Mechanical forces, such as tension on a wound closure, have long been suspected to play a critical role in scar formation but the precise mechanisms by which this occurs remains poorly understood. Recent studies have demonstrated that mechanical forces activates hundreds of different pathways leading to increased inflammation and fibrosis. Our laboratory has identified a critical role for fibroblast specific focal adhesion kinase (FAK) in the development of hypertrophic scars. Blocking FAK mediated mechanical signaling by device or pharmacologic approaches is able to prevent hypertrophic scar formation in humans.
