Iron homeostasis is critical for multiple physiological and pathological processes. DMT1, a core iron transporter, is expressed in almost all cells and organs and altered in response to various conditions, whereas, there is few reviews focusing on DMT1 in diseases associated with aberrant iron metabolism. Based on available knowledge, this review described a full view of DMT1 and summarized the roles of DMT1 and DMT1-mediated iron metabolism in the onset and development of inflammatory and degenerative diseases. This review also provided an overview of DMT1-related treatment in these disorders, highlighting its therapeutic potential in chronic inflammatory and degenerative diseases.

BACKGROUND:Z-DNA binding protein 1 (ZBP1) is a nucleic acid sensor that is involved in multiple inflammatory diseases, but whether and how it contributes to osteoarthritis (OA) are unclear. METHODS:Cartilage tissues were harvested from patients with OA and a murine model of OA to evaluate ZBP1 expression. Subsequently, the functional role and mechanism of ZBP1 were examined in primary chondrocytes, and the role of ZBP1 in OA was explored in mouse models. RESULTS:We showed the upregulation of ZBP1 in articular cartilage originating from OA patients and mice with OA after destabilization of the medial meniscus (DMM) surgery. Specifically, knockdown of ZBP1 alleviated chondrocyte damage and protected mice from DMM-induced OA. Mechanistically, tumor necrosis factor alpha induced ZBP1 overexpression in an interferon regulatory factor 1 (IRF1)-dependent manner and elicited the activation of ZBP1 via mitochondrial DNA (mtDNA) release and ZBP1 binding. The upregulated and activated ZBP1 could interact with receptor-interacting protein kinase 1 and activate the transforming growth factor-beta-activated kinase 1-NF-κB signaling pathway, which led to chondrocyte inflammation and extracellular matrix degradation. Moreover, inhibition of the mtDNA-IRF1-ZBP1 axis with Cyclosporine A, a blocker of mtDNA release, could delay the progression of DMM-induced OA. CONCLUSIONS:Our data revealed the pathological role of the mtDNA-IRF1-ZBP1 axis in OA chondrocytes, suggesting that inhibition of this axis could be a viable therapeutic approach for OA.

Aims: Osteoarthritis (OA) is the most common chronic pathema of human joints. The pathogenesis is complex, involving physiological and mechanical factors. In previous studies, we found that ferroptosis is intimately related to OA, while the role of Sat1 in chondrocyte ferroptosis and OA, as well as the underlying mechanism, remains unclear. Methods: In this study, interleukin-1β (IL-1β) was used to simulate inflammation and Erastin was used to simulate ferroptosis in vitro. We used small interfering RNA (siRNA) to knock down the spermidine/spermine N1-acetyltransferase 1 (Sat1) and arachidonate 15-lipoxygenase (Alox15), and examined damage-associated events including inflammation, ferroptosis, and oxidative stress of chondrocytes. In addition, a destabilization of the medial meniscus (DMM) mouse model of OA induced by surgery was established to investigate the role of Sat1 inhibition in OA progression. Results: The results showed that inhibition of Sat1 expression can reduce inflammation, ferroptosis changes, reactive oxygen species (ROS) level, and lipid-ROS accumulation induced by IL-1β and Erastin. Knockdown of Sat1 promotes nuclear factor-E2-related factor 2 (Nrf2) signalling. Additionally, knockdown Alox15 can alleviate the inflammation-related protein expression induced by IL-1β and ferroptosis-related protein expression induced by Erastin. Furthermore, knockdown Nrf2 can reverse these protein expression alterations. Finally, intra-articular injection of diminazene aceturate (DA), an inhibitor of Sat1, enhanced type II collagen (collagen II) and increased Sat1 and Alox15 expression. Conclusion: Our results demonstrate that inhibition of Sat1 could alleviate chondrocyte ferroptosis and inflammation by downregulating Alox15 activating the Nrf2 system, and delaying the progression of OA. These findings suggest that Sat1 provides a new approach for studying and treating OA. Cite this article: Bone Joint Res 2024;13(3):110–123.

