Fracture healing: the diamond concept.

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Abstract

[Indexed for MEDLINE] 2. J Clin Invest. 2024 Jun 17;134(12):e181974. doi: 10.1172/JCI181974. Targeting senescent cells to boost bone fracture healing. Hofbauer LC(1)(2), Baschant U(1), Hofbauer C(3)(4). Author information: (1)Division of Endocrinology, Diabetes and Bone Diseases, Department of Medicine III & University Center for Healthy Aging, Technische Universität Dresden Medical Center, Dresden, Germany. (2)Center for Regenerative Therapies Dresden, Technische Universität Dresden, Dresden, Germany. (3)Division of Endocrinology, Orthopedic, Trauma and Plastic Surgery Center, Technische Universität Dresden Medical Center, Dresden, Germany. (4)Nationales Zentrum für Tumorerkrankungen (NCT/UCC), Technische Universität Dresden Medical Center, Dresden, Germany. Comment on J Clin Invest. 2024 May 16;134(12):e179834. doi: 10.1172/JCI179834. Bone fracture healing is a complex process with distinct phases: the inflammatory phase, the soft and hard callus formation, and the remodeling phase. In older individuals, bone healing can be delayed or disturbed, leading to non-union fractures at worst. The initial healing phases require communication between immune cells and osteoprogenitor cells. However, senescence in these cell types impedes fracture healing by unknown mechanisms. In this issue of the JCI, Saul et al. showed that two distinct senescent p21-expressing cell populations, an osteochondroprogenitor cell and a neutrophil subpopulation, intrinsically impair fracture healing in mice irrespective of age. Genetic ablation of p21-positive cells accelerated fracture healing, while removal of a different senescent cell population, p16-positive cells, made no difference. Conceptually, this view of senescence in fracture healing with a spotlight on osteoimmune cross-talk provides a promising rationale for therapies to boost bone repair at all ages. DOI: 10.1172/JCI181974 PMCID: PMC11178528