King Justin S, Wan Matthew, Kim Adam, Prabhu Shagun, Novak Sanja, Kalajzic Ivo, Delany Anne M, Sanjay Archana
Department of Orthopedic Surgery, United States of America; UConn Musculoskeletal Institute, United States of America.
Department of Medicine, United States of America.
Bone. 2025 Sep;198:117524. doi: 10.1016/j.bone.2025.117524. Epub 2025 May 15.
Aging predisposes individuals to reduced bone mass and fragility fractures, which are costly and linked to high mortality. Understanding how aging affects fracture healing is essential for developing therapies to enhance bone regeneration in older adults. During the inflammatory phase of fracture healing, immune cells are recruited to the injury site as periosteal skeletal stem/progenitor cells (pSSPCs) rapidly proliferate and differentiate into osteochondral lineages, allowing for fibrocartilaginous callus formation and, subsequently, complete bone healing. Irrespective of age, how periosteal mesenchymal and immune cells interact during early fracture healing is incompletely understood, limiting our ability to modulate this process. To address this, we directly analyzed, in parallel, at a single-cell level, isolated murine CD45(+) and CD45(-) periosteal cells dissected from intact and fractured bones, collected three days after injury. Comprehensive analysis, corroborated by bulk RNA-sequencing, flow cytometry, and histology, demonstrated that aging decreased pSSPC proliferation, markedly reduced expression of genes required for callus formation, and increased senescence signature. During the regeneration phase, at 14 days post injury, aged mice demonstrated reduced mineralization of the callus, accompanied by elevated Sox9 expression and increased cartilage content, suggesting delayed repair. We also found that the chemokine Cxcl9 was highly upregulated in aged intact Prrx1+ pSSPCs, which has the potential to directly regulate other pSSPCs, and was associated with increased recruitment of CD8+ T cells at the fracture site. Cell-to-cell communication analysis provided further appreciation of the complex interactions among the many mesenchymal and hematopoietic cell types regulating fracture healing and highlighted the impact of aging on these interactions. Together, these results provide insight into age-induced alterations in early fracture healing, which could facilitate the development of improved therapeutic approaches for fracture repair in the elderly.
衰老使个体易患骨量减少和脆性骨折,这些不仅代价高昂,还与高死亡率相关。了解衰老如何影响骨折愈合对于开发增强老年人骨再生的疗法至关重要。在骨折愈合的炎症阶段,免疫细胞被募集到损伤部位,同时骨膜骨骼干/祖细胞(pSSPCs)迅速增殖并分化为骨软骨谱系,从而形成纤维软骨痂,随后实现完全骨愈合。无论年龄如何,骨膜间充质细胞和免疫细胞在骨折早期愈合过程中如何相互作用仍不完全清楚,这限制了我们调节这一过程的能力。为了解决这个问题,我们在单细胞水平上直接并行分析了从完整和骨折骨骼中分离出的小鼠CD45(+)和CD45(-)骨膜细胞,这些细胞是在损伤后三天收集的。通过大量RNA测序、流式细胞术和组织学证实的综合分析表明,衰老会降低pSSPC的增殖,显著降低痂形成所需基因的表达,并增加衰老特征。在再生阶段,即损伤后14天,老年小鼠的痂矿化减少,同时Sox9表达升高且软骨含量增加,提示修复延迟。我们还发现趋化因子Cxcl9在老年完整的Prrx1+ pSSPC中高度上调,它有可能直接调节其他pSSPC,并与骨折部位CD8+ T细胞的募集增加有关。细胞间通讯分析进一步揭示了调节骨折愈合的多种间充质和造血细胞类型之间的复杂相互作用,并突出了衰老对这些相互作用的影响。总之,这些结果为早期骨折愈合中年龄诱导的变化提供了见解,这可能有助于开发改进的老年骨折修复治疗方法。