Current role of magnetic resonance imaging on assessing and monitoring the efficacy of phototherapy.

Phototherapy, also known as photobiological therapy, is a non-invasive and highly effective physical treatment method. Its broad use in clinics has led to significant therapeutic results. Phototherapy parameters, such as intensity, wavelength, and duration, can be adjusted to create specific therapeutic effects for various medical conditions. Meanwhile, Magnetic Resonance Imaging (MRI), with its diverse imaging sequences and excellent soft-tissue contrast, provides a valuable tool to understand the therapeutic effects and mechanisms of phototherapy. This review explores the clinical applications of commonly used phototherapy techniques, gives a brief overview of how phototherapy impacts different diseases, and examines MRI's role in various phototherapeutic scenarios. We argue that MRI is crucial for precise targeting, treatment monitoring, and prognosis assessment in phototherapy. Future research and applications will focus on personalized diagnosis and monitoring of phototherapy, expanding its applications in treatment and exploring multimodal imaging technology to enhance diagnostic and therapeutic precision and effectiveness.

A novel adhesive dual-sensitive hydrogel for sustained release of exosomes derived from M2 macrophages promotes repair of bone defects.

The repair of bone defects remains a huge clinical challenge. M2 macrophage-derived exosomes (M2-Exos) can act as immunomodulators to promote fracture healing; however, how to retain the sustained release of exosomes to the target area remains a challenge. Here, we report a composite hydrogel loaded with M2-Exos aiming to accelerate bone defect healing. It was verified that the F127/HA-NB hydrogel had a dense network structure, tissue adhesiveness, and dual sensitivity to temperature and light. F127/HA-NB loaded with M2-Exos (M2-Exos@F127/HA-NB) exhibited good biocompatibility and achieved sustained release of exosomes for up to two weeks. The study showed that both M0-Exos and M2-Exos@F127/HA-NB significantly promoted osteogenic differentiation of rat bone marrow mesenchymal stem cells. The mechanism study implied that M2-Exos activates the Wnt/ß-catenin signaling pathway to promote osteogenic differentiation of BMSCs. Finally, we evaluated the osteogenetic effects of M2-Exos@F127/HA-NB in a rat cranial defect model, and the results showed that M2-Exos@F127/HA-NB had superior bone regeneration-promoting effects. This study provides a new strategy for cell-free treatment of bone defects.

Exosomal microRNA-140-3p from human umbilical cord mesenchymal stem cells attenuates joint injury of rats with rheumatoid arthritis by silencing SGK1.

OBJECTIVE: Over the years, microRNAs (miRNAs) have been involved in the pathogenesis of rheumatoid arthritis (RA). We aim to investigate the role of human umbilical cord mesenchymal stem cells (HUCMSCs)-derived exosomal miR-140-3p in RA development. METHODS: Exosomes(exo) were isolated from human umbilical cord-derived mesenchymal stem cells (HUCMSCs), and this isolation was followed by the transfer of miR-140-3p. RA rat models were constructed by collagen II adjuvant and respectively treated with HUCMSCs-exo or HUCMSCs-exo carrying miR-140-3p mimic/inhibitor, and expression of miR-140-3p and serum- and glucocorticoid-inducible kinase 1 (SGK1) was assessed. Then, RA score and inflammation scoring, fibrosis degree and apoptosis, serum inflammatory response and oxidative stress in joint tissues were determined. The RA synovial fibroblasts (RASFs) were extracted from rats and identified. Conducted with relative treatment, the migration, proliferation and apoptosis in RASFs were determined. RESULTS: MiR-140-3p was decreased while SGK1 was increased in RA rats. HUCMSCs-exo or upregulated exosomal miR-140-3p improved pathological changes and suppressed inflammation, oxidative stress and fibrosis in RA rats, and also constrained and RASF growth. Overexpression of SGK1 reversed the inhibition of RASF growth caused by overexpression of miR-140-3p. CONCLUSION: Upregulated exosomal miR-140-3p attenuated joint injury of RA rats by silencing SGK1. This research provided further understanding of the role of exosomal miR-140-3p in RA development.

Modified double-pulley suture-bridge techniques with or without medial knot tying show comparable clinical and radiological outcomes in arthroscopic rotator cuff repair.