The most common joint disease in the elderly is osteoarthritis (OA), which is characterized by synovitis, cartilage degeneration, and osteophytes, for which there are currently no effective therapies. Chondrocytes, responsible for extracellular matrix (ECM) synthesis and degradation, undergo changes in OA, leading to ECM disruption and disease progression. There is no clear role for the Mechanistic target of rapamycin complex 2 (mTORC2) in OA, but it is known to regulate cellular functions, such as proliferation, metabolism, motility, and apoptosis. The purpose of this study was to determine the molecular mechanism by which Rapamycin-insensitive companion of mTOR (RICTOR), a component of mTORC2, contributes to OA progression. The results demonstrate that IL-1β induces high expression of RICTOR in chondrocytes, promoting downregulation of collagen II expression and impairing autophagy. Silencing RICTOR reverses IL-1β-induced downregulating of collagen II expression and mitochondrial dysfunction. RICTOR inhibits chondrocyte autophagy by inhibiting autophagosome formation and preventing autophagosome-lysosome fusion. Additionally, RICTOR promotes oxidative stress in chondrocytes, leading to disruption of normal mitochondrial structure and disturbance of the articular cartilage microenvironment. This study reveals the potential of RICTOR to treat OA. Specifically, blocking mTORC2 might be an effective treatment strategy.

INTRODUCTION:Excess iron contributes to Hemophilic Arthropathy (HA) development. Divalent metal transporter 1 (DMT1) delivers iron into the cytoplasm, thus regulating iron homeostasis. OBJECTIVES:We aimed to investigate whether DMT1-mediated iron homeostasis is involved in bleeding-induced cartilage degeneration and the molecular mechanisms underlying iron overload-induced chondrocyte damage. METHODS:This study established an in vivo HA model by puncturing knee joints of coagulation factor VIII gene knockout mice with a needle, and mimicked iron overload conditions in vitro by treatment of Ferric ammonium citrate (FAC). RESULTS:We demonstrated that blood exposure caused iron overload and cartilage degeneration, as well as elevated expression of DMT1. Furthermore, DMT1 silencing alleviated blood-induced iron overload and cartilage degeneration. In hemophilic mice, articular cartilage degeneration was also suppressed by intro-articularly injection of DMT1 adeno-associated virus 9 (AAV9). Mechanistically, RNA-sequencing analysis indicated the association between iron overload and cGAS-STING pathway. Further, iron overload triggered mtDNA-cGAS-STING pathway activation, which could be effectively mitigated by DMT1 silencing. Additionally, we discovered that RU.521, a potent Cyclic GMP-AMP Synthase (cGAS) inhibitor, successfully suppressed the downward cascades of cGAS-STING, thereby protecting against chondrocyte damage. CONCLUSION:Taken together, DMT1-mediated iron overload promotes chondrocyte damage and murine HA development, and targeted DMT1 may provide therapeutic and preventive approaches in HA.

