BACKGROUND AND AIMS: Pulsed electromagnetic fields (PEMF) have proven to be an effective noninvasive method in the prevention and treatment of osteoporosis. This study evaluated the effects of PEMF on the expression of the NFATc1, CAII and RANK genes in mouse osteoclast-like cells. METHODS: Bone marrow from bilateral tibiae and femurs was cultured in differentiation medium in the presence of soluble macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor kappa-B ligand (RANKL). After 5 days, the osteoclast-like cells were confirmed by both tartrate-resistant acid phosphatase (TRAP) staining and bone resorption assays. The osteoclast-like cells were divided into five groups and exposed to the following treatments for 3 days: M-CSF; M-CSF + RANKL; M-CSF + RANKL + osteoprotegerin (OPG), M-CSF + RANKL + premarin (E2); and M-CSF + RANKL + PEMF. The numbers of multinucleated, TRAP-positive osteoclast-like cells and resorption pits formed were determined. The expression of NFATc1, CAII and RANK mRNA was determined with real-time fluorescent quantitative polymerase chain reaction. RESULTS: PEMF substantially reduced the number of osteoclast-like cells in the culture with M-CSF + RANKL. The level of NFATc1, CAII, and RANK mRNA expression was decreased in the M-CSF + RANKL + PEMF group compared to the M-CSF + RANKL group (p = 0.007, p = 0.039, p = 0.001, respectively). The mRNA expression of NFATc1, CAII, and RANK was not higher in the M-CSF + RANKL + OPG group compared to the M-CSF + RANKL + PEMF group (p = 0.682, p = 0.200, p = 0.924, respectively). In addition, there was no difference in the expression of mRNA from NFATc1, CAII, and RANK between the M-CSF + RANKL + PEMF group and the M-CSF + RANKL + E2 group (p = 0.853, p = 0.509, p = 0.664, respectively). CONCLUSIONS: These data suggest that PEMF might modulate the process of osteoclastogenesis and subsequent bone resorption, at least partially, through NFATc1, CAII and RANK.
BACKGROUND AND AIMS: Pulsed electromagnetic fields (PEMF) have proven to be an effective noninvasive method in the prevention and treatment of osteoporosis. This study evaluated the effects of PEMF on the expression of the NFATc1, CAII and RANK genes in mouse osteoclast-like cells. METHODS: Bone marrow from bilateral tibiae and femurs was cultured in differentiation medium in the presence of soluble macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor kappa-B ligand (RANKL). After 5 days, the osteoclast-like cells were confirmed by both tartrate-resistant acid phosphatase (TRAP) staining and bone resorption assays. The osteoclast-like cells were divided into five groups and exposed to the following treatments for 3 days: M-CSF; M-CSF + RANKL; M-CSF + RANKL + osteoprotegerin (OPG), M-CSF + RANKL + premarin (E2); and M-CSF + RANKL + PEMF. The numbers of multinucleated, TRAP-positive osteoclast-like cells and resorption pits formed were determined. The expression of NFATc1, CAII and RANK mRNA was determined with real-time fluorescent quantitative polymerase chain reaction. RESULTS: PEMF substantially reduced the number of osteoclast-like cells in the culture with M-CSF + RANKL. The level of NFATc1, CAII, and RANK mRNA expression was decreased in the M-CSF + RANKL + PEMF group compared to the M-CSF + RANKL group (p = 0.007, p = 0.039, p = 0.001, respectively). The mRNA expression of NFATc1, CAII, and RANK was not higher in the M-CSF + RANKL + OPG group compared to the M-CSF + RANKL + PEMF group (p = 0.682, p = 0.200, p = 0.924, respectively). In addition, there was no difference in the expression of mRNA from NFATc1, CAII, and RANK between the M-CSF + RANKL + PEMF group and the M-CSF + RANKL + E2 group (p = 0.853, p = 0.509, p = 0.664, respectively). CONCLUSIONS: These data suggest that PEMF might modulate the process of osteoclastogenesis and subsequent bone resorption, at least partially, through NFATc1, CAII and RANK.