Effect of ProRoot MTA® and Biodentine® on osteoclastic differentiation and activity of mouse bone marrow macrophages.

OBJECTIVES: This investigation aimed to assess the differentiation inhibitory effects of ProRoot MTA® (PMTA) and Biodentine® (BIOD) on osteoclasts originated from murine bone marrow macrophages (BMMs) and compare these effects with those of alendronate (ALD). MATERIALS AND METHODS: Mouse BMMs were cultured to differentiate into osteoclasts with macrophage colony-stimulating factor and receptor activator of NF-κB (RANKL), treated with lipopolysaccharide. After application with PMTA, BIOD, or ALD, cell toxicities were examined using WST-1 assay kit, and RANKL-induced osteoclast differentiation and activities were determined by resorption pit formation assay and tartrate-resistant acid phosphate (TRAP) staining. The mRNA levels of osteoclast activity-related genes were detected with quantitative real time polymerase chain reaction. Expressions of molecular signaling pathways were assessed by western blot. All data were statistically analyzed with one-way ANOVA and Tukey's post-hoc test (p<0.05). RESULTS: Mouse BMMs applied with PMTA, BIOD, or ALD showed highly reduced levels of TRAP-positive osteoclasts. The BIOD treated specimens suppressed mRNA expressions of cathepsin K, TRAP, and c-Fos. Nonetheless, it showed a lower effect than PMTA or ALD applications. Compared with ALD, PMTA and BIOD decreased RANKL-mediated phosphorylation of ERK1/2 and IκBα. CONCLUSIONS: PMTA and BIOD showed the inhibitory effect on osteoclast differentiation and activities similar to that of ALD through IκB phosphorylation and suppression of ERK signaling pathways.

Effect of ProRoot MTA® and Biodentine® on osteoclastic differentiation and activity of mouse bone marrow macrophages

Abstract Objectives This investigation aimed to assess the differentiation inhibitory effects of ProRoot MTA® (PMTA) and Biodentine® (BIOD) on osteoclasts originated from murine bone marrow macrophages (BMMs) and compare these effects with those of alendronate (ALD). Materials and Methods Mouse BMMs were cultured to differentiate into osteoclasts with macrophage colony-stimulating factor and receptor activator of NF-κB (RANKL), treated with lipopolysaccharide. After application with PMTA, BIOD, or ALD, cell toxicities were examined using WST-1 assay kit, and RANKL-induced osteoclast differentiation and activities were determined by resorption pit formation assay and tartrate-resistant acid phosphate (TRAP) staining. The mRNA levels of osteoclast activity-related genes were detected with quantitative real time polymerase chain reaction. Expressions of molecular signaling pathways were assessed by western blot. All data were statistically analyzed with one-way ANOVA and Tukey's post-hoc test (p<0.05). Results Mouse BMMs applied with PMTA, BIOD, or ALD showed highly reduced levels of TRAP-positive osteoclasts. The BIOD treated specimens suppressed mRNA expressions of cathepsin K, TRAP, and c-Fos. Nonetheless, it showed a lower effect than PMTA or ALD applications. Compared with ALD, PMTA and BIOD decreased RANKL-mediated phosphorylation of ERK1/2 and IκBα. Conclusions PMTA and BIOD showed the inhibitory effect on osteoclast differentiation and activities similar to that of ALD through IκB phosphorylation and suppression of ERK signaling pathways.

Effects of the Ultra-High-Frequency Electrical Field Radiofrequency Device on Mouse Skin: A Histologic and Molecular Study.

BACKGROUND: Radiofrequency technology is one of the most recently developed methods for noninvasive skin tightening and facial contouring, and works by generating thermal energy in the deep dermis. Although clinical improvements have been reported using radiofrequency devices, there are few histologic and molecular studies about the mechanisms of dermal collagen remodeling. The authors investigated the histologic effects of an ultra-high-frequency electrical field (40.68 MHz) radiofrequency device (Polargen) on collagen remodeling in hairless mouse skin and evaluated its relative molecular mechanism. METHODS: The radiofrequency was applied to the dorsal skin of hairless mice three times per week for 2 weeks. At 21 days after initial treatment, treated skin and nontreated control skin samples were excised for semiquantitative analysis of histologic features, including collagen. The authors also checked the mRNA expression levels of collagen type 1, transforming growth factor (TGF)-ß, matrix metalloproteinase-1, vascular endothelial growth factor, tumor necrosis factor-α, and interleukin-1. RESULTS: Histologic examination revealed epidermal hyperplasia, increased collagen staining, and fat atrophy in treated skin area compared with the nontreated skin area. In addition, mRNA expression of collagen type І, TGF-ß, and vascular endothelial growth factor in radiofrequency-treated areas was significantly increased compared with that in untreated control areas (p < 0.05, p < 0.05, and p < 0.01, respectively). CONCLUSIONS: These results suggest that the device may facilitate replacement of subcutaneous fat tissue with new collagen in association with the increased mRNA levels in TGF-ß and vascular endothelial growth factor. Therefore, this device may effectively reduce adipose tissue and achieve facial contouring in addition to skin tightening.