Bone defects pose a high risk of non-union and permanent disability, making effective bone regeneration a critical focus in the development of bone repair materials. Current research primarily emphasizes enhancing the single osteogenic function of bone repair materials, while neglecting the impact of the complex microenvironment in bone defect areas. This has resulted in the failure of many developed bone repair materials to achieve effective in vivo bone regeneration. In this study, a multifunctional near-infrared light-responsive black phosphorus (BP) bone repair scaffold was fabricated via low-temperature deposition 3D printing. In vitro characterization demonstrated that the scaffold possesses a cancellous bonelike structure, moderate compressive strength, and cytocompatibility, with the ability to promote osteogenesis under inflammatory conditions. In vivo studies further confirmed its favorable photothermal responsiveness, enabling photothermal therapy (PTT) to accelerate bone regeneration while reducing inflammation in the defect area. These findings indicate that the multifunctional BP scaffold achieves superior bone repair outcomes through synergistic effects of anti-inflammation, promotion of osteogenic differentiation, and PTT, thereby improving the success rate of defect repair. Moreover, the simple fabrication process and satisfactory therapeutic efficacy of this multifunctional BP scaffold highlight its high potential for clinical translation.

Lateral meniscus posterior root tears lead to disruption of hoop tension, elevation of contact pressure, increased knee instability, and accelerated cartilage degeneration of articular cartilage. Anatomical repair is required to re-establish normal knee biomechanics and to slow the progression of osteoarthritis. A modified transtibial pull-out technique using an all-suture anchor is described. The tail suture is applied for root fixation, creating a suture ball on the meniscal surface, while a 2 mm tibial tunnel is created at the anatomic footprint to achieve refixation. This technique provides stable, minimally invasive, and anatomical repair, minimizing bone loss, avoiding tunnel interference with anterior cruciate ligament grafts, and promoting biological healing.

随着全球人口老龄化的加剧,伴随着关节退行性疾病发病率的增长,髋膝关节置换的数量不断增加.在美国,预计到2030年,初次全膝关节置换(total knee arthroplasty,TKA)数量将达到348万,初次全髋关节置换(total hip arthroplasty,THA)数量将达到57.2万[1].我国虽没有人工关节登记系统,但据不完全统计,截至2019年,我国关节置换的数量已经超过每年95万例,年均增长率达19.96％[2].

OBJECTIVES:The aim of this study was to investigate whether proximal tibial cortex transverse distraction (PTCTD) could result in nerve regeneration in diabetic Charcot foot via electromyography (EMG). PATIENTS AND METHODS:Between March 2015 and June 2021, a total of six patients (4 males, 2 females; mean age: 58.8±15.5 years; range, 32 to 75 years) with diabetic Charcot foot treated with PTCTD were retrospectively analyzed. Electromyography was performed preoperatively and six months postoperatively to evaluate nerve regeneration. Healing time, wound area and limb salvage rates were also recorded. RESULTS:The mean time to wound healing in all patients was 155.17±19.13 (range, 135 to 189) days. The mean wound area was 4.44±2.58 (range, 2.52 to 9.52) cm2. No cases of low limb amputation occurred, with a limb salvage rate of 100%. The EMG revealed spontaneous potentials and decreased recruitment in all patients preoperatively. Motor unit potentials were found only in some of the tested muscles. At the final follow-up, the extensor digitorum brevis in four patients (67.7%) had a simple recruitment phase. Three patients (50%) and four patients (67.7%) had increased compound muscle action potential (CMAP) amplitudes in muscles innervated by the nervus peroneus communis and tibial nerve, respectively. In one patient (16.7%), the CMAP was found only at the peroneal head segment of the nervus peroneus communis, but not at the distal end. CONCLUSION:Our results indicate that nerve regeneration can be confirmed by EMG after PTCTD in patients with diabetic Charcot foot. However, further multi-center, large-scale, long-term prospective studies are needed to draw more reliable conclusions on this subject.