Introductions Osteoarthritis (OA) is a significant contributor to disability in the elderly population. However, current therapeutic options are limited. The transient receptor potential melastatin 2 (TRPM2) is involved in a range of disease processes, yet its role in OA remains unclear. Objectives To investigate the role of TRPM2 in OA. Methods Cartilage samples were collected from patients with osteoarthritis (OA) and mice with OA to examine TRPM2 expression levels. To investigate the effects of TRPM2 modulation on the destabilization of the medial meniscus (DMM) induced knee OA in mice, we utilized TRPM2 knockout mice and employed adenovirus-mediated overexpression of TRPM2. Furthermore, siRNA-mediated TRPM2 knockdown or plasmid-mediated TRPM2 overexpression was conducted to explore the role of TRPM2 in IL-1β-induced chondrocytes. The regulatory mechanism of IL-1β on TRPM2 expression was screened by signaling pathway inhibitors, and the transcription factors and binding sites of TRPM2 were predicted using the database. The binding of RELA (NF-κB-p65) to the Trpm2 promoter was verified by chip-PCR and ChIP-qPCR. The therapeutic potential of Ca2+ chelation with BAPTA-AM for the treatment of osteoarthritis (OA) was investigated. Results An increased expression of TRPM2 was observed in the cartilage of OA patients and OA mice. Furthermore, mice deficient in Trpm2 exhibited a protective effect against DMM-induced OA progression. In contrast, TRPM2 overexpression resulted in exacerbation of DMM-induced OA and thepromotion of an OA-like phenotype of chondrocytes. TRPM2 was upregulated by IL-1β in an NF-κB-p65-dependent manner. Subsequently, the TRPM2-Ca2+-mtDNA-cGAS-STING-NF-κB axis in the progression of OA was validated. Furthermore, inhibition of the TRPM2-Ca2+ axis with BAPTA-AM effectively attenuated established OA. Conclusions Our data collectively revealed a pathological feedback loop involving TRPM2, Ca2+, mtDNA, cGAS, STING, and NF-κB in OA chondrocytes. This suggests that disrupting this loop could be a viable therapeutic approach for OA.

BackgroundOsteosarcoma (OS), the most prevalent primary malignant bone tumor in children and adolescents, arises from bone-forming mesenchymal cells. Despite advancements in surgical resection and neoadjuvant chemotherapy (cisplatin, doxorubicin, and methotrexate), chemotherapy resistance remains a significant challenge, leading to poor survival rates in patients with metastatic or recurrent OS.MethodsIn this study, we focused on the role of OTULIN, a key linear deubiquitinating enzyme, in OS chemoresistance. In addition, mechanistic investigations were carried out to identify potential downstream targets of OTULIN involved in cisplatin resistance.ResultsOur results demonstrated that OTULIN expression was significantly upregulated in OS tissues and cell lines following cisplatin treatment but not in response to doxorubicin or methotrexate. High OTULIN expression was associated with reduced survival in sarcoma patients. Furthermore, immunohistochemical analysis of prechemotherapy and postchemotherapy OS tissues revealed increased OTULIN expression in postchemotherapy samples. In vitro results demonstrated that OTULIN plays a critical role in mediating cisplatin resistance in OS. Mechanistically, GPX4 could be a downstream target of OTULIN, conferring cisplatin resistance to OS by blocking the mitochondrial apoptotic pathway but not ferroptosis. Specifically, OTULIN prevents the proteasomal degradation of GPX4 by reducing its ubiquitin level, thereby conferring resistance to cisplatin in OS cells.ConclusionThis study highlights the importance of OTULIN in OS chemoresistance and provides a promising approach for targeting the OTULIN-GPX4 axis to improve the prognosis of OS patients. Our findings offer new insights into the molecular mechanisms underlying OS chemoresistance and suggest potential therapeutic targets for future clinical interventions.

Ferroptosis is involved in the pathogenesis of osteoarthritis (OA) while suppression of chondrocyte ferroptosis has a beneficial effect on OA. However, the molecular mechanism of ferroptosis in OA remains to be elucidated. P21, an indicator of aging, has been reported to inhibit ferroptosis, but the relationship between P21 and ferroptosis in OA remains unclear. Here, we aimed to investigate the expression and function of P21 in OA chondrocytes, and the involvement of P21 in the regulation of ferroptosis in chondrocytes. First, we demonstrated that high P21 expression was observed in the cartilage from OA patients and destabilized medial meniscus (DMM) mice, and in osteoarthritic chondrocytes induced by IL-1β, FAC and erastin. P21 knockdown exacerbated the reduction of Col2a1 and promoted the upregulation of MMP13 in osteoarthritic chondrocytes. Meanwhile, P21 knockdown exacerbated cartilage degradation in DMM-induced OA mouse models and decreased GPX4 expression in vivo. Furthermore, P21 knockdown sensitized chondrocytes to ferroptosis induced by erastin, which was closely associated with the accumulation of lipid peroxides. In mechanism, we demonstrated that P21 regulated the stability of GPX4 protein, and the regulation was independent of NRF2. Meanwhile, we found that P21 significantly affected the recruitment of GPX4 to linear ubiquitin chain assembly complex (LUBAC) and regulated the level of M1-linked ubiquitination of GPX4. Overall, our results suggest that P21 plays an essential anti-ferroptosis role in OA by regulating the stability of GPX4.

