Tendon injury can occur from activity-induced overuse, complete laceration or aging-related degeneration and these injuries commonly fail to wound heal without clinical treatment. Moreover, activity-induced overuse accounts for approximately half of all sports injuries and has highest occurrence rates in athletes playing football, baseball and basketball. Current non invasive technique to rest and ice the damaged tissue in combination with either oral NSAIDS or corticosteroid injections has shown little promise with only ~60% of cases regaining functionality of the tendon (Paterno et al., 2013).

From the literature, this seems to be caused by a combination of poorly perfused tissue along with a lack of cellular control throughout the inflammatory and remodeling phases of wound healing. Because of this, new generations of experimental therapies involve implementing a cocktail of growth factors and cytokines in an effort to control and perhaps expedite the wound healing process. In order for this approach to become clinically effective, improvements must be made in our understanding of TIMP-MMP-COL interaction as well as chemokine-induced differentiation of involved macrophages (Morita et al., 2017; Martinez et al., 2014). This thesis considers the differential gene expressions between healthy and diseased tendons for further insight into tendon pathophysiology and possible improvements in therapeutic approach.