Macrophage apoptosis, along with inflammation in the interface membrane, has been demonstrated to be significant in the pathogenesis and development of particle-induced periprosthetic osteolysis and aseptic loosening. Additionally, the apoptosis of macrophages is considered an indicator of the resolution phase of inflammation and the transition to normal tissue healing. Therefore, targeting macrophages presents a promising strategy for both the prevention and therapeutic management of periprosthetic osteolysis. In this study, we explored the therapeutic potential of chemical chaperone 4-phenylbutyrate (4-PBA) as a pharmacological intervention aimed at modulating macrophage behaviors, particularly focusing on the processes of apoptosis, inflammation, and osteoclastogenesis in a murine model of TiAl6V4 nanoparticle (TiNP)-induced osteolysis. The results derived from in vivo studies conducted on the murine model provide compelling evidence that TiNPs could trigger osteolysis, activate inflammatory cell infiltration, and promote the differentiation of osteoclasts, accompanied by a notable rise in apoptosis at the osteolytic interface periosteum. The severity of TiNP-induced osteolysis, chaotic bone morphology, extensive bone erosion and destruction, occurrence of infiltrating inflammatory cells, and quantity of osteoclasts were attenuated following co-intervention with 4-PBA. Furthermore, the levels of apoptosis, in conjunction with apoptosis-regulated proteins Bcl-2 and Bax, were accentuated following 4-PBA co-intervention, indicating that the TiNP-induced osteolytic interface periosteum environment exhibited a greater propensity for apoptosis due to the pharmacological intervention of 4-PBA. Notably, the use of 4-PBA as a standalone treatment demonstrated comparatively low levels of toxicity and was deemed to be experimentally safe in mice. These findings indicated that 4-PBA may ameliorate the severity of particle-induced osteolysis by inhibiting the inflammatory response and promoting macrophage apoptosis in a manner that may be beneficial for therapeutic strategies. Thus, pharmacological intervention with 4-PBA appears to be a viable option for addressing osteolysis and aseptic loosening resulting from exposure to wear particles, combining efficacy in promoting apoptosis with a favorable safety profile.

Bionic bioelectronics has promising applications in bone defect repair, with current research primarily focusing on the development of electroactive biomaterials and self-powered systems, which can mimic the electrophysiological microenvironment of natural bone tissue, accelerating bone healing by promoting osteoblast proliferation and differentiation through electrical stimulation. However, the biological mechanisms of bionic electrical stimulation in bone defect repair remain incompletely understood. Here, the study developed a self-sustained biomimetic bioelectronic system comprising a triboelectric/piezoelectric hybrid nanogenerator (TP-hNG) and a multifunctional gold-coated polymer internal fixation plate (GP-IFP), which utilizes the natural biomechanical properties of rat heartbeat and respiratory movements to generate bionic electric signals (Bio-SIG) that are closely related to physiological neurofeedback signals. The Bio-SIG can disrupt the glucose metabolic homeostasis in osteoblasts, enhancing the osteoblasts' dependence on aerobic glycolysis while attenuating dependence on oxidative phosphorylation (OXPHOS). This metabolic shift triggers critical steps in osteogenic differentiation, bone formation and mineralization, effectively facilitating the repair of bone defects. This work reveals the key role of glucose metabolic reprogramming in osteogenesis mediated by bionic electrical stimulation, elucidates the complex regulatory mechanisms of bionics in bone regenerative medicine and deepens the understanding of how biofeedback electrical stimulation precisely regulates the bone regeneration process, which provides a solid theoretical basis for clinical personalized treatment.

A central focus of bone tissue engineering is the construction of vascular systems, which provide nutrients for cell survival, remove metabolic waste, and accelerate tissue regeneration. Platelet-derived growth factor-BB (PDGFB) has the ability to stimulate both vascularization and bone regeneration; however, its clinical application has been hindered by side effects and low efficacy due to suboptimal delivery systems. In this study, a biomimetic vascular scaffold crosslinked with heparan sulfate (HS) is developed to enable sustained delivery of the PDGFB-LG4 fusion protein, targeting the regeneration of critically sized bone defects. The scaffold is designed with a vascular-like hierarchical structure, incorporating a customized 3D framework, multibranched microchannels, and permeable porous walls, which facilitates mass exchange and cell infiltration. PDGFB-LG4 exhibits superior osteoinductive and angiogenic activity compared to PDGFB. In a calvarial defect model, the composite scaffold (PCLHS-PDGFB-LG4) significantly enhances both vascularization and bone regeneration, demonstrating improved efficacy at lower doses compared to PDGFB. This approach may be applicable to other growth factors and gelatin-based materials, offering the potential for a wide range of applications in regenerative medicine.

