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Research article2004Peer reviewedOpen access

Experimental ischemia of porcine growth cartilage produces lesions of osteochondrosis

Ytrehus B, Haga HA, Mellum CN, Mathisen L, Carlson CS, Ekman S, Teige J, Reinholt FP

Abstract

Osteochondrosis is a disorder of growth cartilage in which a focal failure of blood supply has been proposed as an important initiating factor. In the present study we investigated the effect on epiphyseal growth cartilage of experimentally interrupting the blood supply to a limited area of the distal femur of growing pigs. In 12 pigs, a thin full-thickness cartilage slab was removed from the abaxial margin of the medial condyle, thereby transecting a limited number of cartilage canals. The pigs were culled 1, 2, 3, 7, 14, 21 and 29 days post-surgery. The condylar cartilage was studied histologically, immunohistologically and by use of the TUNEL method. The transection induced cellular death of cartilage canal elements followed by cellular death of chondrocytes within the deep layers of the resting zone of the epiphyseal growth cartilage. However, in the superficial layers of the resting zone, chondrocytes appeared to proliferate into and subsequently chondrify some of the necrotic cartilage canals. The dying and dead cells were TUNEL-positive, but active caspase 3-negative. The loss of vascular supply induced increased VEGF-immunostaining in chondrocytes surrounding the affected area. We conclude that transection of cartilage canals produces chondronecrosis in the deep resting zone of the epiphyseal growth cartilage similar to that observed in spontaneously occurring osteochondrosis. (C) 2004 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved

Keywords

ischemia; porcine growth cartilage; lesions; osteochondrosis

Published in

Journal of Orthopaedic Research
2004, Volume: 22, number: 6, pages: 1201-1209
Publisher: ELSEVIER SCI LTD

    Publication identifier

    DOI: https://doi.org/10.1016/j.orthres.2004.03.006

    Permanent link to this page (URI)

    https://res.slu.se/id/publ/5432