The Pathogenesis of Osteochondrosis in Humans and Animals

Abstract

Osteochondrosis is a disease involving failure of endochondral ossification that occurs in growing animals and children in highly specific predilection sites, resulting in the formation of a cartilaginous or osseocartilaginous flap that causes pain and locking of the joint. In veterinary medicine, the term “osteochondrosis” (OC) is used for all stages of the disease and all affected sites. In human medicine, “osteochondritis dissecans” (OCD), is the preferred term for clinical disease involving the distal femur/knee joint. In other affected sites in humans, the disease is named after the physician(s) who first recognized it at that site; the disease in humans is further subdivided into adult and juvenile forms. Until very recently, subclinical disease was not recognized in humans as the only available tissue for study was the flap removed surgically from the affected joint, which often had been present for months to years. Subclinical disease, however, is well recognized in animals due to study of predilection sites at ages prior to the age of onset of clinical disease, work that are not possible in humans. Because the appearances of the subclinical and clinical disease are completely different, and because only end‐state tissue has been available for study of the disease in humans, the pathogenesis of the disease has been poorly understood in human medicine. In pigs and horses, it has been well demonstrated that subclinical lesions of osteochondrosis involving the articular‐epiphyseal cartilage complex are composed of areas of necrotic epiphyseal cartilage that often surround necrotic cartilage canal blood vessels. The overlying articular cartilage and subjacent subchondral bone are not initially affected; however, as endochondral ossification proceeds these areas of necrotic cartilage cause a delay in the ossification front that is visible in imaging studies. Study of both naturally‐occurring and surgically‐induced disease in animals have unequivocally demonstrated that failure of cartilage canal blood supply is the cause of these lesions. Traumatic forces to the surface of the articular cartilage, even when minimal in severity, may result in collapse of the necrotic epiphyseal cartilage and cleft formation through the overlying articular cartilage, resulting in the well‐recognized clinical disease. Recent development of magnetic resonance imaging methods to identify cartilage canal vessels and areas of cartilage necrosis, as well as access to human cadaveric knee specimens, have provided strong evidence that the pathogenesis of OC/OCD in animals and humans is identical and that subclinical disease in humans occurs years before clinical disease is evident. This work provides the potential for the development of new methods of early detection of disease in humans and methods for monitoring its response to treatment.Support or Funding InformationNIH/NIAMS R01AR070020; NIH/OD K01OD021293; WM Keck FoundationThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.