An update on the advances in the field of nanostructured drug delivery systems for a variety of orthopedic applications.

Nanotechnology has made significant progress in various fields, including medicine, in recent times. The application of nanotechnology in drug delivery has sparked a lot of research interest, especially due to its potential to revolutionize the field. Researchers have been working on developing nanomaterials with distinctive characteristics that can be utilized in the improvement of drug delivery systems (DDS) for the local, targeted, and sustained release of drugs. This approach has shown great potential in managing diseases more effectively with reduced toxicity. In the medical field of orthopedics, the use of nanotechnology is also being explored, and there is extensive research being conducted to determine its potential benefits in treatment, diagnostics, and research. Specifically, nanophase drug delivery is a promising technique that has demonstrated the capability of delivering medications on a nanoscale for various orthopedic applications. In this article, we will explore current advancements in the area of nanostructured DDS for orthopedic use.

Knowledge Mapping of Macrophage in Spinal Cord Injury: A Bibliometric Analysis.

BACKGROUND: Spinal cord injury (SCI) is a devastating condition, often leading to significant disability and impairment. As crucial immune cells, macrophages play a critical role in the pathophysiology of SCI. Understanding the current state of knowledge and research trends related to macrophages in SCI is crucial for developing effective therapeutic interventions. METHODS: Using search strategies, we retrieved relevant articles from the Web of Science Core Collection (WOSCC), resulting in a robust dataset for analysis. VOSviewer, Citespace, and PRISM were employed for analysis and visualization. Various bibliometric indicators, including publication trends, citation analysis, co-authorship networks, and keyword analysis, were utilized to assess the scholarly landscape of macrophage research in SCI. RESULTS: Our findings revealed a steady increase in publications over the past 33 years, indicating a growing interest in this field. We identified Popovich Phillip G was the most influential author, Ohio State University was the most influential institution, and identification of 2 distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord was the most influential paper in this field. CONCLUSIONS: This bibliometric analysis provides a comprehensive overview of the current knowledge landscape and research trends regarding macrophages in SCI. Neuroinflammation and macrophage polarization, transplation and molecular mechanism were emerging research areas and novel directions. Our study serves as a valuable resource for researchers in spinal cord injury research and therapeutic development.

Comparative study of the modified transtibial technique and the transportal technique in anterior cruciate ligament reconstruction.

BACKGROUND: This study sought to compare the efficacy of the modified transtibial (TT) technique and the transportal (TP) technique in arthroscopic anterior cruciate ligament (ACL) reconstruction. METHODS: This study retrospectively analyzed the clinical data of 74 patients (74 knees) who underwent ACL reconstruction using a single bundle of autologous hamstring tendon graft from October 2013 to September 2017. Forty-one knees were reconstructed using the TT technique (the TT group), and 33 were reconstructed using the TP technique (the TP group). There was no statistically significant difference between the two groups (P>0.05) in terms of age, sex, follow-up time, time from injury to operation, left and right knees, body mass index, and preoperative International Knee Documentation Committee (IKDC) score, Tegner Activity score (Tegner score), Lysholm score, Lachman test results, and Pivot-Shift test results. RESULTS: The incisions in both groups were healed by first intention, and no early postoperative complications occurred. All patients attended follow-up appointments. The TT group had a follow-up period of 24-46 months (average follow-up time: 27.3 months). The TT group had a follow-up period of 24-38 months (average follow-up time: 26.3 months). Two years after surgery, the IKDC, Lysholm, and Tegner scores of the two groups were significantly improved compared to those before surgery (P<0.05), and there was no statistically significant difference between the two groups in relation to these scores (P>0.05). There was also no statistically significant difference in the Lachman and Pivot-Shift test results between the two groups (P>0.05). CONCLUSIONS: Both the TT and TP techniques provide satisfactory efficacy in ACL reconstruction.

Carvacrol Suppresses Human Osteosarcoma Cells via the Wnt/ß-Catenin Signaling Pathway.

BACKGROUND: Carvacrol is a monoterpenic phenol extracted from traditional Chinese herbs, including oregano and thyme. Currently, carvacrol has been widely studied for its therapeutic role in central nervous system diseases, liver diseases and digestive system cancer. OBJECTIVE: However, the role of carvacrol in osteosarcoma and its underlying molecular mechanism remain elusive. Here, we aimed to examine the anticancer effects of carvacrol on osteosarcoma. METHODS: The effects of carvacrol on the osteosarcoma proliferation capacity were revealed by CCK-8 and colony formation assays. Flow cytometry and Hoechst assays were used to determine the effects of carvacrol on osteosarcoma cell apoptosis. The effect of carvacrol on migration and invasion of osteosarcoma cells was determined by wound healing and transwell tests. Protein expression was evaluated by WB assays. The suppressive effects of carvacrol on osteosarcoma in vivo were examined by a xenograft animal model, immunohistochemistry and HE staining. RESULTS: We demonstrated that carvacrol treatment reduced viability and inhibited the colony formation of U2OS and 143B cells in a concentration-dependent manner. Apoptotic cell number increased after exposure to carvacrol. Meanwhile, the expression of Bax increased, and that of Bcl-2 decreased by carvacrol treatment. In addition, the MMP-9 expression and migration and invasion of 143B and U2OS cells were inhibited by carvacrol. We also found that these carvacrol-induced effects on osteosarcoma are associated with the regulation of the Wnt/ß-catenin signaling pathway. CONCLUSION: Our findings suggest that carvacrol suppresses proliferation, migration, invasion and promotes apoptosis in osteosarcoma cells, in part by regulating the Wnt/ß-catenin signaling pathway.

Clinical Study on Different Methods of Internal Fixation for Treatment of Lisfranc Joint Injury.

