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.