Osteoarthritis (OA) is a degenerative joint disease marked by irreversible cartilage destruction, lacking effective disease-modifying therapies. Plant-derived exosome-like nanoparticles (PELNs) have emerged as promising natural nanocarriers. Here, we successfully isolated exosome-like nanoparticles from ginseng (GELNs) and evaluated their therapeutic potential for OA. GELNs were efficiently internalized by chondrocyte-derived SW1353 cells and mitigated IL-1β-induced apoptosis, inflammation, extracellular matrix degradation, and ferroptosis. Integrated transcriptomic and small RNA sequencing revealed significant enrichment of ferroptosis-related pathways and identified ginseng-specific miR-2118 as a key functional cargo within GELNs. Mechanistically, miR-2118 directly targeted the 3′-UTR of the zinc transporter SLC39A7. This targeting downregulated SLC39A7 expression, thereby restoring intracellular zinc homeostasis, improving mitochondrial dysfunction, and ultimately blocking the ferroptosis cascade. These cytoprotective effects were reversed by a miR-2118 inhibitor. In a mouse OA model induced by anterior cruciate ligament transection, intra-articular injection of GELNs markedly attenuated cartilage degradation and subchondral bone destruction. Our findings reveals that GELNs inhibit chondrocyte ferroptosis through the delivery of ginseng-specific miR-2118, which targets the SLC39A7/zinc homeostasis axis, underscoring the unique medicinal value of ginseng. Furthermore, these findings highlight the potential of PELNs as carriers for endogenous miRNAs capable of cross-species communication, providing an expandable nanotherapeutic platform for the treatment of OA.

OBJECTIVE:To investigate the role of endothelin receptor B (Ednrb/ETB) in tranexamic acid (TXA)-induced post-traumatic osteoarthritis (PTOA) and to elucidate the underlying molecular mechanisms. METHODS:Adult rats were assigned to four groups: control + TXA (T), cartilage scratch + TXA (CT), subchondral fracture + TXA (ST), and combined cartilage-subchondral fracture + TXA (CST). RNA sequencing combined with Venn analysis was used to identify candidate genes, including Ednrb. Molecular docking was performed to evaluate the binding affinity between TXA and ETB. Rats were subsequently regrouped for histological, immunohistochemical, and biochemical analyses of cartilage. ATDC5 chondrocytes were transfected with si-Ednrb-1/2 and co-treated with TXA to assess cell viability and pathway activation. RESULTS:RNA sequencing identified Ednrb as a core upregulated gene in the CT and CST groups. Molecular docking demonstrated strong binding between TXA and ETB (binding energy: -5.1 kcal/mol). In the rat PTOA model, TXA significantly increased OARSI scores in the NCT and NCST groups (P < 0.0001), upregulating the expression of ETB, matrix metalloproteinase 13 (MMP13), RXFP1, endothelin-1 (ET-1), phosphorylated nuclear factor-kappa B, and phosphorylated AKT, as well as the inflammatory mediators interleukin-1 beta, tumor necrosis factor alpha, and interleukin-6. In ATDC5 cells, Ednrb knockdown significantly increased cell viability, reduced apoptosis, and downregulated ETB, MMP13, and pathway-related signaling molecules, thereby attenuating inflammatory responses. TXA treatment significantly reversed these protective effects. CONCLUSION:Ednrb functions as a key mediator in TXA-induced PTOA progression. The binding of TXA to ETB activates the relaxin and ET-1/ETB pathways, thereby promoting cartilage degradation and inflammation. Targeting Ednrb may represent a promising therapeutic strategy for preventing TXA-associated PTOA.

