Biomechanical study on parallel cannulated compression screw combined with medial buttress plate fixation and F-type cannulated compression screw fixation in Pauwels III femoral neck fracture：A finite element analysis. / å¹³è¡Œç©ºå¿ƒåŠ åŽ‹èžºé’‰è”åˆå† ä¾§æ”¯æ’‘é’¢æ¿ä¸ŽFåž‹ç©ºå¿ƒåŠ åŽ‹èžºé’‰å›ºå®šPauwels IIIåž‹è‚¡éª¨é¢ˆéª¨æŠ˜ç”Ÿç‰©åŠ›å­¦ç‰¹æ€§çš„æœ‰é™å ƒåˆ†æž.

OBJECTIVES: Pauwels III fracture is a kind of femoral neck fractures, in which the angle of the fracture line in the coronal plane and the upper edge of the acetabulum is more than 50°. Internal fixation for the treatment of femoral neck fractures is largely performed by cannulated compression screw (CCS), dynamic hip screw, or locking plate. This study aims to compare the biomechanical properties of parallel CCS combined with medial buttress plate fixation and F-type CCS fixation in the treatment of Pauwels III femoral neck fracture by finite element modeling and to determinate the most suitable procedure for such fractures. METHODS: A 52-year-old male volunteer, 176 cm in height and 72 kg in weight, with no history of hip joint, was selected. X-ray and CT examination confirmed that the morphology and bone condition of the right hip of the volunteer were normal. A simulation model of Pauwels III femoral neck fracture was established from the collected CT data of the right proximal femur of the volunteer by the finite element method. Four internal fixations were developed to treat the finite element model: Three CCSs in an inverted triangular parallel configuration combined with medial buttress plate model served as Group A, 2 CCSs in a vertical parallel configuration combined with medial buttress plate model served as Group B, 2 CCSs in a horizontal parallel configuration combined with medial buttress model served as Group C, and the "F" shaped CCS model served as Group D. The distribution of stress, the peak stress, the distribution and maximum of displacement of internal fixations and fracture ends in different models were evaluated. RESULTS: For Groups A, B, C, and D, the peak stresses on the internal fixation were 362.74, 586.84, 558.25, and 208.66 mPa, respectively, all of which occurred near the fractures and the stress distribution in Group D was the most uniform. The maximum displacements of internal fixations in Groups A, B, C, and D were 0.39, 0.45, 0.44, and 0.41 mm, respectively; the peak stresses on the fracture ends were 70.62, 98.48, 55.84, and 65.39 mPa, respectively, all of which were concentrated on the base of femoral neck and lateral cortex of the femoral shaft, and the stresses of Groups C and D were more evenly distributed than those of Groups A and B. The maximum displacements of fracture ends in Groups A, B, C, and D were 0.44, 0.52, 0.50, and 0.44 mm, respectively. CONCLUSIONS: The biomechanical stability of F-type CCS fixation is similar to that of 3 CCSs in an inverted triangular parallel configuration combined with medial buttress plate, with a better dispersion of stress. F-type CCS fixation may be a well option for the treatment of femoral neck fracture of Pauwels III.

Long non-coding RNA CIR inhibits chondrogenic differentiation of mesenchymal stem cells by epigenetically suppressing ATOH8 via methyltransferase EZH2.

BACKGROUND: Osteoarthritis (OA) is the most common articular disorder, leading to joint malfunction and disability. Although the incidence of OA is increasing globally, the treatment of OA is very limited. LncRNA CIR has been implicated in OA through unclear mechanisms. Here, we investigated the role of lncRNA CIR in chondrogenic differentiation. METHODS: Human umbilical-cord-derived mesenchymal stem cells (hUC-MSCs) were obtained from human umbilical cords. Flow cytometry was used to analyze the surface markers of hUC-MSCs. Various culture conditions and corresponding staining assays were employed to assess the differentiation abilities of hUC-MSC. qRT-PCR, western blot, and immunostaining were used to measure expression levels of related genes and proteins such as lncRNA CIR, ATOH8, EZH2, and H3K27me3. RNA immunoprecipitation assay, biotin pull-down, and chromatin immunoprecipitaion assay were performed to analyze the interactions of lncRNA CIR, EZH2, H3K27me3 and ATOH8 promoter. RESULTS: hUC-MSCs exhibited MSCs features and could differentiate into chondrocytes under specific conditions. LncRNA CIR was downregulated while ATOH8 was upregulated during the chondrogenic differentiation of hUC-MSCs. Knockdown lncRNA CIR or overexpression of ATOH8 promoted chondrogenic differentiation. Further, lncRNA CIR bound to EZH2 and repressed ATOH8 expression via EZH2-mediated H3K27me3, which promotes the methylation of ATOH8. Inhibition of ATOH8 reversed the effects of knockdown lncRNA CIR on chondrogenic differentiation. CONCLUSION: LncRNA CIR suppresses chondrogenic differentiation of hUC-MSCs. Mechanistically, lncRNA CIR could inhibit ATOH8 expression that functions to promote chondrogenic differentiation through EZH2-mediated epigenetic modifications.