PURPOSE: The optimal technique for arthroscopic rotator cuff repair is still controversial. The aim of this study was to compare modified arthroscopic double-pulley suture-bridge (DPSB) technique with medial knot tying to those without tying, considering clinical and radiological outcomes. METHODS: This study included 292 patients with large full-thickness rotator cuff tears treated with modified DPSB technique. The patients were divided into 158 cases with medial knot tying (knot-tying group) and 134 without tying (knotless group). At follow-up, clinical outcome was assessed by the Constant score, American Shoulder and Elbow Surgeons (ASES) score, and Shoulder Rating Scale of the University of California at Los Angeles (UCLA) score. The assessment of tendon healing was performed with magnetic resonance imaging (MRI) at a minimum of 12 months postoperatively. RESULTS: The Constant score, ASES score and UCLA score in the knot-tying and knotless groups all improved significantly from before surgery to 12 months postoperatively (P < 0.05, respectively). No significant differences were observed between groups for each phase evaluated (n.s.). Tendon healing was categorised according to Sugaya's classification. The retearing rate was 27/158 (17.0%) in the knot-tying group and 20/134 (14.9%) in the knotless group, with no statistically significant difference between groups (n.s.). Additionally, the retear was classified using the Cho's classification. When comparing the retear rates of different types independently, no statistically significant differences were found between groups (n.s.). CONCLUSIONS: The knotless modified DPSB technique showed comparable short-term functional outcomes to those of the knot tying method in large full-thickness rotator cuff tears. Additionally, no significant differences in repair integrity were observed between the two methods. Both techniques can be considered effective treatments for patients with large-sized full-thickness rotator cuff tears. LEVEL OF EVIDENCE: III.

α-Cyperone (CYP) down-regulates NF-κB and MAPKs signaling, attenuating inflammation and extracellular matrix degradation in chondrocytes, to ameliorate osteoarthritis in mice.

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-1ß-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.

Clinical Outcomes of Arthroscopic Tenodesis Versus Tenotomy for Long Head of the Biceps Tendon Lesions: A Systematic Review and Meta-analysis of Randomized Clinical Trials and Cohort Studies.

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.

LncRNA MEG3 Protects Chondrocytes From IL-1ß-Induced Inflammation via Regulating miR-9-5p/KLF4 Axis.

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-1ß (IL-1ß) 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-1ß, 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.

The use of 2-octyl cyanoacrylate as an adjuvant to wound closure in total knee arthroplasty.

PURPOSE: The efficacy of the use of 2-octyl cyanoacrylate (OCA) as an adjuvant to wound closure in preventing wound complications after total knee arthroplasty (TKA) is rarely reported. This study was aimed to determine whether the use of OCA as a supplement to conventional wound closure reduces the incidence of wound complications following TKA. PATIENTS AND METHODS: This retrospective study reviewed 1106 consecutive patients who underwent TKA for symptomatic end-stage osteoarthritis (OA) between 2012 and 2017. The first 562 patients who did not receive OCA were grouped into the Control group, and the subsequent 544 patients who received OCA as an adjuvant to wound closure were grouped into the OCA group. All patients were followed up for at least 2 years. The main outcome was the development of operative site complications, including aseptic and infectious complications. Aseptic wound complications were wound leakage, hematoma, wound dehiscence and delayed wound healing, and infectious complication was mainly referred to the superficial infection. RESULTS: No significant difference with regard to hematoma was observed between groups (3.0% vs. 3.7%, P = 0.617, φ = - 0.02). The incidences were significantly higher in the Control group versus the OCA group in regard to wound leakage (9.4% vs. 2.0%, P = 0.000, φ = 0.16), wound dehiscence (5.7% vs. 1.3%, P = 0.000, φ = 0.12), delayed wound healing (4.4% vs. 1.5%, P = 0.004, φ = 0.09) and superficial infection (2.0% vs. 0.4%, P = 0.022, φ = 0.07). No serious adverse events (AEs) occurred. CONCLUSIONS: The present study showed that the addition of OCA reduced the incidence of wound leakage, wound dehiscence, delayed wound healing and superficial infection after TKA compared to conventional wound closure. Based on the outcomes above, we decide to use OCA routinely for wound closure after TKA. LEVEL OF EVIDENCE: III, retrospective, cohort study.

Preliminary study of icariin indicating prevention of steroid-induced osteonecrosis of femoral head by regulating abnormal expression of miRNA-335 and protecting the functions of bone microvascular endothelial cells in rats.

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.

