ABSTRACT
BACKGROUND: In clinical treatment, patients with traumatic nerve injury and fractures show accelerated fracturehealing and excessive osteophyte growth, and even heterotopic ossification in the muscle, all of which seriously affect the therapeutic efficacy on such fractures. The specific causes and mechanisms for the acceleration of fracture healing after denervation are currently unclear. OBJECTIVE: To investigate the role and expression of fibroblast growth factor receptors 3 (FGFR3) inhibitor in the process of fracture healing. METHODS: The study protocol was approved by the Animal Ethics Committee of Second Hospital of Lanzhou University. Sixty female Sprague-Dawley rats were used to make a transverse humeral fracture model of sciatic nerve injury. They were randomly divided into two groups, experimental group and control group. The experimental group received intraperitoneal injection of FGFR3 blocker; the control group received an equal dose of normal saline. The X-ray films were taken at 4, 7, 10, 14 and 21 days after surgery, and tibia specimens for six animals were subsequently taken at each time point, followed by histological observations using hematoxylin-eosin staining and Masson’s trichrome staining. Osteocyte density and trabecular bone density of the rat tibia were calculated; and the fiber rate of the tibia was determined. RESULTS AND CONCLUSION: There were no significant differences in the X-ray findings of the tibia between the two groups. The experimental group had better bone repair than the control group, shown by hematoxylin-eosin staining and Masson’s trichrome staining. Osteocyte density, trabecular bone density, and fiber rate of the rat tibia were significantly higher in the experimental group than the control group at 7-14 days after treatment. Inhibition of FGFR3 can accelerate fracture healing and promote the shaping of callus in the case of peripheral nerve denervation. FGFR3 is most active at 7-14 days after fracture.