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BackgroundAlthough researchers have adopted various methods for the resection and reconstruction of periacetabular tumors, the total incidence rate of complications remains high. Aiming for preserving the acetabulum and reducing the risk of complications, we applied a surgery method using tumor-free autologous femoral head to reconstruct the defective acetabulum after resection of periacetabular tumors followed by performing a conventional total hip arthroplasty (THA). Moreover, we proposed a preliminary classification system for these surgery methods.MethodsWe retrospectively reviewed 6 patients treated with acetabulum reconstruction combined with autologous femoral head following peri-acetabulum resection between April 2010 and May 2018. All patients were diagnosed as periacetabular tumors including chondrosarcoma (n= 5) and chondroblastoma (n= 1). Clinical data such as age, diagnosis, complications, local recurrence or metastasis, and function (Musculoskeletal Tumor Society 1993, MSTS93) were documented. The average time of follow-up was 62.5 months (range, 17 to 106 months).ResultsA total of 5 patients survive with average MSTS93 score of 27.8 points (range, 26–30). One patient, suffering from multiple bone metastasis prior treatment, ended up dying. One who had received radiotherapy before surgery had poor incision healing. Further, a classification system was preliminary proposed in 2 patients involving the pubis (type A) and 4 patients involving ischium (type B).ConclusionsBased on the results, we preliminary proposed a classification system for reconstruction with autologous femoral head after periacetabular low malignant tumors resection. The clinical results suggested that surgery methods involving pubis (type A) and ischium (Type B) are safe and feasible. However, further researches should be conducted to verify our classification system.

This study is focussed on evaluating and comparing two mediators of osteoclast, osteoprotegerin (OPG) and nuclear factor-κB ligand (RANKL), in plasma and tissue levels in patients with steroid-induced osteonecrosis of femoral head (SIONFH). Subjects were included in this cross-sectional case-control study in 2016. Bone histomorphology, immunohistochemistry, Western blotting, OPG and RANKL plasma levels, post-hoc statistical power and receiver-operating characteristic (ROC) curves were evaluated. Eighty-six patients diagnosed with SIONFH and 51 healthy subjects were included. OPG expression levels in bone samples increased with ARCO stage, and RANKL expression levels decreased with ARCO stages. Plasma OPG and RANKL levels were significantly higher in the SIONFH group compared with the healthy control group. The plasma OPG level and ratio of OPG and RANKL were positively associated with ARCO stages and significantly higher in stages III and IV. Plasma RANKL levels were negatively associated with ARCO stage and were significantly higher in ARCO stages II and III. Plasma OPG and RANKL may represent potential biomarkers during SIONFH at different stages. Higher plasma OPG levels indicated late-stage SIONFH, and higher plasma RANKL levels indicated early stage. Our findings may provide a clue for the development of diagnostic tools and therapies for SIONFH.

Sclerostin is an osteocyte-derived protein that has a potent inhibitory effect on osteoblast activity. The osteocyte apoptosis induced by various causes of osteonecrosis of the femoral head (ONFH) plays a key role in the promotion of femoral head collapse. But the effect of altering sclerostin level on the collapse of ONFH has not been studied. Our aim was to assess the role of sclerostin level in the collapse of ONFH. Between May 2016 and November 2016, 236 subjects were enrolled in the present study. The patients were classified according to the Association Research Circulation Osseous (ARCO) classification. The clinical bone histomorphology, the expression position, and level of sclerostin as well as the plasma sclerostin level were evaluated. The sclerostin level was significantly lower in the non-traumatic ONFH group than those in the healthy control group (P = 0.002). The sclerostin level was negatively associated with ARCO stages (r = − 0.239, P = 0.009) and significantly lower in the postcollapse group (P = 0.025). The reduced expression of sclerostin may play a key role in the collapse process of ONFH and be predictive of the disease progression of ONFH.

