Epiphyseal cartilage canal blood supply to the tarsus of foals and relationship to osteochondrosis

Authors: Olstad, K.; Ytrehus, B.; Ekman, S.; Carlson, C.S.; Dolvik, N.I.

Source: Equine Veterinary Journal, Volume 40, Number 1, January 2008 , pp. 30-39(10)

Publisher: Equine Veterinary Journal Ltd.

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Abstract:

Reasons for performing study: Pathological changes in the blood supply to growth cartilage have been implicated in the pathogenesis of osteochondrosis (OC) in horses, but have not been reported using vascular perfusion techniques.

Objective: To describe the developmental pattern of cartilage canal vessels in the distal tibial epiphysis and talar growth cartilage of foals.

Methods: Nine foals bred from parents with OC were sacrificed between the ages of 0 and 7 weeks to undergo a barium perfusion procedure. The distal end of the tibia and the entire talus were cleared in methyl salicylate and perfused vessels studied in the intact bones. Slabs with a thickness of 4-5 mm from 3 predilection sites for OC were examined in the stereomicroscope and with light microscopy.

Results: Cartilage canals were present for a limited period of growth. Perfused vessels initially entered canals from the perichondrium. Vessels in the proximal portion of canals retained their perichondrial arterial source throughout. With time, the ossification front advanced to incorporate the mid-portion of canals; and anastomoses formed between canal vessels and subchondral vessels. A shift occurred and vessels in the distal terminus of canals came to use subchondral vessels as their arterial source. Twelve histological lesions were found in 7 foals. All contained necrotic vessels surrounded by necrotic growth cartilage and 3 caused macroscopically visible delay in endochondral ossification. Lesions were located where vessels traversed the ossification front to enter the distal terminus of canals.

Conclusion: Cartilage canal vessels are particularly susceptible to failure at the point where they cross the ossification front, with consequences for the viability of those chondrocytes that depend on them.

Potential relevance: A better understanding of how lesions of OC arise may improve the ability to identify, monitor, prevent and treat this disorder. Involvement of cartilage canals in the pathogenesis of equine tarsal OC plausibly explains several clinical features of this disease.

Keywords: HORSE; FOAL; TARSUS; CARTILAGE CANALS; ISCHAEMIC NECROSIS; OSTEOCHONDROSIS

Document Type: Research article

DOI: 10.2746/042516407X239836

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