Table of Contents Author Guidelines Submit a Manuscript
Stem Cells International
Volume 2016 (2016), Article ID 1908365, 13 pages
Review Article

The Modulatory Effects of Mesenchymal Stem Cells on Osteoclastogenesis

1Center of Excellence of Stem Cells and Regenerative Medicine, Zewail City of Science and Technology, Sheikh Zayed District, 6th of October City, Giza 12566, Egypt
2Medical Molecular Genetics Department, Human Genetics and Genome Research Division, National Research Centre, Cairo 12411, Egypt
3Stem Cells Research Group, Centre of Excellence for Advanced Sciences, National Research Centre, Cairo 12411, Egypt

Received 12 July 2015; Accepted 21 September 2015

Academic Editor: Joel C. Glover

Copyright © 2016 Wessam E. Sharaf-Eldin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The effect of mesenchymal stem cells (MSCs) on bone formation has been extensively demonstrated through several in vitro and in vivo studies. However, few studies addressed the effect of MSCs on osteoclastogenesis and bone resorption. Under physiological conditions, MSCs support osteoclastogenesis through producing the main osteoclastogenic cytokines, RANKL and M-CSF. However, during inflammation, MSCs suppress osteoclast formation and activity, partly via secretion of the key anti-osteoclastogenic factor, osteoprotegerin (OPG). In vitro, co-culture of MSCs with osteoclasts in the presence of high concentrations of osteoclast-inducing factors might reflect the in vivo inflammatory pathology and prompt MSCs to exert an osteoclastogenic suppressive effect. MSCs thus seem to have a dual effect, by stimulating or inhibiting osteoclastogenesis, depending on the inflammatory milieu. This effect of MSCs on osteoclast formation seems to mirror the effect of MSCs on other immune cells, and may be exploited for the therapeutic potential of MSCs in bone loss associated inflammatory diseases.