Epiphyseal Etiology for Juvenile Osteochondritis Dissecans?

Most patients with clinically apparent juvenile osteochondritis dissecans (JOCD) are between 12 and 19 years of age. Often the disease can be treated successfully with nonoperative modalities, but even in cases where the initial lesion resolves, patients may be predisposed to osteoarthritis later in life. While repetitive microtrauma is suspected to be involved in the development of JOCD, the exact etiology remains poorly understood, even 130 years after the condition was first described.

In the December 19, 2018 issue of The Journal, Toth et al. histologically examined 59 biopsy samples from the central condyles of 26 pediatric cadavers to look for areas of epiphyseal cartilage necrosis. Hypothesizing that such evaluation would reveal some lesions similar to those found in animals, the authors did indeed identify 6 samples with 1 or more areas of necrotic cartilage, which were either incorporated into subchondral bone or associated with focal failure of endochondral ossification. Those characteristics are consistent with a similar disease process called osteochondrosis manifesta seen in pigs and horses.  While the clinical significance of these findings remains to be determined, the authors suggest that they may help explain an epiphyseal etiology of JOCD, and the data suggest that these microscopic changes (some of which are rendered in this article as whole-slide images) are probably present in young people 5 to 10 years prior to the clinical manifestations of JOCD.

These findings lend credence to the theory that the underlying etiology of JOCD primarily involves the epiphyseal growth plate rather than subchondral bone. Furthermore, the similarities between these cadaveric specimens and osteochondrosis manifesta lesions in porcine and equine femoral condyles may help us develop improved models to better diagnose, prevent, and treat this pathology.

Chad A. Krueger, MD
JBJS Deputy Editor for Social Media

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One response to “Epiphyseal Etiology for Juvenile Osteochondritis Dissecans?”

  1. Ludwig Meiss, Hamburg, Germany says :

    “… existence of these purported precursor lesions of JOCD in human subjects, 5 to 10 years prior to the onset of clinical symptoms …”.
    How can these lesions depicted in primary cancellous bone of the circumferential epiphyseal growth cartilage zone (and moving away from it during growth) play a role for JOCD when a long bone is completely remodeled (probably several times) within 5 to 10 years?

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