ID Number		2201
Study Type		In Vitro
Model		50 Hz (PEMF) and ultrasound exposure to osteogenic sarcoma cells and analysis of gene expression indicating osteolytic activity
Details		Saos-2 osteogenic sarcoma cells were exposed to 50 Hz pulsed electromagnetic fields (PEMF) or low intensity pulsed ultrasound for either 10 minutes or 3 hours, and gene expression and secreted protein expression in the supernatant examined at 4, 8, and 12 hours post-exposure. The authors report increased OPG protein with low intensity pulsed ultrasound after 4 hours and PEMF after 8 hours, and increased RANKL and OPG mRNA with PEMF. The authors suggest the cellular response to low intensity ultrasound was rapid, while the response to PEMF was more delayed. The respose was indicative of osteolysis. AUTHOR'S ABSTRACT: Song et al. 2014 (IEEE #5794): Although glucocorticoids provide benefits for inflammation or autoimmune disorders, high-dose and long-term use could cause osteonecrosis or osteoporosis as adverse effect for patients. Electromagnetic field (EMF) treatments have been clinically used for many years to promote fracture healing, but whether EMF can attenuate the deleterious effects of glucocorticoids is not clear. In this study, the effects of different concentrations of dexamethasone (DEX) on proliferation and adipogenic or osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) were detected and compared, and the effects of EMF treatment (15 Hz, 1 mT, 4 h/day) on 0.1 µM DEX-modulated BMSCs' proliferation and adipogenic or osteogenic differentiation were investigated. Higher concentrations of DEX (0.1 and 1 µM) inhibited proliferation of BMSCs but promoted expression of adipogenic-related genes, increasing the number of lipid droplets. In the early stage of differentiation, DEX restrained expression of RUNX2 and alkaline phosphatase (ALP), but amplified expression of ALP and osteopontin (OPN) in the late stage. EMF treatment of BMSCs influenced by 0.1 µM DEX inhibited the high expression of adipogenic-related genes, stimulated the expression of RUNX2, ALP, OPN, and osteocalcin, and increased the activity of ALP. EMF exposure augmented the expression of p-ERK, which DEX reduced. After using mitogen-activated protein/extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK signaling pathway inhibitor, U0126, the effect of EMF was reduced. In conclusion, EMF exposure accelerates BMSCs proliferation, inhibits adipogenic differentiation, and promotes osteogenic differentiation of BMSCs modulated by DEX, and these effects are mediated at least in part by MEK/ERK signaling pathway.
Findings		Effects
Status		Completed With Publication
Principal Investigator		University of Groningen, The Netherlands
Funding Agency		Private/Instit.
Country		NETHERLANDS
References		Borsje, MA et al. Angle Orthod, (2010) 80:498-503
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