The vacuum-assisted closure device is widely used clinically, yet its mechanisms of action are incompletely understood. In this study, the authors designed a partially splinted full-thickness murine vacuum-assisted closure model to better understand the mechanism of action of the vacuum-assisted closure device.
Full-thickness wounds (n = 10 per group) were excised in diabetic mice and treated with the vacuum-assisted closure device or its isolated components: an occlusive dressing, subatmospheric pressure at 125 mmHg (suction), and a polyurethane foam without and with downward compression. Results were quantified with a two-dimensional immunohistochemical staging system based on blood vessel density (CD31) and cell proliferation (Ki67) 7 days after wounding. Microscopic strain was measured by fixing in situ all dressing modalities.
Wounds exposed to polyurethane foam in compressed and uncompressed dressings or to the vacuum-assisted closure device showed a 2-fold increase in vascularity compared with the occlusive dressing group (p < 0.05). The vacuum-assisted closure device in addition stimulated cell proliferation, with up to 82 percent Ki67-positive nuclei, compared with the other groups. Direct measurements of wound surface deformations showed significant microstrains in the vacuum-assisted closure and foam in compressed dressing groups (60 percent and 16 percent, respectively) compared with all other groups.
These data provide profound insights into the mechanism of action of the vacuum-assisted closure device, providing an explanation for the increases in wound bed vascularity and cell proliferation based on its components. Results suggest that the vascular response is related to the polyurethane foam, whereas tissue strains induced by the vacuum-assisted closure device stimulated cell proliferation.