Abstract
Numerous studies have reported on the positive effects of silicon (Si) on bone metabolism, particularly on the stimulatory effects of Si on osteoblast cells and on bone formation. Inhibitory effects of Si on osteoclast formation and bone resorption have also been demonstrated in vitro and are suggested to be mediated indirectly via stromal and osteoblast cells. Direct effects of Si on osteoclasts have been less studied and mostly using soluble Si, but no characterisation of the Si treatment solutions are provided. The aims of the present study were to (a) further investigate the direct inhibitory effects of Si on osteoclastogenesis in RANKL-stimulated RAW264.7 cells, (b) determine at what stage during osteoclastogenesis Si acts upon, and (c) determine if these effects can be attributed to the biologically relevant soluble orthosilicic acid specie. Our results demonstrate that silicon, at 50 μg/ml (or 1.8 mM), does not affect cell viability but directly inhibits the formation of TRAP+ multinucleated cells and the expression of osteoclast phenotypic genes in RAW264.7 cells. The inhibitory effect of Si was clearly associated with the early stages (first 24 hr) of osteoclastogenesis. Moreover, these effects can be attributed to the soluble orthosilicic acid specie.
Highlights
Impaired bone metabolism and remodelling, due to age or disease, may affect healing and reconstruction of bone after pathologies or traumatic injuries
In 2014, reported that Si inhibits bone resorption in vitro and dose-dependently reduced the number of tartrate-resistant acid phosphatase (TRAP)+ multinucleated cells that were differentiated from bone marrow cultures and cultures of RAW264.7 cells.[22]
RANKL was used to stimulate osteoclastogenesis in RAW264.7 cells and this was confirmed by the expression of osteoclast markers (RANK, TRAP, Cathepsin K (CtsK), and Calcitonin Receptor (CalcR))
Summary
Impaired bone metabolism and remodelling, due to age or disease, may affect healing and reconstruction of bone after pathologies or traumatic injuries. In 2014, reported that Si inhibits bone resorption in vitro and dose-dependently reduced the number of TRAP+ multinucleated cells that were differentiated from bone marrow cultures and cultures of RAW264.7 cells.[22] This inhibitory effect of Si on osteoclastogenesis has been confirmed by others, in stimulated hCD14+ osteoclast precursors and in mouse bone marrow macrophages.[24,28] mechanisms have not been established. It is not known at what stage(s) of osteoclastogenesis Si acts on to inhibit osteoclast differentiation. We used RAW264.7 cells, an established cell line that does not require co-culture with mesenchymal/osteoblast cells for osteoclast formation.[30,31] RANKL was used to stimulate osteoclastogenesis in RAW264.7 cells and this was confirmed by the expression of osteoclast markers (RANK, TRAP, CtsK, and CalcR)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
