Objective: To explore the effect of diabetes mellitus (DM) on implant osseointegration of titanium screws.Methods: Sixty rats were randomly divided into a DM group and a control group (each group, n = 30). DM group rats were injected with 1% Streptozotocin solution at 65 mg/kg to establish a DM model. Titanium screws were implanted into the rats' distal femurs in both groups. The rats were sacrificed for micro‐CT scanning, micro‐indentation, biomechanical detection, confocal Raman microspectroscopy, and histological and histomorphometric analysis at 4, 8, and 12 weeks post‐implantation, respectively. Messenger RNA (mRNA) expression and protein expression of the related growth factors around the implant were analyzed using real‐time polymerase chain reaction and Western blots.Results: At 4, 8 and 12 weeks, micro‐CT scanning, hematoxylin‐eosin (HE) staining, Gieson's acid‐magenta staining, and fluorescent labeled staining showed disorder in the bone tissue arrangement, a lack of new bone tissue, poor maturity and continuity, and poor trabecular bone parameters around the implant in the DM group. At 4, 8, and 12 weeks, the interfacial bone binding rate in the DM group was significantly lower (16.2% ± 4.8%, 25.7% ± 5.7%, 42.5% ± 5.8%, respectively) than that in the control group (23.6% ± 5.2%, 40.8% ± 6.3%, 64.2% ± 7.3%, respectively; P < 0.05). At 8 and 12 weeks, the elastic modulus (17.0 ± 1.8 and 15.1 ± 1.5 GPa, respectively) and trabecular bone hardness (571 ± 39 and 401 ± 37 MPa, respectively) in the DM group were significantly lower than the elastic modulus (23.4 ± 2.3 and 23.8 ± 1.8 GPa, respectively) and trabecular bone hardness (711 ± 45 and 719 ± 46 MPa, respectively) in the control group (P < 0.05). The maximum load required for the prosthesis pull‐out experiment in the DM group at 4, 8, and 12 weeks (55.14 ± 6.74 N, 73.34 ± 8.43 N, and 83.45 ± 8.32 N, respectively) was significantly lower than that in the control group (77.45 ± 7.48 N, 93.28 ± 8.29 N, and 123.62 ± 9.43 N, respectively, P < 0.05). At 8 and 12 weeks, the mineral‐to‐collagen ratio in the DM group (6.56 % ± 1.35% and 4.45%± 1.25%, respectively) was significantly higher than that in the control group (5.31% ± 1.42% and 3.62% ± 1.33%, respectively, P < 0.05). At 12 weeks, mRNA and protein expression levels of bone morphogenetic protein 2, transforming growth factor‐β1, vascular endothelial growth factor, osteopontin, osteocalcin, and runt‐related transcription factor 2 in the DM group were significantly lower than that in the control group.Conclusions: DM can negatively affect bone osseointegration, manifesting as disorder in bone tissue arrangement around the implant, a lack of new bone tissue, poor maturity and continuity, poor trabecular bone parameters and lower expression of the related growth factors.

Objective: To explore the biomechanical efficacy of arthroscopic all-inside anterior talofibular ligament (ATFL) suture augmentation repair, plus suture augmentation repair and anterior tibiofibular ligament-distal fascicle (ATiFL-DF) transfer augmentation repair, so as to provide a basis for the accurate selection of ATFL repair in clinical practice. Methods: Twenty-four (12 pairs) fresh frozen human cadaver ankle specimens were used. Six of the ankle specimens were set as the normal group, and the other 18 ankle specimens were used to establish ATFL injury models. The ATFL was then repaired using arthroscopic all-inside ATFL suture augmentation repair (suture augmentation group), plus suture augmentation repair (plus suture augmentation group) and ATiFL-DF transfer augmentation repair (biological augmentation group), respectively. After the repaired ATFL was separated, the ankle specimens were fixed on an electronic universal testing machine with a customized fixture for the tensile test, and the ultimate failure load (N) and stiffness (N/mm) of the ankle specimens were compared. Results: The ultimate failure load of the plus suture augmentation group (229.3 ± 66.7 N) was significantly higher than that in the normal group (148.2 ± 39.4 N, p = 0.045) and the biological augmentation group (131.3 ± 38.8 N, p = 0.013). There was no statistical difference in ultimate failure load between the suture augmentation group (167.2 ± 47.2 N), the normal group and the biological augmentation group. The stiffness of the plus suture augmentation group (26.2 ± 8.2 N/mm) was significantly higher than that in the normal group (12.1 ± 3.8 N/mm, p = 0.005) and the biological augmentation group (12.7 ± 5.2 N/mm, p = 0.007). The stiffness of the suture augmentation group (23.6 ± 7.0 N/mm) was significantly higher than that in the normal group (p = 0.024) and the biological augmentation group (p = 0.033). There was no statistical difference in stiffness between the plus suture augmentation group and the suture augmentation group, and no statistical difference in stiffness between the normal group and the biological augmentation group. Conclusion s: The tensile strength and rigidity of plus suture augmentation repair were significantly better than those of normal ATFL, suture augmentation repair and ATiFL-DF transfer augmentation repair. Suture augmentation repair can obtain tensile strength similar to normal ATFL and ATiFL-DF transfer augmentation repair, and suture augmentation repair can obtain rigidity significantly better than normal ATFL and ATiFL-DF transfer augmentation repair. ATiFL-DF transfer augmentation repair can obtain tensile strength and rigidity similar to normal ATFL.

Osteosarcoma is a primary malignant bone tumor that primarily affects adolescents and children, is highly metastatic and invasive, and has a poor survival prognosis. P3H2 is a basement membrane-associated tumor suppressor gene that is down-regulated in some types of tumors. Although some studies have shown that P3H2 has a tumor suppressive effect in some cancers, its role and specific mechanism in osteosarcoma remain unclear. Further analysis of the function and mechanism of the basement membrane-related gene P3H2 in osteosarcoma is expected to provide new insights for early diagnosis and treatment, prognosis evaluation, and targeted drug development. In this study, we first investigated the dysregulation of P3H2 in osteosarcoma and pan-cancer by using public databases and bioinformatics analysis. Further, we confirmed the expression of P3H2 in osteosarcoma cell lines. Subsequently, we investigated the effect of P3H2 on proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of osteosarcoma cells through in vitro and in vivo experiments. Finally, we investigated the mechanism by which P3H2 affects the malignant behavior of osteosarcoma through a response experiment. Through comprehensive bioinformatic analysis, this study revealed the expression, prognostic value, and immunomodulatory role of P3H2 in a variety of tumors. Subsequent experiments showed that P3H2 could inhibit the proliferation, migration, invasion, and EMT of osteosarcoma cells, and inhibit the growth of subcutaneous tumors. Mechanistically, P3H2 inactivates AKT/mTOR signaling by inhibiting AKT and mTOR phosphorylation, thereby inhibiting proliferation, migration, invasion, and EMT of osteosarcoma cells. As a tumor suppressor gene in osteosarcoma, P3H2 inhibits the malignant biological behavior of osteosarcoma by inhibiting the AKT/mTOR signaling axis.