Chlamydia muridarum Induces Pathology in the Female Upper Genital Tract via Distinct Mechanisms.

Sexually transmitted infection with Chlamydia trachomatis may lead to fibrotic blockage in women's upper genital tracts, resulting in tubal infertility. Intravaginal inoculation with C. muridarum readily induces fibrotic blockage or hydrosalpinx in mice and is used for investigating C. trachomatis pathogenicity. Using this model in combination with an antibody depletion approach, we confirmed CD4+ T cell-mediated protective immunity and a CD8+ T cell-dependent pathogenic mechanism during chlamydial infection in C57BL/6J mice. However, when mice genetically deficient in CD8+ T cells were evaluated, we found, surprisingly, that these mice were still able to develop robust hydrosalpinx following C. muridarum infection, both contradicting the observation made in C57BL/6J mice and suggesting a pathogenic mechanism that is independent of CD8+ T cells. We further found that depletion of CD4+ T cells from CD8+ T cell-deficient mice significantly reduced chlamydial induction of hydrosalpinx, indicating that CD4+ T cells became pathogenic in mice genetically deficient in CD8+ T cells. Since depletion of CD4+ T cells both promoted chlamydial infection and reduced chlamydial pathogenicity in CD8+ T cell-deficient mice, we propose that in the absence of CD8+ T cells, some CD4+ T cells may remain protective (as in C57BL/6J mice), while others may directly contribute to chlamydial pathogenicity. Thus, chlamydial pathogenicity can be mediated by distinct host mechanisms, depending upon host genetics and infection conditions. The CD8+ T cell-deficient mouse model may be useful for further investigating the mechanisms by which CD4+ T cells promote chlamydial pathogenicity.

Effects of AURKA-mediated degradation of SOD2 on mitochondrial dysfunction and cartilage homeostasis in osteoarthritis.

This study aimed to investigate the mechanism of the ubiquitinase Aurora kinase A (AURKA) in the occurrence of osteoarthritis (OA) by mediating mitochondrial stress. Bioinformatic predictions revealed 2247 differentially expressed genes (DEGs) in the normal and OA tissues. According to the UbiNet database, 39 DEGs that code for ubiquitination enzymes was screened. AURKA was highly expressed in OA tissues and cells. AURKA interference inhibited the elevation of matrix metalloproteinase-13 (MMP-13). (MMP13), sex determining region Y-box 9 (Sox9), and a disintegrin and metalloproteinase with thrombospondin motifs-5 (ADAMTS5) expression and the reduction of collagen type IIα (Col2a1) and Aggrecan expression in interleukin-1 ß (IL-1ß) induced chondrocytes. The animal experiments proved that depleting AURKA could repress the occurrence of OA. Superoxide dismutase 2 (SOD2) was determined to be AURKA ubiquitination substrate via AURKA expression and bioinformatic prediction experiments. SOD2 expression was lower in OA tissues, but higher in normal joint tissues. AURKA interference activates SOD2. Meanwhile, the IP results confirmed that AURKA could bind to SOD2 and degrade it through K48 ubiquitination. Modification and overexpression of AURKA reduce SOD2 levels. AURKA interference can reverse the reactive oxygen species elevation caused by SOD2 overexpression or lysine-48 (K48) mutation, respectively, leading to mitochondrial dysfunction. Furthermore, AURKA silencing suppressed the occurrence of OA induced by mitochondrial activation. These findings suggest that ubiquitination of AURKA lowers SOD2 expression and affects mitochondrial dysfunction to repress the occurrence of OA. The results of the current study reveal that AURKA ubiquitination influences mitochondrial dysfunction and suppresses the occurrence of OA via degradation of SOD2. These data reveal novel potential targets for OA treatment.