Aims: Hemophilic arthropathy (HA) is a typically iron overload induced joint disease secondary to continuous joint bleeding, however, the exact role of iron chelators in HA has not been fully elucidated. In the present study, we investigated whether desferoxamine (DFO), an iron chelator, could limit the development of HA and the underlying mechanisms. Materials and methods: A HA mice model was established by needle puncture in the left knees of FVIII-deficient hemophilic mice. HA progression was evaluated at 8 weeks after DFO administration. Moreover, chondrocytes were treated with ferric ammonium citrate (FAC) to mimic iron overload in vitro. Modulating effect of DFO on iron overload induced oxidative stress, chondrocytes apoptosis and extracellular matrix (ECM) degradation and the role of HIF-1 alpha-BNIP3 mediated mitophagy were examined. Key findings: We found that DFO limited the development of HA and protected iron overload induced ECM degradation, chondrocytes apoptosis and oxidative stress. Besides chelating Fe2+, we found that HIF-1 alpha-BNIP3 mediated mitophagy played important roles in the protective effect of DFO. HIF-1 alpha inhibition suppressed chondrocytes mitophagy process and partly diminished the protective effect of DFO on chondrocytes iron overload. Significance: In conclusion, DFO could protect against HA development via HIF-1 alpha-BNIP3 mediated mitophagy, suggesting DFO might be a potential therapeutic supplement for HA treatment.

Osteoarthritis (OA) is a multifactorial and increasingly prevalent degenerative disease that affects the whole joint. The pathogenesis of OA is poorly understood and there is a lack of therapeutic interventions to reverse the pathological process of this disease. Accumulating studies have shown that the overproduction of reactive oxygen species (ROS) and ROS-induced lipid peroxidation are involved in the pathogenesis of OA. 4-Hydroxy-2-nonenal (4-HNE) and malondialdehyde (MDA) have received considerable attention for their role in cartilage degeneration and subchondral bone remodeling during OA development. Ferroptosis is a form of cell death characterized by a lack of control of membrane lipid peroxidation and recent studies have suggested that chondrocyte ferroptosis contributes to OA progression. In this review, we aim to discuss lipid peroxidation-derived 4-HNE and MDA in the progression of OA. In addition, the therapeutic potential for OA by controlling the accumulation of lipid peroxidation and inhibiting chondrocyte ferroptosis are discussed.

Transiliac-transsacral screw fixation is challenging in clinical practice as the screws need to break through six layers of cortical bone. Transiliac-transsacral screws provide a longer lever arm to withstand the perpendicular vertical shear forces. However, the screw channel is so long that a minor discrepancy can lead to iatrogenic neurovascular injuries. The development of medical robots has improved the precision of surgery. The present protocol describes how to use a new teleoperated robotic system to execute transiliac-transacral screw fixation. The Robot was operated remotely to position the entry point and adjust the orientation of the sleeve. The screw positions were evaluated using postoperative computed tomography (CT). All the screws were safely implanted, as confirmed using intraoperative fluoroscopy. Postoperative CT confirmed that all the screws were in the cancellous bone. This system combines the doctor's initiative with the Robot's stability. The remote control of this procedure is possible. Robot-assisted surgery has a higher position-retention capacity compared with conventional methods. In contrast to active robotic systems, surgeons have full control over the operation. The robot system is fully compatible with operating room systems and does not require additional equipment.

