Endochondral resorption of chick sterna in culture
- 1 July 1995
- journal article
- Published by Wiley in Journal of Orthopaedic Research
- Vol. 13 (4) , 542-552
- https://doi.org/10.1002/jor.1100130409
Abstract
Endochondral resorption is most clearly recognized at the metaphyseal interface of the growth plate with the adjacent vasculature: however, apparently identical processes of endochondral resorption are seen in sites of primary and secondary ossification of the cartilaginous anlage of bones and in ossifying fracture callus. Recent evidence of the expression of the hypertrophic phenotype in osteoarthrotic articular cartilage suggests that endochondral resorption also may be a factor in the loss of articular cartilage in this condition. To investigate the mechanism of endochondral resorption, a model culture system was developed and characterized. The two primary centers of ossification with surrounding cartilage were dissected from embryonic chick sterna prior to (18‐day‐old embryos) or after (20‐day‐old embryos) the initiation of resorption. They were cultured either in plastic culture dishes or on chorioallantoic membranes, and resorption was detected by analysis of the loss of types II and X collagen and by histological characterization. Only sterna showing active resorption in vivo were resorbed when cultured on chorioallantoic membrane. The histological appearance of the resorption site and the specificity of resorption to the primary ossification center, seen from both the analysis of loss of collagen and histological observation, suggested that the resorption of sterna cultured on chorioallantoic membrane was similar to that observed in vivo. These studies further indicated that both vascular cells and viable chondrocytes were required for resorption. Susceptibility to resorption could be induced in resistant primary ossification centers by prior culture in the absence of vascular cells, and it is suggested that it results from the accumulation of resorption‐susceptible cells and matrix as a result of continued chondrocyte development.Keywords
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