11507 Background: Patients (pts) with relapsed and refractory (R/R) osteosarcoma have a poor prognosis with limited therapeutic options. HS-20093 is a novel antibody-drug conjugate (ADC) targeting B7-H3, which showed preliminary anti-tumor activity in phase 1 ARTEMIS-001 study (NCT05276609). Here we report results in R/R osteosarcoma pts treated with HS-20093 from ARTEMIS-002 study (NCT05830123). Methods: ARTEMIS-002 trial is an open label, two-arm phase 2 trial in pts with R/R osteosarcoma or other sarcomas progressed upon standard systemic treatment. Based on the results of the phase 1 trial that the maximum tolerated dose was 12 mg/kg once every 3 weeks (Q3W) intravenous infusion, the osteosarcoma pts in the phase 2 trial were randomized to receiving HS-20093 either at 8 mg/kg or 12 mg/kg Q3W at a ratio of 1:1. The primary endpoint was objective response rate (ORR) according to RECIST1.1. B7-H3 expression was retrospectively evaluated by IHC in osteosarcoma FFPE tissue. Results: A total of 34 pts with R/R osteosarcoma were enrolled from June to December in 2023, receiving HS-20093 at the dose of either 8.0 mg/kg (N = 15) or 12.0 mg/kg (N = 19). Median age was 21.5 years (range: 18~65). At baseline, most pts were evaluated with clinical stage IV disease (32/34, 94.1%) and pulmonary metastasis (28/34, 82.4%). Twenty-two pts (64.7%) had received ≥3 prior lines therapy. Twenty-six pts (76.5%) had received 4 types of standard chemotherapies consisting of platinum, anthracyclines, ifosfamide and methotrexate. Treatment emergent adverse event (TEAEs) occurred in 33 pts (97.1%). The common grade 3/4 TEAEs (≥5%) were: neutropenia, leukopenia, thrombocytopenia, lymphopenia and anemia. The incidences of discontinuations, dose withhold and dose reductions were 2.9%, 11.8% and 23.5%, respectively. There was no TEAE leading to death. As of cut-off date (25 December, 2023), the median follow-up time was 4.1 months (95% CI: 1.4~5.5) among 21 response-evaluable pts (11 treated with 8 mg/kg and 10 with 12.0 mg/kg). The ORR of 12.0 mg/kg HS-20093 was 20.0%. Two confirmed partial responses were observed in pts with 12.0 mg/kg and remained on response until last follow-up, of which the longest duration of response was 4.0 months. The disease control rate was 81.8% (9/11) and 100% (10/10) in pts with 8 mg/kg and 12.0 mg/kg. The median progression-free survival of all 21 pts was not mature. B7-H3 is highly expressed in osteosarcoma with median H-score 185 (0~260). No correlation was observed between tumor response and B7-H3 expression level. The PK exposure of HS-20093 ADC, total Ab and payload increased with dose, approximately proportional to dose, with a half-life of 4 to 6 days, and no or minor accumulation after multiple doses of Q3W. Conclusions: The data has demonstrated that HS-20093 exhibited promising antitumor activity with acceptable toxicity in pts of heavily-pretreated R/R osteosarcoma. The enrollment of ARTEMIS-002 is continuing. Clinical trial information: NCT05830123 .

Osteoarthritis (OA) is the most common joint disease with high prevalence and incidence. Increasing reports has indicated that circular RNAs (circRNAs) are implicated in OA progression. Nevertheless, the roles and functions of most circRNAs in OA remain to be elucidated. In this study, we emphatically discussed circ-IQGAP1 (circ_0104873) in OA. Firstly, we discovered that circ_0104873 was dramatically overexpressed during osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). Several functional assays demonstrated that circ_0104873 inhibition repressed BMSCs proliferation and osteogenic differentiation. Moreover, mechanism assays also revealed that circ_0104873 sponged microRNA-875-5p (miR-875-5p) to up-regulate notch receptor 3 (NOTCH3), thereby activating the Notch signaling pathway. Rescue assays disclosed that circ_0104873 contributed to the development of OA via targeting miR-875-5p/NOTCH3 axis. In conclusion, circ_0104873 promoted the progression of OA by miR-875-5p/NOTCH3/Notch signaling pathway, which might provide a promising target for OA treatment.

