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Background Repair of large-sized bone defects is a challengeable obstacle in orthopedics and evoked the demand for the development of biomaterials that could induce bone repair in such defects. Recently, UiO-66 has emerged as an attractive metal–organic framework (MOF) nanostructure that is incorporated in biomedical applications due to its biocompatibility, porosity, and stability. In addition, its osteogenic properties have earned a great interest as a promising field of research. Thus, the UiO-66 was prepared in this study and assessed for its potential to stimulate and support osteogenesis in vitro and in vivo in a rabbit femoral condyle defect model. The nanomaterial was fabricated and characterized using x-ray diffraction (XRD) and transmission electron microscopy (TEM). Afterward, in vitro cytotoxicity and hemolysis assays were performed to investigate UiO-66 biocompatibility. Furthermore, the material in vitro capability to upregulate osteoblast marker genes was assessed using qPCR. Next, the in vivo new bone formation potential of the UiO-66 nanomaterial was evaluated after induction of bone defects in rabbit femoral condyles. These defects were left empty or filled with UiO-66 nanomaterial and monitored at weeks 4, 8, and 12 after bone defect induction using x-ray, computed tomography (CT), histological examinations, and qPCR analysis of osteocalcin (OC) and osteopontin (OP) expressions. Results The designed UiO-66 nanomaterial showed excellent cytocompatibility and hemocompatibility and stimulated the in vitro osteoblast functions. The in vivo osteogenesis was enhanced in the UiO-66 treated group compared to the control group, whereas evidence of healing of the treated bone defects was observed grossly and histologically. Interestingly, UiO-66 implanted defects displayed a significant osteoid tissue and collagen deposition compared to control defects. Moreover, the UiO-66 nanomaterial demonstrated the potential to upregulate OC and OP in vivo. Conclusions The UiO-66 nanomaterial implantation possesses a stimulatory impact on the healing process of critical-sized bone defects indicating that UiO-66 is a promising biomaterial for application in bone tissue engineering.

Various biomaterials have been evaluated to enhance bone formation in critical-sized bone defects; however, the ideal scaffold is still missing. The objective of this study was to investigate the in vitro and in vivo regenerative capacity of graphitic carbon nitride (g-C3N4) and graphene oxide (GO) nanomaterials to stimulate critical-sized bone defect regeneration. The in vitro cytotoxicity and hemocompatibility of g-C3N4 and GO were evaluated, and their potential to induce the in vitro osteogenesis of human fetal osteoblast (hFOB) cells was assessed using qPCR. Then, bone defect in femoral condyles was created in rabbits and left empty as control or filled with either g-C3N4 or GO. The osteogenesis of the different implanted scaffolds was evaluated after 4, 8, and 12 weeks of surgery using X-ray, computed tomography (CT), macro/microscopic examinations, and qPCR analysis of osteocalcin (OC) and osteopontin (OP) expressions. Both materials displayed good cell viability and hemocompatibility with enhanced collagen type-I (Col-I), OC, and OP expressions of the hFOB cells. Compared to the control group, the bone healing process in g-C3N4 and GO groups was promoted in vivo. Moreover, complete healing of the bone defect was observed radiologically and grossly in g-C3N4 implanted group. Additionally, g-C3N4 implanted group showed higher percentages of osteoid tissue, mature collagen, biodegradation, and expressions of OC and OP. In conclusion, our results revealed that g-C3N4 and GO nanomaterials could induce osteogenesis in critical-sized bone defects.

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Single intra-articular (IA) injection of long-acting local anesthetics such as bupivacaine is commonly used clinically for postoperative analgesia, in particular, after arthroscopic surgery. Despite their widespread use, the side effects of IA bupivacaine on joint cartilage as well as hepatotoxic and nephrotoxic effects remain to be elucidated. The aim of this study is to assess the in vitro effect of bupivacaine 5% on donkey chondrocytes at different time points, in addition to the in vivo effects of a single IA bupivacaine injection on the middle carpal joint in a group of 10 clinically healthy adult male donkeys. In phase I, the effect of in vitro treatment with bupivacaine 5% or saline 0.9% on freshly isolated donkey chondrocytes for 30, 60 min, 24, 48, and 96 h was investigated using MTT and LIVE/DEAD assay. In phase II, in vivo effects of single injection of bupivacaine on the middle carpal joint of the donkey were evaluated compared with saline 0.9%. Biochemical analysis of collected serum and synovia was performed. Additionally, articular cartilage damage was evaluated using radiography, computed tomography (CT), catabolic marker expression via quantitative polymerase chain reaction (qPCR), and histopathological examination 96 h after injection. Our results showed that after a 30-min exposure to bupivacaine 5%, the viability of donkey chondrocytes was 97.3 ± 4.4% and was not significantly affected at the indicated time points (n = 8, p < 0.05). No significant changes in biochemical analytes of serum and synovial fluid following IA bupivacaine injection were observed, compared with saline injection (n = 5 for each group, p < 0.05). Furthermore, in vivo IA injection of bupivacaine revealed no significant differences in radiography, CT scan, gene expression of cartilage catabolic biomarkers, and histopathological examination. These results provide an evidence for the safety of bupivacaine on the donkey cartilage.