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健康和炎症状态下的骨折愈合。

Fracture healing under healthy and inflammatory conditions.

机构信息

Institute of Orthopedic Research and Biomechanics, Center of Musculoskeletal Research, University of Ulm, Helmholtzstraße 14, 89081 Ulm, Germany.

出版信息

Nat Rev Rheumatol. 2012 Jan 31;8(3):133-43. doi: 10.1038/nrrheum.2012.1.

DOI:10.1038/nrrheum.2012.1
PMID:22293759
Abstract

Optimal fracture treatment requires knowledge of the complex physiological process of bone healing. The course of bone healing is mainly influenced by fracture fixation stability (biomechanics) and the blood supply to the healing site (revascularization after trauma). The repair process proceeds via a characteristic sequence of events, described as the inflammatory, repair and remodeling phases. An inflammatory reaction involving immune cells and molecular factors is activated immediately in response to tissue damage and is thought to initiate the repair cascade. Immune cells also have a major role in the repair phase, exhibiting important crosstalk with bone cells. After bony bridging of the fragments, a slow remodeling process eventually leads to the reconstitution of the original bone structure. Systemic inflammation, as observed in patients with rheumatoid arthritis, diabetes mellitus, multiple trauma or sepsis, can increase fracture healing time and the rate of complications, including non-unions. In addition, evidence suggests that insufficient biomechanical conditions within the fracture zone can influence early local inflammation and impair bone healing. In this Review, we discuss the main factors that influence fracture healing, with particular emphasis on the role of inflammation.

摘要

最佳的骨折治疗需要了解骨骼愈合这一复杂的生理过程。骨折愈合的过程主要受骨折固定稳定性(生物力学)和愈合部位的血液供应(创伤后再血管化)的影响。修复过程通过一系列特征性事件进行,可描述为炎症、修复和重塑阶段。组织损伤会立即引发涉及免疫细胞和分子因子的炎症反应,被认为是修复级联反应的启动因素。免疫细胞在修复阶段也发挥着重要作用,与骨细胞之间存在重要的串扰。在骨碎片桥接后,一个缓慢的重塑过程最终会导致恢复原始骨结构。在类风湿关节炎、糖尿病、多发创伤或脓毒症患者中观察到的全身性炎症,会增加骨折愈合时间和并发症(包括骨不连)的发生率。此外,有证据表明,骨折部位内不足够的生物力学条件会影响早期局部炎症,并损害骨骼愈合。在本综述中,我们讨论了影响骨折愈合的主要因素,特别强调了炎症的作用。

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Increased callus mass and enhanced strength during fracture healing in mice lacking the sclerostin gene.
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