Mechanisms of the Analgesic Effect of Low Energy Laser

Abstract

Low energy lasers are widely used in the treatment of various chronic pain syndromes in dentistry, pain clinics and orthopedics. It is generally agreed that low energy laser irradiation is effective for improving blood circulation, reducing pain and promoting wound healing. Although there have been many fundamental studies on the effects of lasers, the mechanism of laser-induced analgesic effects remains unknown. This report describes the effects of low energy laser irradiation on nerve cells in vitro, and demonstrates the mechanism of analgesic effect. A GaAlAs diode laser (trinpl D, YOSHIDA) and the neurosecretory PC12 cell line were used. After short-term laser irradiation (0.3-0.5 J/cm²) on PC12 cells differentiated by treatment with nerve growth factor, terminals of neurites swelled within a few minutes and the number of synaptic vesicles decreased. After long-term laser irradiation (15.0 J/cm²), synaptic vesicles completely disappeared from the swollen terminals, whereas cell bodies were still well preserved. Some of the cells appeared to be in degeneration and retracted their neurites accompanied with the alteration of F-Actin structures. The laser irradiation induced a temporary increase in intracellular free calcium ion concentration ([Ca²⁺]i) and enhanced the amplitude of calcium oscillation.
Thus, it is clearly demonstrated that the mechanism of laser-induced analgesic effects is that the laser stimulates calcium ion influx and neurotransmitter release, and then degenerates the terminals and processes of neurites, according to the alteration of F-Actin organization. These findings suggest that low energy laser attenuates the sensitivity of nerve cells to painful stimuli and produces analgesic effects.