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Research article2004Peer reviewed

Focal changes in blood supply during normal epiphyseal growth are central in the pathogenesis of osteochondrosis in pigs

Ytrehus B, Ekman S, Carlson CS, Teige J, Reinholt FP


Cartilage canals are temporary vessel-containing structures within the growth cartilage. The canals gradually regress with age in a process designated 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 and relationship between chondrification of cartilage canals and the initial steps in the pathogenesis of osteochondrosis with respect to morphology, presence of factors influencing the processes, and mode of cellular death. The articular-epiphyseal cartilage complexes of the distal femur of 48 pigs were studied, combining a technique of perfusion and tissue clearing with histological and immunohistological methods. The results provided strong evidence that the process of chondrification occurs at the terminations of the cartilage canals and is characterized by disintegration of the endothelial cells and transformation of perivascular cells into matrix-producing chondrocytes. Lesions of osteochondrosis, however, 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 of the cartilage canal blood supply occurs at the junction between cartilage and bone where anastomoses are formed between cartilage canal vessels and vessels from the bone marrow. It is possible that microfractures occurring secondary to minor trauma at a vulnerable time in the development of the cartilage may be the initial event in pathogenesis of osteochondrosis. (C) 2004 Elsevier Inc. All rights reserved


Cartilage canals; Osteochondrosis; Pigs; VEGF; Apoptosis

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2004, Volume: 35, number: 6, pages: 1294-1306

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