Baker Courtney E, Moore-Lotridge Stephanie N, Hysong Alexander A, Posey Samuel L, Robinette J Patton, Blum Deke M, Benvenuti Michael A, Cole Heather A, Egawa Satoru, Okawa Atsushi, Saito Masanori, McCarthy Jason R, Nyman Jeffry S, Yuasa Masato, Schoenecker Jonathan G
1Department of Orthopaedics, Mayo Clinic, 200 1st Ave SW, Rochester, MN 55903 USA.
2Department of Orthopaedics and Rehabilitation, Vanderbilt University Medical Center, 1215 21st Ave. South, Suite 4200 MCE, South Tower, Nashville, TN 37232 USA.
Clin Rev Bone Miner Metab. 2018;16(4):142-158. doi: 10.1007/s12018-018-9256-x. Epub 2018 Dec 29.
Bone fractures create five problems that must be resolved: bleeding, risk of infection, hypoxia, disproportionate strain, and inability to bear weight. There have been enormous advancements in our understanding of the molecular mechanisms that resolve these problems after fractures, and in best clinical practices of repairing fractures. We put forth a modern, comprehensive model of fracture repair that synthesizes the literature on the biology and biomechanics of fracture repair to address the primary problems of fractures. This updated model is a framework for both fracture management and future studies aimed at understanding and treating this complex process. This model is based upon the fracture acute phase response (APR), which encompasses the molecular mechanisms that respond to injury. The APR is divided into sequential stages of "survival" and "repair." Early in convalescence, during "survival," bleeding and infection are resolved by collaborative efforts of the hemostatic and inflammatory pathways. Later, in "repair," avascular and biomechanically insufficient bone is replaced by a variable combination of intramembranous and endochondral ossification. Progression to repair cannot occur until survival has been ensured. A disproportionate APR-either insufficient or exuberant-leads to complications of survival (hemorrhage, thrombosis, systemic inflammatory response syndrome, infection, death) and/or repair (delayed- or non-union). The type of ossification utilized for fracture repair is dependent on the relative amounts of strain and vascularity in the fracture microenvironment, but any failure along this process can disrupt or delay fracture healing and result in a similar non-union. Therefore, incomplete understanding of the principles herein can result in mismanagement of fracture care or application of hardware that interferes with fracture repair. This unifying model of fracture repair not only informs clinicians how their interventions fit within the framework of normal biological healing but also instructs investigators about the critical variables and outputs to assess during a study of fracture repair.
出血、感染风险、缺氧、应变失衡以及无法承重。在我们对骨折后解决这些问题的分子机制的理解以及骨折修复的最佳临床实践方面，已经取得了巨大进展。我们提出了一个现代的、全面的骨折修复模型，该模型综合了有关骨折修复生物学和生物力学的文献，以解决骨折的主要问题。这个更新后的模型是骨折管理和未来旨在理解和治疗这一复杂过程的研究的框架。该模型基于骨折急性期反应（APR），它涵盖了对损伤作出反应的分子机制。APR分为“生存”和“修复”两个连续阶段。在康复早期的“生存”阶段，出血和感染通过止血和炎症途径的协同作用得以解决。后来，在“修复”阶段，无血管且生物力学不足的骨被膜内成骨和软骨内成骨的不同组合所替代。在确保生存之前，无法进入修复阶段。APR失调——无论是不足还是过度——都会导致生存并发症（出血、血栓形成、全身炎症反应综合征、感染、死亡）和/或修复并发症（延迟愈合或不愈合）。用于骨折修复的成骨类型取决于骨折微环境中的应变和血管相对量，但这一过程中的任何失败都可能破坏或延迟骨折愈合，并导致类似的不愈合。因此，对本文所述原则的不完全理解可能导致骨折护理管理不当或应用妨碍骨折修复的硬件。这个统一的骨折修复模型不仅告知临床医生他们的干预措施如何适应正常生物愈合的框架，还指导研究人员在骨折修复研究中评估关键变量和结果。
