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. 2020 Oct 6;22:232. doi: 10.1186/s13075-020-02327-4

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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. 4 — TgA86 peripheral disease progression involves features of inflammation, bone erosion, and ectopic new bone formation. a Representative H&E stained sections of hind limbs show the accumulation of cells in the joints of TgA86 mice including features of enthesitis (arrow 1), synovitis (arrow 2), bone erosion (box), and bone destruction (asterisk) highlighted in higher magnification (lower panels). b Representative TRAP-stained sections of hind limbs show the accumulation of active osteoclasts in the joints of 10- and 20-week-old TgA86 mice, while their number is reduced in the joints of 40-week-old TgA86 mice. c, d Safranin O-stained sections of hind limbs of 20-week-old (c) and 40-week-old (d) TgA86 mice show the presence of fibrocartilage and ectopic chondrocytes (black arrows)