sound. We haven’t really improved on that approach much.
When OCD lesions are large and involve a flap of cartilage, surgery is indicated. For less-extensive lesions, surgery may not help. However, the shift from open surgeries to arthroscopic procedures has resulted in improved outcomes.
Otherwise, conservative therapy involves a short period of stall rest, followed by turnout in progressively larger areas at increasing amounts of time.
Oral joint nutraceuticals and/or injectable hyaluronic acid, glucosamine, polysulfated glycosaminoglycans are often recommended, but the benefit is unknown.
Angular Limb Deformities
An angular limb deformity is basically a crooked leg. It may be due to physical immaturity with ligament weakness or incompletely calcified small bones in the hock or knee, possibly combined with problems caused by their position in the uterus.
Some foals will appear knock-kneed and/or wobbly hocked, with their legs splayed out for the first day or two, but eventually straighten out on their own. However, any obvious inward deviation to the leg, or legs obviously crooked even when the foal isn’t bearing weight, warrant your veterinarian’s evaluation immediately.
Make a quick check of your foal’s conformation before he tries to get up for the first time. A deviation that seems to worsen over the first 24 to 48 hours, especially in an immature or premature foal, should be checked out right away.
A foal’s legs may also begin to deviate abnormally from the knee, ankle or hock down later in the first few months of life as a result of the foal being overweight, an injury to the growth plate, inflammation of the growth plate, or a lameness anywhere that causes him to bear weight unevenly.
When the deformity isn’t the result of incomplete calcification of the small bones, treatment may be attempted by trimming the foot to redistribute weight. When the foal doesn’t have enough hoof to work with, or more correction is desired than can be obtained with trimming, special glue-on shoes may be used to wedge up one side.
More severe cases, or those involving incomplete calcification, require a cast and restricted exercise. Foals with incomplete calcification or weak ligaments may correct on their ownif confined to stalls for 10 days to two weeks. Splints or casts may be used as needed, and careful attention paid to feet with frequent trims.
When progressive angular limb deformity strikes older foals, or these measures don’t correct the problem, surgery may be needed. Surgery is performed at the growth plate above the joint where the deviation begins.
Ruptured Common Digital Extensor Tendon
This problem is usually grouped in with flaccid or contracted tendons but really is neither one. The foal is born with swelling over the front and inside of the knee joint, corresponding to the sheath of the extensor tendon. How these tendons become injured is unknown. When the foal walks, he may knuckle over at the fetlock and when standing can appear bow-legged or over at the knee.
Treatment involves splints in the area, and these foals eventually will recover to move normally. It’s not clear whether the tendon heals/scars down, or if they simply learn to move without the benefit of the extensor tendon.
Many foals are born with weaknesses in the flexor muscles and flaccid tendons that cause their fetlocks to drop excessively and, in the extreme cases, the toe may even be elevated, sometimes to the point that the foal is walking on the bulbs of his heels. Prematurity and weakness are the most predominant causes of flaccid tendons in foals.
Tincture of time is usually all that is required. Exercise should be permitted, but the foal may need to be away from other foals until he strengthens. When the weakness is profound or is not improving after a few days, glue-on shoes with long heel extensions will help greatly. Most foals correct by the age of six weeks to near normal.
Contracted tendons may be congenital, although the cause is unknown. Among the things that have been suggested are intrauterine positioning, influenza virus, locoweed, hypothyroidism, some neuromuscular disorder, genetic factors or nutritional imbalances during pregnancy.
Treatment should be instituted as soon as possible. Exercise should be encouraged. Massage and passive extension of the joints helps. Splints can help prevent the fetlocks from knuckling forward and encourage relaxation.
Intravenous oxytetracycline can reverse the condition. Exactly why this works is also unknown, but it may have something to do with tetracycline’s ability to interfere with muscle contraction. A variety of surgical procedures have been attempted, but the prognosis is generally poor.
Acquired contracted tendons also occur for reasons that are poorly understood, possibly involving pain somewhere in the leg, genetics, nutrition, or accelerated/disproportionate bone growth. When the problem involves the deep digital flexor, forward subluxation of the coffin joint may occur, with the eventual development of a classical clubfoot. The horse should be carefully evaluated for sources of pain and the diet carefully examined for nutritional imbalances.
Young horses grow rapidly. Those on a high level of concentrate feeding may benefit from cutting back drastically on the grain, feeding predominantly grass hay, with up to 10% or so alfalfa and a pa latable protein/mineral supplement to correct any imbalances or deficiencies. Maximize turnout, with stall confinement reserved only for horses that require treatment for a painful condition.
Acquired contraction of the superficial flexor tendon may also occur. This is characterized by a knuckling forward at the fetlock joint. The cause is unknown.
Conservative treatment is the same as for contracted tendons except that the usual trimming/shoeing approach is different. The foal’s heels are raised to relax the deep digital flexor and put more pull on the contracted superficial flexor. Shoes with toe extensions are usually employed to delay breakover and prolong the period of stretch.
When the horse doesn’t respond to these measures, a variety of surgeries have been proposed and tried, but the prognosis is guarded at best.
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