OBJECTIVE:To establish the finite element model of spinal canal reconstruction and internal fixation,analysis influence of spinal canal reconstruction and internal fixation on spinal stability,and verify the effectiveness and reliability of spinal canal reconstruction and internal fixation in spinal canal surgery. METHODS:A 30-year-old male healthy volunteer with a height of 172 cm and weight of 75 kg was selected and his lumbar CT data were collected to establish a finite element model of normal lumbar L3-L5,and the results were compared with in vitro solid results and published finite element analysis results to verify the validity of the model. They were divided into normal group,laminectomy group and spinal canal reconstruction group according to different treatment methods. Under the same boundary fixation and physiological load conditions,six kinds of activities were performed,including forward bending,backward extension,left bending,right bending,left rotation and right rotation,and the changes of range of motion (ROM) of L3-L4,L4-L5 segments and overall maximum ROM of L3-L5 were analyzed under the six conditions. RESULTS:The ROM displacement range of each segment of the constructed L3-L5 finite element model was consistent with the in vitro solid results and previous literature data,which confirms the validity of the model. In L3-L4,ROM of spinal canal reconstruction group was slightly increased than that of normal group during posterior extension(>5% difference),and ROM of other conditions was similar to that of normal group(<5% difference). ROM in laminectomy group was significantly increase than that in normal group and spinal canal reconstruction group under the condition of flexion,extension,left and right rotation. In L4-L5,ROM in spinal canal reconstruction group was similar to that in normal group(<5% difference),while ROM in laminectomy group was significantly higher than that in normal group and spinal canal reconstruction group(>5% difference). In the overall maximum ROM of L3-L5,spinal canal reconstruction group was only slightly higher than normal group under the condition of posterior extension(>5% difference),while laminectomy was significantly higher than normal group and spinal canal reconstruction group under the condition of anterior flexion,posterior extension,left and right rotation(>5% difference). The changes of each segment ROM and overall ROM of L3-L5 showed laminectomy group>spinal canal reconstruction group>normal group. CONCLUSION:Laminectomy could seriously affect biomechanical stability of the spine,but application of spinal canal reconstruction and internal fixation could effectively reduce ROM displacement of the responsible segment of spine and maintain its biomechanical stability.

Effective antitumor agents with concurrent osteogenic properties are essential for comprehensive osteosarcoma (OS) treatment. However, the current clinical therapeutic strategies of OS fail to completely eradicate tumors while simultaneously encouraging bone formation. To address this issue, a switchable strategy for dynamic OS ablation and static bone regeneration is developed by integrating piezoelectric BaTiO 3 (BTO) with atomic‐thin Ti 3 C 2 (TC) through a Schottky heterojunction, resulting in the formation of TC@BTO. Under sequential ultrasound and near‐infrared irradiation, the optimized carrier transport of TC@BTO, based on Schottky heterojunction, exhibits excellent characteristics of photothermal conversion and reactive oxygen species generation. This results in ferroptosis of tumor cells and eventual elimination of OS. Moreover, in the static state, the interfacial Schottky heterojunction facilitates the carriers’ directed transfer from the semiconductor to the metal. The Schottky heterojunction‐enhanced static electrical stimulation enhances the osteogenic differentiation of bone marrow‐derived mesenchymal stem cells and repair of bone defects. Furthermore, RNA‐sequencing analysis reveals that static TC@BTO promotes bone regeneration by activating Wnt signaling pathway, and remarkably, pharmacological inhibition of Wnt signaling suppresses the TC@BTO‐induced osteogenesis. Overall, this work broadens the biomedical potential of Schottky heterojunction‐based therapies and provides a comprehensive strategy for overall OS ablation and bone regeneration.

