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No study has evaluated the effect of topical powdered vancomycin in patients undergoing primary total knee arthroplasty (TKA). The goal of this study is to determine if this method reduces postoperative infection rates following primary TKA.This retrospective study reviewed 855 consecutive patients undergoing TKA. The first 418 patients, who did not receive topical vancomycin, were grouped into the control group and the subsequent 437 patients, who received powdered vancomycin applied to the target joint prior to wound closure, were grouped into the treatment group.The control group was found to have 18 infectious complications (4.3%) compared with 6 (1.4%) in the treatment group, which differed significantly (p0.05). When comparing the rates of infectious complications independently, there was no significant difference in the rate of superficial infection (3.1% vs. 1.4%; p0.05), while the difference in prevalence of periprosthetic joint infection (PJI) was statistically significant (1.2% vs. 0; p0.05). No serious adverse events (AEs) occurred.Topical application of powdered vancomycin may present a reasonable means of decreasing the risk of infectious complications following TKA. There were no serious AEs associated with topical vancomycin. Further research is needed to focus on its long-term efficacy and safety.III, retrospective, cohort study.

Objective Nontraumatic osteonecrosis of the femoral head (ONFH) is one of the most common diseases in orthopaedics. The damage to vascular endothelial (VE) cells caused by glucocorticoids (GC) has been reported as a possible mechanism of pathogenesis for ONFH. Junction‐mediating and regulatory protein (JMY), originally identified as a p53 coactivator, plays prominent roles in the DNA damage response and in cell motility. This study aimed to discover the role of JMY in the pathogenesis of GC‐induced endothelial cell lesions. Methods High‐throughput RNA sequencing was performed to identify the differentially expressed genes between GC‐treated human umbilical vein endothelial cells (HUVEC) and control cells. JMY knockdown and overexpressing HUVEC lines were treated with GC. Cell proliferation was examined with a survival cell count assay (Cell Counting Kit‐8, CCK‐8); cell apoptosis was measured by flow cytometry; a scarification assay was used to detect the capability of cell migration; a Transwell chamber assay was done to detect the cell motility . Differential expression of cell protein was detected by western blot. Results A total of 1561 differential genes were obtained through transcription sequencing, of which 789 mRNA were upregulated and 772 mRNA were downregulated in the GC‐treated HUVEC compared with the control cells. CCK‐8 assay results showed that: without GC treatment, overexpression or knockdown of JMY did not affect the proliferation activity of HUVEC. In the presence of GC treatment, the proliferation activity of HUVEC in the JMY knockdown group was significantly higher than that in the control group (P

Rheumatoid arthritis (RA) is a chronic and inflammatory synovitis systemic disease. Due to the unknown pathogenesis, this study was to investigate the effect of microRNA (miR)-411 on apoptosis and joint function of synoviocytes in RA mice via RIPK1-mediated NF-κB signaling pathway. The collagen-induced arthritis model mice were induced via collagen type II and Freund’s adjuvant. The mice were injected with miR-411 mimics, si-RIPK1 or miR-411 mimics + oe-RIPK1 to figure out their roles in cell apoptosis and inflammation of synovial tissues. Synoviocytes were grouped as in animal experiments. Proliferation and apoptosis of synoviocytes were detected upon treatment with overexpressed miR-411 and silenced RIPK1. The expression of miR-411, RIPK1 and NF-κB in synovial tissues and synoviocytes of RA mice was detected by RT-qPCR and Western blot analysis. Poorly expressed miR-411, and highly expressed NF-κB and RIPK1 existed in synovial tissue and synoviocytes of RA. Additionally, it was found that si-RIPK1 decreased NF-κB expression, and miR-411 mimics decreased both RIPK1 and NF-κB. MiR-411 had a targeted relationship with RIPK1. si-RIPK1 or miR-411 mimics promoted cell apoptosis and strained inflammation in synovial tissues of mice with RA. Overexpressed miR-411 or silencing RIPK1 inhibited the proliferation and promoted apoptosis of synoviocytes of RA mice. Up-regulation of miR-411 or down-regulation of RIPK1 had a certain inhibitory effect on RA. This study suggests that up-regulated miR-411 or down-regulated RIPK1 promoted apoptosis and inhibited proliferation of synoviocytes of RA mice, which may be related to the inhibition of NF-κB activation.

