Developmental Orthopaedic Conditions (DODs) are conditions that affect young, growing horses. These conditions can impact the skeletal system, especially the growth plates, joints, and spine, as well as tendons in the distal limbs. As Veterinary Rehabilitation Therapists, an understanding of these conditions and their causes as well as treatment strategies can help us to better support owners, growing foals, and the veterinary team.
We will discuss the following equine conditions:
- Physitis or Physeal Dysplasia
- Incomplete Cuboidal Bone Ossification
- Angular Limb Deformities (ALD)
- Flexural Limb Deformities (Contracture & Laxity)
- Osteochondrosis Dissecans (OCD)
- Subchondral Bone Cysts
- Cervical Stenotic Myelopathy (Wobbler Syndrome)
Shared Beginning
Many DOD’s are a result of abnormal or disrupted endochondral ossification. This refers to the process where cartilage is replaced by bone at the physes or growth plates of young horses during the normal growth process. Endochondral ossification can be disrupted by a number of factors, including rapid growth, nutritional imbalances, inappropriate exercise, or poor limb conformation. In young horses, there is often a mismatch between pain levels and the degree of visible pathology on imaging, which makes objective outcome measures and intentional load management important in the treatment of these conditions.
Physitis (Physeal Dysplasia)
Physitis, or physeal dysplasia, is an inflammatory condition that affects the growth plates or physes in young, rapidly growing horses. It primarily affects the distal radius, distal tibia, and distal metatarsals or metacarpals.
Signalment:
This condition commonly occurs in fast growing large breed horses. While it can occur as young as 4 months, it is more common in yearlings and 2 year olds that are undergoing a growth spurt or have entered early training.
Excess dietary energy, protein and carbohydrates as well as a Ca:P imbalance increases the risk of development.
Conformation such as varus or valgus can increase the risk of development.
Presentation:
Firm, occasionally warm bony enlargements above the fetlock, carpus or hock. Pain on palpation. Varying degrees of lameness.
Chronic cases may predispose to the development of ALD and early joint disease.
Diagnostics:
Radiography to assess physeal widening and irregularity.
Treatment options:
Dietary correction is essential – reduce protein and carbohydrate intake, correct the Ca:P balance. In foals at foot, the mares milk production may need to be slowed to decrease calorie intake.
Controlled activity and turnout to reduce load on the affected area and allow bone remodelling. NSAIDs as prescribed.
Monitor progression to ensure early intervention if ALD starts to develop.
Incomplete Cuboidal Bone Ossification
A condition where the cuboidal bones of the carpus or tarsus have not ossified at or shortly following birth. This is common in premature or dysmature foals. Incomplete ossification of the cuboidal bones can occur with or without collapse of the affected joints.
Signalment:
Foals born prematurely or underdeveloped. Twins can be predisposed.
Presentation:
Foals can present with or without collapse of the affected joint.
When the joint is not collapsed, the condition can be difficult to identify. They may have small, lax or soft joints, and show a reduced level of activity. Horses may reach maturity at which point the condition becomes apparent when they are brought into work.
When joint collapse is present in foals, it appears as an ALD of the carpus or tarsus.
Diagnostics:
Radiography will reveal small, rounded cuboidal bones with wide joint spaces. Compression or crushing may be present. In young foals, serial radiography is necessary to assess ossification progression.
Treatment options:
Load reduction and protection is essential to prevent joint collapse. Stall rest and controlled activity are necessary. Splints or casts may be used if indicated.
As ossification progresses, activity and turnout can be gradually increased.
Angular Limb Deformities (ALD)
Angular Limb Deformities include conditions that result in a frontal plane deviation of the limbs, including varus or valgus. These deviations commonly occur at the carpus, tarsus or fetlock and can affect one or multiple limbs. ALD’s can be caused by peri-physeal imbalance, incomplete cuboidal bone ossification, or soft tissue laxity or contracture.
Signalment:
Foals and weanlings during rapid growth phases. The presence of physitis or incomplete cuboidal bone ossification. Lameness in the contralateral limb can cause ALD in the weightbearing limb. Excess activity in young foals, or poor farriery leading to hoof imbalances.
Presentation:
Visible limb deviation in stance and in motion when viewed from the cranial aspect. A joint wobble or instability may be seen. ALDs can be non-painful and horses may not show any lameness.
Diagnostics:
Radiographs are necessary to evaluate growth plates and to identify underlying conditions. Measurement of deviation angles.
Treatment options:
Conservative treatment includes corrective farriery, and controlled activity. Kinesiotape can be used in the early stages of conservative treatment.
Surgical correction can include periosteal stripping to stimulate growth, or transphyseal bridging to delay growth. Both surgical procedures need to be implemented during specific growth windows.
Flexural Limb Deformities (Contracture & Laxity)
Flexural limb deformities affect the tendons and ligaments of the distal limbs, and can be grouped into either a contracture or a laxity.
