The effectiveness of photobiomodulation in the management of temporomandibular pain sensitivity in rats: behavioral and neurochemical effects.

This study analyzed the effects of photobiomodulation (PBM) with low-level laser therapy on nociceptive behavior and neuronal activity in the trigeminal nucleus after experimental unilateral temporomandibular joint (TMJ) disc injury. The animals were divided into 4 groups (n = 10 each): group 1, surgical injury of the articular disc and PBM; group 2, sham-operated subjected to PBM; group 3, surgical injury of the articular disc; and group 4, control (Naïve). Ten sessions of PBM were performed using GaAs laser with a wavelength of 904 nm, power of 75 W pico, average power of 0.043 W, area of the beam of 0.13 cm2, duration of the pulses of 60 nseg (in the frequency of 9500 Hz), energy density of 5.95 J/cm2, energy per point of 0.7 J, and power density of 333.8 mW/cm2, and the irradiation was done for 18 s per point. Neuropathic symptoms were evaluated using the von Frey test. Trigeminal ganglion samples underwent immunoblotting to examine the expression of substance P, vanilloid transient potential receptor of subtype-1 (TRPV-1), and peptide related to the calcitonin gene (CGRP). There was a total decrease in pain sensitivity after the second session of PBM in operated animals, and this decrease remains until the last session. There was a significant decrease in the expression of SP, TRPV-1, and CGRP after PBM. Photobiomodulation therapy was effective in reducing nociceptive behavior and trigeminal nucleus neuronal activity after TMJ disc injury.

Laser therapy and pain-related behavior after injury of the inferior alveolar nerve: possible involvement of neurotrophins.

Nerve-related complications have been frequently reported in dental procedures, and a very frequent type of occurrence involves the inferior alveolar nerve (IAN). The nerve injury in humans often results in persistent pain accompanied by allodynia and hyperalgesia. In this investigation, we used an experimental IAN injury in rats, which was induced by a Crile hemostatic clamp, to evaluate the effects of laser therapy on nerve repair. We also studied the nociceptive behavior (von Frey hair test) before and after the injury and the behavioral effects of treatment with laser therapy (emitting a wavelength of 904 nm, output power of 70 Wpk, a spot area of ∼0.1 cm², frequency of 9500 Hz, pulse time 60 ns and an energy density of 6 J/cm²). As neurotrophins are essential for the process of nerve regeneration, we used immunoblotting techniques to preliminarily examine the effects of laser therapy on the expression of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF). The injured animals treated with laser exhibited an improved nociceptive behavior. In irradiated animals, there was an enhanced expression of NGF (53%) and a decreased BDNF expression (40%) after laser therapy. These results indicate that BDNF plays a locally crucial role in pain-related behavior development after IAN injury, increasing after lesions (in parallel to the installation of pain behavior) and decreasing with laser therapy (in parallel to the improvement of pain behavior). On the other hand, NGF probably contributes to the repair of nerve tissue, in addition to improving the pain-related behavior.