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. 2020 Dec 9;8:42. doi: 10.1038/s41413-020-00119-9

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© The Author(s) 2020

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. 3 — Key pathways/mechanisms implicated in the development of NHO highlighting potential and existing therapeutic targets to mitigate NHO. a Substance P receptor (NK-₁R) antagonists (e.g. RP67580) have been found to reduce NHO volume in murine models. b Downstream of the BMP pathway, RAR-_γ agonists such as palovarotene have been reported to prevent early stages of NHO development by disrupting OPC differentiation, chondrogenesis and osteogenesis by downregulating mRNA expression of SOX-9 and RUNX2. c OSM is a potential therapeutic target and may serve as a biomarker for NHO. Blocking OSM has been found to reduce NHO likely by inhibiting downstream transcription factor, STAT3, which is known to trigger bone formation. d NSAID, indomethacin is currently the preferred prophylaxis for NHO/HO. It targets COX-1 and COX-2 non-selectively, inhibiting the production of prostaglandins and osteogenesis (created with BioRender.com)