Myositis ossificans.

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Abstract

[Indexed for MEDLINE] 3. Biomolecules. 2024 Apr 16;14(4):485. doi: 10.3390/biom14040485. Cell Senescence in Heterotopic Ossification. Pignolo RJ(1)(2)(3), Kaplan FS(4)(5)(6), Wang H(3)(7). Author information: (1)Department of Medicine, Section of Geriatric Medicine & Gerontology, Mayo Clinic, Rochester, MN 55905, USA. (2)Divisions of Endocrinology and Hospital Internal Medicine, Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA. (3)Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN 55905, USA. (4)Department of Orthopaedic Surgery, The Perelman School of Medicine of the University of Pennsylvania, Philadelphia, PA 19104, USA. (5)Department of Medicine, The Perelman School of Medicine of the University of Pennsylvania, Philadelphia, PA 19104, USA. (6)The Center for Research in FOP and Related Disorders, The Perelman School of Medicine of the University of Pennsylvania, Philadelphia, PA 19104, USA. (7)Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA. The formation of bone outside the normal skeleton, or heterotopic ossification (HO), occurs through genetic and acquired mechanisms. Fibrodysplasia ossificans progressiva (FOP), the most devastating genetic condition of HO, is due to mutations in the ACVR1/ALK2 gene and is relentlessly progressive. Acquired HO is mostly precipitated by injury or orthopedic surgical procedures but can also be associated with certain conditions related to aging. Cellular senescence is a hallmark of aging and thought to be a tumor-suppressive mechanism with characteristic features such as irreversible growth arrest, apoptosis resistance, and an inflammatory senescence-associated secretory phenotype (SASP). Here, we review possible roles for cellular senescence in HO and how targeting senescent cells may provide new therapeutic approaches to both FOP and acquired forms of HO. DOI: 10.3390/biom14040485 PMCID: PMC11047966