IntroductionIn the present research, we formulated a modern chemotherapeutic drug by silver nanoparticles (AgNPs) containing Nigella sativa aqueous extract for the treatment of bone tumor.Material and methodsCharacterization of AgNPs was done by UV–Visible Spectroscopy (UV-Vis), Fourier Transformed Infrared Spectroscopy (FT‐IR), Transmission Electron Microscopy (TEM), and Field Emission Scanning Electron Microscopy (FE‐SEM). For investigating the antioxidant properties of AgNO3, N. sativa, and AgNPs, the DPPH test was used in the presence of butylated hydroxytoluene as the positive control. To survey the cytotoxicity and anti-bone tumor effects of AgNO3, N. sativa, and AgNPs, MTT assay was used on the human bone Ewing’s sarcoma (CADO-ES1 and MHH-ES1), human bone osteosarcoma (HOS and MG-63), and human bone chondrosarcoma (SW-1353 and CH-3573) cell lines.ResultsDPPH test revealed similar antioxidant potentials for N. sativa, AgNPs, and butylated hydroxytoluene. Silver nanoparticles had very low cell viability and anti-bone tumor properties dose-dependently against CADO-ES1, MHH-ES1, HOS, MG-63, SW-1353, and CH-3573 cell lines without any cytotoxicity on the normal cell line. The best result of anti-bone tumor properties of AgNPs against the above cell lines was seen in the case of the MG-63 cell line.ConclusionsAccording to the above findings, the silver nanoparticles containing N. sativa aqueous extract can be administrated in humans for the treatment of several types of bone tumors.

The injury and dysfunction of the femoral head microvascular endothelial cells are associated with the pathogenesis of glucocorticoid‐induced osteonecrosis of the femoral head (ONFH). Reports indicate that icariin (ICA) can enhance vascular roles and also inhibit endothelial cell dysfunction. However, it still remains unclear whether ICA can promote angiogenesis in glucocorticoid‐induced ONFH. In this study, we investigate this hypothesis through in vitro and in vivo experiments. Results showed that 0.1 mg/mL hydrocortisone significantly suppressed bone microvascular endothelial cells (BMECs) proliferation while ICA at 10−5 mol/L reversed this inhibition. ICA significantly promoted BMECs migration, tube formation, the angiogenesis‐related cytokines expression and the activation of Akt. Furthermore, ICA enhanced Bcl‐2 expression but diminished Bax expression. According to in vivo results, rats with ICA treatment exhibited a lower ratio of empty lacunae, higher volume of blood vessels and more CD31‐positive cells. This study revealed that ICA promotes angiogenesis of BMECs in vitro and improves femoral head blood vessel volume of rats treated with glucocorticoid, suggesting the efficacy of ICA in the prevention of glucocorticoid‐induced ONFH.

Inflammation and extracellular matrix (ECM) degradation have been implicated in the pathological process of osteoarthritis (OA). α-Cyperone is the main active component of the traditional Chinese medicine Cyperus rotundus L. In this study, we found that α-Cyperone abolished the IL-1β-induced production of inflammatory cytokines in isolated rat chondrocytes, such as cyclooxygenase-2 (COX-2), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and inducible nitric oxide synthase (iNOS), in a dose-dependent manner (0.75, 1.5 or 3 μM). Also, the results showed that α-Cyperone downregulated the expression of metalloproteinases (MMPs) and thrombospondin motifs 5 (ADAMTS5), and upregulated the expression of type-2 collagen. Mechanistically, molecular docking tests revealed that α-Cyperone stably and effectively binds to p65, p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK). α-Cyperone inhibited NF-κB activation by blocking its nuclear transfer, and decreasing the phosphorylation of mitogen-activated protein kinase (MAPKs). In addition, in vivo studies based on a mouse model of arthritis showed that α-Cyperone prevented the development of osteoarthritis. Therefore, α-Cyperone may be a potential anti-OA drug.