Decreased angiogenic and increased apoptotic activities of bone microvascular endothelial cells in patients with glucocorticoid-induced osteonecrosis of the femoral head.

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.

Role of Junction-Mediating and Regulatory Protein in the Pathogenesis of Glucocorticoid-Induced Endothelial Cell Lesions.

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 < 0.01). The proliferation activity of HUVEC in the overexpression JMY group was significantly lower than that in the control group (P < 0.01). The results of flow cytometry showed that without GC treatment, overexpression or knockdown of JMY did not affect the apoptosis proportion of HUVEC. With GC treatment, the apoptosis proportion of HUVEC in the JMY knockdown group was significantly lower than that in the control group (P < 0.01), and the apoptosis proportion of HUVEC in the overexpression JMY group was significantly higher than that in the control group (P < 0.01). Western blot results showed that with GC treatment, the JMY expression level of HUVEC increased with the reaction time. Moreover, the distribution of JMY was mainly concentrated in the nucleus. The expression level of Bax also increased with the reaction time. With GC treatment, overexpression of JMY could significantly increase the expression of Bax in HUVEC. JMY knockdown could reduce the expression of Bax in HUVEC. In the absence of GC treatment, HUVEC overexpression or knockdown of JMY did not affect the expression of Bax. The results of scarification and Transwell chamber assays showed that: without GC treatment, JMY knockdown could significantly decrease the cell motility and increase the expression level of VE-cadherin in HUVEC; with GC treatment, JMY knockdown in HUVEC had lower cell motility compared with the control group (P < 0.01). CONCLUSION: Glucocorticoids can induce the HUVEC apoptosis, and reduce its proliferation, cell motility. Our results mainly confirmed the role of JMY in the pathogenesis of GC-inducing lesions in HUVEC. GC act on HUVEC, inducing cell damage. Following the event of cell damage, JMY levels upregulate in the nucleus to induce transcription of Bax, triggering apoptosis. JMY can also regulate HUVEC motility via its regulation of VE-cadherin levels.

High failure rate after Beta-tricalcium phosphate grafting for the treatment of femoral head osteonecrosis: a retrospective analysis.

BACKGROUND: 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 (ß-TCP) for the treatment of pre-collapse and early post-collapse lesions NONFH. METHODS: 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. RESULTS: The 5-years survival rate of using ß-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 <  0.05). Two hips collapsed more than 2 mm were awaiting for THA, and 33 of the 47 hips had converted to THAs in an average time to failure of 24.24 months postoperatively. Meanwhile, only 4 hips survived without collapse, and 8 hips collapsed less than 2 mm. After surgery, the time onset of head collapse was 3.65 months on average, and the first conversion to THA was performed at 5 months postoperative. CONCLUSIONS: Our results suggest that "light-bulb" procedure grafting with ß-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.

Role of intra-wound powdered vancomycin in primary total knee arthroplasty.

BACKGROUND: 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. PATIENTS AND METHODS: 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. RESULTS: The control group was found to have 18 infectious complications (4.3%) compared with 6 (1.4%) in the treatment group, which differed significantly (p<0.05). When comparing the rates of infectious complications independently, there was no significant difference in the rate of superficial infection (3.1% vs. 1.4%; p>0.05), while the difference in prevalence of periprosthetic joint infection (PJI) was statistically significant (1.2% vs. 0; p<0.05). No serious adverse events (AEs) occurred. DISCUSSION: 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. LEVEL OF EVIDENCE: III, retrospective, cohort study.

Safety and efficacy of tranexamic acid with epinephrine for prevention of blood loss following surgery for trochanteric femoral fractures.

