A central role for synovial inflammation and inflammatory pathway activation in mediating the effects of biomechanical joint injury has been implicated in post-traumatic OA.  We have taken a bedside-to-bench approach to focus our preclinical work on mechanisms relevant to human disease. Our lab has identified several pathways and mediators associated with synovial pathology, macrophage activation, and pain in patients with OA, including chemokine and Toll-like receptor-mediated pathways. We are now exploring a functional role for these pathways on structural and symptomatic outcomes, including structural and functional joint degeneration and joint pain-related behavior in preclinical models. In these studies, we aim to better understand the inflammatory response to joint tissue injuries resulting from a variety of insults, and in doing so understand the factors that allow the post-injury inflammatory response to become chronic, perpetuating chronic joint pain and degeneration.  We anticipate that these investigations will be applicable not only to OA, but to a broad range of musculoskeletal disorders characterized by tissue injury, chronic inflammation, and pain. The ultimate goal of the laboratory is to get back to the bedside, by developing novel targeted approaches to modulate the inflammatory environment of the joint to prevent arthritis development after a joint injury and to treat existing OA.

Current Openings:

We currently have positions available for a research assistant and a postdoctoral fellow.   

If interested, please contact Dr. Scanzello at cscanz@pennmedicine.upenn.edu.