Equine osteochondrosis

What it is

Osteochondrosis is a failure of endochondral ossification: in an area of the growth cartilage beneath the articular cartilage, cartilage is not converted into bone. In the horse the initial lesion is a focal necrosis of the growth cartilage caused by failure of the blood supply through the cartilage canals, which supply the cartilage at that stage. The cartilage that does not ossify thickens and weakens, cracks under load and can detach as an osteochondral fragment: this is osteochondritis dissecans (OCD). At other sites the lesion forms a subchondral cyst.

Lesions appear very early, in the first months of life, and many regress on their own: in a study of warmblood foals, hock lesions were permanent by 5 months and stifle lesions by 8 months. The disease is multifactorial: genetics, rapid growth and large size, diet (excess energy, mineral imbalances such as copper deficiency), exercise and trauma to immature cartilage all play a part.

Who it affects

Foals and young horses, more often of large, fast-growing sport breeds: warmbloods, Standardbreds and Thoroughbreds; it is less common in ponies and small breeds. Many lesions are found in horses aged 1 to 3 years on sale or selection radiographs, sometimes without clinical signs.

Anatomy involved

• Tibia: the most common site in the hock is the distal intermediate ridge of the tibia, in the tarsocrural joint; also the medial malleolus.
• Tarsus: the lateral trochlear ridge of the talus, especially its distal end, in the same tarsocrural joint.
• Femur: in the stifle, the lateral trochlear ridge of the femur is the typical site in the femoropatellar joint; the medial trochlear ridge and the patella are affected less often. In the femorotibial joint, the medial femoral condyle is the classic site of subchondral cysts.
• Metacarpus and metatarsus: in the fetlock, the sagittal ridge of the distal end of the third metacarpal and third metatarsal bones. Fragments from the dorsoproximal aspect of the first phalanx are often included in this group too.
• Less often, the shoulder joint and the cervical vertebrae are affected, where osteochondrosis of the articular processes is linked to cervical myelopathy (wobbler syndrome).

Clinical signs

The most typical sign is painless joint effusion, often bilateral: in the hock it appears as a soft distension of the tarsocrural joint (bog spavin), and in the stifle as a distension of the femoropatellar joint. Lameness is usually mild or absent and appears or worsens when training starts. Large stifle lesions in foals can cause more obvious lameness, with difficulty getting up. Many lesions are radiographic findings without clinical signs.

Diagnosis

• Radiographs of the typical joints, often of both sides because lesions are frequently bilateral: flattening or defects of the subchondral outline, fragments and cysts.
• Ultrasonography of the stifle to assess the cartilage and fragments that have not yet ossified.
• Arthroscopy: confirms the lesion, assesses the cartilage and allows treatment in the same procedure.
• In young foals, serial radiographs show whether a lesion regresses or progresses before treatment is decided.

Treatment and prevention

• Arthroscopic surgery: removal of fragments and debridement of the affected cartilage and bone; it is the usual treatment in horses with effusion or lameness and for hock and fetlock fragments before training starts.
• Conservative treatment with rest and controlled exercise in young foals with small stifle lesions, which can heal; large lesions or loose fragments need surgery.
• Prevention: avoiding excess dietary energy and overly rapid growth, balancing minerals, providing regular exercise in a paddock of moderate size and selecting breeding stock; some studbooks require radiographs of stallions. Because heritability is low to moderate, selection alone does not eliminate the disease.
• The horse is a food-producing animal in many countries and drug use is subject to national regulations and withdrawal periods.

Key studies

• Lepeule et al. (2009), cohort study on 21 farms in Normandy (France) with 378 foals of 3 breeds followed from gestation to weaning. At 6 months, 47% had developmental orthopaedic lesions and 36% had osteochondrosis. Warmblood foals were at higher risk than Thoroughbreds (OR 2.9; 95% CI 1.1–7.5 for osteochondrosis), as were foals with greater wither height at one month. Some exercise conditions, such as large pastures or irregular exercise, also increased the risk, but no association with feeding was found, possibly because of little variation between farms. The farms were a convenience sample.
• Denoix et al. (2013), radiographic study of 392 six-month-old French Trotter, Selle Français (warmblood) and Thoroughbred foals from the same population. The most affected site was the hind fetlock (28.3% of foals), followed by the fore fetlock in Thoroughbreds and Selle Français and by the carpus and proximal tarsus in Trotters; Selle Français foals were the most affected. It is a descriptive study at a single age, and many lesions at this age may still regress.
• Russell et al. (2017), retrospective cohort with radiographs of 1,962 Thoroughbred yearlings in Australia. The prevalence of osteochondrosis was 23%: 10% of stifles, 6% of hocks and 8% of fetlocks. Heritabilities were low, from 0 to 0.21, highest for the lateral trochlear ridge of the femur, and a meta-analysis with earlier studies gave values of 0.10 to 0.20 depending on the joint. The estimates have wide standard errors.
• Grøndahl and Engeland (1995), cohort of 753 Standardbred trotters radiographed as yearlings and followed through their racing careers. Horses with hock osteochondrosis, palmar or plantar fetlock fragments or other fetlock changes (including osteochondrosis of the sagittal ridge) had fewer starts and somewhat lower earnings than horses without radiographic changes. It is a single breed and the abstract does not give the effect size.
• Laws et al. (1993), retrospective study of 114 Standardbreds with osteochondrosis of the distal intermediate ridge of the tibia, 58 treated arthroscopically and 56 conservatively, compared with 456 controls matched by year of birth, sex and sire. Overall, affected horses had fewer starts than controls but similar earnings and no difference in record time; females did perform worse. It is retrospective and treatment was not randomised.