Immune cells play a crucial role in the onset and progression of rheumatoid Arthritis (RA). we leveraged publicly available Genome-Wide Association Studies (GWAS) data to explore the causal relationship between 731 immune cell traits and RA using the Bidirectional MR analysis. The primary method for causal analysis relies on Inverse Variance Weighting (IVW). To ensure robustness, sensitivity analyses include the Cochran Q test, MR-Egger intercept test, MR-PRESSO, and leave-one-out analysis. Additionally, gene colocalization analysis and drug target MR are employed to enhance the comprehensiveness of the study.In the forward MR analysis, after FDR correction, 731 immune cell traits had no statistically significant effect on RA. Notably, some phenotypes showed lower P values before adjustment, including 12 different immune cell traits. After gene colocalisation analysis only CD4 on HLA DR+ CD4+ T cells and CD45RA- CD28- CD8+ T cell %T cell shared the same genetic variant as RA. Inverse MR analysis showed that RA was associated with 12 immune cell traits. After gene colocalisation analysis RA was associated with CD28- CD8+ T cell %T cell, Effector Memory CD8+ T cell %T cell, CD8+ Natural Killer T Absolute Count, CD8+ Natural Killer T %lymphocyte, and CD8+ Natural Killer T %T cell share the same genetic variant. No evidence of horizontal pleiotropy or heterogeneity between genetic variants was found (P>0.05), and the "leave-one-out" test confirmed the stability and robustness of the associations. MR analyses of drug targets suggested that CCHCR1 may play an important role in the pathogenesis of RA.This study suggests that specific immune cell traits may play a key role in RA development and could serve as new biomarkers for its diagnosis. Notably, identifying CCHCR1 as a drug target unveils new paths for research and treatment, offering promising opportunities in the field.

BACKGROUND:Periprosthetic osteolysis and subsequent aseptic loosening are the leading causes of failure following total joint arthroplasty. Osteogenic impairment induced by wear particles is regarded as a crucial contributing factor in the development of osteolysis, with endoplasmic reticulum (ER) stress identified as a key underlying mechanism. Therefore, identifying potential therapeutic targets and agents that can regulate ER stress adaption in osteoblasts is necessary for arresting aseptic loosening. Osthole (OST), a natural coumarin derivative, has demonstrated promising osteogenic properties and the ability to modulate ER stress adaption in various diseases. However, the impact of OST on ER stress-mediated osteogenic impairment caused by wear particles remains unclear. METHODS:TiAl6V4 particles (TiPs) were sourced from the prosthesis of patients who underwent revision hip arthroplasty due to aseptic loosening. A mouse calvarial osteolysis model was utilized to explore the effects of OST on TiPs-induced osteogenic impairment in vivo. Primary mouse osteoblasts were employed to investigate the impact of OST on ER stress-mediated osteoblast apoptosis and osteogenic inhibition induced by TiPs in vitro. The mechanisms underlying OST-modulated alleviation of ER stress induced by TiPs were elucidated through Molecular docking, immunochemistry, PCR, and Western blot analysis. RESULTS:In this study, we found that OST treatment effectively mitigated TiAl6V4 particles (TiPs)-induced osteolysis by enhancing osteogenesis in a mouse calvarial model. Furthermore, we observed that OST could attenuate ER stress-mediated apoptosis and osteogenic reduction in osteoblasts exposed to TiPs in vitro and in vivo. Mechanistically, we demonstrated that OST exerts bone-sparing effects on stressed osteoblasts upon TiPs exposure by specifically suppressing the ER stress-dependent PERK signaling cascade. CONCLUSION:Osthole ameliorates wear particle-induced osteogenic impairment by mitigating endoplasmic reticulum stress via PERK signaling cascade. These findings suggest that OST may serve as a potential therapeutic agent for combating wear particle-induced osteogenic impairment, offering a novel alternative strategy for managing aseptic prosthesis loosening.

Background/Objective Brain metastasis in osteosarcoma (BMO) is rare and its clinical characteristics are often buried among studies on brain metastasis of bone and soft tissue sarcomas. The aim of the present study was to summarize the incidence, clinical characteristics, treatment and outcomes of patients with BMO.Methods This retrospective study included 7 patients with BMO who received treatment in our center between 2005 and 2019. The clinical medical records of the 7 patients, together with data of 70 BMO patients published in 33 articles and retrieved by means of PubMed and Medline, were analyzed, retrospectively.Results Data analysis of the 97 BMO patients showed a high correlation between the interval from the primary diagnosis to BMO occurrence and the interval from the primary diagnosis to prior metastases. Multivariate analysis showed that chemotherapy, radiotherapy and surgery were three main factors affecting the overall survival of BMO patients (HR = 0.427; HR = 0.372; HR = 0.296). Surgery combined with chemotherapy or radiotherapy offered a better overall survival than surgery alone.Conclusion Patients with BMO may obtain survival benefits from regular neuroimaging and early aggressive multi-disciplinary interventions including surgical resection, postoperative radiotherapy and chemotherapy.Synopsis This is a retrospective study describing the characteristics of metastasic intervals, locations, clinical features and prognosis in 97 patients with brain metastasis of osteosarcoma (BMO). Multivariate analysis showed that chemotherapy was effective as surgery and radiotherapy for the treatment of BMO. Our findings emphasize the importance of regular neuroimaging and early aggressive multi-disciplinary interventions including surgical resection, postoperative radiotherapy and chemotherapy.

