Juvenile Osteochondritis dissecans (JOCD) in humans and subchondral cystic lesions (SCL) in horses (also termed radiolucencies) share similarities: they develop in skeletally immature individuals at the same location in the medial femoral condyle (MFC) and their etiology is only partially understood but trauma is suspected to be involved. JOCD is relatively uncommon in people whereas SCLs arise in 6% of young horses leading to lameness. Ischemic chondronecrosis is speculated to have a role in both osteochondrosis and SCL pathogenesis. We hypothesize that MFC radiolucencies develop very early in life following a focal internal trauma to the osteochondral junction. Our aims were to characterize early MFC radioluciencies in foals from 0 to 2 years old. Distal femurs (n=182) from Thoroughbred horses (n=91, 0–2 years old), presented for post-mortem examination for reasons unrelated to this study, were collected. Radiographs and clinical tomodensitometry were performed to identify lesions defined as a focal delay of ossification. Micro-tomodensitometry (m-CT) and histology was then performed on the MFCs (CT lesions and age-matched subset of controls). Images were constructed in 3D. The thawed condyles, following fixation, were sectioned within the region of interest, determined by CT lesion sites. Hematoxylin eosin phloxin and safran (HEPS) and Martius-Scarlet-Blue (MSB) stains were performed. Histological parameters assessed included presence of chondronecrosis, fibrin, fibroplasia and osteochondral fracture. An additional subset of CT control (lesion-free) MFCs (less 6 months old) were studied to identify early chondronecrosis lesions distant from the osteochondral junction. One MFC in clinical CT triages controls had a small lesion on m-CT and was placed in the lesion group. All m-CT and histologic lesions (n=23) had a focal delay of ossification located in the same site, a weight bearing area on craniomedial condyle. The youngest specimen with lesions was less than 2 months old. On m-CT 3D image analysis, the lesions seemed to progressively move in a craniolateral to caudomedial direction with advancing age and development. Seventy-four percent (n=17/23) of the lesions had bone-cartilage separation (considered to be osteochondral fractures) confirmed by the identification of fibrin/clot on MSB stains, representing an acute focal bleed. Fibroplasia, indicating chronicity, was also identified (74%, n=17/23). In four cases, the chondrocytes in the adjacent cartilage were healthy and no chondronecrosis was identified in any sections in the lesions. Nineteen cases had chondronecrosis and always on the surface adjacent to the bone, at the osteochondral junction. None of the subset of control specimens, less than 6 months old (n=44), had chondronecrosis within the growth cartilage. Early subchondral cystic lesions of the medial femoral condyle may arise secondary to focal internal trauma at the osteochondral junction. The presence of fibrin/clot is compatible with a recent focal bleed in the lesion. Medial femorotibial joint internal forces related to geometry could be the cause of repetitive trauma and lesion progression. In the juvenile horse, and potentially humans, the early diagnosis of MFC lesions and rest during the susceptible period may reduce progression and promote healing by prevention of repetitive trauma, but requires further study