Background: Controversy exists concerning whether tenotomy or tenodesis is the optimal surgical treatment option for proximal biceps tendon lesions. Purpose: To evaluate the clinical outcomes after arthroscopic tenodesis and tenotomy in the treatment of long head of the biceps tendon (LHBT) lesions. Study Design: Systematic review; Level of evidence, 4. Methods: A systematic review was performed by searching PubMed, the Cochrane Library, Web of Science, and Embase to identify randomized controlled trials (RCTs) and cohort studies that compared the clinical efficacy of tenotomy with that of tenodesis for LHBT lesions. A standardized data extraction form was predesigned to obtain bibliographic information of the study as well as patient, intervention, comparison, and outcome data. A random-effects model was used to pool quantitative data from the primary outcomes. Results: A total of 21 eligible studies were separated into 3 methodological groups: (1) 4 RCTs with level 1 evidence, (2) 3 RCTs and 4 prospective cohort studies with level 2 evidence, and (3) 10 retrospective cohort studies with level 3 to 4 evidence. Analysis of the 3 groups demonstrated a significantly higher risk of the Popeye sign after tenotomy versus tenodesis (group 1: risk ratio [RR], 3.29 [95% CI, 1.92-5.49]; group 2: RR, 2.35 [95% CI, 1.43-3.85]; and group 3: RR, 2.57 [95% CI, 1.33-4.98]). Arm cramping pain remained significantly higher after tenotomy only in the retrospective cohort group (RR, 2.17 [95% CI, 1.20-3.95]). The Constant score for tenotomy was significantly worse than that for tenodesis in the prospective cohort group (standardized mean difference [SMD], –0.47 [95% CI, –0.73 to –0.21]), as were the forearm supination strength index (SMD, –0.75 [95% CI, –1.28 to –0.21]) and the Simple Shoulder Test (SST) score (SMD, –0.60 [95% CI, –0.94 to –0.27]). Conclusion: The results demonstrated that compared with tenodesis, tenotomy had a higher risk of a Popeye deformity in all 3 study groups; worse functional outcomes in terms of the Constant score, forearm supination strength index, and SST score according to prospective cohort studies; and a higher incidence of arm cramping pain according to retrospective cohort studies.

Background Osteoarthritis (OA) is a chronic degenerative disease of the joints characterized by articular cartilage damage, subchondral bone remodeling, osteophyte formation, and inflammatory changes. This work aims to investigate the protective role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) against the apoptosis of chondrocytes. Methods Chondrocyte cell lines, CHON-001, and ATDC5 were treated with different doses of interleukin-1β (IL-1β) to mimic the inflammatory response during OA pathogenesis. Quantitative real-time polymerase chain reaction was performed to measure MEG3, miR-9-5p, and Krüppel-like factor 4 (KLF4) mRNA expression levels. MEG3 and KLF4 overexpression plasmids, MEG3 shRNA, miR-9-5p mimics, and miR-9-5p inhibitors were transfected into the cells. Cell counting kit-8, wound healing assay, and flow cytometry were conducted to determine cell viability, migration, and apoptotic rate. Dual-luciferase reporter assay was adopted to verify the targeting relationships among MEG3, miR-9-5p, and KLF4. Western blot was used to detect KLF4 protein expression. Enzyme-linked immunosorbent assay was employed to measure the levels of inflammatory factors. Results MEG3 expression in chondrocytes was down-regulated by the stimulation of IL-1β, and MEG3 negatively regulated miR-9-5p expression but positively regulated KLF4 expression. MEG3 overexpression strengthened the viability and migration of CHON-001 and ATDC5 cells but restrained the apoptosis and inflammatory response, while MEG3 knockdown had opposite effects. miR-9-5p inhibition or KLF4 overexpression could counteract the effects of MEG3 knockdown on chondrocytes. Besides that, MEG3 was proved to be a molecular sponge for miR-9-5p, and KLF4 was verified as the target of miR-9-5p. Conclusion MEG3 can promote chondrocyte proliferation and migration and inhibit apoptosis and inflammation by sponging miR-9-5p to induce KLF4 expression, which provides a promising therapy target for OA treatment.

