ABSTRACT

Applications of low-level laser therapy (LLLT) on muscle skeletal

disorders are probably higher than any other type of laser therapy

applications in health sciences. This is easily visible from the dose

table of the World Association for Laser Therapy (WALT). This

dose table adresses different irradiation protocols according to the

lesion area, which was only described referring to muscle skeletal

disorders, and among them, the rheumatoid arthritis. Although a

reasonable number of studies show the anti-inflammatory effect

of LLLT in a variety of arthritis animal models induced for

different pathways, there is no action mechanism for describing

exactly what cellular signaling is responsible for low-level laser

effects. In fact, diverse authors have found different cellular

mechanisms for describing the beneficial effects of LLLT. This does

not mean that experimental designs from studies with animal

model for arthritis have been poorly delineated; the viewpoint is

that LLLT reveals different signaling pathways according to the

inflammatory environment. For this reason, an increasing number

of authors have reported that instead of LLLT reducing all chemical

mediators of inflammatory process similar to what happens in

treatment with glucocorticoid, laser therapy can modulate the pro-

inflammatory response, increasing both the mRNA expression and

the protein concentration of anti-inflammatory mediators such

as IL-10 (tendinitis model) and heat shock protein-72 (HSP72)

(chondrocytes in rheumatoid arthritis). Thus, these effects suggest

that LLLT, in models of joint inflammation, acts as a homeostasis

regulator to maintain balance between anti-and pro-inflammatory

responses. Naturally, experimental studies reported in this chapter

deserve caution when extrapolated to cellular response in humans.

However, these different signals responsible for laser effect on

rheumatoid arthritis have an important role in the process for

understanding the laser therapy effect in clinical trials as well as the

adjustment of better dosimetry to be used. Another important point

is the resemblance between animal models and clinical symptoms

of rheumatoid arthritis observed in humans. Surely, this gives

reason for trusting experimental results. Moreover, regardless of

the method used to induce rheumatoid arthritis (auto-immune or

septic) in animal models, a majority of studies describe that LLLT

is efficient in attenuating at least one of the symptoms of joint

inflammation without producing any side effect.