Abstract

Cartilage canals are temporary vascular structures within the growth cartilage. They were described as early as 1736 and the first perfusion study performed already in 1743. In its most complex form, the vascular structure consists of an arteriole, originating in the perichondrial plexus and branching out into an anastomosing network of capillaries. The capillaries circle back along the arteriole and rejoin into a venule that follows the course of the arteriole back to the plexus. The canals regress with age in a process designated as chondrification, where the content of the canals is replaced by cartilage. The process of chondrification is considered physiological; however, premature regression has been associated with the formation of lesions of osteochondrosis. The purpose of the present study was to gain further insight into the nature of chondrification and the initial steps in the pathogenesis of osteochondrosis and the relationship between these events and age, growth rate, weight and femoral shape of the individual animals. This involved studies of the distribution and pattern of regression of the cartilage canals. The articular‐epiphyseal cartilage complexes of the distal femur of 48 half‐siblings of the Norwegian Landrace pig breed were studied, combining techniques of perfusion and tissue clearing with histological and immunohistological methods. The results of this study indicate that the physiological regression of the cartilage canals is an orderly and time‐dependent process in which the endothelial cells at the termination of the vessels die by apoptosis, while perivascular cells differentiate into chondrocytes that fill in the cartilage canal with matrix. However, as the ossification front advances, the deepest portion of some of the canals form anastomoses with vessels of the subchondral bone, giving the axial portion of the growth cartilage a new source of blood supply. Lesions of osteochondrosis, typically occurring in the axial growth cartilage, are characterized by necrosis of the portion of the affected cartilage canal distal to a point of interruption, with subsequent necrosis of adjacent resting zone growth cartilage. This interruption occurs at the junction between cartilage and bone where anastomoses are formed between cartilage canal vessels and subchondral vessels.

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