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. 2019 Aug 15;7:25. doi: 10.1038/s41413-019-0066-7

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© The Author(s) 2019

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Static and dynamic changes in osteoporotic bone. An osteoporotic fracture is the macroscopic result of microstructural alterations that change the response of bone to the applied load. The aging process in osteoporotic bone would lead to overaccumulation of PPi, AGEs, and nonenzymatic crosslinking of collagen, which disturb the normal organization of bone material. With the increase of bone resorption and low rate osteogenesis, the osteocyte lacunae reduction leads to decreased trabecular thickness and more porous cortical bone. PTH parathyroid hormone, M-CSF macrophage colony-stimulating factor, RANKL receptor activator of nuclear factor kappa-B ligand, PPi inorganic pyrophosphate, AGEs advanced glycation end-products, MSCs mesenchymal stem cells. “Red” refers to upregulation; “Green” refers to downregulation