Repository logo
 

Inhibitory effects of orthosilicic acid on osteoclastogenesis in RANKL-stimulated RAW264.7 cells.

Published version
Peer-reviewed

Change log

Authors

Magnusson, Catarina  ORCID logo  https://orcid.org/0000-0002-1069-1859
Uribe, Pamela 
Jugdaohsingh, Ravin 
Powell, Jonathan J 
Johansson, Anders 

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.

Description

Funder: Swedish Dental Society

Keywords

RAW264.7 cells, bioceramics, bone metabolism, orthosilicic acid, osteoclast differentiation, Animals, Culture Media, Gene Expression Regulation, Mice, Neutral Red, Osteoclasts, Osteogenesis, RANK Ligand, RAW 264.7 Cells, Silicic Acid, Silicon, Solubility

Journal Title

J Biomed Mater Res A

Conference Name

Journal ISSN

1549-3296
1552-4965

Volume Title

109

Publisher

Wiley
Sponsorship
Medical Research Council (MR/R005699/1)