• 国家药监局综合司 国家卫生健康委办公厅
  • 国家药监局综合司 国家卫生健康委办公厅

[title missed]

Corresponding author: chengpeng, 1415047901@qq.com
DOI: 10.12201/bmr.202506.00002
Statement: This article is a preprint and has not been peer-reviewed. It reports new research that has yet to be evaluated and so should not be used to guide clinical practice.
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    Abstract: Heterotopic Ossification (HO) is a phenomenon of pathological bone tissue formation in soft tissues, and its pathological feature is a mature lamellar bone structure. HO is commonly seen after joint replacement surgery, spinal cord injury, blast injury and genetic diseases (such as fibrodysplasia progressive ossification FOP), etc. The clinical manifestations are pain, joint dysfunction and decreased quality of life. Its pathogenesis involves the abnormal differentiation of osteogenic precursor cells, the activation of the BMP/SMAD signaling pathway, the imbalance of the inflammatory microenvironment, and the interaction of multiple signaling pathways (such as Hedgehog, Wnt/β-catenin, mTOR). At present, non-steroidal anti-inflammatory drugs (NSAIDs) and radiotherapy are the main preventive measures. Surgical resection is the only effective treatment method, but there is a risk of recurrence. Emerging targeted therapies (such as BMP inhibitor DLN-193189 and Hedgehog inhibitor Gant58) and gene therapy have shown potential, but further clinical verification is still needed. This article systematically reviews the etiology, molecular mechanism and therapeutic progress of HO, providing a direction for future research.

    Key words: Heterotopic; Ossification, Ectopic; ossification, BMP/SMAD; signaling pathway, Inflammatory; microenvironment, Targeted; therapy

    Submit time: 3 June 2025

    Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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  • ID Submit time Number Download
    2 2025-04-18

    bmr.202506.00002V2

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    1 2025-04-15

    bmr.202506.00002V1

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chen haiwei, wangzhiqiang, chengpeng. [title missed]. 2025. biomedRxiv.202506.00002

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