BackgroundArticular cartilage defects (ACD) are injuries with a diameter greater than 3 mm, resulting from wear and tear on joints. When the diameter of the defect exceeds 6 mm, it can further damage the surrounding joint cartilage, causing osteoarthritis (OA). Try to explain why OA is an irreversible disease, we hypothesize that damaged articular chondrocytes (DAC) may have reduced capacities to repair cartilage because its extracellular vesicle (EVs) that might directly contribute to OA formation.MethodsIn this study, DAC-EVs and AC-EVs were isolated using ultracentrifugation. Next-generation sequencing was employed to screen for a pathogenic long non-coding RNA (lncRNA). After verifying its function in vitro, the corresponding small interfering RNA (siRNA) was constructed and loaded into extracellular vesicles, which were then injected into the knee joint cavities of rats.ResultsThe results revealed that DAC-EVs packaged lncRNA LOC102546541 acts as a competitive endogenous RNA (ceRNA) of MMP13, down-regulating miR-632. Consequently, the function of MMP13 in degrading the extracellular matrix is enhanced, promoting the development of osteoarthritis.ConclusionsThis study uncovered a novel mode of OA pathogenesis using rat models, which DAC deliver pathogenic LOC102546541 packaged EVs to normal articular chondrocytes, amplifying the degradation of the extracellular matrix. Nonetheless, the functions of highly homologous human gene of LOC102546541 need to be verified in the future.

OBJECTIVE:To analyze the hip joint biomechanics of the acetabular anatomical reconstruction and nonanatomical reconstruction in total hip arthroplasty (THA) for Crowe type Ⅲ developmental dysplasia of the hip (DDH) by finite element method, which provided theoretical foundation and experimental basis for the anatomical acetabular reconstruction during THA in clinical practice.METHODS:One patient with left end-stage hip arthritis secondary to Crowe type Ⅲ DDH was selected in this study, who underwent total hip arthroplasty in the orthopedic department of the First Affiliated Hospital of Bengbu Medical College in April 2020. This patient was female, 57 years old. The preoperative and postoperative three dimentional CT scan of the patient's pelvis were performed. Fourteen acetabular cup models with different anteversion, inclination and rotation center height were established in Mimics and 3-Matic software. The boundary and load conditions were set in Abaqus software. The Von Mises and stress distribution of the hip joint were calculated and observed.RESULTS:In the Crowe type Ⅲ DDH THA, if the hip rotation center was restored anatomically and the acetabular cup's inclination was set as 40°, the cup's anteversion varied from 5° to 25°, the lowest Von Mises value of acetabular cup and polyethylene liner occured in 20°anteversioin;if the hip rotation center was restored anatomically and the acetabular cup's anteversion was set as 15°, the cup's inclination varied from 35° to 55°, the lowest Von Mises value of acetabular cup and polyethylene liner occured in 35° inclination;if the acetabular cup's anteversion and inclination were set as 15°and 40°respectively, the up migration of hip rotaion center varied from 0 mm to 20 mm, the lowest Von Mises value of acetabular cup and polyethylene liner occured in 10 mm up migration. In all fourteen models, the Von Mises value of the acetabulum, acetabulum cup and polyethylene liner were lowest when the acetabular cup's anteversion and inlcination were 15°, 35° respectively, as well as the rotation center was restored anatomically.CONCLUSION:In total hip arthroplasty for Crowe type Ⅲ DDH, the anatomical restoration of hip rotation center with 15° anteversion and 35° inclination of the acetabular cup are suggested, bone graft above the acetabular cup and additional screws are recommended simultaneously to further reduce the Von Mises of hip joint.

