Laser therapy has the potential to be an effective, minimally invasive procedure in periodontal therapy. The aim of the present review was to survey the relevant literature on the clinical application of lasers as a minimally invasive treatment for periodontitis and peri-implant disease. Currently, there are a large number of published clinical studies and case reports that evaluate the adjunctive use of diode, carbon dioxide, neodymium-doped yttrium aluminium garnet (Nd:YAG), erbium-doped yttrium aluminium garnet (Er:YAG) and erbium, chromium-doped: yttrium, scandium, gallium, garnet (Er,Cr:YSGG) lasers or antimicrobial photodynamic therapy for nonsurgical and minimally invasive surgical treatment of periodontal pockets. These procedures are expected not only to control inflammation but also to provide biostimulation effects with photonic energy. Recent meta-analyses did not show statistically significant differences in pocket reduction and clinical attachment gain compared with mechanical debridement alone, although limited positive effects of adjunctive laser therapy were reported. At present, systematic literature approaches suggest that more evidence-based studies need to be performed to support the integration of various laser therapies into the treatment of periodontal and peri-implant diseases. The disparity between previous statistical analyses and individual successful clinical outcomes of laser applications might reveal the necessity of developing optimal laser-treatment modalities of different wavelengths and better-defined indications for each protocol.
Although the use of high-level Er:YAG laser irradiation has been increasing in periodontal and peri-implant therapy, the effects of low-level Er:YAG laser on surrounding tissues and cells remain unclear. In the present study, the effects of low-level Er:YAG laser irradiation on osteoblast proliferation were investigated. Cells of the osteoblastic cell line MC3T3-E1 were treated with low-level Er:YAG laser irradiation with various combinations of laser settings (fluence 0.7-17.2 J/cm(2)) and in the absence or presence of culture medium during irradiation. On day 1 and/or day 3, cell proliferation and death were determined by cell counting and by measurement of lactate dehydrogenase (LDH) levels. Further, the role of mitogen-activated protein kinase (MAPK) pathways in laser-enhanced cell proliferation was investigated by inhibiting the MAPK pathways and then measuring MAPK phosphorylation by Western blotting. Higher proliferation rates were found with various combinations of irradiation parameters on days 1 and 3. Significantly higher proliferation was also observed in laser-irradiated MC3T3-E1 cells at a fluence of approximately 1.0-15.1 J/cm(2), whereas no increase in LDH activity was observed. Further, low-level Er:YAG irradiation induced the phosphorylation of extracellular signal-regulated protein kinase (MAPK/ERK) 5 to 30 min after irradiation. Although MAPK/ERK 1/2 inhibitor U0126 significantly inhibited laser-enhanced cell proliferation, activation of stress-activated protein kinases/Jun N-terminal kinase (SAPK/JNK) and p38 MAPK was not clearly detected. These results suggest that low-level Er:YAG laser irradiation increases osteoblast proliferation mainly by activation of MAPK/ERK, suggesting that the Er:YAG laser may be able to promote bone healing following periodontal and peri-implant therapy.
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