Objective: The aim of this study was to review the biological and clinical short-term effects of low-level laser therapy(LLLT) in acute pain from soft-tissue injury. Background Data: It is unclear if and how LLLT can reduce acute pain. Methods: Literature search of (i) controlled laboratory trials investigating potential biological mechanisms for pain relief and (ii) randomized placebo-controlled clinical trials which measure outcomes within the first 7 days after acute soft-tissue injury. Results: There is strong evidence from 19 out of 22 controlled laboratory studies that LLLT can modulate inflammatory pain by reducing levels of biochemical markers (PGE ₂ , mRNA Cox 2, IL-1β, TNFα), neutrophil cell influx, oxidative stress, and formation of edema and hemorrhage in a dosedependent manner (median dose 7.5 J/cm ² , range 0.3–19 J/cm ² ). Four comparisons with non-steroidal anti-inflammatory drugs (NSAIDs) in animal studies found optimal doses of LLLT and NSAIDs to be equally effective. Seven randomized placebo-controlled trials found no significant results after irradiating only a single point on the skin overlying the site of injury, or after using a total energy dose below 5 Joules. Nine randomized placebo-controlled trials ( n = 609) were of acceptable methodological quality, and irradiated three or more points and/or more than 2.5 cm2 at site of injury or surgical incision, with a total energy of 5.0–19.5 Joules. Results in these nine trials were significantly in favor of LLLT groups over placebo groups in 15 out of 18 outcome comparisons. Poor and heterogeneous data presentation hampered statistical pooling of continuous data. Categorical data of subjective improvement were homogeneous (Q-value = 7.1) and could be calculated from four trials ( n = 379) giving a significant relative risk for improvement of 2.7 (95% confidence interval [CI], 1.8–3.9) in a fixed effects model. Conclusion: LLLT can modulate inflammatory processes in a dose-dependent manner and can be titrated to significantly reduce acute inflammatory pain in clinical settings. Further clinical trials with adequate LLLT doses are needed to precisely estimate the effect size for LLLT in acute pain.

Objective: The aim of this study was to investigate if low-level laser therapy (LLLT) can modulate acute inflammation and tumor necrosis factor (TNFα) levels. Background Data: Drug therapy with TNFα-inhibitors has become standard treatment for rheumatoid arthritis, but it is unknown if LLLT can reduce or modulate TNFα levels in inflammatory disorders. Methods: Two controlled animal studies were undertaken, with 35 male Wistar rats randomly divided into five groups each. Rabbit antiserum to ovalbumin was instilled intrabronchially in one of the lobes, followed by the intravenous injection of 10 mg of ovalbumin in 0.5 mL to induce acute lung injury. The first study served to define the time profile of TNFα activity for the first 4 h, while the second study compared three different LLLT doses to a control group and a chlorpromazine group at a timepoint where TNFα activity was increased. The rats in LLLT groups were irradiated within 5 min at the site of injury by a 650-nm Ga-Al-As laser. Results: There was a time-lag before TNFα activity increased after BSA injection. TNFα levels increased from ≤6.9 (95% confidence interval [CI], 5.6–8.2) units/mL in the first 3 h to 62.1 (95% CI, 60.8–63.4) units/mL ( p < 0.001) at 4 h. An LLLT dose of 0.11 Joules administered with a power density of 31.3 mW/cm ² in 42 sec significantly reduced TNFα level to 50.2 (95% CI, 49.4–51.0), p < 0.01 units/mL versus control. Chlorpromazine reduced TNFα level to 45.3 (95% CI, 44.0–46.6) units/mL, p < 0.001 versus control. Conclusion: LLLT can reduce TNFα expression after acute immunocomplex lung injury in rats, but LLLT dose appears to be critical for reducing TNFα release.

We investigated whether low-level laser therapy (LLLT) can reduce muscular fatigue during tetanic contractions in rats. Thirty-two male Wistar rats were divided into four groups receiving either one of three different LLLT doses (0.5, 1.0, and 2.5 J/cm²) or a no-treatment control group. Electrical stimulation was used to induce six tetanic muscle contractions in the tibial anterior muscle. Contractions were stopped when the muscle force fell to 50% of the initial value for each contraction (T50%). There was no significant difference between the 2.5 J/cm² laser-irradiated group and the control group in mean T50% values. Laser-irradiated groups (0.5 and 1.0 J/cm²) had significantly longer T50% values than the control group. The relative peak force for the sixth contraction in the laser-irradiated groups were significantly higher at 92.2% (SD 12.6) for 0.5 J/cm², 83.2% (SD 20.5) for 1.0 J/cm², and 82.9% (SD 18.3) for 2.5 J/cm² than for the control group [50% (SD 15)]. Laser groups receiving 0.5 and 1.0 J/cm² showed significant increases in mean performed work compared with both the control group and their first contraction values. Muscle damage was indirectly measured by creatine kinase levels in plasma. A distinct dose-response pattern was found in which 1.0 and 2.5 J/cm² LLLT groups had significantly lower creatine kinase levels than the 0.5 J/cm² LLLT group and the control group. We conclude that LLLT doses of 0.5 and 1.0 J/cm² can prevent development of muscular fatigue in rats during repeated tetanic contractions.