Contractures result in one or more joints of the distal limb being held in permanent flexion – often the carpus, fetlock, pastern and coffin joint. When the coffin joint is affected, we recognise a club foot.
Laxity results in hyperextension of the distal limb at one or more joints, including the coffin and fetlock joints.
These conditions often occur bilaterally.
Signalment:
Young foals experiencing pain or rapid growth. They may have a history of immobilisation.
These conditions can be congenital, developmental or acquired.
Presentation:
Contractures: Club foot when the DDFT is shortened presents as a raised heel or walking on the toe. A contracted fetlock presents when the SDFT is shortened. Carpal flexion can occur when pain is present.
Laxity: Hyperextension will be seen at one or more distal joints during stance, usually bilaterally. We may see the heel contact the ground prematurely in coffin joint hyperextension, or the fetlock drop low or contacting the ground during weightbearing.
Diagnostics:
Radiographs to assess joint alignment and US to assess tendons if injury is suspected.
Treatment options:
Corrective farriery can be essential for both contractures and laxity.
Splinting or bandaging joints into proper alignment, coupled with controlled activity.
Stretching protocols for contracted tendons may be implemented.
Surgical correction for severe or non-responsive cases may include a tendon desmotomy of the inferior check ligament for an SDFT contracture, or a DDFT tenotomy for a severe club foot contracture.
Osteochondrosis Dissecans (OCD)
OCD occurs when endochondral ossification fails, resulting in an area of cartilage that can fissure off into a flap or fragment inside the joint space. This generally occurs on a weightbearing surface of the joint. In horses, the shoulder, fetlock, hock and stifle are commonly affected.
Signalment:
Rapidly growing large breed horses, especially sport horses. Nutrition can be a contributing factor.
Presentation:
Horses may present with joint effusion, varying degrees of lameness that is worse after rest.
Diagnostics:
Radiography, ultrasound and arthroscopy.
Treatment options:
Arthroscopic debridement of OCD flaps and fragments can be indicated.
Conservative management focuses on treating synovitis and osteoarthritis.
Subchondral Bone Cysts
Cystic lesions within subchondral bone that generate pain with load and can communicate with the joint. Often occurs on the medial femoral condyle of the stifle, distal radius and tibia, proximal phalanx, and the fetlock.
Signalment:
Young, large breed horses, often sport horses. Lameness can be intermittent and mild.
Presentation:
Joint effusion, reduced range of motion, pain on flexion or compression of the joint, and a reduction in performance. Lameness may be worse on hard surfaces.
Diagnostics:
Radiographs can identify a radiolucent subchondral defect. US to identify cartilage or synovium damage.
Treatment options:
Rest and controlled exercise;
intra-articular therapies;
surgical intervention can include arthroscopic debridement of cyst lining, insertion of biologics or corticosteroids, and grafting or cyst filling in severe cases.
Cervical Stenotic Myelopathy (Wobbler Syndrome)
A developmental or degenerative narrowing of the cervical canal that compresses the spinal cord. That compression disrupts motor and sensory signaling, so what we see is ataxia, weakness and a loss of coordination. In many horses the compression is dynamic or position-dependent.
Signalment:
Type 1: Large breed sport horses during periods of rapid growth where neck pain is absent. Generally 2-4 years of age. This type usually affects cranial cervical levels, C2-4. Neurological signs will worsen during flexion of the cervical spine, as compression is dynamic.
Type 2: In older working horses of 7-12 years, cervical facet OA can develop leading to compression of the spinal cord. Neck pain is likely present. Usually affects the caudal cervical levels, C5-7.
Presentation:
Neurological deficits in the hindlimb may be seen, including truncal sway, delayed protraction, circumduction on circles, inconsistent foot placement, toe scuffing, stumbling.
Caution must be exercised during evaluation as a loss of balance can occur suddenly.
Diagnostics:
Full neurological exam followed by cervical radiographs, including stress radiographs, to identify malformation or malalignment of vertebra. Myelography can be used to identify spinal cord compression.
Treatment options:
Young horses: nutrition management (balanced minerals; avoid excess energy/protein), controlled turnout, moderate growth and BCS targets; consider genetics in breeding decisions. Prioritize environmental safety and handling safety.
Older horses: work modification (avoid over-flexion and compression of neck), NSAIDs, targeted facet joint corticosteroid injections; some cases need workload reduction or retirement.
Surgery: selected cases may be candidates for ventral interbody fusion to stabilize and decompress.
Therapeutic exercise programs should prioritise safety while improving proprioception, coordination, and postural strength and stability.
Conclusion
Developmental Orthopedic Diseases are complex, but with the right knowledge, we can play a vital role in supporting foals and young horses as they grow. By working closely with veterinarians, farriers, and owners, and by staying curious about emerging techniques like kinesiotaping, we can help improve outcomes and set our patients up for healthy futures.
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