Low-level laser therapy in collagenase-induced Achilles tendinitis in rats: analyses of biochemical and biomechanical aspects

J Orthop Res. 2012 Dec;30(12):1945-51. doi: 10.1002/jor.22156. Epub 2012 Jun 5.


NSAIDs are widely prescribed and used over the years to treat tendon injuries despite its well-known long-term side effects. In the last years several animal and human trials have shown that low-level laser therapy (LLLT) presents modulatory effects on inflammatory markers, however the mechanisms involved are not fully understood. The aim of this study was to evaluate the short-term effects of LLLT or sodium diclofenac treatments on biochemical markers and biomechanical properties of inflamed Achilles tendons. Wistar rats Achilles tendons (n = 6/group) were injected with saline (control) or collagenase at peritendinous area of Achilles tendons. After 1 h animals were treated with two different doses of LLLT (810 nm, 1 and 3 J) at the sites of the injections, or with intramuscular sodium diclofenac. Regarding biochemical analyses, LLLT significantly decreased (p < 0.05) COX-2, TNF-α, MMP-3, MMP-9, and MMP-13 gene expression, as well as prostaglandin E(2) (PGE(2) ) production when compared to collagenase group. Interestingly, diclofenac treatment only decreased PGE(2) levels. Biomechanical properties were preserved in the laser-treated groups when compared to collagenase and diclofenac groups. We conclude that LLLT was able to reduce tendon inflammation and to preserve tendon resistance and elasticity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Achilles Tendon / pathology*
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Biochemistry / methods
  • Biomechanical Phenomena
  • Collagenases / chemistry
  • Collagenases / metabolism*
  • Cyclooxygenase 2 / metabolism
  • Diclofenac / pharmacology
  • Dinoprostone / metabolism
  • Inflammation
  • Low-Level Light Therapy / methods*
  • Male
  • Matrix Metalloproteinases / biosynthesis
  • Rats
  • Rats, Wistar
  • Tendinopathy / etiology
  • Tendinopathy / radiotherapy*
  • Tumor Necrosis Factor-alpha / biosynthesis


  • Anti-Inflammatory Agents, Non-Steroidal
  • Tumor Necrosis Factor-alpha
  • Diclofenac
  • Cyclooxygenase 2
  • Collagenases
  • Matrix Metalloproteinases
  • Dinoprostone