ObjectiveThis study aimed to identify genes and signaling pathways associated with acute cartilage injury using RNA sequencing (RNA-seq).MethodsKnee joint cartilage samples were collected from normal mice and 2 models of acute cartilage injury (non-invasive and groove models) within an 8-hour time limit. RNA-seq revealed differential gene expression between the injury models and controls, with subsequent validation using real-time quantitative polymerase chain reaction (RT-qPCR) for 9 representative genes.ResultsCompared to controls, the non-invasive model showed 36 differentially expressed genes (DEGs) (13 up-regulated, 23 down-regulated), with Gm14648 and Gm35438 showing the most significant upregulation and downregulation, respectively. The groove model exhibited 255 DEGs (13 up-regulated, 23 down-regulated), with Gm14648 and Gm35438 showing the (222 up-regulated, 33 down-regulated). Six overlapping genes were identified between the non-invasive and groove models, including up-regulated genes (Igfn1, Muc6, Hmox1) and down-regulated genes (Pthlh, Cyp1a1, Gm13490), validated by RT-qPCR. Gene ontology (GO) analysis highlighted involvement in environmental information processing and cartilage organ system function, while Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis implicated the JAK-STAT signaling pathway. RT-qPCR and immunohistochemistry confirmed downregulation of Fhl1 in the non-invasive model, supported by Western blotting of p-JAK2/t-JAK2 levels.ConclusionsThis study identifies DEGs (13 up-regulated, 23 down-regulated), with Gm14648 and Gm35438 showing the in acute cartilage injury, suggesting potential therapeutic targets. The role of Fhl1 in cartilage protection via the JAK-STAT pathway warrants further investigation in acute cartilage injury research.

Posttraumatic osteoarthritis (PTOA) is directly associated with early acute articular cartilage injury. Inhibition of cartilage destruction immediately following joint damage can effectively slow or prevent PTOA progression. Therefore, we sought to determine intervention targets and therapeutic strategies in the acute stage of cartilage injury. The benefits of chronic intermittent hypobaric hypoxia (CIHH) extend to various body tissues, but its impact on acute cartilage injury remains unclear. We selected PTOA initiation as the therapeutic window and administered CIHH treatment immediately following cartilage injury initiation to investigate its protective effect on cartilage and molecular mechanism changing with time-varying. The non-invasive PTOA mouse model was established by applying a single rapid specific impact force to the right knee’s tibial plateau, initiating load-induced PTOA development, closely resembling the pathological changes in human diseases. Following loading, we inhibited cartilage destruction by treating mice immediately in a hypobaric chamber with a hypobaric hypoxia mimic at 5000 m altitude. Cohorts of mice subjected to distinct experimental conditions were monitored for 3, 7, 14 or 28 days. Safranin O-Fast Green staining, Immunohistochemistry, immunofluorescence, ELISA, and western blotting were performed to evaluate the therapeutic effects of CIHH on cartilage in vivo. The nuclear translocation of NF-κB p65 and Nrf2 were detected by immunofluorescence. The results showed that inhibiting cartilage destruction using CIHH immediately following acute articular cartilage injury initiation delayed the progression of PTOA, decreased the Mankin score and suppressed the expression of proinflammatory factors, including iNOS, NO, TNF-α, and IL-1β. Meanwhile, immediate CIHH treatment reduced levels of the catabolic enzymes ADAMTS5 and MMP13 in the cartilage matrix, reversed degradation of Collagen II and COMP, and inhibited oxidative stress by decreasing ROS levels. Moreover, CIHH suppressed NF-κB signaling by activating the Nrf2 in vivo studies. Our study demonstrated that immediate CIHH treatment following cartilage injury initiation can attenuate load-induced cartilage damage by activating Nrf2/HO-1 and inhibiting the NF-κB p65 signalling pathways to counteract oxidative stress and inflammatory reactions, enhance the metabolic balance of the cartilage matrix and delay cartilage degeneration. This treatment may represent a potential therapeutic strategy for limiting PTOA progression.

Abstract Purpose The study’s objective was to assess the effect of the screw insertion depth into fractured vertebrae in treating thoracolumbar fractures. Materials and methods This was a retrospective analysis of 92 patients with thoracolumbar fractures from December 2018 to February 2020. Patients had AO type A2, A3 thoracolumbar fractures. The patients were divided into two groups according to the screw insertion depth. The vertebral wedge angle (VWA), Cobb angle (CA), anterior vertebral body height (AVBH), middle vertebral body height (MVBH), visual analog scale (VAS) score, and Oswestry Disability Index (ODI) were compared preoperatively and at one week and 12 months postoperatively. The correlation between Vertebral height loss and potential risk factors, such as sex, age, BMD and BMI was evaluated. Results Compared with the preoperative data, the postoperative clinical and radiographic findings were significantly different in both groups, But no significant difference between the two groups at 1 week. At 1 year postoperatively, there was a significant difference in the CA (p < 0.0001), VWA (p = 0.047), AVBH (p < 0.0001), MVBH (p < 0.0001), VAS score (p < 0.0001), and ODI (p < 0.0001) between the two groups, Except for age, bone density and other influencing factors the long screw group had better treatment results than the short screw group. Conclusion A longer screw provides greater grip on the fractured vertebral body and stronger support to the vertebral plate. The optimal screw placement depth exceeds 60% of the vertebral body length on the lateral view.

