Department of Orthopaedic Surgery, University of Michigan, Ann Arbor, MI, United States.
Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI, United States.
Front Immunol. 2024 Feb 22;15:1352819. doi: 10.3389/fimmu.2024.1352819. eCollection 2024.
Bone fracture repair is a complex, multi-step process that involves communication between immune and stromal cells to coordinate the repair and regeneration of damaged tissue. In the US, 10% of all bone fractures do not heal properly without intervention, resulting in non-union. Complications from non-union fractures are physically and financially debilitating. We now appreciate the important role that immune cells play in tissue repair, and the necessity of the inflammatory response in initiating healing after skeletal trauma. The temporal dynamics of immune and stromal cell populations have been well characterized across the stages of fracture healing. Recent studies have begun to untangle the intricate mechanisms driving the immune response during normal or atypical, delayed healing. Various models of fracture healing, including genetic knockouts, as well as models of the fracture callus, have been implemented to enable experimental manipulation of the heterogeneous cellular environment. The goals of this review are to (1): summarize our current understanding of immune cell involvement in fracture healing (2); describe state-of-the art approaches to study inflammatory cells in fracture healing, including computational and models; and (3) identify gaps in our knowledge concerning immune-stromal crosstalk during bone healing.
骨骨折修复是一个复杂的、多步骤的过程，涉及免疫细胞和基质细胞之间的通讯，以协调受损组织的修复和再生。在美国，未经干预，10%的骨折无法正常愈合，导致骨折不愈合。骨折不愈合的并发症会使人身体和经济上衰弱。我们现在认识到免疫细胞在组织修复中起着重要作用，炎症反应对于骨骼创伤后启动愈合是必要的。在骨折愈合的各个阶段，免疫细胞和基质细胞群体的时间动态已经得到了很好的描述。最近的研究开始揭示在正常或非典型、延迟愈合过程中驱动免疫反应的复杂机制。各种骨折愈合模型，包括基因敲除以及骨折痂模型，已经被实施，以实现对异质细胞环境的实验操作。本综述的目的是：（1）总结我们目前对免疫细胞参与骨折愈合的理解；（2）描述研究骨折愈合中炎症细胞的最新方法，包括计算和模型；（3）确定在骨愈合过程中免疫-基质细胞相互作用方面的知识空白。
