The overarching goal of our research program is to identify novel strategies to improve flexor tendon healing by reducing the formation of range of motion (ROM) limiting adhesions, without compromising mechanical strength. Flexor tendons glide through a synovial sheath to facilitate digit ROM and movement of the hand. Following injury, up to 40% of primary flexor tendon repairs will heal with unsatisfactory outcomes. The primary complication involves a robust scar tissue response, which forms adhesions between the tendon and synovial sheath, resulting impaired gliding function.
We have developed a novel murine model of intrasynovial FT healing, which mimics many aspects of healing in humans including abundant adhesion formation, impaired ROM and early decrements in tendon strength. We continue to use this model to gain a greater understanding of the cell and molecular processes involved in scar and adhesion formation in order to identify therapeutic targets to improve FT healing