[This corrects the article DOI: 10.1016/j.isci.2023.107647.].

Abstract purpose Osteoarthritis (OA) is one of the most common causes of disability in the elderly. Ubiquitin-like modifier-activated enzyme 5 (UBA5) is a critical factor in preventing cellular autophagy and causing endoplasmic reticulum stress but has not been studied in OA. We aimed and explored the involvement of the UBA5-GABARAP-PERK axis in regulating cartilage matrix metabolism and apoptosis in osteoarthritis. Methods Oxidative stress was induced using IL-1β, which disrupted the homeostatic balance of cartilage. In in vivo and in vitro experiments, Western blot, qt-QPCR, scanning electron microscopy, immunofluorescence, and mCherry-GFP-LC3 plasmid were applied to observe OA-associated cartilage degeneration, ROS production, mitochondrial function, autophagic flux, endoplasmic reticulum stress and matrix after application of UBA5 selective inhibitor DKM2-93, knockdown or overexpression of UBA5 changes in metabolic indicators. UBA5 adeno-associated virus was injected into the cavity of mice, and a mouse OA model was induced by DMM surgery. Histological analysis of cartilage degeneration was performed using immunohistochemistry, Safranin-O staining, HE staining, Micro-CT, OARSI, and synovitis score. Results Expression of UBA5 was increased in chondrocytes receiving IL-1β intervention. Knockdown of UBA5 in vivo and in vitro inhibited OA-related chondrogenic degeneration, alleviated mitochondrial dysfunction, stimulated autophagy, inhibited endoplasmic reticulum stress, reduced catabolism, and increased anabolism. Overexpression of UBA5 also promotes oxidative stress and disrupts the molecular signature of healthy chondrocytes. Mechanistically, the destructive function of UBA5 may be attributed to the activation of the PERK/ATF4 signaling pathway. Through immunoprecipitation experiments, UBA5 was shown to inhibit autophagy by interacting with GABARAP to activate the PERK signaling pathway. Inhibition of PERK attenuated UBA5-induced osteoarthritis. Our findings suggest that Jun-B and C-Jun transcription factors may promote UBA5 expression and inhibition of UBA5 expression by in vivo application of adeno-associated virus, reduce chondrocyte death, attenuate cartilage degeneration, and promote subchondral bone remodeling. Conclusions This study revealed that UBA5 might regulate chondrocyte matrix catabolism and anabolism through the UBA5-GABARAP-PERK axis, suggesting a potential role for UBA5 in OA cartilage injury.

Abstract Background The use of interlocked intramedullary nail has become the preferred method of treatment for intertrochanteric fracture of the femur. This study explored a new guide awl with a distal positioner assisting the guide wire insertion and opening canal, and verification the accuracy and security of our new guide awl.Methods 42 patients with intertrochanteric fracture treated by locking intramedullary nailing were retrospectively analyzed. Three patients with insufficient follow-up were excluded from analysis. 19 patients underwent the operation using the new guide awl, the other 20 patients in the control group were operated with the help of the conventional guide apparatus. Describe the new guide awl with a distal positioner usage in the operations. Operation time, the success rate of one-time insertion, fluoroscopy time, blood loss and bone healing time were recorded.Results 42 patients (25 males and 17 females) were treated with Gamma 3 and PFNA with the help of the new guide awl with a distal positioner or the conventional conventional guide apparatus. The surgical time in new guide awl group was significantly shorter compared to the control group. The success rate of one-time needle insertion in the new guide apparatus group was 89.5%, which was higher than the 65% of the control group. The fluoroscopy time in new guide apparatus group is obviously lower than in the control group. There was no significant difference in intraoperative blood loss and bone healing time.Conclusion The new guide awl with a distal positioner we designed could reduce the difficulty in opening the femur for inserting the interlocked intramedullary nail. It is especially suitable for obese patients.

