Bibliographical noteFunding Information:
IT IS well-established that damaged articular cartilage has only a limited ability to repair itself \[1\]. Recently, Brittburg et al. reported the treatment of full-thickness articular defects in the human knee by transplantation of cultured autologous chondrocytes \[2\].T his work was an extension of animal studies involving the transplantation of chondrocytes or their progenitors into similar defects \[3-11\]. However, the success of all of these techniques has been variable, and limited in that none were able to demonstrate long-term repair of the damaged cartilage with tissue that was histologically, biochemically, and biomechanically identical to normal cartilage. Several cytokines, including transforming growth factor ~-1 (TGF-~I) and insulin-like growth factor-1 (IGF-1), have been found to play significant roles in promoting chondrocyte anabolism and inhibiting chondrocyte catabolism (reviewed in \[12\]).T hus, the presence of one or more of these cytokines during repair may be the key to regenerating normal cartilage \[3\]H. owever, sustained delivery of sufficient quantities of a cytokine(s) to transplanted cells bound within a three-dimensional matrix would be difficult and impractical using conventional methods. Gene therapy offers an elegant solution to this delivery problem \[13\]B. y introducing an exogenous gene(s) into cells prior to transplantation, a therapeutic cytokine(s) may be expressed in vivo at Received 25 June 1996; accepted 3 October 1996. Supported, in part, by the Ferguson Foundation and NIH Grant PO1 DK44935 Address correspondence to: C. H. Evans, Ph.D, 986 Scaife Hall, Ferguson laboratory, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, U.S.A.
- cartilage injury
- gene therapy