Periprosthetic osteolysis and subsequent aseptic loosening are the primary causes of failure following total joint arthroplasty. Wear particle-induced - induced osteogenic impairment is recognized as an important contributing factor in the development of osteolysis, with endoplasmic reticulum (ER) stress emerging as a pivotal underlying mechanism. Hence, searching for potential therapeutic targets and agents capable of modulating ER stress in osteoblasts is crucial for preventing aseptic loosening. Kaempferol (KAE), a natural fl avonol compound, has shown promising osteoprotective effects and anti-ER stress properties in diverse diseases. However, the influence fl uence of KAE on ER stress-mediated osteogenic impairment induced by wear particles remains unclear. In this study, we observed that KAE effectively relieved TiAl6V4 6 V 4 particles-induced - induced osteolysis by improving osteogenesis in a mouse calvarial model. Furthermore, we demonstrated that KAE could attenuate ER stress- mediated apoptosis in osteoblasts exposed to TiAl6V4 6 V 4 particles, both in vitro and in vivo. . Mechanistically, our results revealed that KAE mitigated ER stress-mediated apoptosis by upregulating the IRE1a-XBP1s a - XBP1s pathway while concurrently partially inhibiting the IRE1a-regulated a-regulated RIDD and JNK activation. Collectively, our fi ndings suggest that KAE is a prospective therapeutic agent for treating wear particle-induced - induced osteolysis and highlight the IRE1a-XBP1s a - XBP1s pathway as a potential therapeutic target for preventing aseptic loosening.

A bony Bankart lesion is a condition where the labroligamentous complex is detached from the anterior glenoid rim, often accompanied by a fracture. It is a common occurrence found in up to 70% of traumatic shoulder dislocations. Arthroscopic surgery has become the mainstream approach for treating this condition. However, the commonly used techniques, such as labrum alone, transosseous, and double-row, can encounter difficulties passing sutures and may cause damage to the surrounding tissues, especially when dealing with large bony fragments. In this technical note, we describe our preferred technique for fixing bony Bankart lesions, which involves fixing the bony Bankart fragment through the bone tunnel using an all-suture anchor. The surgery is performed with the patient in the lateral decubitus position. Our technique offers a reliable and effective approach to treat bony Bankart lesions while minimizing the risks of complications associated with conventional techniques.

OBJECTIVE:To investigate the biomechanical properties of H-shaped and L-shaped miniplate fixation systems (H-MFS and L-MFS, respectively) in restorative laminoplasty for spinal canal reconstruction (RL-SCR). METHODS:Laminectomy was performed in a 3D printed L4 vertebral model followed by RL-SCR using H-MFS or L-MFS, and the biomechanical properties of the reconstructed models were evaluated using static and dynamic compression tests. Biomechanical analyses of RL-SCR were also conducted in finite element models of the L3-L5 vertebrae with normal assignment (NA), laminectomy, or fixation with H-MFS or L-MFS, and the range of motion (ROM) of L3-L4 and L4-L5 was evaluated. RESULTS:In static compression test, the sustained yield load, compression stiffness, yield displacement and axial displacement- axial load were all significantly greater in H-MFS group (P < 0.05). Door closing, lamina collapse and plate breakage occurred in all the models in L-MFS group, and only some models in H-MFS group showed plate cracks and screw loosening. In dynamic compression tests, the peak load in H-MFS group reached 873 N (which was 95% of the average yield load in static compression), significantly greater than that in L-MFS group (P < 0.05). The ultimate load in L-MFS group was only 46.59% of that in H-MFS group (P>0.05). In finite element analysis, the ROM of the L3-L4 and L4- L5 segments were significantly smaller in NA, H-MFS and L-MFS groups than in laminectomy group. Compared with NA group, H-MFS group showed a greater ROM during extension, and L-MFS group showed greater ROM in flexion, extension, bending, and rotation; The overall ROM of the vertebral segments decreased in the order of laminectomy group, L-MFS group, H-MFS group, and NA group. CONCLUSION:Laminectomy causes structural destruction of the posterior column of the spine to affect its biomechanical stability. RL-SCR can effectively maintain the biomechanical stability of the spine, and H-MFS is superior to L-MFS in maintaining the integrity and biomechanical properties of the reconstructed spinal canal.