Abstract
Dear Editor,
The authors discussed the effect of low-level laser therapy (LLLT) in two different rat experimental models. 2,3 In both, the restorative actions of LLLT were tested, as the therapy was accomplished after the tissue damage. In one lesion, the injury was achieved in muscle tissues and, as a result, there was a better preservation of the tissue architecture and, subsequently, a more effective injury resolution with subsequent regeneration. In our model of renal injury, the animals were subjected to unilateral ureteral obstruction, which was maintained during the study. Without any treatment, the expected answer in the kidney after unilateral ureteral obstruction is characterized by a chronic inflammation, widespread tissue fibrosis, and upregulation of fibrosis mediators. Our results showed an attenuation of the three major aspects of the injury. We could see less fibrosis, decreased expression of inflammation, and pro-fibrosis mediators (monocyte chemotactic protein-1 [MCP-1], interleukin 6 [IL-6], and SMAD3). We did not specifically evaluate tubular cell regeneration, because considering the nature of the lesion, which is very intense and destructive, it is significant to achieve even a decreased fibrosis.
Those two kinds of effects on rat fibrosis do not seem to be different. LLLT is now used to treat a wide variety of ailments, 4 –6 and the therapeutic effect of LLLT in these diseases is very similar when analyzed from the primary or biochemical viewpoint. The irradiation parameters and the irradiation time, adjusted individually, define the therapeutic effects performed successfully in different organs and tissues. 7,8 Specifically, in regeneration of injured muscle after rat muscular contusion or rat muscular cryolesion, the selected irradiation probably prevented oxidative stress, decreasing inflammation and reducing or inhibiting fibrosis formation, independent of the irradiated tissue. 4,5
The molecular and cellular mechanisms of LLLT suggest that photons are absorbed by the mitochondria; they stimulate more adenosine triphosphate (ATP) production, subsequently lowering the levels of reactive oxygen species (ROS), which in turn activate transcription factors to induce many gene transcript products responsible for the beneficial effects of LLLT. 7,8 However, when the dose parameters are used incorrectly, without knowledge of the pathophysiology of the model studied, to establish the ranges of laser application, the effects may be similar to those of placebo, or may even be negative. Another important variable related to this process is the time of the treatment. After an acute insult or during a chronic lesion, many tissue mechanisms are activated to limit the damage. Each tissue and each injury seems to bring its own orchestrated sequence of events—inflammatory, regenerative, or only restorative. The nature of the injury, mainly the degree of damage, the specific ability of the tissue to regenerate, the extension of damage, measured by the acute or chronic nature of the insult and also the time the LLLT is given, are all determinants of the potential benefit. 9 That means if LLLT is used early, or before the injury, it could result in a better outcome, with more preserved tissue. Or if the treatment is delayed, the best result is, at least, less fibrosis.
As an example, Oron et al. 5 demonstrated that elevated antioxidant activity of LLLT in the dog ischemic myocardium was probably one of the mechanisms inhibiting cardiomyocyte degeneration and asserting a cardioprotective effect on these cells in the ischemic zone. Thus, the antioxidant effect of laser, in addition to reducing or inhibiting the development of the inflammatory process, also activated specialized cells in the tissue, increasing their survival in the injured zone. When compared with celecoxib, laser shows, when handled properly, better results in tissue repair.
Therefore, these findings suggest that LLLT acts by modulating the stress oxidative and inflammatory processes, and subsequent tissue regeneration. Therefore, LLLT-treated tissue may respond better to injury, thereby making its repair more structured, in a different manner.