Although the etiology of osteoarthritis (0A) may differ, the outcome is the same: degeneration of joint tissues, characterized by the loss of articular cartilage. In addition, it is established that articular cartilage has a limited repair/regeneration potential in the normal joint as well as once the 0A process has begun. Two important elements may contribute to the long-term joint failure: the milieu of cytolines in the degenerating joint and their effects on cartilage and the poor regenerative capacity of the cartilage cells themselves. We propose to experimentally alter these two parameters by genetically manipulating cells with cartilage regenerative capacity, so that they also produce molecular agents that inhibit the degenerative 0A process and stimulate the reparative process. The hypothesis to be tested is that with the continuous introduction of specific bioactive factor(s), it will be possible to optimize cartilage regeneration and stop cartilage degeneration. Two independent groups of researchers have joined together for this endeavor: the CWRU group has extensive experience in the rabbit 0A model and in the use of reparative cells to repair articular cartilage and bone in the joint. The University of Pittsburgh group has wide experience in gene transduction into connective tissue cells. The first specific aim of this proposal is to optimize the transduction of cartilage reparative cells with cytokine genes. The second aim is to introduce cells with the appropriate transgene into full-thickness defects and the third aim is to introduce the appropriate cell into the 0A joint under conditions either including full-thickness defect repair or not. The overall objective is to modify the degenerative ambiance of the 0A joint while cartilage regeneration/repair is being effected by implantation of reparative cells.
|Effective start/end date||9/25/95 → 8/31/00|
- National Institutes of Health: $195,116.00
- National Institutes of Health: $198,185.00
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