ABSTRACT
Tissue repair is an excellent example of pathophysiological model for studying the role of cyclooxygenase-2 (COX-2) on eukaryotic cells. It has been established that two COX isoforms are expressed in human tissues: constitutive or induced. COX-1 activity is constitutive, present in nearly all cell types at a constant level; COX-2 activity is normally absent from cells, and when induced, the protein levels increase and decrease in a matter of hours after a single stimulus. Thus, the purpose of this review was to describe the role of COX-2 during tissue repair induced by low level laser therapy (LLLT) in humans and experimental models. COX-2 expression has been implicated in the onset or the exacerbation of inflammation during tissue repair induced by LLLT in a number of studies, Many studies are conducted to investigate the role of COX-2 during tissue repair induced by LLLT using different experimental protocols and dosages. Therefore, this is an area that warrants investigation, since the estimation of COX-2 expression from using such important techniques in therapeutics with respect to tissue repair will be added to those already established in the literature as a way to improve health status and prevention of side effects.
Subject(s)
Cyclooxygenase 2/metabolism , Low-Level Light Therapy/adverse effects , Rejuvenation/physiology , Wound Healing/physiology , Animals , Cyclooxygenase 1/metabolism , Humans , Inflammation/metabolism , Inflammation Mediators/metabolism , RatsABSTRACT
Skin flaps are still a matter of concern among surgeons, as failures can occur leading to flap necrosis. However, low-level laser irradiation has been reported as an effective tool to improve the viability of ischemic flaps, yet its mechanisms of action remain unclear. We investigated the effect of low-level laser irradiation on the viability of random skin flaps in rats and determined COX-2 expression in the flap pedicle. The study animals comprised 24 EPM-1 Wistar rats which were randomly allocated into three equal groups. A cranially based dorsal random skin flap measuring 10 × 4 cm was created in all the animals. In one group, laser irradiation was simulated (sham group), and in the other two groups the animals were irradiated at 12 points with 0.29 J at 20 mW (energy density 10.36 J/cm(2), irradiance 0.71 W/cm(2)), or with 7.3 J at 100 mW (energy density 260.7 J/cm(2), irradiance 3.57 W/cm(2)). These procedures were applied to the cranial half of the flap immediately after surgery and were repeated on days 2 and 5 after surgery. The percentage necrotic area was determined on day 7 after surgery by the paper template method. The immunohistochemical expression of COX-2 in the samples was given scores from 0 to 3. The necrotic area was smaller in group irradiated at 7.3 J compared to sham-treated group and to the group irradiated at 0.29 J (P < 0.05); there was no difference between the sham-treated group and group irradiated at 0.29 J. COX-2 expression was lower in the group irradiated at 7.3 J than in the sham-treated group and the group irradiated at 0.29 J (P < 0.001). Low-level laser therapy was effective in decreasing random skin flap necrosis in rats using a laser energy of 7.30 J per point. Laser irradiation also decreased the expression of COX-2 in the flap pedicle.