Proanthocyanidins attenuate breast cancer-induced bone metastasis by inhibiting Irf-3/c-jun activation.

We have previously demonstrated the pivotal role of Jnk-mediated Irf-3/c-Jun in regulating nuclear factor kappa-Β ligand (RANKL)-induced osteoclastogenesis. Here, we demonstrated that proanthocyanidins (PACs) target Irf-3 to alleviate breast cancer-induced activation of osteoclasts. We also found that PACs induced apoptosis of osteoclast precursors by upregulating the ratio of bax/bcl-2 and activating caspase-3 activity. Such bone protective effect also could be observed in a bone metastasis model of breast cancer. These findings provided a novel therapeutic intervention targeting abnormal bone metabolism to alleviate bone metastasis of breast cancer.

[Suppression of miR-30a/HMGA2-mediated autophagy in osteosarcoma cells impacts chemotherapeutics-induced apoptosis].

OBJECTIVE: To investigate the effect of miR-30a/HMGA2-mediated autophagy in osteosarcoma cells on apoptosis induced by chemotherapeutics. 
 Methods: A total of 30 osteosarcoma tissues of sensitive and resistant to chemotherapeutics were divided into a chemotherapy-sensitive group and a chemotherapy-resistant group. The mRNA expression levels of miR-30a and high mobility group protein A2 (HMGA2) in the chemotherapy-sensitive group and the chemotherapy-resistant group, and the mRNA expression levels of miR-30a in osteosarcoma U2-OS cells treated by cisplatin, doxorubicin and methotrexate at different concentrations were detected by real-time PCR. The expression levels of autophagy related protein Beclin 1, microtubule associated protein 1 light chain 3B (LC3B) and autophagy factor P62 were detected by Western blotting. The osteosarcoma U2-OS cells were transfected with miR-30a mimics and miR-30a inhibitors to construct a miR-30a high expression group, a miR-30a low expression group and a control group. The expression levels of Beclin 1, LC3B and P62 in osteosarcoma U2-OS cells after treatment of cisplatin and doxorubicin in these 3 groups were detected by Western blotting; the level of autophagy was detected by monodansylcada (MDC) staining; the level of ROS was detected by dihydroethidium (DHE); the level of cell surviving rate was detected by cell counting kit-8 (CCK-8); the level of apoptosis was detected by annexin APC/PI double staining; the level of mitochondria oxidative damage was detected by mitochondrial membrane potential assay kit with JC-1 (JC-1 method). The interaction between miR-30a and HMGA2 was detected by dual luciferase reporter assay. The osteosarcoma U2-OS cells were transfected with HMGA2 mimics and HMGA2-shRNA to construct a high HMGA2 group, a low HMGA2 group, and a control group. The expression levels of Beclin 1, LC3B and P62 in osteosarcoma U2-OS cells after the treatment of cisplatin were detected by Western blotting.
 Results: The level of miR-30a in the chemotherapy-resistant tissues was significantly lower than that in the chemotherapy-sensitive tissues (P<0.05), and the expression of HMGA2 was opposite comparing to that of miR-30a (P<0.05). After the treatment by low concentration (5 µmol/L) of chemotherapeutics, the level of miR-30a was down-regulated in osteosarcoma U2-OS cells, accompanied with up-regulation of Beclin 1 and LC3B (P<0.01) and down-regulation of P62 (P<0.01). Compared with the control group, the expression levels of Beclin 1 and LC3B were significantly decreased (P<0.05), and the expression level of P62 was significantly increased (P<0.05) in the miR-30a high expression group, which was opposite in the miR-30a low expression group. In the miR-30a high expression group treated by chemotherapeutics, the level of autophagy and the cell survival rate were lower than those in group with low expression of miR-30a, while the levels of ROS, the mitochondrial oxidative damage and the apoptosis were higher than those in group with low expression of miR-30a (all P<0.05). The targeting interaction between HMGA2 and miR-30a were verified by dual luciferase reporter assay. Compared with the control group, the expression levels of Beclin 1 and LC3B were significantly increased (P<0.05), and the expression level of P62 was significantly decreased (P<0.05) in the HMGA2 high expression group, which was opposite in the HMGA2 low expression group.
 Conclusion: Suppression of miR-30a/HMGA2-mediated autophagy in osteosarcoma cells is likely to enhance the therapeutic effect of chemotherapeutics.

