BACKGROUND: The pathogenesis of human juvenile osteochondritis dissecans (JOCD) remains poorly understood, with multiple factors implicated, including ischemia, repetitive trauma, and genetic predisposition. Similarities in the predilection site and the diagnostic and clinical features of JOCD to the well-characterized veterinary counterpart, osteochondrosis dissecans, suggest that, similar to the animal disease, the pathogenesis JOCD may also be initiated in the first few years of life, when disruption of blood supply to the epiphyseal growth cartilage leads to failure of endochondral ossification. To gather data in support of the hypothesis that JOCD and osteochondrosis dissecans have a shared pathogenesis, biopsy specimens obtained from predilection sites of JOCD in juvenile human cadavers were histologically examined to determine whether they contained lesions similar to those found in animals diagnosed with subclinical osteochondrosis dissecans. METHODS: In this descriptive laboratory study, 59 biopsy specimens (6 mm in diameter) were harvested from the central aspect (i.e., the notch side) of the femoral condyles of 26 human cadavers (1 month to 11 years old). Specimens were histologically evaluated for the presence of areas of cartilage necrosis and the morphology of cartilage canal blood vessels. RESULTS: Locally extensive areas of necrotic epiphyseal cartilage were identified in 4 specimens obtained from 3 donors (ages 2 to 4 years). Areas of cartilage necrosis accompanied by focal failure of endochondral ossification or surrounded by subchondral bone were identified in biopsy specimens from 4 donors (ages 4 to 9 years). CONCLUSIONS: The identification of epiphyseal cartilage necrosis identical to that described in animals with subclinical osteochondrosis, found in biopsy specimens obtained from femoral predilection sites of JOCD in pediatric cadavers, suggests a shared pathogenesis of JOCD in humans and osteochondrosis dissecans in animals. CLINICAL RELEVANCE: These findings imply that the pathogenesis of human JOCD likely starts 5 to 10 years prior to the development of clinical symptoms. Enhanced understanding of the temporal features of JOCD pathogenesis provides an opportunity for earlier diagnosis and treatment, likely resulting in improved outcomes for this condition in the future.