Mechanisms of the Analgesic Effect of a Low Level Laser

Abstract

Low level laser therapy (LLLT) has been used widely in the treatment of various chronic painsyndromes in dentistry, pain clinics, and orthopedics. In particular, in dentistry the application of LLLT isincreasing in many cases, such as dentin hyperesthesia, aphtha, and temporomandibular joint dysfunction.There is general agreement that LLLT is effective for improving blood circulation, for pain attenuation, andfor wound healing. Although a large number of studies have been done on laser effects, most of them areclinical reports, and only a few studies have so far focused on cell biological research. As such, themechanism of laser-induced analgesic effects remains unknown. In this report, we describe the effects of lowlevel laser irradiation on nerve cells in vitro, and demonstrate the mechanism of the analgesic effect in LLLT.
A Ga-Al-As diode laser (trinpl D, YOSHIDA, Japan) was used as the laser apparatus. The experimentalcells were from the neurosecretory PC12 cell line, established from rat adrenal pheochromocytoma by Greeneand Tischler in 1976. After short-term laser irradiations (0.3-0.5J/cm²) to PC12 cells differentiated bytreatment with nerve growth factor, terminals of neurites underwent swelling within a few minutes. At thesesites, the density of the cytoplasmic matrix was reduced, and the number of synaptic vesicles was decreased.After long-term laser irradiations (15.0J/cm²), synaptic vesicles completely disappeared from terminals thatwere extremely swollen, and the density of the cytoplasmic matrix was greatly reduced, whereas cell bodieswere still well preserved. Some of the cells appeared to be in degeneration and had retracted their neurites, accompanied by alterations of F-Actin structures.
The laser irradiation induced a temporary increase in intracellular free calcium ion concentrations ([Ca²⁺] i), making them 1.7-fold higher in terminals and 2.7-fold higher in cell bodies, and enhanced the amplitude ofcalcium oscillation. In terminals, the peak level of [Ca²⁺] i. was 1400nM, and the interval time of each peak wasabout 200 ms, but in cell bodies, calcium oscillation was not clear.
Thus, the mechanism of the laser-induced analgesic effect is clearly demonstrated to be that the laserstimulates calcium ion influx and neurotransmitter release, and then degenerates terminals and processes ofneurites, according to alterations of actin organization. These findings suggest that LLLT attenuates thesensibility of nerve cells to painful stimuli and produces analgesic effects.