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作 者:李怀任 韩凤平 孟静[2] 常文利[2] 冯立[2] LI Huairen;HAN Fengping;MENG Jing;CHANG Wenli;FENG Li(School of Clinical Medicine,Jining Medical University,Jining Shandong,272000,P.R.China;Department of Emergency Trauma Surgery,the First People’s Hospital of Jining,Jining Shandong,272000,P.R.China)
机构地区:[1]济宁医学院临床医学院,山东济宁272000 [2]济宁市第一人民医院急诊创伤外科,山东济宁272000
出 处:《中国修复重建外科杂志》2024年第1期125-132,共8页Chinese Journal of Reparative and Reconstructive Surgery
基 金:山东省中医药科技项目(M-2023157);济宁市重点研发计划项目(2021YXNS125);济宁市第一人民医院博士基金(2022-BS-005)。
摘 要:目的总结创伤性脑损伤(traumatic brain injury,TBI)促进骨折愈合相关机制的研究进展,为临床治疗骨折不愈合提供理论依据。方法查阅国内外关于TBI促进骨折愈合的研究文献,从神经、体液及免疫3个方面总结TBI在骨折愈合中的作用,探讨骨折不愈合治疗新思路。结果大量研究表明,骨折合并TBI患者的骨折愈合速度较单纯骨折患者更快。骨折合并TBI患者体液中各种细胞因子、激素的表达量明显高于单纯骨折患者;神经系统释放的神经因子透过受损血脑屏障到达骨折部位,同时合并TBI的骨折端炎症细胞和炎症因子的趋化、聚集与单纯骨折患者也有显著差异。复杂的体液、神经及免疫调节网络共同促进骨折端血管再生、成骨细胞分化并抑制破骨细胞活性。结论TBI通过复杂的神经、体液及免疫调节网络促进骨折愈合,提示通过干预骨折周围微环境可以治疗骨折不愈合。Objective To summarize the research progress on the mechanism related to traumatic brain injury(TBI)to promote fracture healing,and to provide theoretical basis for clinical treatment of fracture non-union.Methods The research literature on TBI to promote fracture healing at home and abroad was reviewed,the role of TBI in fracture healing was summarized from three aspects of nerves,body fluids,and immunity,to explore new ideas for the treatment of fracture non-union.Results Numerous studies have shown that fracture healing is faster in patients with fracture combined with TBI than in patients with simple fracture.It is found that the expression of various cytokines and hormones in the body fluids of patients with fracture and TBI is significantly higher than that of patients with simple fracture,and the neurofactors released by the nervous system reaches the fracture site through the damaged blood-brain barrier,and the chemotaxis and aggregation of inflammatory cells and inflammatory factors at the fracture end of patients with combined TBI also differs significantly from those of patients with simple fracture.A complex network of humoral,neural,and immunomodulatory networks together promote regeneration of blood vessels at the fracture site,osteoblasts differentiation,and inhibition of osteoclasts activity.Conclusion TBI promotes fracture healing through a complex network of neural,humoral,and immunomodulatory,and can treat fracture non-union by intervening in the perifracture microenvironment.
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