Objective To investigate the ability of the biodegradable polycaprolactone (PCL) material to repair bone defect and to evaluate the feasibility ofusing the PCL as the scaffold in tissue engineering bone. Methods The bone defect models of 4.5 mm×12 mm were made in the bilateral femoral condyle of 65 NewZealand white rabbits. The PCL cylinder was implanted into the right side of defect(experimental group, n=60), the high dense crystality hydroxyapatite was implanted into the left side of defect (control group, n=60), and the incision was sutured without any implants (blank group, n=5). The samples were harvested and observed by examinations of gross, X-ray, bone density,99mTc-MDP bone scanning, γ-display ratio and scanning electron microscope (SEM) after 3, 6, 9 and 12 months of operation. The results were compared between the experimental group and control group. Results At 3, 6, 9 and 12 months after operation, the gross and X-ray examinations indicated that the bone defect filled with the new bone onthe PCL-tissue surface, and no delayed inflammatory reaction appeared. The average bone mineral density was greater in the experimental group than that in the control group, and the difference had statistical significance(P＜0.05). Theresults of 99mTc-MDP bone scanning and γ-display ratio showed that thenuclide uptake was more in the PCL group than that in the control group. The SEM result proved that the new compact bone formed on the PCL migrating surface as the PCL degraded gradually，but the collagen fiber sheathe formed around the hydroxyapatitein the control group. Conclusion PCL possesses good biocompatibility and high bone inductive potentiality, it can be used to repair bone defect.
【Abstract】ObjectiveTo investigate the effects of high molecular bio-degradable film on preventing peritoneal adhesion. MethodsOne hundred and twenty rats were divided into control group, non-bio-degradable film group and polycaprolactone (PCL) group. Animal models of peritoneal adhesion made by operations on rats serve as control group. In the study, non-bio-degradable film and biodegradable, namely PCL films sensitive to pseudomonas enzyme, were put into the opening of peritoneum. The effect of the films on peritoneal adhesion was examined on 1, 3, 7 and 30 d after operation. ResultsPeritoneal adhesion was found in all the rats of control group and very low in PCL group and non-bio-degradable film group. ConclusionPCL film can effectively prevent the formation of postoperative peritoneal adhesion.
ObjectiveTo fabricate salidroside/collagen/polycaprolactone (PCL) nerve conduit composite and to investigate the effect of composite nerve conduits for repairing sciatic nerve defect. MethodsThe salidroside microspheres were prepared by W/O/W method, and the sustained release rate of microspheres was detected. The microspheres containing 10, 20, and 40 μg salidroside were mixed with collagen to prepare the nerve conduit core layer by freeze-drying method. The shell layer of collagen/PCL scaffold material was fabricated by electrospinning technology. The genipin cross-linked salidroside/collagen/PCL nerve conduit composite was prepared. The structure of nerve conduit was observed before and after cross-linked by scanning electron microscope. Thirty-eight Wistar rats were used to make the right sciatic nerve defect model of 15 mm in length, and randomly divided into groups A, B, C, D (n=9), and group E (n=2), then defect was repaired with the collagen/PCL conduit in group A, autologous nerve in group E, the 10, 20, and 40 μg/mL salidroside/collagen/PCL conduit in groups B, C, and D, respectively. The survival of rats was observed. The sciatic functional index (SFI) was evaluated at 1, 3, and 6 months after operation. At 6 months, the tissue of defect area was harvested for the general, electrophysiology, histological, and immunohistochemical[S-100 and peripheral myelin protein 0(P0)] staining observations. ResultsSalidroside microspheres showed burst release at 3 days, and then it tended to be stable at 13 days and lasted for 16 days, with a cumulative release rate of 76.59%. SEM showed that the disordered fiber of nerve conduit shell layer after crosslinking became conglutination, shrinkage, and density, and had void. The channels of core layer were clearly visible before and after crosslinking. The rats had no infection or death after operation. The SFI of group E was significantly higher than that of groups A, B, C, and D at 1, 3, and 6 months (P<0.05); it was significantly higher in groups B, C, and D than group A (P<0.05), but no significant difference was found among groups B, C, and D at 1 month (P>0.05); there was no significant difference in SFI among groups A, B, C, and D at 3 months (P>0.05); SFI was significantly higher in group C than groups A, B, and D and in groups A and B than group D (P<0.05), but no significant difference between groups A and B (P>0.05) at 6 months. In addition, no significant difference was shown among different time points in the other groups (P>0.05) except groups C and E at 1, 3, and 6 months (P<0.05). The general observation showed that good connection with the thick nerve in groups B and C, and connection with the fine nerves in groups A and D. The conduit materials obviously degraded. Nerve electrophysiological examination showed that the latency/conduction velocity of groups C and E were significantly lower than those of groups A, B, and D (P<0.05), but difference was not significant between groups C and E, and among groups A, B, and D (P>0.05). The histological observation showed that the nerve fiber tissue of groups B, C, and E was obviously more than that of groups A and D, and group C was similar to group E in the nerve fiber arrangement, and the core layer material of each group was completely degraded. Immunohistochemical staining showed that S-100 and P0 proteins expressed in all groups; and the expression level of groups B, C, and E was significantly higher than that of groups A and D, and gradually increased (P<0.05); difference in S-100 expression level was not significant between groups A and D (P>0.05), and P0 expression level of group A was significantly lower than that of group D (P<0.05). ConclusionSalidroside/collagen/PCL nerve conduit can promote sciatic nerve defect repair.