The Role of Global Femoral Offset in Total Hip Arthroplasty with High Hip Center Technique.

OBJECTIVE: The high hip center (HHC) technique has been proposed for the treatment of patients with developmental dysplaisa of the hip (DDH) who have an acetabular bone defect. However, the importance of global femoral offset (FO) in the application of this technique has not been sufficiently appreciated. Our goals were to confirm that the HHC technique is feasible in the treatment of patients with DDH and to assess the function of global FO in this procedure. METHODS: We retrospectively analyzed 73 patients who underwent total hip arthroplasty using high hip center technique for unilateral DDH at our hospital between January 2014 and June 2019. According to global FO, the patients were split into three groups: increased FO group (increment greater than 5 mm), restored FO group (restoration within 5 mm) and decreased FO group (reduction greater than 5 mm). Patients' medical records and plain radiographs were reviewed. One-way ANOVA was used to compare radiographic outcomes and Harris hip score (HHS). Paired t-test was used to assess preoperative and postoperative HHS and leg length discrepancy. Trochanteric pain syndrome, Trendelenburg sign and postoperative limp was evaluated with Fisher's exact test. RESULTS: The average follow-up time was 7.5 ± 1.4 years. The patients' HHS and leg length discrepancy were significantly improved (p < 0.05). In terms of vertical acetabular height, abductor arm, postoperative leg length difference, and acetabular cup inclination, there was no statistically significant difference between the three groups. At the last follow-up, HHS was significantly higher in the restored FO group than in the decreased FO and increased FO groups. Trochanteric pain syndrome occurred in 15.0% and Trendelenburg sign and postoperative limp in 8.2% of all patients, respectively. Trochanteric pain syndrome, Trendelenburg sign and postoperative limp did not differ significantly across the three groups. One patient in increased FO group underwent revision for dislocation 6 years after surgery. CONCLUSION: The HHC technique is an alternative technique for total hip arthroplasty in patients with acetabular bone abnormalities, according to the results of the mid-term follow-up. Also, controlling the correction of the global femoral offset to within 5 mm may lead to better clinical outcomes.

Evaluation of Biodegradable Alloy Fe30Mn0.6N in Rabbit Femur and Cartilage through Detecting Osteogenesis and Autophagy.

Biodegradable iron alloy implants have become one of the most ideal possible candidates because of their biocompatibility and comprehensive mechanical properties. Iron alloy's impact on chondrocytes is still unknown, though. This investigation looked at the biocompatibility and degradation of the Fe30Mn0.6N alloy as well as how it affected bone formation and chondrocyte autophagy. In vivo implantation of Fe30Mn0.6N and Ti6Al4V rods into rabbit femoral cartilage and femoral shaft was carried out to evaluate the degradation of the alloy and the cartilage and bone response at different intervals. After 8 weeks of implantation, the cross-sectional area of the Fe30Mn0.6N alloys lowered by 50.79 ± 9.59%. More Ca and P element deposition was found on the surface Fe30Mn0.6N rods by using energy dispersive spectroscopy (EDS) and scanning electron microscopy (P < 0.05). After 2, 4, and 8 weeks of implantation, no evident inflammatory infiltration was seen in peri-implant cartilage and bone tissue of Fe30Mn0.6N and Ti6Al4V alloys. Also, implantation of Fe30Mn0.6N alloy promoted autophagy in cartilage by detecting expression of LC3-II compared with Ti6Al4V after implantation (P < 0.05). Fe30Mn0.6N alloy also stimulated early osteogenesis at the peri-implant interface compared with Ti6Al4V after implantation (P < 0.05). In the in vitro test, we found that low concentrations of Fe30Mn0.6N extracts had no influence on cell viability. 15% and 30% extracts of Fe30Mn0.6N could upregulate autophagy compared to the control group by detecting beclin-1, LC3, Atg3, and P62 on the basis of WB and IHC (P < 0.05). Also, the PI3K-AKT-mTOR signaling pathway mediated in the upregulation of autophagy of chondrocytes resulting in exposure to extract of Fe30Mn0.6N alloy. It is concluded that Fe30Mn0.6N showed degradability and biocompatibility in vivo and upregulated autophagy activity in chondrocytes.

Circular RNA CircSLC8A1 contributes to osteogenic differentiation in hBMSCs via CircSLC8A1/miR-144-3p/RUNX1 in periprosthetic osteolysis.

Circular RNAs (circRNAs) are often found in eukaryocyte and have a role in the pathogenesis of a variety of human disorders. Our related research has shown the differential expression of circRNAs in periprosthetic osteolysis (PPOL). However, the involvement of circRNAs in the exact process is yet unknown. CircSLC8A1 expression was evaluated in clinical samples and human bone marrow mesenchymal stem cells (hBMSCs) in this investigation using quantitative real-time PCR. In vitro and in vivo studies were conducted to explicate its functional role and pathway. We demonstrated CircSLC8A1 is involved in PPOL using gain- and loss-of-function methods. The association of CircSLC8A1 and miR-144-3p, along with miR-144-3p and RUNX1, was predicted using bioinformatics. RNA pull-down and luciferase assays confirmed it. The impact of CircSLC8A1 in the PPOL-mouse model was also investigated using adeno-associated virus. CircSLC8A1 was found to be downregulated in PPOL patients' periprosthetic tissues. Overexpression of CircSLC8A1 promoted osteogenic differentiation (OD) and inhibited apoptosis of hBMSCs in vitro. The osteogenic markers of RUNX1, osteopontin (OPN) and osteocalcin (OCN) were significantly upregulated in hBMSCs after miR-144-3p inhibitor was transferred. Mechanistic analysis demonstrated that CircSLC8A1 directly bound to miR-144-3p and participated in PPOL through the miR-144-3p/RUNX1 pathway in hBMSCs. Micro-CT and quantitative analysis showed that CircSLC8A1 markedly inhibited PPOL, and osteogenic markers (RUNX1, OPN and OCN) were significantly increased (P<0.05) in the mice model. Our findings prove that CircSLC8A1 exerted a regulatory role in promoting osteogenic differentiation in hBMSCs, and CircSLC8A1/miR-144-3p/RUNX1 pathway may provide a potential target for prevention of PPOL.