IL-1ß-induced miR-34a up-regulation inhibits Cyr61 to modulate osteoarthritis chondrocyte proliferation through ADAMTS-4.

Osteoarthritis (OA) is the most prevalent degenerative joint disease with multifactorial etiology caused by risk factors. The degradation of aggrecan by upregulated ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) is the key event in the development of OA. ADAMTS-4 contributes to aggrecan degradation in human OA. Cysteine-rich angiogenic inducer 61 (Cyr61), which is associated with diseases related to chronic inflammation, is found in articular cartilage from patients with osteoarthritis and appears to suppress ADAMTS-4 activity, possibly leading to chondrocyte cloning. Herein, we first revealed that Cyr61 and ADAMTS-4 protein levels were remarkably increased in OA cartilage tissues and OA chondrocytes, and verified Cyr61 regulation of ADAMTS-4 in normal and OA chondrocyte. Further, we revealed that Cyr61 could promote OA chondrocyte proliferation through inhibiting ADAMTS-4. Overproduction of inflammatory cytokines plays a vital role in the pathological development of OA; herein, we demonstrated that IL-1ß inhibited Cyr61, while promoted ADAMTS-4 expression. By using online tools and luciferase assays, we confirmed that miR-34a, a regulatory miRNA of chondrocyte proliferation, could directly bind to the 3'-UTR of Cyr61 to inhibit its expression; further, IL-1ß regulated Cyr61 and ADAMTS-4 expression through miR-34a. In OA cartilage tissues, miR-34a, and IL-1ß mRNA expression was up-regulated and positively correlated; miR-34a and Cyr61 mRNA was positively correlated, further indicating that suppressing miR-34a expression might rescue IL-1ß-induced Cyr61 suppression, and promote OA chondrocyte proliferation. Taken together, we provided novel experimental basis for rescuing OA chondrocyte proliferation through miR-34a/Cyr61 axis.

[Repair of articular cartilage defects by autologous bone mesenchymal stem cells and allogeneic costal chondrocytes in the knee of Wuzhishan miniature pigs].

OBJECTIVE: To investigate the feasibility of construction of tissue engineered cartilage by co-culture of bone marrow mesenchymal stem cells (BMSCs) and costal chondrocytes (CCs), and to provide theoretical basis and experimental basis for clinical repair of articular cartilage defects by Wuzhishan miniature pig knee cartilage defects with co-cultured cells.
 Methods: Density gradient centrifugation method was used to isolate BMSCs from Wuzhishan miniature pig. The double enzyme digestion method was used to isolate CCs. The passage 3 generation of BMSCs and passage 2 generation of CCs were randomly divided into 3 groups: a co-culture group of BMSCs:CCs for 1:2 (Group A), a simple CCs (Group B), and a simple BMSCs (Group C). The cell growth curve was drawn, and the content of glycosaminoglycan (GAG) of external separation in chondrocytes was determined. The 12 Wuzhishan miniature pigs were randomly divided into a co-culture cells/collagen membrane experimental group, a collagen membrane control group and the blank group. In the co-culture cells/collagen membrane experimental group, the co-cultured cells/collagen membrane were implanted into the cartilage defects of the mandibular condyle; in the collagen membrane control group, only collagen membrane was implanted; while in the blank group, nothing was implanted. Six animals were sacrificed at 8 and 16 weeks after surgery respectively (2 animals in each group). General observation, cartilage histological score and histopathological examination were carried out.
 Results: The BMSCs and co-culture cells grew well. The biological activity of CCs was good. After 16 weeks of operation, the repair tissues in the co-cultured cells/collagen membrane experimental group showed hyaline cartilage features: smooth, flat, and integrated well with the surrounding cartilage and subchondral bone. The collagen membrane in the collagen membrane control group was fibrously repaired. Repair tissue gross score in the co-culture cells/collagen membrane experimental group was significantly better than that in the collagen membrane control group and the blank group (both P<0.05), but there was no significant difference between the collagen membrane control group and the blank group (P>0.05).
 Conclusion: BMSCs, CCs and co-cultured cells can function as the seed cells for cartilage tissue engineering, and the co-culture cells (BMSCs:CCs=1:2) possess more advantages; the short-term effect of co-culture cells with collagen membrane on repairing cartilage defects is satisfied.

Krüppel-like factor 4 promotes high-mobility group box 1-induced chemotherapy resistance in osteosarcoma cells.