Icariin, the major ingredient of Herba Epimedii, promotes the osteogenic differentiation of rat bone marrow stromal cells (rBMSCs) and exerts protective effects against bone loss and increases bone regeneration, but the underlying signaling pathway by which icariin affects osteogenic differentiation remain unclear. Transcriptional coactivator with PDZ-binding motif (TAZ) is a transcriptional modulator of the Hippo signaling pathway, which plays an important role in the osteogenic differentiation of BMSCs by activating Runx2 gene during the terminal osteogenic differentiation. In this study, we found that 0.1μM icariin markedly promoted the proliferation, calcium depositions, and osteogenic genes expression of rBMSCs. Icariin (0.1μM) upregulated TAZ, Runx2, β-catenin, Osteopotin, and Dlx5 expression mainly at the early stage of osteogenic differentiation, and increased osteocalcin expression at the late stage. Our result further demonstrated that knockdown TAZ expression by lentivirus-mediated TAZ shRNA inhibited the icariin-induced osteogenic differentiation. Moreover, ICI 182780 (the estrogen receptor alpha inhibitor) or DKK1 (the Wnt/β-catenin pathway inhibitor), inhibited the icariin-induced increase in TAZ expression. Furthermore, icariin stimulated the activation of TAZ as evidenced by increased total TAZ protein and nuclear translocation, but these effects of icariin were blocked by ICI 182780 or DKK1. Taken together, our results demonstrate that icariin promotes the osteogenic differentiation of rBMSCs by increasing TAZ expression, and that the increased TAZ expression induced by icariin is mostly mediated by the ERα and Wnt/β-catenin pathway.

Steroid-induced osteonecrosis of the femoral head (SONFH) is a refractory disease induced by glucocorticoids. Marrow mesenchymal stem cells (MSCs) differentiate into multiple bone matrix cells and have been used as cell-based therapies to treat ONFH. However, the osteogenesis of MSCs isolated from patients with SONFH is significantly decreased. Polydatin has been widely used in traditional Chinese remedies due to its multiple pharmacological actions. As shown in our previous study, Polydatin protects from oxidative stress and promotes BMSC migration. However, little is known about its role in BMSC (Bone marrow mesenchymal stem cells) osteogenesis; therefore, we further investigated the effect and mechanism of Polydatin in hBMSC osteogenesis. The ability of Polydatin to promote the proliferation and osteogenic differentiation of hBMSCs was determined using the MTT assay, ALP staining and the ALP activity assay. Next, qPCR and western blotting were performed to measure the levels of genes and proteins related to the osteogenesis of hBMSCs. Then, the effect of Polydatin on the nuclear translocation of β-catenin was determined using immunofluorescence staining. Polydatin (30 μM) markedly enhanced the proliferation of hBMSCs and alkaline phosphatase (ALP) activity. Additionally, it also significantly upregulated the expression of osteogenic genes (Runx2, osteopontin, DLX5, osteocalcin, collagen type I and BMP2) and components of the Wnt signaling pathway (β-catenin, Lef1, TCF7, c-jun, c-myc and cyclin D). These osteogenesis-potentiating effects of Polydatin were blocked by Noggin, an inhibitor of the BMP pathway, and DKK1, an inhibitor of the Wnt/β-catenin pathway. However, DKK1 did not affect Polydatin-induced BMP2 expression. Based on our results, Polydatin promotes the proliferation and osteogenic differentiation of hBMSCs through the BMP2-Wnt/β-catenin signaling pathway.

Aim: The aim of this study is to investigate the potential role of C-terminal cross-linking telopeptide of type II collagen (CTX-II) in the development of femoral head osteonecrosis (FHN).Materials and methodsOne hundred and thirty-two patients diagnosed with FHN and 66 age- and sex-matched healthy subjects were included in this cross-sectional case-control study between May 2016 and November 2016. Bone histomorphology, cartilaginous immunohistochemistry, Western blotting, and level of plasma CTX-II, as well as the receiver operating characteristic (ROC) curve, were evaluated. ResultsImmunohistochemistry and Western blotting showed that CTX-II was abundantly detected in the cartilage of FHN samples in stages III & IV. Plasma CTX-II levels were significantly higher in FHN patients in the advanced stages (III & IV) than was the level in the control group (164.81% and 198.15% higher in stages III & IV, respectively). However, the levels of CTX-II did not differ significantly among the FHN patients with different etiology or other clinical data. ConclusionOur result suggests that the degeneration of cartilage has already begun in stage III, even though a relatively normal articular gap can be found in the X-ray. Plasma CTX-II level may be a biomarker of the development of FHN.