Objective:To evaluate the significance of S1 posterior edge inlet view for placement of percutaneous sacroiliac screws.Methods:1. CT data of the pelvis were collected from 134 normal adults and introduced into Mimics Medical 21.0 system. Anatomical parameters of sacral vertebrae were measured and analyzed to observe the anatomical disparities between the anterior and posterior edges of S1 vertebral body. A mathematical model was established using the data acquired. 2. Manual placement of sacroiliac screws was performed using a conventional S1 posterior edge inlet view on the pelvic specimens from 5 adult cadavers in simulation of actual surgical situations. After placement, the inlet views from both the S1 anterior and posterior edges were taken to observe the imaging differences and to check if the screws had pierced the sacral canal. 3. A retrospective study was conducted of the 11 patients with posterior pelvic ring fracture who had been treated at Department of Orthopaedics, Tongji Hospital from January 2019 to October 2020. Their fractures were fixated by percutaneous sacroiliac screws under the guidance of a C-arm X-ray machine. The manual placement of the screws was guided intraoperatively by the inlet views from both the S1 anterior and posterior edges to secure a safe placement. Pelvic CT examinations were performed to check any screw dislocation.Results:1. CT measurements in the normal adults showed that the angle of S1 anterior edge inlet view (20.71°±11.89°) was smaller than that of S1 posterior edge inlet view (41.99°±11.67°) and the width of S1 upper end plate [(32.22±3.41) mm] greater than that of S1 lower end plate [(20.10±3.28) mm], showing significant disparities in anatomy between the anterior and posterior edges of S1 vertebral body ( P<0.05). 2. In 2 of the 5 cadaveric specimens, imaging differences were observed between the inlet views of the anterior and posterior edges of S1 and the screws pierced out of the sacral canal. 3. Satisfactory closed reduction was achieved in all the 11 patients. A total of 17 screws were placed, with 12 ones into S1 and 5 ones into S2. Operation time ranged from 84 to 141 min (average, 114.4 min), fluoroscopy frequency from 69 to 101 times (average, 89.6 times), and intraoperative blood loss from 110 to 463 mL(average, 296.6 mL). No screw dislocation was observed on postoperative CT. Conclusion:As there is a difference between the inlet views of the anterior and posterior edges of S1 vertebral body, the inlet view of the posterior edge of S1 can display the posterior edge of S1 more clearly so as to improve the safety of placement of percutaneous sacroiliac screws.

BACKGROUND:The transiliac-transsacral screw placement is a clinical challenge for surgeons. This study explored a point-to-point coaxial guide apparatus assisting the transiliac-transsacral screw insertion and aimed to investigate the feasibility and accuracy of the guide apparatus in the treatment of posterior ring unstable pelvic fracture compared with a free-hand technique.METHODS:A retrospective study was performed to evaluate patients treated with transiliac-transsacral screws assisted by the point-to-point coaxial guide apparatus or free-hand technique. The intraoperative data of operative time and radiation exposure times were recorded. Postoperative radiographs and CT scans were performed to scrutinize the accuracy of screws position. The quality of the postoperative fracture reduction was assessed according to Matta radiology criteria. The pelvic function was assessed according to the Majeed scoring criteria at 6 months postoperatively.RESULTS:From July 2017 to December 2019, a total of 38 patients were included in this study, 20 from the point-to-point guide apparatus group and 18 from the free-hand group. There were no significant differences between the two groups in gender, age, injury causes, pelvic fracture type, screws level, and follow-up time (P > 0.05). The average operative time of the guide apparatus group for each screw was significantly less than that in the free-hand group (25.8 ± 4.7 min vs 40.5 ± 5.1, P < 0.001). The radiation exposure times were significantly lower in the guide apparatus group than that in the free-hand group (24.4 ± 6.0 vs 51.6 ± 8.4, P < 0.001). The intraosseous and juxtacortical rate of screw placement (100%) higher than in the free-hand group (94.4%).CONCLUSION:The point-to-point coaxial guide apparatus is feasible for assisting the transiliac-transsacral screw in the treatment of posterior unstable pelvic fractures. It has the advantages of simple operation, reasonable design and no need for expensive equipment, and provides an additional surgical strategy for the insertion of the transiliac-transsacral screw.