Osteosarcoma is the most common primary malignant bone tumor, and the frequent acquisition of chemoresistance is often an obstacle to achieving favorable outcomes during chemotherapy. Recently, Krüppel-like factor 4 (KLF4) has been shown to be associated with chemotherapy resistance in a few tumors; however, the involvement of KLF4 in chemotherapy resistance in osteosarcoma cells remains unknown. In this study, quantitative real-time PCR and western blot analysis revealed that KLF4 expression was significantly increased in response to cisplatin, methotrexate and doxorubicin treatment in osteosarcoma cells, and knockdown of KLF4 increased sensitivity to these anticancer drugs by decreasing cellular clonogenic ability and increasing apoptosis. Moreover, our data suggest that KLF4-regulated drug resistance might, at least partially, positively regulate high-mobility group box 1 (HMGB1), which was found to be a significant contributor to chemoresistance in osteosarcoma cells in our previous study. In summary, this study highlights the significance of KLF4/HMGB1 interaction in regulating chemotherapy resistance, and suggests that targeting KLF4/high-mobility group box 1 may be a therapeutic strategy for osteosarcoma chemotherapy.

A Modified Technique to Improve Reliability of Distally Based Sural Fasciocutaneous Flap for Reconstruction of Soft Tissue Defects Longitudinal in Distal Pretibial Region or Transverse in Heel and Ankle.

Partial flap loss is a common complication of the distally based sural fasciocutaneous flap. We present a modified technique of a sloped skin island design to improve the reliability of the flap when used to reconstruct a longitudinal distal pretibial defect or transverse heel and ankle defect. Thirty-one flaps with the slope-designed skin island were used to reconstruct such defects in 30 patients. In the modified technique, the skin island was rotated toward the vascular axis of the flap. The defects were located in the distal pretibial region in 7 cases and the ankle and heel region in 24. The horizontal dimension of the skin island decreased by an average of 5.6 (range 2.5 to 14.8) cm with the sloped design, and the rotation angle varied from 42° to 90° (mean 69°). Of the 31 flaps, 29 survived, 1 developed marginal necrosis, and 1 developed lateral partial necrosis. The sloped design of the skin island is applicable to reconstruction of longitudinal distal pretibial or transverse heel and ankle defects. The modified technique can decrease the horizontal dimension and increase perfusion of the skin island, thus improving the reliability of the flap.

iNOS expression and osteocyte apoptosis in idiopathic, non-traumatic osteonecrosis.

BACKGROUND AND PURPOSE: Non-traumatic osteonecrosis is a progressive disease with multiple etiologies. It affects younger individuals more and more, often leading to total hip arthroplasty. We investigated whether there is a correlation between inducible nitric oxide synthase (iNOS) expression and osteocyte apoptosis in non-traumatic osteonecrosis. PATIENTS AND METHODS: We collected and studied 20 human idiopathic, non-traumatic osteonecrosis femoral heads. Subchondral bone samples in the non-sclerotic region (n = 30), collected from osteoarthritis patients, were used as controls. Spontaneously hypertensive rats were used as a model for osteonecrosis in the study. We used scanning electron microscopy, TUNEL assay, and immunohistochemical staining to study osteocyte changes and apoptosis. RESULTS: The morphology of osteocytes in the areas close to the necrotic region changed and the number of apoptotic osteocytes increased in comparison with the same region in control groups. The expression of iNOS and cytochrome C in osteocytes increased while Bax expression was not detectable in osteonecrosis samples. Using spontaneously hypertensive rats, we found a positive correlation between iNOS expression and osteocyte apoptosis in the osteonecrotic region. iNOS inhibitor (aminoguanidine) added to the drinking water for 5 weeks reduced the production of iNOS and osteonecrosis compared to a control group without aminoguanidine. INTERPRETATION: Our findings show that increased iNOS expression can lead to osteocyte apopotosis in idiopathic, non-traumatic osteonecrosis and that an iNOS inhibitor may prevent the progression of the disease.

Endothelin-1 gene polymorphisms and risk of chemoresistant pediatric osteosarcoma.

