The role of inflammation in chronic tendinopathy has been a topic of great controversy. While inflammatory cells have been observed in clinical discards, it is unclear whether inflammation plays any role in the pathogenesis or the attempted (albeit ineffective) repair response of tendinopathy. Inflammation is a necessary first step in healing any type of injury; it is during this stage that circulating inflammatory cells are recruited to the injury site to clear debris, phagocytose dead cells, degrade damaged ECM, and recruit fibroblasts. In chronic injuries, there is some low-level molecular inflammation at onset of injury, though it is not significant enough to trigger the remainder of the healing cascade, which partially explains the lack of repair seen in these injuries. Inducing cell necrosis in tendon will result in heightened recruitment of macrophages and will yield more effective repair in the absence of matrix damage, as matrix damage creates a catabolic environment that stifles the inflammatory response and impedes the healing cascade. We are investigating the potential role and therapeutic potential of modulating inflammation in tendinopathy using various approaches.
Graduate Researchers
Diane Stonestreet