Fibrosis is a major cause of loss of organ function and death. Fibrosis, the excessive deposition of scar tissue, is hallmark of connective tissue diseases such as scleroderma and osteoarthritis. Moreover, fibrosis is a major cause of complications resulting from arthroplasty. All of these processes have a significant result on mobility and pain, but can also result in deaths. Our objective is to identify the cell types specifically responsible for fibrosis and to develop methods of altering the local microenvironment to block and reverse the fibrotic process. Specifically, we are focusing on how resident mesenchymal cells and mesenchymal precursors show highly reactive adhesive signaling and how this process modifies responses to growth factors and the surrounding extracellular matrix to generate fibrogenic responses and scar tissue.