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. 2020 May 1;40:7. doi: 10.1186/s41232-020-00115-w

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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/.

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Fig. 5 — Hypertrophic chondrocytes express Runx2, Sox9, and Col10a1. In situ hybridization was performed [16]. a, bSox9 (red), Runx2 (white), and Col10a1 (green) mRNA signals in hypertrophic chondrocytes (a) and osteocytes (b) in bColII-D1BC inflamed joints. c In pannus, OCs in bone, HCs, and synovial fibroblasts express podoplanin (green), vimentin (red), and S100A4 (yellow), respectively. Scale bar = 20 μm (yellow) and 50 μm (white). d, e Joint space narrowing, erosion, and osteoporosis in bColII-D1BC mice. D1BC and DBA/1J mice were injected with a low-dose of bColII to induce joint inflammation. Whole-mount bone and cartilage staining with alizarin red S and alcian blue, for bone (red) and cartilage (blue), respectively. All mouse limbs at 1 year after the first immunization. No ankylosis in CIA-induced DBA/1J mouse (d). Note, the complete destruction of all joints (ankylosis, allow) and shortening of the phalanges in bColII-D1BC mouse joints (e)