BACKGROUND: Osteosarcoma (OS) is the most common childhood bone cancer. Chemoresistance is the principal reason for poor survival and disease recurrence in OS patients, and ET-1 reportedly plays an important role in the development of chemoresistance in OS cells. In the present study, we for the first time explored the association of endothelin-1 (ET-1) SNPs and haplotypes with the risk of chemoresistant pediatric OS. PROCEDURE: We genotyped three SNPs (rs1800541, rs2070699, and rs5370) in the ET-1 gene in a case-control study, using 350 pairs of age, sex, and tumor location and stage matched pediatric patients with OS. Patients who showed <90% tumor necrosis after neochemotherapy were defined as poor responders (cases), and those who showed ≥90% tumor necrosis were defined as good responders (controls). RESULTS: The G allele at rs1800541 and the G allele at rs2070699 were associated with reduced and increased risk of chemoresistant OS, respectively. The rs1800541-rs2070699 haplotypes TG and GT were respectively associated with increased (P = 0.012; adjusted OR, 1.82; 95% CI, 1.10-5.65) and reduced (P = 0.009; adjusted OR, 0.25; 95% CI, 0.14-0.84) risk of chemoresistant OS. The TG and the GT haplotypes have a gene-dosage effect on increasing and decreasing the ET-1 expression in primary OS tumor cells from chemoresistant pediatric OS subjects, respectively. CONCLUSIONS: This study provides the first evidence of an association between the ET-1 gene SNPs and haplotypes and the risk of chemoresistant pediatric OS, potentially adding new insights into the pathophysiology and treatment of chemoresistant OS.

Distally based perforator-plus sural fasciocutaneous flap for soft-tissue reconstruction of the distal lower leg, ankle, and foot: comparison between pediatric and adult patients.

There are no large series comparing the distally based perforator-plus sural fasciocutaneous flap used in pediatric and adult populations. The flaps were divided into two groups: the children (patient's age<14 years) group (n=53) and the adults (patient's age ≥ 18 years) group (n=148). We compared flap-viability-related complications and their potential risk factors. In the patients with at least 12-month postoperative follow-up, the reconstruction outcomes, donor-site morbidities, and transitory and permanent swelling of the affected lower limb were compared. Partial necrosis, marginal necrosis, and overall complication rates were 13.2, 3.8, and 17.0% in the pediatric group, and 12.2, 1.4, and 13.6% in the adult group, respectively; the differences were not statistically significant (p>0.05). Incidences of hypertrophic scar and pruritus at the donor site were significantly higher, while incidence of transitory swelling of the affected lower limb was significantly lower in the pediatric group. This flap in children is similar to that in adults in the reliability.

[Advance of adipose-derived stem cells in tendon tissue engineering].

Tendon tissue engineering is a novel therapeutic strategy for severe tendon injury and loss. Adipose derived stem cells (ASCs) have been studied extensively, due to their potency to differentiate into musculoskeletal tissue precursors such as osteoblasts, chondrocytes, adipocytes, and tendocytes under specific cues and high ability of proliferation. Resources of ASCs are ubiquitous and isolation of ASCs is secure, simple and minimally invasive. Mounting evidences demonstrate that ASCs may be involved in tendon tissue engineering and repair the severe injury of tendon under stimulation of various growth factors and other appropriate fittings.

[Effect of alendronate amount on the static mechanical properties of bone cement].

OBJECTIVE: To determine the effect of alendronate amount on the static mechanical properties of bone cement before elution and 4 weeks after elution, and determine suitable amount of alendronate in cement from the perspective of biomechanics. METHODS: Samples of compression strength and bending strength (modulus) were prepared with bone cement adding 0, 10, 50, 100, 500 and 1000 mg alendronate in 50 g Cemex®XL bone cement powders respectively (named as G0-G5 groups). The compression strength, bending strength, and bending modulus of bone cement were examinated by INSTRON 8032 tester before the elution and 4 weeks after the elution. Some broken samples of 4-point bending test were examinated by scanning electronic microscopy (SEM), and some other samples of bending strength (modulus) tests by micro-CT. RESULTS: No significant difference was found in the compression strength before the elution,4 weeks after elution in the 6 groups, and before and after the elution in the respective groups (P>0.05). Compared with G0 group, G1-G4 groups had no obvious difference in the bending strength before the elution and 4 weeks after the elution (P>0.05), while G5 group had difference (P<0.05). There was no significant difference in the bending strength before and after the elution in the respective groups (P>0.05). Taken G0 group as the control group, G1-G4 groups had no visible effects on the bending modulus 4 weeks after the elution (P>0.05), while G5 group decreased it significantly (P<0.05). Bending modulus before the elution in the 6 groups didn't show obvious difference (P>0.05), while bending modulus before and after the elution in the respective groups displayed a marked difference (P<0.05). CONCLUSION: Less than 500 mg alendronate added in Cemex?XL 50 g bone cement powder does not decrease the compressive strength, flexural strength and flexural modulus before the elution and 4 weeks after the elution.

