创伤性脑损伤促进骨痂形成及骨折愈合的机制  

Mechanisms by which traumatic brain injury promotes bone callus formation and fracture healing

作　　者：刘涵菲 蔡振存[1] 周雪婷 温航 陈振军 Liu Hanfei;Cai Zhencun;Zhou Xueting;Wen Hang;Chen Zhenjun(Central Hospital of Shenyang Medical College,Shenyang 110024,Liaoning Province,China)

机构地区：[1]沈阳医学院附属中心医院,辽宁省沈阳市110024

出　　处：《中国组织工程研究》2025年第29期6260-6268,共9页Chinese Journal of Tissue Engineering Research

基　　金：沈阳市科技计划项目(22-321-32-13),项目负责人:蔡振存;2023年度辽宁省教育厅基本科研项目(JYTMS20231396),项目负责人:蔡振存。

摘　　要：背景:骨折延迟愈合和不愈合是常见的临床问题。在临床观察中,常见到合并创伤性脑损伤的四肢骨折患者的骨折愈合速度明显快于无脑损伤的患者。这一现象背后的可能机制已成为当前研究的重要焦点。近年来的研究表明,创伤性脑损伤通过调控细胞因子、激素、神经信号以及干细胞等机制,显著加速了骨痂形成和骨折愈合过程。目的:总结创伤性脑损伤促进骨痂形成及骨折愈合机制的最新研究进展,为临床应用提供理论依据。方法:文章第一作者通过检索中国知网、万方、维普、PubMed、Embase、Web of Science及Cochrane Library数据库2013年1月至2024年10月相关文献,个别文献追溯至20年前。检索词为“创伤性脑损伤,骨痂,骨折愈合,炎症反应,细胞因子,激素,神经肽,基因,干细胞”“traumatic brain injury,callus,fracture healing,inflammatory response,cytokines,hormones,neuropeptides,genes,stem cells”,最终选取符合纳入标准的文献共计83篇。结果与结论:创伤性脑损伤对骨痂形成及骨折愈合的促进作用机制极其复杂,涉及细胞因子、激素、神经系统和干细胞等多个调节环节。然而,目前关于创伤性脑损伤促进骨痂形成及骨折愈合的具体机制尚未得到全面、清晰的理解,仍需进一步深入研究。现有研究表明,创伤性脑损伤主要通过促进细胞因子(如胰岛素样生长因子1)和激素(如生长激素及瘦素)的释放,调控神经系统,促进干细胞的增殖与分化等机制来加速骨痂形成和骨组织再生。此外,创伤性脑损伤会引发一系列免疫反应,包括炎症因子的释放和免疫细胞的激活,这些反应能够调节骨折修复的过程。具体而言,免疫反应通过增强局部血流、促进细胞迁移和激活成纤维细胞,从而支持骨愈合的不同阶段。同时,创伤性脑损伤诱发的干细胞活化也在骨折修复中发挥了关键作用。活化的干细胞能够分化为�BACKGROUND:Delayed healing and nonunion of fractures are common clinical issues.Clinical observations have shown that patients with limb fractures combined with traumatic brain injury experience significantly faster fracture healing compared with those without brain injury.The potential mechanisms behind this phenomenon have become a crucial focus of current research.Recent studies indicate that traumatic brain injury significantly accelerates callus formation and fracture healing processes by regulating cytokines,hormones,neural signals,and stem cell mechanisms.OBJECTIVE:To summarize the latest research progress in the mechanisms by which traumatic brain injury promotes callus formation and fracture healing,thereby providing a theoretical basis for clinical applications.METHODS:The first author conducted a search of CNKI,WanFang,VIP,PubMed,Embase,Web of Science,and Cochrane Library databases for literature published from January 2013 to October 2024,with some references traced back up to 20 years.The search terms used were“traumatic brain injury,callus,fracture healing,inflammatory response,cytokines,hormones,neuropeptides,genes,stem cells”in Chinese and English.A total of 83 articles meeting the inclusion criteria were ultimately selected.RESULTS AND CONCLUSION:The mechanism by which traumatic brain injury promotes callus formation and fracture healing is highly complex,involving multiple regulatory pathways such as cytokines,hormones,the nervous system,and stem cells.However,the precise mechanisms are still not fully understood and require further investigation.Current research suggests that traumatic brain injury accelerates bone callus formation and bone tissue regeneration by promoting the release of cytokines(e.g.,insulin-like growth factor-1)and hormones(e.g.,growth hormone and leptin),regulating the nervous system,and promoting stem cell proliferation and differentiation.Additionally,traumatic brain injury triggers a series of immune responses,including the release of inflammatory factors and activat

关 键 词：创伤性脑损伤 骨痂 骨折愈合 炎症反应 细胞因子 激素 神经肽 基因 干细胞 

分 类 号：R459.9[医药卫生—治疗学] R363[医药卫生—临床医学] R651.15