Chondrocyte outgrowth into a gelatin scaffold in a single impact load model of damage/repair - effect of BMP-2
Vincent, Thea A
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Henson, F., & Vincent, T. A. (2007). Chondrocyte outgrowth into a gelatin scaffold in a single impact load model of damage/repair - effect of BMP-2. https://doi.org/10.1186/1471-2474-8-120
Abstract Background Articular cartilage has little capacity for repair in vivo, however, a small number of studies have shown that, in vitro, a damage/repair response can be induced. Recent work by our group has shown that cartilage can respond to single impact load and culture by producing repair cells on the articular surface. The purpose of this study was to identify whether chondrocyte outgrowth into a 3D scaffold could be observed following single impact load and culture. The effect of bone morphogenic-2 (BMP-2) on this process was investigated. Methods Cartilage explants were single impact loaded, placed within a scaffold and cultured for up to 20 days +/- BMP-2. Cell numbers in the scaffold, on and extruding from the articular surface were quantified and the immunohistochemistry used to identify the cellular phenotype. Results Following single impact load and culture, chondrocytes were observed in a 3D gelatin scaffold under all culture conditions. Chondrocytes were also observed on the articular surface of the cartilage and extruding out of the parent cartilage and on to the cartilage surface. BMP-2 was demonstrated to quantitatively inhibit these events. Conclusion These studies demonstrate that articular chondrocytes can be stimulated to migrate out of parent cartilage following single impact load and culture. The addition of BMP-2 to the culture medium quantitatively reduced the repair response. It may be that the inhibitory effect of BMP-2 in this experimental model provides a clue to the apparent inability of articular cartilage to heal itself following damage in vivo.
External DOI: https://doi.org/10.1186/1471-2474-8-120
This record's URL: http://www.dspace.cam.ac.uk/handle/1810/237998
Rights Holder: Henson et al.; licensee BioMed Central Ltd.