Etiology

• Unknown.
• Multifactorial - may be a complex interaction of environmental, nutritional, biomechanical and genetic influences. 
• The following factors may have a primary or contributory role in the etiopathogenesis.

Growth rate

• Large, rapidly growing animals are typically associated with osteochondrosis, but a clear association between body size/growth rate and disease incidence has not been shown.

Nutrition

• When foals are fed according to requirements, there is a lower incidence of osteochondrosis.
• Excess energy intake (easily digestible carbohydrate and/or fat) may → cause abnormal development of cartilage through disturbances in hormonal balance and excessive growth rates. The latter may come as growth spurts during which the animal is particularly vulnerable to the formation of osteochondrosis lesions. The timing of these vulnerable growth spurts is variable depending on the individual joint and the site within it.
• Mineral homeostasis - excess phosphorus, excess calcium and copper deficiency have been implicated.
• Excess carbohydrate can influence endocrine factors affecting cartilage development, eg hyperinsulinemia Pancreas: hyperinsulinemia/hyperglycemia, hypothyroxemia → chondrocyte maturation and differentiation → affecting endochondral ossification.
• High dietary phosphorus can → abnormal endochondral ossification.

Hereditary

• Several studies suggest an influence of genetics on the development of connective tissue disorders.
• Heritability estimates vary enormously but have been cited at 0.0-0.52.
• The genetic basis of osteochondrosis is highly complex and polygenic. It's thought that affected chromosomes may occupy up to 20 chromosomes out of the 33 in the horse.
• Selection of certain traits in some horse breeds has led to a much higher incidence in some. Pony breeds are rarely affected.
• No appropriate program for screening dams, sires or progeny has been developed.

Exercise

• Lesions occur in sites of high biomechanical loading within specific joints. This trauma may exert excessive forces on normal tissue or normal forces on abnormal tissue within a joint(s).
• These forces may lead to disruption of the vascular supply of the cartilage undergoing endochondral ossification or shearing of cartilage flaps.
• Other factors may include body size, conformation, and exercise (too little, irregular or excessive), all of which affect biomechanical loading.
• Direct trauma or excessive loading of growth plates over time may lead to damage and clinical manifestations.
• A relationship appears to exist between the intensity of exercise, the level of nutrition and the incidence of osteochondrosis.

Predisposing factors

General

• Nutrition Nutrition: growth.
• Conformation Musculoskeletal: conformation.
• Familial incidence.

Pathophysiology

• The pathophysiology of osteochondrosis has not been resolved, although it is most commonly regarded as a developmental condition. Several theories have emerged, including failure of the cartilage canals, biomechanical shearing of the osteochondral junction, molecular alterations in endochondral ossification, and genetic basis.
• A primary failure of endochondral ossification, and specifically failure of cartilage canals, during the early postnatal period is thought to be a major factor in osteochondrosis. This is most likely to occur along the ossification front and involves the failure of vessel anastomosis between those involving the canals and the front. This leads to chondronecrosis and cartilage fissuring.
• Biomechanical forces are also involved in the development of osteochondrosis with the specific sites in joints where lesions of OCD occur often related to regions of high shear stress or impact. Shearing may occur as a primary event particularly at the cartilage-to-bone interface, a known biomechanically weak region in 4-month-old foals. Secondary shearing may occur after canal failure and chondronecrosis or other causes of cartilage weakening. Lack of exercise, irregular exercise or excessive exercise in the early developmental period (<6 months) has a negative effect on osteochondral status and may be a contributing factor in some cases of osteochondrosis.
• Other theories of pathogenesis include molecular alterations within the cartilage matrix and/or cell signaling pathways occurring prior to osteochondrosis developing, eg altered type 2 collagen synthesis weakening cartilage matrix near to cartilage canals and osteochondral junction.
• Changes in gene expression of multiple growth factors and paracrine factors in chondrocytes close to cartilage canals and osteochondral junctions may cause a delay in endochondral ossification. 
• Increased expression of MMP-13 and MMP-3 may also result in biomechanical weakness in the cartilage in these areas.
• Numerous studies have confirmed genetic loci linked to osteochondrosis and the heritability estimates range from low to high depending on the affected joint and breed of horse.
• Multiple sites and types of lesions are possible due to the variation in types of bone surfaces and the three areas in which endochondral ossification takes place (articular epiphysis complex, metaphyseal growth plate, secondary centers of ossification).
• Early osteochondrosis lesions have the potential to heal intrinsically or develop into more advanced OCD lesions and clinical disease. Healing is most likely to occur in younger foals when the blood supply to the developing cartilage is greatest. Decreasing contributory factors such as biomechanical stress during this healing phase is essential. If healing does not occur by one year of age, it's unlikely it will happen, and surgery becomes necessary.
• The primary lesion may not be recognized, and cycles of repair and remodeling may go unnoticed. If re-injury does occur or the repair is inadequate, the lesion remains and continues to compromise the joint function. Continued use of the joint as the animal matures and eventually enters work may → ongoing synovitis and degenerative joint disease Musculoskeletal: osteoarthritis (joint disease).
• Osteochondrosis is a disorder of cartilage development which leads to cartilage injury but also in some cases damage to subchondral injury.
• It is a developmental orthopedic disease and may be a precursor for other developmental orthopedic conditions, see also:
  • Acquired angular limb deformities Musculoskeletal: angular deformity.
  • Subchondral bone cysts Stifle: femorotibial subchondral bone cyst.
  • Flexural deformities Musculoskeletal: flexural deformity.
  • Cuboidal bone malformation Musculoskeletal: angular deformity.
  • Cervical vertebral malformation Spine: occipitoatlantoaxial malformation.

