Mechanistic model of wound contraction.

The interplay between cellular, biochemical, and biomechanical phenomena which result in wound contraction is examined with the aid of a mathematical model. The model accounts for fibroblasts repopulating the wound extracellular matrix (ECM) by a combination of migration and proliferation and, in the course of exerting traction forces associated with their motility, their deformation of the local ECM, which has a viscoelastic character. A base model, which assumes that cell and tissue properties are the same irrespective of position with respect to the wound center, is found to be inconsistent with wound contraction. Extensions of the base model which account for the possible influence of a concentration gradient of an inflammation-derived mediator on the traction, growth, or chemotactic properties of the fibroblasts do predict the qualitative features of a contracting wound. In particular, the case where traction is prescribed to increase as fibroblasts approach the wound center is shown to obey the commonly observed exponential rate contraction law and to be largely consistent with the findings of McGrath and Simon (Plast. Reconstr. Surg. 72, 66, 1983) concerning the independence of the contraction rate constant and final extent of contraction from initial wound size and geometry.