|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:
Expected Feed Consumption
||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
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
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
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