Abstract Objective The intra-articular injection of tranexamic acid (TXA) has been shown to be effective at reducing perioperative bleeding. However, the damage to human articular cartilage caused by TXA could contribute to posttraumatic osteoarthritis (PTOA) after acute cartilage injury. In the present study, we aimed to investigate the genes and molecular programmes controlling PTOA pathogenesis associated with TXA using RNA sequencing (RNA-seq). Methods We performed RNA-seq and computational analyses of cartilage tissues obtained from various groups of rats. The differentially expressed genes between the control group and each experimental group were collated to identify those genes that were regulated by TXA. We investigated the role of TXA in cartilage tissue degeneration using RT‒qPCR analysis and histological assays. Results We identified 3113 genes (1834 upregulated and 1279 downregulated) that were differentially expressed between the cartilage-subchondral bone damage group and the control group. Furthermore, 57 genes were differentially expressed (45 upregulated and 12 downregulated) between the cartilage damage group and the control group. EDNRB was identified in both sets of differentially expressed genes and was thus considered a gene specifically regulated by TXA. Upregulation of EDNRB mRNA in the TXA injection model was confirmed by RT‒qPCR. Notably, immunohistochemistry analysis revealed that EDNRB is involved in PTOA pathogenesis. Conclusion These study results suggest that the ETB receptor plays a pivotal role in cartilage degeneration after acute injury induced by topical administration of TXA and may be a new target for the development of therapies for this condition.

目的 比较CT三维重建引导下双平面克氏针撬拨辅助复位与有限切开复位治疗难复性股骨颈骨折的临床疗效.方法 回顾性分析2019 年1 月～2021 年6 月我院创伤急救中心采用CT三维重建引导下双平面克氏针撬拨辅助复位与有限切开复位治疗难复位性股骨颈骨折 44 例(Garden Ⅲ型 19 例和Ⅳ型 25 例),采用双平面克氏针撬拨辅助复位 25 例(撬拨复位组),切开复位 19 例(切开复位组),比较 2 组患者手术时间、术中出血量、术后复位质量、术后并发症情况.结果 撬拨复位组手术时间(102.6±13.4)min,明显短于切开复位组(128.9±13.0)min(t =-6.546,P =0.000);术中出血量(66.7±11.5)ml,明显少于切开复位组(103.6±12.4)ml(t =-10.185,P =0.000).撬拨复位组复位质量Ⅰ级20 例,Ⅱ级5 例,切开复位组Ⅰ级 16 例,Ⅱ级 3 例,2 组复位质量差异无统计学意义(Z =-0.355,P =0.723).44 例平均随访 2.1 年(1.5～2.5 年),骨折均愈合,撬拨复位组无术后并发症发生,切开复位组1 例术后切口感染,1 例随访1 年后发生股骨头坏死.结论 与切开复位相比,CT三维重建引导下双平面克氏针撬拨辅助复位治疗难复性股骨颈骨折,复位快捷,手术创伤小,是切开复位前值得尝试的方法.

Objective This study aimed to examine the effect of the endplate reduction (EPR) technique combined with bone grafting for treating thoracolumbar burst fractures using posterior short-segmental fixation. Methods Patients with thoracolumbar fractures admitted between January 2018 and October 2021 were retrospectively analyzed, and those meeting the criteria were assigned to the EPR group and the intermediate screws (IS) group. The vertebral wedge angle (VWA), Cobb angle (CA), anterior vertebral body height (AVBH), middle vertebral body height (MVBH), upper endplate line (UEPL), upper intervertebral angle (UIVA), and upper intervertebral disc height (UIDH) indices were examined and compared preoperatively, first day postoperatively, as well as at 12 months postoperatively. Results The result indicated that the EPR group achieved better MVBH reduction (p<0.001), UEPL reduction (p<0.001), vertebral body fracture healing (p=0.006), as well as implant breakage (p=0.04) than the IS group; VWA (p<0.001), CA (p=0.005), AVBH (p<0.001), MVBH (p<0.001), UEPL (p<0.001), and UIDH (p<0.001) were lost after reduction less than those in the IS group. There was no significant difference in operative time (p=0.315) and intraoperative bleeding (p=0.274) between the 2 groups. Conclusion The EPR group achieved better results in repositioning and maintaining MVBH and endplate morphology, with less correction loss after the reduction of the VWA, CA, AVBH, and endplate morphology. The EPR group exhibited a better healing pattern after vertebral fracture and disc degeneration was better relieved.

