Osteochondrosis (OC) represents a disturbance in the process of endochondral ossification without a clearly understood aetiology. This disturbance can eventually lead to the formation of semi loose or even completely loose fragments within a joint. The term osteochondritis dissecans was originally coined by Konig in 1887 and used to describe loose or semi loose bodies in joints of young persons that could have 3 causes: very severe trauma, lesser trauma and necrosis or minimal trauma inducing an underlying lesion. 

Endochondral ossification is the process of transformation from the primordial cartilaginous skeleton into bone coupled with simultaneous growth. Ossification of the primary centres of ossification in the diaphysis of long bones occurs early in foetal life, however ossification of the secondary centres of ossification at the epiphysis continues after birth (the apophyses and cuboidal bones remaining cartilaginous at birth). The cartilage cells of the physis and epiphysis proliferate and hypertrophy then undergo apoptosis. This is followed by calcification of the cartilage and deposition of primary bone which is subsequently modelled into trabeculae according to Wolf’s Law. 

1. Ischaemic. Failures of vascularisation; the blood supply to growth cartilage is provided

   by the cartilage canals. It has been suggested that disruption of this blood supply can lead to cartilage necrosis where vessels traverse the ossification front. The regions that remain perfused the longest coincide with the predilection sites for OC (Olstad et al. 2008).

2. Cartilage type II collagen metabolism (Lecocq et al. 2008) identified changes in the collagen structure from a more dense structure to one with thinner fibrils paralleling cellular changes at the predilection sites. Thus rendering the articular epiphyseal cartilage complex (AECC) susceptible to traumatic injury and blood vessel injury. 

3. Biomechanical; biomechanical loading plays a role in the pathogenesis of OC,

   consistency of predilection sites within specific joints, OC lesions have not been

   identified in the foetus. 

3. Exercise; this is known to steer the functional adaptation of cartilage to its

   topographically heterogenous character during the first year of life. Studies demonstrate that exercised foals have a lower incidence of OC. Exercise may be a factor determining the final appearance of lesions but does not seem to be important in the primary pathogenesis. 

3. Nutrition, hormonal factors and growth rate; dietary copper is thought to have an effect on the final outcome of lesions as several studies have shown increased OC with low copper but there is not sufficient evidence to pinpoint copper as the sole cause of OC. High calcium did not increased levels of OC but high levels of phosphorus resulted in significantly more lesions. Dietary energy levels have been implicated in the pathogenesis of OC for decades, mostly in relation to high growth rate. Easily digestible carbohydrates result in post-prandial hyperinsulinaemia. Insulin and its derivatives have direct effects on the process of endochondral ossification (stimulating chondrocyte survival and suppressing apoptosis). 

Genetics; lesions are rarely found in ponies and feral horses. OC has a polygenetic trait with a complex method of inheritance with various candidate genes being identified that differ even between joints. Heritabilities of 0.25 in KWPN Warmbloods have initiated the implementation of selection programmes but these have thus far been unsuccessful due to the complicated genetic nature of OC. 

OC is most commonly seen in the tarsus, stifle and metocarpophalangeal joints, but it has been described in almost every diarthrodial joint. Breed differences do occur, the tarsocrural being the most affected in Warmbloods, yet the femoropatellar joint is common in the racing Thoroughbred. The hallmark of OC is that lesions ALWAYS occur at certain predilection sites within a joint:

- tarsal

- stifle

- metacarpophalangeal joint  

Tarsal predilection sites

Cranial end of the distal intermediate ridge of the tibia (DIRT lesions), distal end of the lateral trochlear ridge of the talus, medial malleoulus of the tibia, medial trochlear ridge of the talus. 

Lateral trochlear ridge of the femur >>> medial trochlear ridge of the femur, trochlear groove, distal end of the patella. Subchondral bone cysts of the medial femoral condyle are also a manifestation of OC.

Metacarpophalangeal joint predilection sites

Dorsal edge of sagittal ridge of the metacarpus. Opinions differ on the aetiology of dorsoproximal proximal phalanx fragments. Plantar osteochondral fragments of the proximal phalanx are now considered traumatic in origin. 

