Background: For periacetabular osteotomy, traditional approaches usually have a long learning curve. We aimed to evaluate the postoperative results and complications of periacetabular osteotomy under a new double-incision approach. Methods: The records of 58 consecutive patients (65 hips) who underwent periacetabular osteotomy using the new approach were retrospectively reviewed and evaluated. There were 52 women and 6 men with a mean age of 28.1 years at the time of surgery. Results: The average follow-up period was 35.2 months, during which no patients were converted to total hip arthroplasty. Complications included 6 hips (9.2%) with nerve dysesthesias and 1 hip (1.5%) with delayed wound healing. The mean operative time and intraoperative blood loss were 88.6 min and 402.8 ml, respectively. The mean modified Harris hip score had improved from 72.2 points preoperatively to 91.3 points at the last follow-up. Fifty-five patients (62 hips, 95.4%) were satisfied to their outcomes, and good preoperative functional score was associated with a satisfactory outcome. Furthermore, the average lateral center–edge angle, anterior center–edge angle and acetabular index angle were corrected well after surgery. Conclusion: Periacetabular osteotomy using modified Smith-Petersen or Bikini approach with posterolateral assisted small incision can be performed safely and with satisfactory results. In addition, this technique shortens the learning curve, and reduces the operating complexity, especially for beginner.

Background The copper metabolism may play a role in angiogenesis and osteogenesis. However, the relationship between copper metabolism and steroid-induced osteonecrosis of the femoral head (SONFH) still remains unclear. Methods The GSE123568 dataset and 2062 copper metabolism-related genes (CMRGs) were downloaded from the Gene Expression Omnibus (GEO) and GeneCards databases, respectively. The differentially expressed copper metabolism-related SONFH genes (DE-CMR-SONFHGs) were identified by differential analysis and weighted gene coexpression network analysis (WGCNA). The Least-Absolute Shrinkage and Selection Operator (LASSO) and Support Vector Machine (SVM) algorithms were employed to screen key DE-CMR-SONFHGs. Receiver operating characteristic (ROC) analysis and functional enrichment analysis were performed on the key genes. Targeting drugs were predicted with The Drug Gene Interaction Database (DGIdb). The correlation between key SONFH genes and copper death-related genes was calculated by Pearson method. The result of bioinformatics analysis were confirmed by quantitative real-time polymerase chain reaction (qRT‒PCR). Results A total of 106 DE-CMR-SONFHGs were identified. Then, 2 key genes (PNP and SLC2A1) were identified by LASSO and SVM algorithms. The ROC curves of PNP and SLC2A1 indicated that they had diagnostic value in distinguishing SONFH from control samples. Additionally, 20 immune cell populations had notably different abundances between the SONFH and control samples. PNP showed the most significant correlations with plasmacytoid dendritic cells and CD56bright natural killer cells, and SLC2A1 expression showed the most significant correlations with T follicular helper cells and T helper 17 cells. Moreover, 11 drugs that target PNP and 5 drugs that target SLC2A1 were identified. Four copper death-related genes (LIPT1, DLD, PDHB, and MTF1) were upregulated in the disease samples. The qRT‒PCR results showed that PNP and SLC2A1 expression was downregulated and that the copper death-related genes DLD, PDHB and MTF1, which are closely related to these two key genes, were notably highly expressed in the peripheral blood of SONFH patients. These findings were consistent with the bioinformatics analysis results. Conclusions Copper homeostatic imbalance may be involved in the process of SONFH. PNP and SLC2A1 were confirmed to be key genes related to SONFH, and these genes may provide insights for the treatment of SONFH.

Objectives: The present work studied the mechanism of action of Wen-Dan decoction in treating steroid-induced necrosis of the femoral head (SINFH) via network pharmacology and in vivo experiments. Methods: The active compounds of Wen-Dan decoction and SINFH-related target genes were identified through public databases. Based on the results, further network pharmacological analysis was conducted to explore the potential key active compounds, core targets and biological processes of Wen-Dan decoction in SINFH. Subsequently, the potential mechanisms of action of Wen-Dan decoction in the treatment of SINFH obtained by network pharmacology analyses were validated through in vivo experiments. Results: A total of 608 DEGs (230 upregulated and 378 downregulated) in SINFH were identified. A GO functional enrichment analysis revealed that the SINFH-related genes were mainly involved in neutrophil activation and the immune response, and a KEGG pathway analysis showed that the SINFH-related genes were mainly associated with cytokine receptor interactions, lipids and atherosclerosis, and tuberculosis. In addition, a total of 147 active ingredients of Wen-Dan decoction were identified; of these, the core ingredient was quercetin, and licorice was an active ingredient. Moreover, 277 target genes in the treatment of SINFH with Wen-Dan decoction were identified, and NCF1, PTGS2, and RUNX2 were selected as core target genes. A quantitative real-time polymerase chain reaction (qRT–PCR) assay of peripheral blood from SINFH patients and control individuals showed that the patients exhibited highest levels of PGTS2 and NCF1 in blood. The qRT–PCR analysis of peripheral blood and femoral bone tissue from a mouse model of SINFH and control mice treated with quercetin showed that the PGTS2 and NCF1 levels revealed lower levels in the experimental animals compared with the controls, which was consistent with the bioinformatics analysis results. HE staining, immunohistochemistry and TUNEL staining confirmed significant improvement in hormone-induced femoral head necrosis in the mice treated with quercetin. Conclusions: This study provides new insights into the genes and related pathways involved in SINFH and shows that PTGS2 and NCF1 could be used as potential drug targets in SINFH. Quercetin could improve SINFH by promoting osteogenesis and inhibiting apoptosis.