Pulsed radiofrequency energy accelerates wound healing in diabetic mice. Academic Article uri icon

Overview

abstract

  • BACKGROUND: Impaired healing is a problematic and common complication of chronic wounds. Although pulsed radiofrequency energy has been used in the treatment of chronic wounds with promising efficacy, its mechanism is still poorly characterized. In this study, the authors used a diabetic mouse model to illustrate the action of pulsed radiofrequency energy on cutaneous wounds and set the stage to begin to understand its mechanism. METHODS: Full-thickness cutaneous wounds were created in diabetic mice (n = 26). The experimental group (n = 13) was subject to pulsed radiofrequency energy treatment two times per day, whereas the sham group (n = 13) was subjected to sham devices. The rate of wound closure was evaluated by digital analysis of surface area of the wound bed, zone of reepithelialization, and rate of contraction. Mice were euthanized on days 7, 10, 22, and 42 and wounds were evaluated qualitatively and quantitatively by hematoxylin and eosin, Masson's trichrome, and Ki-67 assay for cell proliferation. RESULTS: In the experimental group, the rate of wound closure was significantly accelerated, particularly beyond day 17. Contraction contributed to the wound healing process rather than reepithelialization. This was also associated with increased granulation tissue that was most prominent by day 22 and with enhanced dermal cell proliferation, with 25 percent and 45 percent Ki-67-positive nuclei on days 10 and 22, respectively, as compared with control animals. CONCLUSION: These results indicate that pulsed radiofrequency energy accelerates impaired wound healing mainly through wound contraction by means of stimulating cell proliferation, granulation tissue formation, and collagen deposition.

publication date

  • June 1, 2011

Research

keywords

  • Diabetes Mellitus, Experimental
  • Radiofrequency Therapy
  • Skin
  • Wound Healing

Identity

Scopus Document Identifier

  • 79958717526

Digital Object Identifier (DOI)

  • 10.1097/PRS.0b013e3182131bb5

PubMed ID

  • 21311391

Additional Document Info

volume

  • 127

issue

  • 6