Background Glucocorticoid-induced osteonecrosis of the femoral head (ONFH) is closely associated with the dysfunction of the bone microvascular endothelial cells (BMECs). The present study investigated the angiogenic and apoptotic activity of the BMECs in glucocorticoid-induced ONFH. Methods This study enrolled a total of 12 patients, six of whom were assigned to the ONFH group whereas the other six served as the control group. The ONFH group was composed of patients with glucocorticoid-induced ONFH while the control group had femoral neck fractures. BMECs were isolated from the subchondral region of the femoral head. Cell proliferation, cell viability, tube formation assay, Transwell assay, TUNEL assay, and Western blot analysis were performed. Results BMECs of the two groups were successfully isolated and identified. No significant differences were noticed in BMECs proliferation between the two groups. However, compared to the control, cell viability, tube formation, and migration of BMECs were significantly decreased and the number of TUNEL positive cells was markedly increased in the ONFH group. In the ONFH group, it was also noted that the amount of Bax and cleaved-caspase3 was elevated while that of Bcl-2 was reduced. Conclusion The findings of our study revealed that BMECs obtained from the glucocorticoid-induced ONFH patients had decreased angiogenic and increased apoptotic activities, which could explain the pathogenesis and progression of glucocorticoid-induced ONFH.

BackgroundNon-vascularized bone grafting is a promising head-preserving technique for younger patients diagnosed as non-traumatic osteonecrosis of the femoral head (NONFH). Among the various types of bone grafting techniques, “light-bulb” procedure grafting with synthetic bone substitute is an attractive option. We aimed to assess the effectiveness of using beta-tricalcium phosphate (β-TCP) for the treatment of pre-collapse and early post-collapse lesions NONFH.MethodsFrom April 2010 to June 2014, 33 patients (47 hips) with NONFH were treated using the afore-mentioned technique. The clinical and radiological outcomes were recorded and compared statistically between pre- and post-operation. Harris hip score (HHS) was used to evaluate the clinical results, and Association Research Circulation Osseous (ARCO) stage was applied to assess the radiological outcomes.ResultsThe 5-years survival rate of using β-TCP grafting was accounting for 25.5%. HHS was decreased from 78.47 to 52.87 points, and a very significant worsening of radiological results were revealed (P ConclusionsOur results suggest that “light-bulb” procedure grafting with β-TCP sticks presented with a high failure rate in the early postoperative period. It is not proposed for the treatment of pre-collapse and early post-collapse lesions NONFH.

Background The pathogenesis of osteonecrosis of the femoral head (ONFH) is unclear. Our previous study demonstrated that upregulated miR-335 in bone microvascular endothelial cells (BMECs) might be associated with the disease of steroid-induced ONFH. Here, we study the preventive effect of ICA on steroid-induced ONFH in rats. Method 90 rats were separated into three groups: control group, methylprednisolone (MPS) group, and MPS + Icariin (ICA) group. Four weeks later, histological analyses were performed. Thrombomodulin (TM) and vascular endothelial growth factor (VEGF) were tested. MiRNA-335 expression was screened in the three groups using Agilent Gene Spring GX software. Target genes of miRNA-335 were detected by bioinformatics analysis. The functions of BMECs were analyzed by scratch, angiogenesis and cell survival rate. Results ICA can prevent the occurrence of steroid-associated ONFH in rats and reduce the amount of TM and VEGF in serum induced by glucocorticoids. ICA could regulate the overexpression of miRNA-335 induced by glucocorticoids. We predicted the Gene ontology (GO) and signaling pathways of target genes. At 24 hours, we found that ICA significantly promoted BMECs migration abilities. We also found that ICA could promote the angioplasty ability of BMECs. ICA could improve the survival rate of BMECs after steroid-induced injury. Conclusions ICA is effective to prevent the occurrence of steroidinduced ONFH. ICA has a protective effect against steroid-induced BMECs injury. ICA regulated the imbalance of miRNA-335 expression induced by the glucocorticoid in BMECs, which provides a new viewpoint to explore the mechanism of ICA in preventing steroid-induced ONFH.

