Background Bernese periacetabular osteotomy (PAO) has been shown to be applicable as a hip-preserving technique for the treatment of developmental dysplasia of the hip (DDH). The approach could be designed preoperatively using various types of reverse-engineering software and finite element analysis, but how to implement it in the actual PAO remains a challenge. This study examines and evaluates a solution to achieve higher accuracy when performing a PAO. Methods A patient-specific cutting and rotating template was predesigned through computer-aided design (CAD) with three-dimensional (3D) modeling programs. The templates were then reproduced with rapid prototyping (RP) technology and used in the actual PAO. Finally, the clinical and radiographic effects were assessed and compared between the newly developed PAO and conventional PAO groups. Results The customized cutting template fit well with the bone surface and served as a guide for surgeons as they slid the osteotome to the precise location that had been determined prior to surgery. A very similar acetabular fragment was reproduced, and no major complications occurred when performing the osteotomy along the edge of the cutting template. The acetabular fragment was then corrected to the predetermined position through one-off manipulation with the customized rotating template. The final position of the acetabular fragment in the new developed PAO group was highly consistent with the planned position, and the postoperative morphological parameters were consistent with the preoperative planned data compared to the conventional PAO group. The duration of the operation and the number of irradiation decreased significantly. The Harris hip score (HHS) and visual analogue scale (VAS) score improved significantly with the use of the new developed PAO. Conclusions We demonstrate that our system, which was based on CAD-RP technology, is feasible and could realize the predicted results accurately during the actual PAO.

Total knee arthroplasty is a commonly performed safe procedure and typically executed in severe knee arthritis, but it also triggers ischemia-reperfusion injury (IRI). More recently, microRNAs (miRs) have been reported to play a contributory role in IRI through the key signaling pathway. Hence, the current study aimed to investigate the effect and specific mechanism of microRNA-23b (miR-23b), murine double minute 4 (MDM4), and the p53 signaling pathway in IRI rat models. First, the IRI model was established, and the expression pattern of miR-23b, MDM4, and the p53 signaling pathway-related genes was characterized in cartilaginous tissues. Then, miR-23b mimics or inhibitors were applied for the elevation or the depletion of the miR-23b expression and siRNA-MDM4 for the depletion of the MDM4 expression in the articular chondrocytes. By means of immunohistochemistry, quantitative real-time polymerase chain reaction, and Western blot analysis, IRI rats exhibited increased miR-23b expression, activated p53 signaling pathway, and decreased MDM4 expression. MDM4 was verified as a target gene of miR-23b through. Downregulated miR-23b increased the expression of MDM4, AKT, and Bcl-2, but decreased the expression of p53, p21, and Bax. In addition, a series of cell experiments demonstrated that downregulated miR-23b promoted articular chondrocyte proliferation and cell cycle entry, but inhibited articular chondrocyte apoptosis. The absence of the effects of miR-23b was observed after MDM4 knocked down. Our results indicate that silencing miR-23b could act to attenuate IRI and reduce the apoptosis of articular chondrocytes through inactivation of the p53 signaling pathway by upregulating MDM4, which provide basic therapeutic considerations for a novel target against IRI. K E Y W O R D S articular chondrocytes, ischemia-reperfusion injury (IRI), murine double minute 4 (MDM4), microRNA-23b (miR-23b), p53 signaling pathway J Cell Biochem. 2019;120:4599-4612.wileyonlinelibrary.com/journal/jcb

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Neobavaisoflavone (NBIF) is a flavonoid, which has a variety of pharmacological activities. However, the mechanism of NBIF in the treatment of osteoporosis still needs further exploration. The differentiation of osteoblast MC‐3T3‐E1 cells after treatment was observed by Alizarin red staining. Cell counting kit‐8 and flow cytometry were used to detect viability, apoptosis, and reactive oxygen species (ROS) levels of treated MC‐3T3‐E1 cells, respectively. Malondialdehyde (MDA), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and glutathione peroxidase (GSH‐Px) were tested by ELISA kits. The expressions of lncRNA MALAT1, MEG3, CRNDE, Runx2, osteocalcin (OCN), osteopontin (OPN), collagen I (col‐I), nuclear Nrf2, cytoplasm Nrf2, heme oxygenase‐1 (HO‐1) and quinone oxidoreductase 1 (NQO1) in treated MC‐3T3‐E1 cells were examined by Quantitative real‐time PCR or Western blot. Dexamethasone (Dex) inhibited the viability of MC‐3T3‐E1 cells, while the appropriate amount of NBIF had no significantly effect on cell viability. Dex downregulated CRNDE expression, whereas NBIF upregulated CRNDE. Overexpressed CRNDE and NBIF reversed the inhibitory effects of Dex on cell viability, differentiation and levels of SOD, GSH‐Px, Runx2, OCN, OPN, col‐I, nuclear Nrf2, HO‐1 and NQO1 while reversing the promoting effect of Dex on apoptosis and the levels of ROS, MDA, LDH and cytoplasm Nrf2 in MC‐3T3‐E1 cells, respectively, but shCRNDE further reversed the effects of NBIF in MC‐3T3‐E1 cells. NBIF protected osteoblasts from Dex‐induced oxidative stress by upregulating the CRNDE‐mediated Nrf2/HO‐1 signaling pathway.