The Lisfranc joints are mainly used to connect the forefoot and midfoot and maintain the stability of the arch of the foot. It is an important part of the arch of the foot. If the Lisfranc joints injury is not treated in time, it will cause poor walking, pain in the back of the foot, and even deformity or disability of the forefoot. The common treatment method is to select the Kirschner wires, screws, or steel plates for incisional repositioning internal fixation surgery. In our study, we used different materials to perform fixation surgery on Lisfranc joint injury patients. We measured the joint recovery, pain condition, complications, and biomechanical indexes of different groups of patients after the operation. The results of the study showed that compared with Kirschner wire and screw internal fixation, the use of shaped arch bridge-type microsteel plate internal fixation for the treatment of metatarsotarsal joint injury patients has better foot function recovery, fewer complications, and more reliable biomechanical strength.

Galangin suppresses RANKL-induced osteoclastogenesis via inhibiting MAPK and NF-κB signalling pathways.

Osteoclasts play a critical role in osteoporosis; thus, inhibiting osteoclastogenesis is a therapeutic strategy for osteoporosis. Galangin, a natural bioflavonoid extracted from a traditional Chinese herb, possesses a variety of biological activities, including anti-inflammation and anti-oxidation. However, its effects on osteoporosis have not been elucidated. In this study, we found that galangin treatment dose-dependently decreased osteoclastogenesis in bone marrow-derived macrophages (BMMs). Moreover, during osteoclastogenesis, osteoclast-specific genes, such as tartrate-resistant acid phosphatase (TRAP), cathepsin K (CtsK), ATPase, H + transporting, lysosomal V0 subunit D2 (V-ATPase d2) and dendritic cell-specific transmembrane protein (DC-STAMP), were down-regulated by galangin treatment. Furthermore, the results of the pit formation assay and F-actin ring staining revealed impaired osteoclastic bone resorption in the galangin-treated group compared with that in the control group. Additionally, galangin treatment also inhibited the phosphorylation of p38 and ERK of MAPK signalling pathway, as well as downstream factors of NFATc1, C-Jun and C-Fos. Consistent with our in vitro results, galangin suppressed lipopolysaccharide (LPS)-induced bone resorption via inhibition of osteoclastogenesis. Taken together, our findings provide evidence that galangin is a promising natural compound for the treatment of osteoporosis and may be associated with the inhibition of MAPK and NF-κB signalling pathways.

Fangchinoline suppresses the proliferation, invasion and tumorigenesis of human osteosarcoma cells through the inhibition of PI3K and downstream signaling pathways.

Osteosarcoma is the most common malignant bone tumor. Most patients diagnosed with osteosarcoma are less than 20 years of age. Osteosarcoma cells proliferate rapidly and invade other tissues. At present, neoadjuvant chemotherapy is the primary pharmacodynamic strategy to prevent the progression of osteosarcoma. However, adverse effects of this strategy limit its long­term application. Previous research has shown that fangchinoline exerts antitumor effects on several types of tumor cells; however, its effect on osteosarcoma cells remains unknown. The present study evaluated the effects of fangchinoline on the proliferation, apoptosis, migration and invasion of osteosarcoma cells in vitro and on their tumorigenesis in vivo and determined the possible underlying mechanism of action. Fangchinoline­treated MG63 and U20S cells showed significantly decreased proliferation and significantly increased apoptosis. Fangchinoline markedly suppressed the migration and invasion of the MG63 cells. Fangchinoline­treated MG63 cells showed significantly decreased expression of phosphoinositide 3­kinase (PI3K) and Aktp­Thr308. Moreover, fangchinoline­treated MG63 cells showed downregulated expression of cyclin D1 and matrix metalloproteinase 2 and 9, which act downstream of PI3K, and upregulated expression of caspase­3 and caspase­8. Furthermore, fangchinoline suppressed the growth of subcutaneous osteosarcoma tumors in Balb/c mice subcutaneously injected with osteosarcoma cells. These findings suggest that fangchinoline inhibits the progression of osteosarcoma by suppressing the proliferation, migration and invasion and by accelerating the apoptosis of osteosarcoma cells. In addition, our results suggest that the mechanism underlying the antitumor effects of fangchinoline involve the inhibition of PI3K and its downstream signaling pathways.

Galangin suppresses human osteosarcoma cells: An exploration of its underlying mechanism.

Osteosarcoma is the most common malignant bone tumor that frequently affects adolescents. Osteosarcoma cells tend to proliferate and invade other tissues such as those of the lungs. Currently, neoadjuvant chemotherapy is the primary strategy to prevent tumor progression. However, its adverse effects result in poor long-term outcomes. Previous research has shown that galangin exhibits antitumor properties on several types of cancer cells; however its effect on osteosarcoma cells is yet unknown. The aims of this study were to evaluate the effects of galangin on the proliferation, apoptosis, migration, and invasion of osteosarcoma cells and to explore the underlying mechanisms. We found that the proliferation of MG63 and U20S osteosarcoma cells decreased significantly, while the apoptosis of MG63 cells accelerated significantly after exposure to galangin. In addition, the migration and invasion of MG63 cells were significantly inhibited by galangin. Moreover, phosphoinositide 3-kinase (PI3K) and Aktp-Thr308 expression levels were found to be significantly lower in galangin-treated MG63 cells than in the control cells, and the protein expression levels of their downstream regulators cyclin D1 and matrix metalloproteinase 2/9 were also downregulated in galangin-treated groups, while those of p27Kip1, caspase-3, and caspase-8 were upregulated. These findings suggest that galangin suppresses osteosarcoma cells by inhibiting their proliferation and invasion and accelerating their apoptosis, and the mechanism may be associated with the inhibition of PI3K and its downstream signaling pathway.