Résumé
Objective@#To evaluate the osteogenic effect of concentrated growth factor (CGF) combined with deproteinated bovine bone mineral (DBBM) in site preservation using clinical and histomorphometric observations.@*Methods @#A total of 26 patients who needed extraction of affected teeth and received staged implantation after site preservation were selected. The patients were randomly divided into the DBBM group (Bio-Oss was implanted simultaneously after extraction) and CGF+DBBM group (CGF+Bio-Oss was implanted simultaneously after extraction), with 13 patients in each group, and both groups were covered with Bio-Gide collagen membrane. Cone beam computed tomography (CBCT) was performed preoperatively and 6 months later to measure the changes in alveolar bone height and width, and the bone specimens were drilled 6 months after site preservation during implant surgery for histological analyses.@*Results@# CBCT showed that the height and width of alveolar bone were absorbed 6 months after site preservation in the CGF+DBBM and DBBM groups, and the reduction in alveolar ridge width in the CGF+DBBM group was statistically less than the DBBM group (P <0.05). The histomorphometry results showed that the percentage of new bone in the CGF+DBBM and DBBM groups were 35.30% ± 3.56% and 26.38% ± 5.04%, respectively, and the amount of new bone in the CGF+DBBM group was statistically higher than the DBBM group (P<0.05). @*Conclusion @#CGF combined with DBBM is superior to DBBM in maintaining the alveolar bone volume and shape in site preservation, which creates favorable conditions for implant restoration.
Résumé
BACKGROUND: Guided bone regeneration technology, as a most widely used method for repairing bone defects, has been extensively used in the field of stomatology. However, there are few reports on the guided bone regeneration technology in long bone defects. OBJECTIVE: To explore the effects of guided bone regeneration combined with kidney-tonifying therapy on the repair of femoral bone defects in rats, and investigate its osteogenic efficacy and underlying mechanism. METHODS: Thirty-six Sprague-Dawley rats were randomly divided into six groups: blank group, guided bone regeneration group, high-, moderate-, and low-dose kidney-tonifying groups, and ossotide tablets group. The femur bone defect model of rats was established, and was treated by guided bone regeneration except for blank group. Bio-Gide collagen membrane combined with autologous bone was implanted by guided bone regeneration. The kidney-tonifying groups were given 0.216, 0.108 and 0.054 g/(kg•d) Qianggu capsule via gavage for 8 weeks. The ossotide tablets group was given 0.58 mg/(kg•d) ossotide tablets via gavage for 8 weeks. At 12 weeks after surgery, the osteogenesis was evaluated by X-ray examination, hematoxylin-eosin staining and Masson staining of bone tissue. The mRNA expression levels of alkaline phosphatase, Runx-2, vascular endothelial growth factor and bone morphogenetic protein-2 in bone tissues were detected by quantitative real-time RT-PCR. RESULTS AND CONCLUSION: Results of X-ray examination and hematoxylin-eosin staining and Masson staining of bone tissue showed that the scores of Lane Sandhu and Huddleston in each group were significantly higher than those in the blank group (P < 0.001). The scores in the high-and moderate-dose kidney-tonifying groups were significantly higher than those in the guided bone regeneration group (P < 0.01). RT-PCR results showed that the mRNA expression levels of alkaline phosphatase, Runx-2, vascular endothelial growth factor and bone morphogenetic protein-2 in bone tissue in the high-and moderate-dose kidney-tonifying groups were significantly higher than those in the blank group (P < 0.01), and were superior to the guided bone regeneration group (P < 0.05). In summary, guided bone regeneration combined with kidney-tonifying can significantly promote the repair of femoral bone defects, reduce bone absorption and improve osteogenic efficacy in rats. The mechanism of promoting bone regeneration and angiogenesis may be by up-regulating the expression of related osteogenic factors and angiogenic factors in the environment where the membrane barrier creates a dominant growth of bone tissue.