BackgroundIt remains unclear whether conservative treatment should be used to treat the common undisplaced femoral neck fractures that develop in the elderly. Herein, we systematically review the rates of union and avascular necrosis after conservative and surgical treatment of undisplaced femoral neck fractures.MethodsWe searched the EMBASE, PubMed, OVID, Cochrane Library, Web of Science, and Scopus databases for randomized controlled trials or observational studies that assessed the outcomes of conservative or surgical treatments of undisplaced femoral neck fractures. No language or publication year limitation was imposed. Statistical analyses were performed with the aid of the chi-squared test. We evaluated the quality of each publication and the risk of bias.ResultsTwenty-nine studies involving 5071 patients were ultimately included; 1120 patients were treated conservatively and 3951 surgically. The union rates were 68.8% (642/933) and 92.6% (635/686) in the former and latter groups, respectively (p < 0.001). The avascular necrosis rate in the conservatively treated group was 10.3% (39/380), while it was 7.7% (159/2074) in the surgically treated group (p = 0.09).ConclusionsSurgery to treat undisplaced femoral neck fractures was associated with a higher union rate and a tendency toward less avascular necrosis than conservative treatment.
Though the occurrence of neuroinflammation after spinal cord injury (SCI) is essential for antigen clearance and tissue repair, excessive inflammation results in cell death and axon dieback. The effect of anti‐inflammatory medicine used in clinical treatment remains debatable owing to the inappropriate therapeutic schedule that does not align with the biological process of immune reaction. A better understanding of the immunity process is critical to promote effective anti‐inflammatory therapeutics. However, cellular heterogeneity, which results in complex cellular functions, is a major challenge. This study performs single‐cell RNA sequencing by profiling the tissue proximity to the injury site at different time points after SCI. Depending on the analysis of single‐cell data and histochemistry observation, an appropriate time window for anti‐inflammatory medicine treatment is proposed. This work also verifies the mechanism of typical anti‐inflammatory medicine methylprednisolone sodium succinate (MPSS), which is found attributable to the activation inhibition of cells with pro‐inflammatory phenotype through the downregulation of pathways such as TNF, IL2, and MIF. These pathways can also be provided as targets for anti‐inflammatory treatment. Collectively, this work provides a therapeutic schedule of 1–3 dpi (days post injury) to argue against classical early pulse therapy and provides some pathways for target therapy in the future.
Neuroinflammation is a necessary response to spinal cord injury (SCI) as it helps to clear antigens and promote tissue repair. However, excessive inflammation can result in the death of cells and axon dieback. The efficacy of anti-inflammatory medication in clinical treatment is still up for debate due to inappropriate therapeutic scheduling that does not align with the biological process of immune response. A better understanding of the immune process is crucial for effective anti-inflammatory therapeutics, but it is challenged by cellular heterogeneity and complex cellular functions. To address this, we conducted a single-cell RNA sequencing study and profiled tissue proximity to the injury site at various time points after SCI. Based on our analysis of single-cell data and histochemistry observations, we recommend an appropriate time window of 1-3 days post-injury for anti-inflammatory medication treatment. We also verified the mechanism of MPSS, a typical anti-inflammatory medication, which was found to inhibit the activation of cells with pro-inflammatory phenotypes by downregulating pathways such as TNF, IL2, and MIF. These pathways could be potential targets for anti-inflammatory treatment. In summary, we recommend a therapeutic schedule of 1-3 days post-injury to argue against classical early pulse therapy and provide potential pathways for target therapy in the future.
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