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. 2017 Oct 17;5:17019. doi: 10.1038/boneres.2017.19

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Copyright © 2017 The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Schematic illustration of the potential phenotypic switching of macrophages. RANKL induces the polarization of macrophages into the M1 phenotype that is present in normal long bones. Conversely, interleukin (IL)-4, IL-10, IL-13, and other glucocorticoids may promote the resolution of inflammation by skewing macrophages toward the M2 phenotype. M1 macrophages may be in a transient state that is similar to the pre-osteoclast state and finally turn into osteoclasts through the persistent induction of RANKL in the physiological environment.