Background: Chronic wounds are biochemically complex and are associated with insufficient cell proliferation, angiogenesis, and extracellular matrix remodeling. The mechanisms by which pulsed radiofrequency energy modulates wound healing are still unclear.
Methods: Db/db mice were wounded and exposed to pulsed radiofrequency energy. Gross closure, cell proliferation, and morphometric analysis of CD31-stained wound cross-sections were assessed. The mRNA expression of profibrotic factors (transforming growth factor-β and platelet-derived growth factor-A), angiogenetic factors (vascular endothelial growth factor and basic fibroblast growth factor), and extracellular matrix components (collagen I and α-smooth muscle actin) were evaluated by quantitative reverse-transcriptase polymerase chain reaction. Collagen protein level of the wound was determined by Western blot analysis. To test the effect of pulsed radiofrequency energy on cell movement in wound healing, cell migration was monitored in monolayer dermal fibroblast cultures. The degree of collagen alignment and gelation time was quantitatively assessed using image analysis techniques.
Results: Pulsed radiofrequency energy–treated wounds were characterized by dermal cell proliferation and increased collagen synthesis. By contrast, the CD31 density and the mRNA expression of vascular endothelial growth factor and basic fibroblast growth factor showed no significant difference between the pulsed radiofrequency energy–treated wounds and the sham group. The pulsed radiofrequency energy–treated dermal fibroblast cultures expressed a significantly longer gelation time compared with the sham-exposed cultures.
Conclusions: Exposing wounds to pulsed radiofrequency accelerated wound healing in this diabetic mouse model by means of significantly increasing dermal cell proliferation and collagen synthesis. A cellular mechanism behind these observations has been proposed.