目的 建立一种可有效、快速获得的小鼠骨髓间充质干细胞(BMSC)衰老细胞模型,为研究衰老BMSC的生物学特性及功能作准备.方法 造模组采用200μmol/L过氧化氢(H2 O2)处理分离培养的第三代小鼠BMSC 2 h,对照组加入等量PBS处理,两组细胞继续培养72 h.MTT法绘制细胞生长曲线,行SA-β-gal染色和端粒功能失调诱导病灶(TIF)分析,提取细胞RNA,Real-time PCR检测衰老相关基因p16、p21、p53的表达.结果 与对照组比较,H2O2处理后的小鼠BMSC生长缓慢(P<0.05),SA-β-gal染色阳性率较高(P<0.05),TIF阳性细胞较多(P<0.05),且Real-time PCR显示,造模组p16、p21、p53基因表达较高(P<0.05).结论 通过H2O2处理可以快速且有效地建立BMSC的衰老细胞模型.

随着人口老龄化的进展,老年人因行动不便容易跌倒,且常伴有骨量丢失[1] ,低暴力引起的老年骨盆脆性骨折发病率逐年上升[2]. 对于老年骨盆脆性骨折,保守治疗往往需要长期卧床,这就不可避免地增加了发生下肢深静脉血栓、坠积性肺炎、压疮等一系列严重并发症的风险[2-5]. 传统骨盆切开复位内固定手术治疗骨盆脆性骨折,需要对骨盆深层结构广泛暴露,对软组织损伤大、出血多、易损伤血管神经、手术时间长,体质较差或患有基础疾病的老年患者大多不能耐受此种手术方式[5]. 微创内固定治疗老年骨盆脆性骨折具有创伤小、手术时间短、术中出血少等优点. 笔者回顾了华中科技大学同济医学院附属同济医院骨科收治的采用微创内固定治疗的16例患者的临床资料,现将结果报告如下.

目的 探讨以大型开放式网络课程(massive open online courses,MOOC)平台为基础的小规模限制性在线课程(small private online course,SPOC)教学模式应用于骨科临床教学中的效果情况.方法 选取2020年3月至5月在我院骨科进行第一年住院医师规范化培训的专业学位硕士研究生和规培生共50人作为教学研究对象,随机分为两组,每组25例,观察组采取基于MOOC平台的SPOC教学模式,对照组采取单一的MOOC教学模式,通过成绩考核和问卷调查的方式来评估两组教学效果和教学满意度,比较两种教学模式的应用效果.结果 观察组教学研究对象的病例分析考试成绩和总成绩分别为(20.04±2.70)分和(84.80±8.35)分,对照组的成绩分别为(13.40±7.54)分和(76.60±10.42)分,两组比较差异均有统计学意义(t=4.146,P<0.001;t=3.069,P=0.004);在成绩考核评级分析中,观察组教学的成绩考核等级明显优于对照组,观察组临床技能教学较对照组有明显优势(χ2=12.054,P=0.002),但是两组的理论知识考核评级的差异无统计学意义(χ2=1.520,P=0.468).在满意度问卷调查中,仅仅只在培养临床思维能力这一项上,观察组与对照组的差异有统计学意义(χ2=4.196,P=0.037),其余四项满意度的差异均无统计学意义.结论 基于MOOC平台的SPOC教学模式能够提高骨科临床教学质量,同时有利于培养学生的临床思维能力.