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.

The ischaemic hypothesis for the pathogenesis of OC has been reproduced experimentally in foals. There are several similarities between OCD in animals and JOCD in children. It should be investigated whether JOCD also occurs due to a focal failure in the cartilage canal blood supply, followed by ischaemic chondronecrosis.

Osteochondrosis is defined as a focal disturbance in endochondral ossification. The cartilage superficial to an osteochondrosis lesion can fracture, giving rise to fragments in joints known as osteochondrosis dissecans (OCD). In pigs and horses, it has been confirmed that the disturbance in ossification is the result of failure of the blood supply to epiphyseal growth cartilage and associated ischemic chondronecrosis. The earliest lesion following vascular failure is an area of ischemic chondronecrosis at an intermediate depth of the growth cartilage (osteochondrosis latens) that is detectable ex vivo, indirectly using contrast-enhanced micro-and conventional computed tomography (CT) or directly using adiabatic T1r magnetic resonance imaging. More chronic lesions of ischemic chondronecrosis within the ossification front (osteochondrosis manifesta) are detectable by the same techniques and have also been followed longitudinally in pigs using plain CT. The results confirm that lesions sometimes undergo spontaneous resolution, and in combination, CT and histology observations indicate that this occurs by filling of radiolucent defects with bone from separate centers of endochondral ossification that form superficial to lesions and by phagocytosis and intramembranous ossification of granulation tissue that forms deep to lesions. Research is currently aimed at discovering the cause of the vascular failure in osteochondrosis, and studies of spontaneous lesions suggest that failure is associated with the process of incorporating blood vessels into the advancing ossification front during growth. Experimental studies also show that bacteremia can lead to vascular occlusion. Future challenges are to differentiate between causes of vascular failure and to discover the nature of the heritable predisposition for osteochondrosis.

Background Osteochondrosis (OC) is a common developmental orthopedic disease affecting both humans and animals. Despite increasing recognition of this disease among children and adolescents, its pathogenesis is incompletely understood because clinical signs are often not apparent until lesions have progressed to end-stage, and examination of cadaveric early lesions is not feasible. In contrast, both naturally-occurring and surgically-induced animal models of disease have been extensively studied, most notably in horses and swine, species in which OC is recognized to have profound health and economic implications. The potential for a translational model of human OC has not been recognized in the existing human literature. Objective The purpose of this review is to highlight the similarities in signalment, predilection sites and clinical presentation of naturally-occurring OC in humans and animals and to propose a common pathogenesis for this condition across species. Study Design Review Methods The published human and veterinary literature for the various manifestations of OC was reviewed. Peer-reviewed original scientific articles and species-specific review articles accessible in PubMed (US National Library of Medicine) were eligible for inclusion. Results A broad range of similarities exists between OC affecting humans and animals, including predilection sites, clinical presentation, radiographic/MRI changes, and histological appearance of the end stage lesion, suggesting a shared pathogenesis across species. Conclusion This proposed shared pathogenesis for OC between species implies that naturally-occurring and surgically-induced models of OC in animals may be useful in determining risk factors and for testing new diagnostic and therapeutic interventions that can be used in humans.

Material available for research into osteochondrosis (OC) in humans tends to represent chronic lesions. Comparative studies of early lesions in young animals are, therefore, important in clarifying the pathogenesis of OC in humans. Recent studies in pigs provide strong evidence that lesions of articular OC are associated with a focal failure in the cartilage canal vascular supply to epiphyseal growth cartilage (articular-epiphyseal cartilage complex excluding the articular cartilage). The purpose of the present study was to examine histological sections from a specific predilection site for articular OC in the distal tibia of a large number of young foals to determine if the same is true in horses. Material from the distal tibiae of 100 foals aged from 191 days of gestation to 153 days old was collected from routine submissions of fetuses and foals for post mortem examination. The tibiae were band-sawed into slabs, and selected slabs were processed for histology, stained with hematoxylin and eosin, and examined using light microscopy. Early subclinical developmental stages of OC were found in the most common site for clinical OC lesions of horses in nine of 100 foals aged 12 to 122 days old. All lesions contained areas of chondrocyte necrosis that were associated with cartilage canal necrosis in five of nine foals. Five of these foals also had focal disruption of enchondral ossification at the chondro-osseous junction in the same site. Early lesions purported to play a role in the initial stages of articular OC in the distal tibia of horses were characterized by chondrocyte necrosis and likely occurred secondary to a failure of cartilage canal vascular supply to epiphyseal growth cartilage. The similarities in appearance between early lesions of piglets and foals suggest that information gained in one species may be transferable to others, including humans. ß