Low-level laser irradiation, cyclooxygenase-2 (COX-2) expression and necrosis of random skin flaps in rats

Ivaldo Esteves Junior1, Igor B Masson, Celina T F Oshima

  • 1Department of Surgery, Division of Operative Technique and Experimental Surgery, Federal University of São Paulo - UNIFESP, São Paulo, SP, Brazil.

Lasers in Medical Science
|October 22, 2011
PubMed

Insights

Low-level laser therapy effectively reduced skin flap necrosis in rats by decreasing cyclooxygenase-2 (COX-2) expression. This study highlights laser irradiation as a promising method to improve flap viability in surgical procedures.

Area of Science:

  • Regenerative Medicine
  • Biomedical Engineering
  • Surgical Innovation

Background:

  • Skin flap necrosis remains a significant surgical complication.
  • Low-level laser irradiation (LLLI) shows potential for improving ischemic flap viability, but mechanisms are unclear.
  • Cyclooxygenase-2 (COX-2) is implicated in inflammatory and healing processes relevant to flap survival.

Purpose of the Study:

  • To investigate the efficacy of LLLI in reducing random skin flap necrosis in a rat model.
  • To determine the effect of LLLI on COX-2 expression in the flap pedicle.
  • To elucidate the potential mechanisms by which LLLI enhances flap viability.

Main Methods:

  • 24 Wistar rats underwent random skin flap creation and were divided into three groups: sham, LLLI (0.29 J), and LLLI (7.3 J).
  • LLLI was applied immediately post-surgery and repeated on days 2 and 5.
  • Necrotic area was measured on day 7, and COX-2 expression was assessed immunohistochemically.

Main Results:

  • The group treated with 7.3 J LLLI exhibited significantly smaller necrotic areas compared to sham and 0.29 J groups (P < 0.05).
  • COX-2 expression was significantly lower in the 7.3 J LLLI group compared to sham and 0.29 J groups (P < 0.001).
  • No significant difference in necrosis was observed between sham and 0.29 J groups.

Conclusions:

  • LLLI, particularly at 7.3 J per point, is effective in reducing random skin flap necrosis in rats.
  • LLLI at this dosage also decreases COX-2 expression in the flap pedicle.
  • These findings suggest LLLI may improve flap survival through modulation of inflammatory pathways involving COX-2.

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