Research progress on mechanism of traumatic brain injury promoting fracture healing.
10.7507/1002-1892.202310045
- Author:
Huairen LI
1
;
Fengping HAN
1
;
Jing MENG
2
;
Wenli CHANG
2
;
Li FENG
2
Author Information
1. School of Clinical Medicine, Jining Medical University, Jining Shandong, 272000, P. R. China.
2. Department of Emergency Trauma Surgery, the First People's Hospital of Jining, Jining Shandong, 272000, P. R. China.
- Publication Type:Journal Article
- Keywords:
Traumatic brain injury;
cytokines;
fracture healing;
hormones;
inflammation;
neurokines
- MeSH:
Humans;
Fracture Healing/physiology*;
Brain Injuries/metabolism*;
Brain Injuries, Traumatic;
Fractures, Bone;
Osteogenesis
- From:
Chinese Journal of Reparative and Reconstructive Surgery
2024;38(1):125-132
- CountryChina
- Language:Chinese
-
Abstract:
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.
