An introduction to the regulation of wound healing by micromechanical forces

It is widely acknowledged that exudate from non-healing wounds contains elevated levels of proteases, such as matrix metalloproteinases and polymorphonuclear elastase (Barrick et al, 1999; Trengove et al, 1999; Yager and Nwomeh, 1999). The excessive action of these proteases leads to considerable reduction in growth factors (He et al, 1999) and proteinase inhibitors; cleavage of matrix components, such as collagens, elastin and fibronectin, and, consequently, to the destruction of the extracellular matrix (ECM; Yager and Nwomeh, 1999). In addition, markedly increased levels of proinflammatory cytokines are released by macrophages and granulocytes in non-healing wounds (Harris et al, 1995) and chronic wounds have comparatively higher concentrations of reactive oxygen and nitrogen species than acute wounds (James et al, 2003). As a consequence, these wounds are trapped in the inflammatory phase and often do not heal for months or even years. It has been suggested that changing the mostly destructive state of chronic wounds to a more physiological wound milieu could re-establish the structural requisites for normal cell proliferation, migration and differentiation and would move the wound towards healing. A literature review was conducted to find and summarise relevant research on micromechanical forces and microdeformation related to wound healing. The following electronic databases were searched: CINHAL, the Cochrane Central Register of Controlled Trials, the Cochrane Database of Systematic Reviews, the Database of Abstracts of Reviews of Effects, Health Technology Assessments, National Health Service Economic Evaluation, Embase, Ovid Medline and PubMed.