The mechanism of action of the Vacuum Assisted Closure Therapy (VAC; KCI, San Antonio, Texas), a recent novel innovation in the care of wounds, remains unknown. In vitro studies have revealed that cells allowed to stretch tend to divide and proliferate in the presence of soluble mitogens, whereas retracted cells remain quiescent. The authors hypothesize that application of micromechanical forces to wounds in vivo can promote wound healing through this cell shape-dependent, mechanical control mechanism. The authors created a computer model (finite element) of a wound and simulated VAC application. Finite element modeling is commonly used to engineer complex systems by breaking them down into simple discrete elements. In this model, the authors altered the pressure, pore diameter, and pore volume fraction to study the effects of vacuum-induced material deformations. The authors compared the morphology of deformation of this wound model with histologic sections of wounds treated with the VAC. The finite element model showed that most elements stretched by VAC application experienced deformations of 5 to 20 percent strain, which are similar to in vitro strain levels shown to promote cellular proliferation. Importantly, the deformation predicted by the model also was similar in morphology to the surface undulations observed in histologic cross-sections of the wounds. The authors hypothesize that this tissue deformation stretches individual cells, thereby promoting proliferation in the wound microenvironment. The application of micromechanical forces may be a useful method with which to stimulate wound healing through promotion of cell division, angiogenesis, and local elaboration of growth factors. Finite element modeling of the VAC device is consistent with this mechanism of action.