PATHOGENESIS

Endochondral ossification is the process of bone formation over a cartilage template; the process results in simultaneous growth and transformation of the initially cartilaginous primordial skeleton into bone. There is little doubt that endochondral ossification plays a role in OC. Although ossification at birth in precocial species like foals is advanced, large cartilaginous sections remain at the transition between diaphysis and epiphysis (the physis) and near the joint surfaces (the articular-epiphyseal cartilage complex), allowing for continued growth in the juvenile animal. Nutrition of these cartilaginous sections is provided through vessels passing through the so-called cartilage canals. During endochondral ossification of the articular-epiphyseal cartilage complex, the cartilage layer on the articular side becomes thinner and is converted into epiphyseal bone and the final articular cartilage layer of the mature animal.

The classic hypothesis of equine OC is that there is disturbance of the physiologic process of endochondral ossification that leads to locally thickened cartilage plugs (Figure 114-1). At the same time, cartilage canals disappear in a physiologic process called chondrification. From that moment, nutrition of the articular cartilage depends exclusively on diffusion of nutrients from the synovial fluid. Excessive thickening of the cartilage layer leads to malnutrition of certain areas and hence to focal necrosis and weakening of the tissue. Together with biomechanical influences, this may result in the formation of fissures, cartilage flaps, and eventually loose fragments or joint mice.

Figure 114-1 Section of bone taken through the articular-epiphyseal cartilage complex revealing thickened retained cartilage.

(Courtesy PR van Weeren, Utrecht University)

This hypothesis seems straightforward, but many concerns, including the fact that thickened cartilage or necrosis is not always seen with typical OC lesions, have been expressed that call into question the accuracy of the single hypothesis for OC. Recent investigations of the molecular mechanisms of OC indicate that the collagen component of the cartilage extracellular matrix is primarily affected. It is hypothesized that a defective collagen network results in disturbed calcification of cartilage, as has been shown in bone, causing delayed endochondral ossification, which is the hallmark of OC. Furthermore, a defective collagen network likely reduces the tensile strength of the cartilage and may, together with or without local cartilage thickening and biomechanical forces, result in the development of characteristic cartilage flaps or fragments. Osteochondrosis is a complex disease of multifactorial origin, and how these factors interrelate to produce the disease remains poorly understood.