The pathophysiology of osteochondrosis.

S. Ekman, C. S. Carlson

Research output: Contribution to journalReview articlepeer-review

121 Scopus citations


Osteochondrosis is a disorder of epiphyseal cartilage about which there is considerable confusion in the literature. We believe that this is due to the fact that osteochondrosis has been studied in the chronic stage when the lesions are morphologically complicated and the initial causative insult is impossible to determine. The etiology of osteochondrosis appears to be multifactorial, with trauma, hereditary factors and rapid growth, nutritional factors, and ischemia all having a role in its pathogenesis. Although predilection sites are variable among species, the morphology of the early lesions is strikingly similar, strongly suggesting that the pathogenesis of osteochondrosis is the same, regardless of the species affected. Based on recent studies in pigs and horses, and supported by observations in dogs and cattle, we believe that local ischemia secondary to defects in cartilage canal blood supply is a key factor in the initiation of lesions of osteochondrosis and explains many of the features of this disease. Local ischemia to the epiphyseal cartilage of the articular-epiphyseal cartilage complex leads to the formation of highly vulnerable zones of necrotic epiphyseal cartilage which later cause a delay in endochondral ossification, with extension of necrotic cartilage into the subchondral bone. Trauma, whether major or minor, to the overlying articular cartilage leads to cartilage cleft formation, clinical signs of pain and lameness, and other chronic sequelae. Studies aimed at further elucidating the pathogenesis of osteochondrosis should attempt to determine the cause of the vascular defect and whether or not it may be modified by experimental manipulations.

Original languageEnglish (US)
Pages (from-to)17-32
Number of pages16
JournalThe Veterinary clinics of North America. Small animal practice
Issue number1
StatePublished - Jan 1998
Externally publishedYes

Bibliographical note

Funding Information:
This work was supported by Professor Sten-Erik Olsson, Laboratory for Comparative Pathology and by Grant RR08562 from the National Institutes of Health.


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