Objective: To observe the change of fibroblast growth factor-2 (FGF-2), insulin-like growth factor-1 (IGF-1) in serum and bone callus after fracture in diabetic rats, and to explore molecular biological mechanism of healing of diabetic fracture.
Methods: Thirty male SD rats were designed into normal (n=15) and control (n=15) groups randomly. Venous blood was extracted on the lst, 2nd, 4th, 6th, 8th week after surgery. It was certificated and the serum was obtained. Left lower extremity was observed by X- ray. Bone callus at broken ends was observed under light microscope. Expressions of FGF-2 and IGF-1 in tissue were detected by immunohistochemistry method, and ELISA was used to detect expression of FGF-2 and IGF-1 in serum.
Results: The results showed a significant increase in the density and area of newly formed bone in the distraction gaps of normal rats compared to control rats. Increased cell proliferation was also found in the distraction gaps of normal rats versus control rats. There was significant difference in serum levels of FGF-2 and IGF-1 between two groups.
Conclusions: The decrease of FGF-2 and IGF-1 both in the serum and in the fracture region is one of the reasons for bad bone healing or delayed union in rats' fracture with diabetes. There are some synergistic effects possibly between FGF-2 and IGF-1.
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