2018 Volume 16 Issue 3-4 Pages 54-61
Purpose: In this study, to elucidate the ability of Ga-Al-As laser treatment to induce hard tissue formation, human dental pulp cells (hDPCs) stimulated with high concentration prostaglandin E2 (PGE2), which inhibits hard tissue formation, were irradiated with lasers at 660 or 810 nm. Differences in the molecular mechanisms underlying hard tissue formation using Ga-Al-As lasers at these wavelengths, including signaling via the bone morphogenetic protein (BMP)/SMAD pathway, were examined and compared.
Methods: hDPCs were harvested from third molars extracted under aseptic conditions from 20-year-old patients undergoing orthodontic treatment. hDPCs were cultured for up to 30 days. After adding PGE2, hDPCs were irradiated with a Ga-Al-As laser at an output of 300 mW and wavelengths of 660 or 810 nm, approximately 10 cm above the culture supernatant. The laser irradiation time period was set to 600 seconds. BMP2, phosphorylated- (p-) SMAD1/5/8 and SMAD6 production were evaluated and calcified nodules stained.
Results: Ga-Al-As laser treatment resulted in decreased SMAD6 mRNA and increased protein expression of p-SMAD1/5/8 in groups irradiated at both wavelengths, compared with hDPCs stimulated with PGE2. Moreover, those irradiated at 810 nm exhibited lower BMP2 mRNA expression, but no definite difference in SMAD6 protein expression,compared with cells stimulated with PGE2.
Conclusion: Using Ga-Al-As lasers at the same output power, our results suggest that irradiation at 660 nm enhanced the ability of hDPCs to form hard tissue by suppressing SMAD6 expression; however, irradiation at 810 nm enhanced hard tissue generation via a different route that did not involve BMP2 and SMAD6.