后踝骨折是临床常见的骨折,也是临床治疗的重难点,本研究首次采用新型特殊构型接骨板固定后踝骨折,完成骨折块的加压及固定,与传统内固定方式相比,具有操作较为简单方便,踝关节后方软组织的损伤较小,避免骨折块的破坏等优势,值得进一步研究和推广.

Objective To determine the effect of endplate reduction on the final healing morphology and degenerative changes in intervertebral discs. Methods Forty-eight patients with single-level thoracolumbar fractures with endplate injury were included. All patients underwent posterior reduction and pedicle screw fixation, and postoperative imaging was used to determine whether endplate reduction was successful. The healing morphology of the endplate was divided into three types: increased endplate curvature, irregular healing and traumatic Schmorl node. MRI was performed at baseline and at the last follow-up evaluation to observe changes in disc degeneration (disc height and nucleus pulposus signal) and Modic changes. Results The reduction rate in the central area was significantly lower than that in the peripheral area (P = 0.017). In patients with successful reduction, 90.9% (20/22) of the endplates healed with increased curvature. In patients with an unsuccessful endplate reduction, 63.4% (26/41) of the endplates healed irregularly, and 34.1% (14/41) of the endplates formed traumatic Schmorl nodes. Endplate reduction was closely related to the final healing morphology of the endplate (P < 0.001), which had a significant protective effect on the degeneration of the intervertebral disc. At the last follow-up evaluation, there was no statistically significant correlation between different endplate healing morphologies and new Modic changes. Conclusions The reduction rate in the central area is significantly lower than that in the peripheral area. Although all of the intervertebral discs corresponding to fractured endplates had degenerated to different degrees, successful endplate fracture reduction can obviously delay the degeneration of intervertebral discs.

Background Tibial plateau fractures (TPFs) are a challenging type of fracture in orthopedic traumatology. We previously designed a plate (Patent Number: CN201520195596.5) for posterolateral TPF combined with posterior lateral collapse.. In this study, finite element analysis was used to compare the biomechanical characteristics of two internal fixation methods for posterolateral TPF. We investigated the support effect of the new steel plate on lateral TPFs combined with posterior TPFs. Methods Two models of complex TPF were established. Model A was fixed with the new type of plate, and model B was fixed without the plate. Three axial loads of 500, 1,000, and 1,500 N were applied using FEA on the two fracture models (A and B) to analyze the data. Results In model A, the maximum displacement at 500, 1,000, and 1,500 N was 0.085797, 0.17043, and 0.25465 mm, respectively; the maximum stress of the bone block was 11.285, 20.648, and 29.227 MPa, respectively; and the maximum strain of the bone block was 0.0012474, 0.007435, and 0.0035769 mm, respectively. The maximum displacement of the internal fixation was 0.096932, 0.18682, and 0.27655 mm, respectively; the maximum stress was 69.54, 112.1, and 155.71 MPa, respectively; and the maximum strain was 0.00066228, 0.0010676, and 0.0014829 mm, respectively. In model B, the maximum displacement of fractures at 500, 1,000, and 1,500 N was 0.15675, 0.29868, and 0.44017 mm, respectively; the maximum stress of the bone block was 6.5519, 12.575, and 18.842 MPa, respectively; and the maximum strain of the bone block was 0.0032554, 0.0074357, and 0.012146 mm, respectively. The maximum displacement of the screw was 0.14177, 0.27109, and 0.39849 mm, respectively; the maximum stress was 48.916, 92.251, and 135.27 MPa, respectively; and the maximum strain was 0.00046608, 0.00087893, and 0.0012887 mm, respectively. Conclusions The fixation method using this type of plates and screws can replace other methods using two plates to fix complex TPF.