OC was originally seen as a largely static condition but this concept has now changed. Repeated radiographic examinations have documented changes in the radiological appearance of OC. Indeed resolution of radiographically apparent lesions has been well documented. The ages at which lesions originated and the ages at which they became undetectable varied for each joint. Lesions within the tarsocrural joint were seen within the first 1-3 months of life and had become undetectable by 5 months. No further changes occurred after this age and lesions remained visible for the tarsocrural joint i.e. a radiographically evident lesion within the tarsocrural joint detected after 5 months is unlikely to spontaneously resolve. In the femoropatellar joint lesions originated later and peaked at about 6 months before declining by about 8 months after which lesions remained stable. OC is an extremely dynamic disease in which lesions appear and apparently heal during the first months of life while the cartilage is still able to heal. Lesions that manifest clinically are those that either originate too late or are too large so that they do not have enough time for repair. 

Clinical signs include lameness and/or synovial effusion usually in yearlings. Sometimes in less severe cases clinical signs coincide with the onset of training. Lameness can vary from subtle (reduced arc of foot flight, shortening of cranial phase) to obvious with owners sometimes reporting that the horse has difficulties getting up. Diagnosis is usually based on clinical signs and radiography. Lesions of the distal intermediate ridge of the tibia are best visualised on the DMPLO (Figure 1); lesions of the lateral trochlear ridge of the talus are best visualised on the DMPLO projection; medial malleolar OC can be identified on DLPMO and DP projections. Femoropatellar OC can be identified on the lateromedial (Figure 2) and CaLCrMO projections. Ultrasound is more sensitive for identifying the less common OC of the medial trochlear ridge of the femur (Bourzac et al. 2009). Ultrasound should be used in combination with radiography as ultrasound has limitations in identifying lesion length for large fragments. 

Non-surgical management consists of rest and controlled exercise. Administration of NSAIDs and intra-articular medications have NOT been shown to be of benefit for OC cases. Given the nature of the disease process conservative management can only be expected to be successful in very young animals or where lesions are mild. 

Peri-operative antibiotics are administerd as necessary. Bilateral tarsocrural arthroscopy is carried out with the horse placed in dorsal recumbency under general anaesthesia. The arthroscope is inserted in the dorsomedial pouch of the tarsocrural joint and an instrument in the dorsolateral pouch of the joint. The fragment is elevated with a periosteal elevator and grasped with Ferris Smith Rongeurs to remove from the joint, the subchondral bed is then debrided to healthy subchondral bone. Sutures are placed through the skin only and the limb is placed in a modified Robert-Jones bandage. Post-operative management consists of 4 weeks box rest and in hand walking followed by 4 weeks turnout and light exercise. Post-operative oral hyaluronan has been shown to reduce effusion in one study (Bergin et al. 2006). 

Recommended for lesions >2cm in length or 0.5cm in depth, or any lesion that contains osseous densities in combination with synovial effusion. Peri-operative antibiosis is administered for a longer period due to the higher occurrence of peri-articular extravasation associated with stifle arthroscopy. Surgery is carried out with the horse in dorsal recumbency under general anaesthesia. The arthroscope is inserted between the middle and lateral patellar ligaments mid way between the tibial crest and the distal aspect of the patella. A spinal needle is used to identify the optimal position for instrument portal placement. The osteochondral fragments are elevated and removed as decribed for the tarsocrural joint. Post-operative management consists of 4 weeks box rest and in hand walking followed by 4 weeks turnout and light exercise can commence 3-4 months post-operatively. 

Tarsocrural joint: The prognosis for athletic function does not appear to be related to lesion size for DIRT lesions with 74-87% returning to athletic function post-surgery. The prognosis for effusion resolution is better for DIRT lesions (75%) than lateral trochlear ridge or medial malleolar lesions (50%).

Femoropatellar joint: The prognosis does appear to be related to lesion size with 78% of horses with lesion <2cm returning to racing, 63% of horses with lesions between 2-4cm and 54% of horses with lesions >4cm returning to racing (Foland et al. 1990). 

The complex nature of the disorder will probably not permit the identification of a single genetic marker, however the identification of osteocalcin (Donabedian et al. 2008) as a very early molecular marker for increased risk of OC may allow the establishment of specific rearing programmes for such animals to reduce the environmental risk for OC.