OBJECTIVE: This study aimed to determine whether the local administration of tranexamic acid (TXA) combined with diluted epinephrine (DEP) reduces blood loss and the need for transfusions compared with the administration of TXA alone following surgery for trochanteric femoral fractures. METHODS: Hundred patients were enrolled in this study. In the target group (TXA/DEP group: n=50; 19 men and 31 women, mean age 72.5±11.1 years), the surgical sites were injected with 35 mL normal saline mixed with 3 g of TXA with 0.2 mg of DEP at a 1:200,000 dilution (TXA/DEP) immediately after musculoaponeurotic closure. In the control group (TXA group: n=50; 22 men and 28 women; mean age: 70.5±12.2 years), the surgical site was injected with 35 mL normal saline containing 3 g of TXA alone. The main outcome measures were postoperative hemoglobin (Hb) levels, hematocrit, drainage volume, and total blood loss (TBL); the secondary measures included transfusion requirements and perioperative complications. RESULTS: The mean Hb levels among patients in theTXA/DEP group were significantly lower than among those in the TXA group, measured on postoperative day 1 at 101.0±14.1 g/L vs. 106.9±10.5 g/L and day 3 as 104.2±8.2 g/L vs. 108.5±9.1 g/L, respectively (p<0.05). Drainage volume from the surgical site and TBL measured on postoperative day 2 were also significantly reduced in the TXA/DEP group vs. the TXA group, measured at 71.4±26.0 mL vs. 82.5±24.6 mL and 343.6±148.0 mL vs. 419.6±165.4 mL, respectively (p<0.05). Furthermore, 11 patients (22%) from the TXA group and 15 (30%) from the TXA/DEP group received blood transfusions; the mean number of transfusion events (1.2±0.4 vs. 1.9±0.7) and the amount of blood transfused (1.7±0.5 Units vs. 2.9±1.0 Units) was also markedly reduced in the TXA/DEP group (p<0.05). Two cases in the TXA/DEP group and three in the TXA group were diagnosed with deep vein thrombosis, a difference that did not reach statistical significance (p>0.05). CONCLUSION: Local administration of TXA with DEP reduced blood loss and limited the need for blood transfusions after surgery for trochanteric femoral fracture without increasing the risk of perioperative complications. Our study indicates that the local administration of TXA/DEP is safe and more effective than the administration of TXA alone in treating trochanteric femoral fractures. LEVEL OF EVIDENCE: Level III, Therapeutic study.

Up-regulated microRNA-411 or declined RIPK1 inhibits proliferation and promotes apoptosis of synoviocytes in rheumatoid arthritis mice via decreased NF-κB pathway.

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.

Icariin promotes angiogenesis in glucocorticoid-induced osteonecrosis of femoral heads: In vitro and in vivo studies.

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.

Should synovectomy be performed in primary total knee arthroplasty for osteoarthritis? A meta-analysis of randomized controlled trials.

BACKGROUND: During primary total knee arthroplasty (TKA), synovectomy as a part of the procedure has been recommended to relieve pain and inflammation of the synovium, but there is a controversy about it due to increased bleeding. In this meta-analysis, the aim is to answer whether synovectomy should be performed routinely during TKA for symptomatic knee osteoarthritis (KOA). METHODS: Relevant randomized controlled trials (RCTs) on synovectomy were retrieved through database searches of PubMed, Embase, Web of Science, and Cochrane Library up to February 2019. Studies that compared postoperative pain, clinical Knee Society Score (KSS), functional KSS, range of motion (ROM), drainage, pre- and postoperative hemoglobin difference, transfusion rate, operative time, and/or complications were included in the meta-analysis. Review Manager 5.3.0 was used for meta-analysis. RESULTS: We included 5 RCTs with 542 knees. Pooled results indicated that the synovectomy group was associated with more blood loss via drainage (WMD = - 99.41, 95% CI - 153.75 to - 45.08, P = 0.0003) and pre- and postoperative hemoglobin difference (WMD = - 0.93, 95% CI - 1.33 to - 0.5, P < 0.00001), compared with the non-synovectomy group. No statistically significant differences were demonstrated between both groups in postoperative pain, clinical KSS, functional KSS, ROM, transfusion rate, or complications (P > 0.05). CONCLUSIONS: The current evidence demonstrates that performing synovectomy in primary TKA for symptomatic KOA does not have any clinical benefit. It increases postsurgical blood loss. Surgeons routinely undertaking synovectomy should deliberate whether this is clinically indicated and consider limiting resection, if possible.

Differences in Intrinsic Brain Abnormalities Between Patients With Left- and Right-Sided Long-Term Hearing Impairment.

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.

Selective medial soft tissue release combined with tibial reduction osteotomy in total knee arthroplasty.

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 < 0.01). Posteromedial release and posteromedial osteotomy contributed to more improvement in extension than in flexion (each p < 0.01). No specific complication related to our technique was identified. CONCLUSION: The technique of the tibial reduction osteotomy combined with medial soft structure release using Patrick's sign is effective, safe, and minimally invasive to obtain balanced mediolateral and extension-flexion gaps in primary TKA.