Based on the construction of an evaluation index system for land urbanization quality, this paper evaluates and analyzes the variability of spatial-temporal in land urbanization quality during 2005-2015 in China. Results shows that: (1) Among the three aspects of land urbanization quality, sustainable development capacity scores the highest, land urbanization development quality follows, land-population coordinated development is the lowest. (2) The quality of land urbanization in China is generally improving, and the spatial distribution has a “gradient difference”, showing a pattern of high east and low west. In conclusion, to improve the quality of land urbanization, all aspects should be considered comprehensively; each region should combine its own conditions to formulate strategies for improving the quality of land urbanization.

Background To obtain the correct coronal alignment and balancing in flexion and extension, we established a selective medial release technique and investigated the effectiveness and safety of the technique during primary total knee arthroplasty (TKA). Methods Four hundred sixty-six primary TKAs with varus deformity were prospectively evaluated between June 2013 and June 2015. A knee joint position similar to Patrick’s sign was used to release the medial structure. The medial release technique consisted of release of the capsule and the deep medial collateral ligament (dMCL) (step1), selective release of superficial medial collateral ligament (sMCL) or posterior oblique ligament (POL) (step 2), and selective tibial reduction osteotomy (step 3). Improvement of medial joint gap at each step and other clinical outcomes were evaluated. Results Among the 466 knees, symmetrical gaps could be achieved by the limited release of the capsule and the dMCcL in 276 (59%) knees. One hundred fifty-two (33%) required additional sMCL release with 2–5 cm from the joint line distally or POL release. Thirty-eight (8%) necessitated an additional tibial reduction osteotomy. Anterior-medial release and 4-mm medial osteotomy contributed to more improvement of medial gap in flexion than in extension (each p

Unilateral hearing impairment is characterized by asymmetric hearing input, which causes bilateral unbalanced auditory afferents and tinnitus of varying degrees. Long-term hearing imbalance can cause functional reorganization in the brain. However, differences between intrinsic functional changes in the brains of patients with left- and those with right-sided long-term hearing impairments are incompletely understood. This study included 67 patients with unilateral hearing impairments (left-sided, 33 patients; right-sided, 34 patients) and 32 healthy controls. All study participants underwent blood oxygenation level dependent resting-state functional magnetic resonance imaging and T1-weighted imaging with three-dimensional fast spoiled gradient-echo sequences. After data preprocessing, fractional amplitude of low frequency (fALFF) and functional connectivity (FC) analyses were used to evaluate differences between patients and healthy controls. When compared with the right-sided hearing impairment group, the left-sided hearing impairment group showed significantly higher fALFF values in the left superior parietal gyrus, right inferior parietal lobule, and right superior frontal gyrus, whereas it showed significantly lower fALFF values in the left Heschl’s gyrus, right supramarginal gyrus, and left superior frontal gyrus. In the left-sided hearing impairment group, paired brain regions with enhanced FC were the left Heschl’s gyrus and right supramarginal gyrus, left Heschl’s gyrus and left superior parietal gyrus, left superior parietal gyrus and right inferior parietal lobule, right inferior parietal lobule and right superior frontal gyrus, and left and right superior frontal gyri. In the left-sided hearing impairment group, the FC of the paired brain regions correlated negatively with the duration and pure tone audiometry were in the left Heschl’s gyrus and right supramarginal gyrus. In the right-sided hearing impairment group, the FC of the paired brain regions correlated negatively with the duration was in the left Heschl’s gyrus and superior parietal gyrus, and with pure tone audiometry was right inferior parietal lobule and superior frontal gyrus. The intrinsic reintegration mechanisms of the brain appeared to differ between patients with left-sided hearing impairment and those with right-sided hearing impairment, and the severity of hearing impairment was associated with differences in functional integration in certain brain regions.

