M2 macrophages are closely associated with accelerated clavicle fracture healing in patients with traumatic brain injury
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RESEARCH ARTICLE
Open Access
M2 macrophages are closely associated with accelerated clavicle fracture healing in patients with traumatic brain injury: a retrospective cohort study Ran Zhang1,2*, Yi Liang1 and Shuxiang Wei1
Abstract Background: Mounting evidence indicate patients with traumatic brain injury (TBI) have an accelerated fracture healing. The healing process of bone fractures is greatly dependent on infiltrated macrophages. The macrophages are categorized into M1 or M2 phenotypes with different functions. This study is aimed to address the potential role of subtypes of macrophages in the process of fracture healing in patients with TBI. Methods: Twenty-five cases of clavicle fracture alone (CF group) and 22 cases of clavicle fracture concomitant with TBI (CFT group) were retrospectively analyzed in this study. Callus tissues were harvested during operations. The expressions of COX-2, CD206, and CD68 were measured with immunohistochemistry. Results: The percentages of M2 macrophages in total macrophages increased after bone fracture in both groups, while the percentages of M1-type macrophages are decreased. Interestingly, the increased percentages of M2 macrophages are significantly higher in CFT group than in CF group. Compared to CF group, the fracture callus volume was much larger (21.9 vs 8.5 cm3) and the fracture healing time was much shorter (82.2 vs 127.0 days) in CFT group. The percentage of M2 macrophages was negatively correlated with fracture healing time in patients (r = − 0.575, p < 0.01). Conclusions: The findings suggest that the percentages of M2 macrophages in callus tissues increased dramatically during the repairing stage in both CF and CFT group. Percentages of M2 macrophages are associated with accelerated fracture healing in patients with TBI. M2 macrophage polarization during the stage of bone regeneration may play a vital role in promoting bone fracture healing. Keywords: Traumatic brain injury, Clavicle fracture, Fracture healing, Macrophages
Background Traumatic brain injury (TBI) is one of the most severe trauma-induced injuries and is one of the leading cause of death and disability. TBI is usually accompanied with peripheral bone fractures. The interaction of TBI and concomitant fracture has been under long-term discussion [1, 2]. In the last decade, multiple clinical and preclinical studies have shown an association between TBI and accelerated fracture healing [3–7]. However, the * Correspondence: [email protected] 1 Department of Orthopedics, Liuzhou General Hospital, 8 Wenchang Rd, Liuzhou 545006, Guangxi, China 2 Guangxi University of Technology, Liuzhou 545006, Guangxi, China
mechanism underlying this relationship needs to be further studied. Fracture healing is a sophisticated biological process involving numerous types of cells and signals. After the bone fracture, immune cells are rapidly recruited to the damage site and secrete inflammatory factors. This intense inflammatory response is required to facilitate the recruitment and activation of hematopoietic and mesen
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