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. 2021 Nov 22;11:22708. doi: 10.1038/s41598-021-02246-7

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© The Author(s) 2021

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 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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MMPs drive osteoclast-mediated cartilage degradation. (a,b) Effect of bafilomycin, E64 and GM6001 on osteoclast-mediated release of GAG from (a) acellular or (b) cellular cartilage after 13 days of differentiation. N varies for each graph, as represented by the number of data points. Statistics: (a): bafilomyin, Kruskal–Wallis ANOVA; E64 and GM6001, one-way ANOVA. (b) bafilomycin and E64, one-way ANOVA; GM6001, Kruskal–Wallis ANOVA. (c) Effect of recombinant human TIMP1 (100 nM) on GAG release from osteoclasts cultured on acellular cartilage (n = 18; T test).