Non-vascularized bone grafting is a promising head-preserving technique for younger patients diagnosed as non-traumatic osteonecrosis of the femoral head (NONFH). Among the various types of bone grafting techniques, “light-bulb” procedure grafting with synthetic bone substitute is an attractive option. We aimed to assess the effectiveness of using beta-tricalcium phosphate (β-TCP) for the treatment of pre-collapse and early post-collapse lesions NONFH. From April 2010 to June 2014, 33 patients (47 hips) with NONFH were treated using the afore-mentioned technique. The clinical and radiological outcomes were recorded and compared statistically between pre- and post-operation. Harris hip score (HHS) was used to evaluate the clinical results, and Association Research Circulation Osseous (ARCO) stage was applied to assess the radiological outcomes. The 5-years survival rate of using β-TCP grafting was accounting for 25.5%. HHS was decreased from 78.47 to 52.87 points, and a very significant worsening of radiological results were revealed (P

Background The aim of this study was to compare clinical and radiological outcomes between a short femoral cementless stem and a conventional femoral cementless stem in total hip arthroplasty in patients 70 years and older. Methods From December 2011 and July 2013, we retrospectively reviewed 50 patients (55 hips) 70 years and older treated with a short femoral cementless stem and 53 patients (58 hips) 70 years and older treated with a conventional femoral cementless stem. Their mean age was 74 ± 13.2 years and 75 ± 10.4 years, respectively. The mean follow-up was 40 ± 3.6 months and 42 ± 5.2 month, respectively. They were pre- and postoperatively evaluated by the clinical and radiological examination. Results There was no difference in terms of average operative time, average estimated blood loss, and average hemoglobin at discharge between the short stem and the conventional stem. No patients with the short stem had intra-operative fracture, but five patients with the conventional stem had intra-operative fracture. At final follow-up, there was no statistically significant difference in Harris Hip Score, and radiographic review level between two stems. No hip with the short stem had thigh pain, but six hips with the conventional stem had thigh pain at the final follow-up. No component was revised for aseptic loosening in either group. Conclusions Our study demonstrated that both short cementless stem and conventional cementless stem provided stable fixation and achieved a satisfactory result in patients 70 years and older and the short cementless stem had a low incidence of thigh pain and intra-operative fracture.

Osteocyte apoptosis is the main manifestation of steroid-induced avascular necrosis of the femoral head (SANFH). STAT1 and caspase 3 participate in the process of apoptosis and STAT1 upregulates the expression of caspase 3. We examined the relationship between the STAT1-caspase 3 pathway and apoptosis in SANFH. All specimens were divided into four groups: the negative control group, Ficat I-II group, Ficat III group, and Ficat IV-V group, and examined histologically, with a TUNEL assay, immunohistochemically, with a caspase 3 activity assay, with ELISAs of STAT1 and phospo-STAT1 (p-STAT1), with a western blotting analysis of p-STAT1 and with real-time RT-PCR. The proportion of empty lacunae increased significantly with the development of SANFH. The proportion of TUNEL-positive cells and immunohistochemical analysis of caspase 3 also increased significantly, although the Ficat I-II group did not differ significantly from the negative control group. Immunohistochemical analysis of STAT1 and p-STAT1, caspase 3 activity all showed significant differences among the groups. An ELISA and a western blotting analysis of p-STAT1 showed significant differences among the groups. An ELISA of STAT1, real-time RT-PCR analysis of caspase 3 and STAT1 all showed significant differences among the groups except between the Ficat I-II and negative control groups. The correlation analysis showed strong positive relationships between the proportion of empty lacunae and the proportion of TUNEL-positive cells between caspase 3 activity and the proportion of TUNEL-positive cells and between the levels of p-STAT1 protein and caspase 3 mRNA. The apoptotic process in SANFH develops with the upregulated expression of caspase 3 via the expression and activation of STAT1. The STATI-caspase 3 pathway plays a critical role in the development of SANFH.

To release extension contracture of the knee, the authors used a minimally invasive technique: percutaneous quadriceps tendon pie-crusting release. Percutaneous pie-crusting release was performed using an 18-gauge needle to puncture the stiff fibrous band of the distal and lateral quadriceps tendon under maximum knee flexion. Quadriceps contracture was gradually released by multiple needle punctures. A knee brace was prescribed for one week and knee flexion exercises were performed on the first postoperative day. This technique was performed in seven post-traumatic stiff knees and five stiff total knee arthroplasties. Mean maximum flexion increased from 37o preoperatively to 50o after arthrolysis and 107o after pie-crusting. At a mean follow-up of eight months, mean maximum flexion was 103o. There were no major complications. The technique of quadriceps tendon pie-crusting release is a simple, minimally invasive and effective treatment for knee extension contracture.