OBJECTIVE: Laser therapy is known to stimulate cell proliferation and differentiation, an effect called "biostimulation". Although many clinical applications of laser therapy take advantage from such positive effect, the underlying molecular mechanisms are not fully understood. The aim of this work was to investigate the effect of near-infrared laser stimulation on rat pre-odontoblast cells (MDPC-23 cells) and the molecular mechanism/s involved. MATERIALS AND METHODS: MDPC-23 cells were stimulated with a near-infrared (980 nm) laser source with different energy settings (1-50 J, corresponding to 0.65-32.47 J/cm2) and cell proliferation was evaluated by manual count. ERK 1/2 pathway activation was evaluated by Western blot analysis. RESULTS: 1-10 J stimulation (corresponding to 0.65-6.5 J/cm2) significantly increase MDPC-23 cell proliferation and such effect seems to be mediated by ERK 1/2 signalling pathway activation, showing a key role of ERK 1/2 pathway in mediating the proliferative response induced by laser stimulation. CONCLUSIONS: Near infrared laser stimulation with low energies (1-10 J) is able to increase cell proliferation through ERK 1/2 signalling pathway activation. At the same time, higher energy stimulation (25-50 J) induces an initial toxic effect, probably activating pro-apoptotic signalling molecules, downstream ERK 1/2 kinase. Such results foster the application of this therapeutic approach in different clinical settings in which a regenerative tissue response is needed.

Pre-odontoblast proliferation induced by near-infrared laser stimulation

RIZZI, Manuela;MIGLIARIO, MARIO;ROCCHETTI, Vincenzo;Tonello, S;RENO', Filippo
2016-01-01

Abstract

OBJECTIVE: Laser therapy is known to stimulate cell proliferation and differentiation, an effect called "biostimulation". Although many clinical applications of laser therapy take advantage from such positive effect, the underlying molecular mechanisms are not fully understood. The aim of this work was to investigate the effect of near-infrared laser stimulation on rat pre-odontoblast cells (MDPC-23 cells) and the molecular mechanism/s involved. MATERIALS AND METHODS: MDPC-23 cells were stimulated with a near-infrared (980 nm) laser source with different energy settings (1-50 J, corresponding to 0.65-32.47 J/cm2) and cell proliferation was evaluated by manual count. ERK 1/2 pathway activation was evaluated by Western blot analysis. RESULTS: 1-10 J stimulation (corresponding to 0.65-6.5 J/cm2) significantly increase MDPC-23 cell proliferation and such effect seems to be mediated by ERK 1/2 signalling pathway activation, showing a key role of ERK 1/2 pathway in mediating the proliferative response induced by laser stimulation. CONCLUSIONS: Near infrared laser stimulation with low energies (1-10 J) is able to increase cell proliferation through ERK 1/2 signalling pathway activation. At the same time, higher energy stimulation (25-50 J) induces an initial toxic effect, probably activating pro-apoptotic signalling molecules, downstream ERK 1/2 kinase. Such results foster the application of this therapeutic approach in different clinical settings in which a regenerative tissue response is needed.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11579/75409
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