Tendinitis,an Open Avenue for Low-Level Laser Therapy

Abstract

The incidence of tendon injuries has increased significantly in recent decades as a result of greater citizen participation in recreational and competitive physical activities. It is estimated that these injuries comprise 50% of all injuries related to sports. Tendinopaties are clinical disorders mostly characterized by pain and swelling in and around the tendon, thus affecting movement and body biomechanics. It is important to note that pain is the main symptom, but the causative mechanism is not yet fully understood. There may be a relationship with inflammation at least in the acute stages, which is possibly caused by breaks in the collagen fibers and crosslinks, or which may arise from a combination of other mechanical and biochemical causes.

Among several risk factors that may predispose to tendinopaties, we can mention gender (more frequent in men), aging, overweight, lack of flexibility, discrepancy in the size of the limbs, joint laxity, and postural changes. Other risk factors described, especially in cases of rupture of the tendon, are the use of antibiotics such as quinolones,¹ and the use of local or systemic corticosteroids,² as well as familial hypercholesterolimia.

Several therapies have been used with the aim of relieving pain and discomfort and promoting improved function of the affected tissue, but the first step after diagnosis is to identify the cause of the injury and the factors that may be involved, so as to avoid the risk of recurrence. The current available treatments includes drug therapy, phototherapy, cryotherapy, ultrasound therapy, stretching, and eccentric exercises, among others.

Animal studies evaluating the effects of anti-inflammatory drugs in tendon repair have been performed since the 1970s. Over the years, many studies have been conducted, but the results found in the literature are conflicting. It is possible that these differences are connected with the wide range of drugs used, dosage, time of treatment, the animal species used, and the site of injury.

In a review of the literature, it seems clear that use of nonsteroidal anti-inflammatory drugs (NSAIDs) for a short period, and physiotherapy sessions, are the first line of treatment for tendinopaties. However, Rees et al.³ describe that despite being widely used, there is little scientific evidence evaluating the efficacy of this class of anti-inflammatory agents in the repair of tendon injury, particularly injury of the calcaneous tendon.

Steroidal anti-inflammatory drugs, or corticosteroids, also represent a class of drugs with wide application in the treatment of painful musculoskeletal injuries, because they are supposed to promote the temporary relief of pain. Their use seems to pose no long-term benefits and may lead to reduction in strength of the treated tendon structure.⁴ The anti-inflammatory action of these drugs may interfere with the repair of the collagen fibers and reduce the tensile strength, thus having negative effects on the tendon. Despite the risks already reported, corticosteroids are used indiscriminately today. There is no doubt that the adverse effects of corticosteroids on tendon cells may affect the responses of tendon injuries to repair.

Therapy with low-level laser (LLLT) has been used in the treatment of tissue damage and inflammatory processes since the 1960s; however, it was in the 1980s that the first reports were published of its beneficial effects on tendon injuries and other overload disorders triggered by physical activity.⁵

Two important biological responses have been reported in clinical studies⁶ as possible mechanisms responsible for the beneficial effects of LLLT on tendon injuries, The first hypothesis is a dose-dependent stimulation of the metabolism of fibroblasts and deposition of collagen. This response has been observed in a variety of controlled cell culture studies and animal studies. The second mechanism is similar to the actions of NSAIDs and steroidal anti-inflammatories, by attenuating inflammation by inhibition of cyclooxygenase-2 enzyme and the resulting reduction in the concentration of prostaglandin E2 (PGE2).^7,8 In addition to these effects, Enwemeka et al.⁹ report that certain laser irradiation doses enhance fibroblast proliferation and increase the release of fibroblast growth factor (FGF). Thus, this effect may act by promoting the balance between production of extracellular matrix (ECM) degradation, culminating in the healing of the injured tendon. Through a meta-analysis, Enwemeka et al.¹⁰ found that phototherapy could produce beneficial responses in injured areas, through the proliferation of fibroblasts and increasing collagen synthesis, which again increases the tensile strength of the tendon. This fact seems to justify the large number of studies with laser and the increasing popularity among clinicians of LLLT in the treatment of musculotendinous injuries.

Bjordal et al.,⁷ in a randomized placebo-controlled clinical study, concluded that laser irradiation of low intensity with a dose of 5.4 J per point reduced the concentration of PGE2 and increased the local pain threshold in individuals with Achilles tendinopathy. Stergioulas et al.¹¹ reported that LLLT associated with a program of eccentric exercises for 12 weeks reduced pain and crepitus during palpation, besides increasing pain-free dorsiflexion of the ankle joint. According to Marcos et al.,⁸ a LLLT dose of 3 J significantly reduced inflammation through decreased cyclooxygenase (COX)-2-derived gene expression and PGE2 production, and less edema formation than unirradiated controls. Diclofenac controls exhibited significantly lower PGE2 cytokine levels. As LLLT seems to act on inflammation through a selective inhibition of the COX-2 isoform in collagenase-induced tendinitis, LLLT may have the potential to become a new and safer non-drug alternative to COX-2 inhibitors (coxibs).

LLLT significantly decreases COX-2, tumor necrosis factor (TNF)-α, matrix metalloproteinase (MMP)-3, MMP-9, and MMP-13 gene expression, as well as PGE2 production in experimental models. Interestingly, diclofenac treatment only decreased PGE2 levels, but not the other cytokines. Biomechanical properties were preserved in the LLLT-treated groups when compared with untreated tendons and diclofenac-treated tendons. In the same context, LLLT-treated tendons preserved resistance and elasticity of the structure.¹²

According to Marcos et al.,¹³ treatment by NSAIDS such as diclofenac sodium only produces a small protective effect, which can affect the short-term biochemical and biomechanical properties. On the contrary, it was also shown that LLLT exhibits the best results in terms of MMP reduction and mechanical property recovery.

Therefore, we consider that there is an open field for promising research in LLLT as a consistent treatment for tendinopathies.

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