Previous studies have indicated that chronic intermittent hypobaric hypoxia (CIHH) preconditioning can inhibit TNF‑α and other related inflammatory cytokines and exerts protective effect on intervertebral disc degeneration disease (IDD) in rats; however, the mechanism is still unclear. The present study aimed to explore the repair mechanisms of CIHH on IDD in rats. In the experiment, 48 adult Sprague‑Dawley rats were selected and randomly divided into an experimental group (CIHH‑IDD), a degenerative group (IDD) and a control group (CON). The CIHH‑IDD group of rats (n=16) were treated with CIHH (simulated 3000 m altitude, 5 h per day, 28 days; PO2=108.8 mmHg) before disc degeneration surgery. The IDD group of rats (n=16) underwent tail‑vertebral intervertebral disc surgery to establish a model of intervertebral disc degeneration. The CON group of rats (n=16) did not receive any treatments. After surgery, the disc height index was calculated using X‑ray analysis of rat tail vertebrae, the degeneration process was observed and repair was evaluated by chemically staining degenerative intervertebral disc tissue slices. The expression levels of basic fibroblast growth factor (bFGF), TGFβ1, Collagen I and Collagen II were measured in the intervertebral disc tissue using western blotting; while the expression levels of bFGF, TGFβ1 and hypoxia‑inducible factor 1‑α (HIF‑1α) were measured in rat serum using ELISA. The results demonstrated that: i) The degree of intervertebral disc height degeneration in CIHH‑IDD rats was significantly lower compared with that in IDD rats (P<0.05); ii) the expression levels of bFGF, TGFβ1 and HIF‑1α were higher in CIHH‑IDD rat serum compared with those in IDD rat serum (P<0.05); iii) optical microscopy revealed that the degree of disc degeneration was relatively mild in CIHH‑IDD rats; and iv) the protein expression levels of bFGF, TGFβ1 and collagen II were increased in CIHH‑IDD rat intervertebral disc tissues compared with those of IDD rats, while the overexpression of collagen I protein was inhibited. Overall, after CIHH pre‑treatment, the expression levels of bFGF and TGFβ1 were up‑regulated, which play notable roles in repairing degenerative intervertebral discs in rats.

Abstract Background In tibial plateau fractures, the posterolateral segment of the tibia plateau is frequently affected and challenging to treat. Although there are many surgical approaches and fixation methods for the treatment of these fractures, all of these methods have limitations. We designed a new rotational support plate (RSP) and a special pressurizer that can fix the fracture directly via the anterolateral approach. This method is advantageous because it leads to little trauma, involves a simple operation, and has a reliable fixation effect. This study details the technique of treating these fractures with the RSP and special pressurizer and provides the outcomes. Methods From May 2016 to January 2019, the data of 12 patients with posterolateral tibial plateau fractures treated with the RSP and special pressurizer in our hospital were retrospectively analyzed. Postoperative rehabilitation was advised, knee X-rays were taken at follow-ups, and fracture healing, complications, and knee range of motion were assessed. The Hospital for Special Surgery (HSS) knee score and Knee Injury and Osteoarthritis Outcome Score (KOOS) were used to evaluate knee function at the last follow-up. Results The average follow-up time of all patients was 16.5 months (range, 12–25 months). The average bony union time was 3.2 months (range, 3–4.5 months). At the last follow-up, the average knee range of motion was 138° (range, 107–145°). The average HSS score was 91 (range, 64–98). The average KOOS Symptoms score was 90 (range, 75–96). The average KOOS Pain score was 91 (range, 72–97). The average KOOS ADL score was 91 (range, 74–97). The average KOOS sport/recreation score was 83 (range, 70–90). The average KOOS QOL score was 88 (range, 69–93). Skin necrosis, incision infections, and fixation failure did not occur during the follow-up period. Conclusions With our newly designed RSP and special pressurizer, posterolateral tibial plateau fractures can be easily and effectively reduced and fixed through the anterolateral approach, which serves as a novel treatment for posterolateral tibial plateau fractures.

胫骨后外侧平台骨折一直是创伤骨科治疗的难题,本研究首次报道采用特制加压器结合旋转支撑接骨板的方式治疗胫骨后外侧平台骨折,术中通过拧入顶推螺钉挤压加压器L形中空框架滑动的方式,完成骨折块的加压及固定,与传统加压方式相比,其具有操作简单、加压固定效果更稳定可靠等优势,经术后影像学检查表明其临床效果满意,值得进一步推广应用.