[Effect of alendronate-loaded bone cement on osteoblast].

OBJECTIVE: To determine the effect of bone cement, with different amounts of alendronate on osteoblast, and determine the cytotoxicity of alendronate-integrated bone cement from the viewpoint of cell biology. METHODS: According to different additions (0, 10, 50, 100, 500, 1 000 mg) of alendronate in 50 g Cemex®XL bone cement powder, the experiments were divided into 6 groups, namely G0-G5 groups. In all groups, the adhesive capacity of osteoblast-like cells MG-63 was evaluated by electron microscope, the optical density (OD) value of cells by MTT colorimetry method, the alkaline phosphatase activity (AKP) by AKP assay kit, the apoptosis rates by Annexin-V-FITC apoptosis detection kit, and the bone mineralization potentiality by phase contrast microscope. RESULTS: The adhesive capacity of MG-63 was good in all groups. Compared with the G0 group, the cell apoptosis was inhibited in G1-G4 groups while in G5 group the cell apoptosis was promoted and cell proliferation was inhibited (P<0.05). In all groups, no significant difference was found in alkaline phosphatase activity and bone mineralization potentiality (P>0.05). CONCLUSION: Less than 500 mg alendronate added in Cemex®XL 50 g bone cement powder has no cytotoxicity on osteoblasts.

Retraction: Strontium-doped gelatin scaffolds promote M2 macrophage switch and angiogenesis through modulating the polarization of neutrophils.

Retraction of 'Strontium-doped gelatin scaffolds promote M2 macrophage switch and angiogenesis through modulating the polarization of neutrophils' by Tao Li et al., Biomater. Sci., 2021, 9, 2931-2946, https://doi.org/10.1039/D0BM02126A.

Overexpression of Wnt7b antagonizes the inhibitory effect of dexamethasone on osteoblastogenesis of ST2 cells.

INTRODUCTION: It is well established that glucocorticoid-induced osteoporosis is highly associated with preosteoblast differentiation and function. This study is based on the premise that Wnt7b can promote bone formation through Wnt signalling pathway because it can stimulate preosteoblast differentiation and increase its activity. However, it is unknown whether Wnt7b can rescue the inhibited osteoblast differentiation and function caused by exogenous glucocorticoid. MATERIAL AND METHODS: In this study we used Wnt7b overexpression ST2 cells to explore whether Wnt7bcan rescue the inhibited osteoblast differentiation and function, which can provide strong proof to investigate a new drug for curing the glucocorticoid induced osteoporosis. RESULTS/CONCLUSION: We found that Wnt7b can rescue the suppressed osteoblast differentiation and function without cell viability caused by dexamethasone.

Distally Based Sural Fasciocutaneous Flaps for Reconstructing Soft Tissue Defects Proximal and Distal to the Tarsometatarsal Joints: A Comparative Analysis.

Distally based sural fasciocutaneous (DBSF) flaps are widely used for reconstructing soft tissue defects of the foot. The purpose of this paper was to compare the clinical efficacy of the use of flaps to repair defects in areas proximal and distal to the level of the tarsometatarsal joints in a relatively large number of patients and to analyze the effects of factors on the risk of developing partial necrosis of the flaps. Between April 2001 and December 2019, a total of 355 DBSF flaps were utilized to cover soft tissue defects in the foot. According to the furthest location of the defects reconstructed with the flaps, the flaps were divided into the proximal foot group (n = 260) and the distal foot group (n = 95). The partial necrosis rates, their influencing factors, and the clinical outcomes of the procedure were compared between the two groups. In the proximal foot group, the partial necrosis rate (6.2%, 16 of 260) was significantly lower than that in the distal foot group (14.7%, 14 of 95) (P < .05). The proportion of successful coverage of the defects using the flaps alone or in combination with a simple salvage treatment was comparable between the groups (P > .05). The ratio of unfavorable conditions in the distal foot group was higher than that in the proximal foot group (P < .05). DBSF flaps can be effectively utilized to repair defects in the proximal and distal areas of the foot. The use of a DBSF flap to repair defects in the proximal areas of the foot is superior to the use of DBSF flaps for repairing defects in the distal areas of the foot in terms of reliable survival of the flap.