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.
Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2024 Jan 15;38(1):125-132. doi: 10.7507/1002-1892.202310045.
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.
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.
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.
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.
总结创伤性脑损伤(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。
回顾国内外关于TBI促进骨折愈合的研究文献,从神经、体液和免疫三个方面总结TBI在骨折愈合中的作用,以探索治疗骨折不愈合的新思路。
大量研究表明,骨折合并TBI患者的骨折愈合速度比单纯骨折患者更快。发现骨折合并TBI患者体液中各种细胞因子和激素的表达明显高于单纯骨折患者,神经系统释放的神经因子通过受损的血脑屏障到达骨折部位,合并TBI患者骨折端炎症细胞和炎症因子的趋化和聚集也与单纯骨折患者有显著差异。体液、神经和免疫调节网络共同促进骨折部位血管再生、成骨细胞分化并抑制破骨细胞活性。
TBI通过神经、体液和免疫调节的复杂网络促进骨折愈合,并可通过干预骨折周围微环境治疗骨折不愈合。