Cannulated screw fixation is widely used in the treatment of femoral neck fractures. During surgery, we often face the situation that a guide wire needs to be adjusted because of poor positioning in the femoral neck. It is difficult to adjust the direction of the guide wire in the neck of the femur due to its elasticity. This study developed a practical technique to adjust the guide wire to the correct position. When the direction of insertion of the guide wire has deviated, first, measure the length of the guide wire. Second, select the appropriate cannulated screw based on the measurement, and screw the cannulated screw in along the direction of the guide wire to Ward's triangle. Then return the guide wire to the front of the cannulated screw. At this time, the cannulated screw can be used as a built‐in guide, and a screwdriver can be used to fine‐tune the position of the screw to the optimal direction under the X‐ray guidance. Finally, the cannulated screw is screwed in in this direction until it passes through the Ward triangle area, and the guide wire is inserted. This technique can help doctors insert a guide wire more quickly and accurately, reducing intraoperative injury and the operation time.

Intervertebral disc degeneration (IDD) is the major pathogenesis of lower back pain. Tyrosol is a polyphenolic compound that exhibits anti-oxidant, anti-apoptotic, and anti-inflammatory effects. Herein, we explored the effects and mechanisms of tyrosol on IDD progression in interleukin (IL)-1β-stimulated human nucleus pulposus cells (HNPCs). Cell viability and apoptosis were detected by CCK-8 and flow cytometry analysis, respectively. The production of tumor necrosis factor-α (TNF-α), IL-6, nitric oxide (NO), and prostaglandin E2 (PGE2) was examined to evaluate inflammation. The mRNA expression of matrix metalloproteinases (MMPs) (MMP-3/9/13), collagen type II, SRY-related high mobility group box 9 (SOX-9), and aggrecan was measured by qRT-PCR. Protein levels of silent information regulator 2 homolog 1 (Sirt1), phosphorylated protein kinase B (p-Akt), Akt, collagen type II, SOX-9, and aggrecan were determined by western blot. Results showed that tyrosol attenuated IL-1β-induced viability reduction, apoptosis, and caspase-3/7 activity in HNPCs. The increase in the production of TNF-α, IL-6, NO, and PGE2 in IL-1β-treated HNPCs was abolished by tyrosol treatment. Tyrosol treatment reversed IL-1β-induced upregulation of MMP-3, MMP-9, and MMP-13, and downregulation of collagen II, SOX-9, and aggrecan in HNPCs. Additionally, tyrosol treatment activated the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in IL-1β-stimulated HNPCs. Sirt1 was upregulated by tyrosol, and Sirt1 silencing inhibited Akt phosphorylation in HNPCs. Sirt1 knockdown attenuated the effects of tyrosol on IL-1β-induced apoptosis, inflammation, and ECM remodeling in HNPCs. In summary, upregulation of Sirt1 by tyrosol suppressed apoptosis and inflammation and regulated ECM remodeling in IL-1β-stimulated HNPCs through activation of PI3K/Akt pathway.

Objective:To compare the biomechanical properties of four-screw diamond internal fixation, traditional three-screw internal fixation and internal fixation with dynamic hip screw plus one anti-rotation screw for femoral neck fracture of Pauwels type Ⅲ.Methods:The CT data of the right femoral neck of a 65-year-old healthy male volunteer and the data of cannulated screw and dynamic hip screw (DHS) provided by Synthes medical-device company were used to create models of femoral neck fracture of Pauwels type Ⅲ and models of 3 modes of internal fixation via Mimics 14.0 software: four-screw diamond internal fixation (group A), three-screw inverted triangle internal fixation (group B) and internal fixation with DHS plus one anti-rotation screw (group C). The 3 kinds of models were input into the finite element analysis software Ansys12.1 to stimulate the fracture site displacements and stress distributions on internal fixation when a human body was in upright position.Results:For groups A, B and C, the peak stresses on the femoral neck screws were 26.95 MPa, 39.48 MPa and 34.57 MPa. The overall stress peak in group C was 50.36 Mpa, concentrated at the distal screw on the femoral shaft plate. For groups A, B and C, the peak stresses at fracture site were 9.55 MPa, 10.07 MPa and 20.10 MPa, and the peak displacements 0.64 mm, 0.65 mm and 0.67 mm.Conclusions:Compared with the other 2 modes of internal fixation, diamond fixation of femoral neck fracture of Pauwels type Ⅲ with 4 cannulated screws may result in better anti-shearing force and dispersion of stresses. In addition, it can provide effective sliding compression and reduce postoperative shortening of the femoral neck.