Classification

• Attempts to classify osteochondrosis have been based on the lesion and etiology.
• Lesion classification:
  • Type 1 - cartilage fragmentation in a typical site(s).
  • Type 2 - fragmentation of cartilage and subchondral bone in a typical site(s).
  • Type 3 - thickened cartilage (?=delayed ossification) in a typical site(s).
  • Type 4 - multiple lesions in typical and atypical sites including growth plates and secondary centers of ossification.
• Some joint conditions have been attributed to osteochondrosis, but have proved to have a traumatic or other specific etiopathogenesis, eg in the fetlock the following conditions have been previously attributed to osteochondrosis: fetlock plantar osteochondral fragmentation (POFs), ununited palmar fragment of the proximal phalanx (UPEs) and plantar condylar necrosis of the cannon bone (MC/MTIII) MCP / MTP joint: developmental orthopedic diseases.
• Osteochondrosis → joint surface susceptible to injury during development → subchondral bone cysts Stifle: femorotibial subchondral bone cyst and degenerative joint disease Musculoskeletal: osteoarthritis (joint disease).

Typical disease pattern

• One or two lesions, bilaterally symmetric, clinical evidence may be unilateral.
• Lesions range from fissures in articular cartilage, variably detached cartilaginous or osteochondral flaps/fragments, cysts and delayed ossification. The term osteochondritis dissecans is used to describe lesions with loose or separated flaps of cartilage.
• Stifle Stifle: femoropatellar osteochondrosis:
  • Lateral trochlea ridge of femur .
  • Lateral facet of patella.
  • Medial trochlear ridge - lesions may occur at any age.
• Hock Tarsus: osteochondrosis:
  • Distal intermediate ridge of tibia .
  • Lateral and medial trochlear ridge of talus.
  • Medial malleolus of tibia.
  • Incomplete ossification of the central tarsal and third tarsal bones.
• Fetlock MCP / MTP joint: developmental orthopedic diseases:
  • Mid-sagittal ridge and condyles of MC3/MT3.
  • Medial condyle proximal phalanx.
• Carpus:
  • Rare.
  • Incomplete ossification of the ulnar, third and fourth carpal bones.
  • Distal medial radius.
  • Distal medial radial carpal bone.
  • Proximal third carpal bone.
• Proximal interphalangeal joint:
  • Lysis of the distal end of the proximal phalanx .
• Elbow:
  • Rare.
  • Medial humeral condyle.
  • Proximal radius.
• Shoulder:
  • Glenoid fossa of scapula.
  • Humeral head.
• Areas uncommonly affected:
  • Hip.
  • Cervical vertebra joints.

Atypical pattern

• Multiple lesions.
• Physeal lesions.
• Uncommonly bilaterally symmetrical.
• Probably nutritional or toxic etiologies.
• Atypical locations within classically affected joint.
• A combination of typical and atypical lesions can occur in the same animal.