Enhanced wound healing associated with Sharpey's fiber-like tissue formation around FGF-2-apatite composite layers on percutaneous titanium screws in rabbits

Background Pin-tract infections are the most common complications of external fixation. To solve the problem, we developed a fibroblast growth factor-2 (FGF-2)-apatite composite layer for coating titanium screws. The purpose of this study was to elucidate the mechanism of the improvement in infection resistance associated with FGF-2-apatite composite layers. Method We analyzed FGF-2 release from the FGF-2-apatite composite layer and the mitogenic activity of the FGF-2-apatite composite layer. We evaluated time-dependent development of macroscopic pin-tract infection around uncoated titanium control screws (n = 10). Screws coated with the apatite layer (n = 16) and FGF-2-apatite composite layer (n = 16) were percutaneously implanted for 4 weeks in the medial proximal tibia in rabbits. Results A FGF-2-apatite composite layer coated on the screws led to the retention of the mitogenic activity of FGF-2. FGF-2 was released from the FGF-2-apatite composite layer in vitro for at least 4 days, which corresponds to a period when 30% of pin-tract infections develop macroscopically in the percutaneous implantation of uncoated titanium control screws. The macroscopic infection rate increased with time, reaching a plateau of 80-90% within 12 days. This value remained unchanged until 4 weeks after implantation. The screws coated with an FGF-2-apatite composite layer showed a significantly higher wound healing rate than those coated with an apatite layer (31.25 vs. 6.25%, p < 0.05). The interfacial soft tissue that bonded to the FGF-2-apatite composite layer is a Sharpey's fiber-like tissue, where collagen fibers are inclined at angles from 30 to 40A degrees to the screw surface. The Sharpey's Wber-like tissue is rich in blood vessels and directly bonds to the FGF-2-apatite composite layer via a thin cell monolayer (0.8-1.7 mu m thick). Conclusion It is suggested that the enhanced wound healing associated with the formation of Sharpey's fiber-like tissue triggered by FGF-2 released from the FGF-2-apatite composite layer leads to the reduction in the pin-tract inflammation rate.