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Journal of Bone and Joint Surgery - British Volume, Vol 87-B, Issue 1, 128-134.
doi: 10.1302/0301-620X.87B1.14154  
Copyright © 2005 by British Editorial Society of Bone and Joint Surgery
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Autologous chondrocyte implantation

CULTURE IN A TGF-ß-CONTAINING MEDIUM ENHANCES THE REEXPRESSION OF A CHONDROCYTIC PHENOTYPE IN PASSAGED HUMAN CHONDROCYTES IN PELLET CULTURE

A. J. Goldberg, FRCS, Specialist Registrar1; D. A. Lee, PhD, Senior Lecturer2; D. L. Bader, PhD, Professor of Mechanical Engineering2; and G. Bentley, ChMFRCS, Professor of Orthopaedic Surgery1

1 Interdisciplinary Research Centre, Institute of Orthopaedics, Royal Free & University College Medical School, Brockley Hill, Stanmore, Middlesex HA7 4LP, UK.
2 Medical Engineering Division and IRC in Biomedical Materials, Department of Engineering, Queen Mary, University of London, Mile End Road, London E1 4NS, UK.

Correspondence should be sent to Mr A. J. Goldberg.

An increasing number of patients are treated by autologous chondrocyte implantation (ACI). This study tests the hypothesis that culture within a defined chondrogenic medium containing TGF-ß enhances the reexpression of a chondrocytic phenotype and the subsequent production of cartilaginous extracellular matrix by human chondrocytes used in ACI. Chondrocytes surplus to clinical requirements for ACI from 24 patients were pelleted and cultured in either DMEM (Dulbecco’s modified eagles medium)/ITS+Premix/TGF-ß1 or DMEM/10%FCS (fetal calf serum) and were subsequently analysed biochemically and morphologically.

Pellets cultured in DMEM/ITS+/TGF-ß1 stained positively for type-II collagen, while those maintained in DMEM/10%FCS expressed type-I collagen. The pellets cultured in DMEM/ITS+/TGF-ß1 were larger and contained significantly greater amounts of DNA and glycosaminoglycans. This study suggests that the use of a defined medium containing TGF-ß is necessary to induce the re-expression of a differentiated chondrocytic phenotype and the subsequent stimulation of glycosaminoglycan and type-II collagen production by human monolayer expanded chondrocytes.




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