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. 2020 Jun 3;21:122. doi: 10.1186/s12881-020-01036-8

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Schematic representation of the cellular and molecular players involved in the RANKL/RANK/OPG signaling axis in bone remodeling. The RANKL from the osteoblast-lineage cells binds to the RANK receptor on osteoclast precursor cells and promotes osteoclasts activation and differentiation, resulting in increased bone resorption. Whereas the OPG decoy receptor binds to RANKL leading to inhibition of osteoclastogenesis. OPG also functions as a decoy receptor for TRAIL, and OPG decreased production mediates the TRAIL-induced apoptosis of osteoblasts leading therefore to bone loss