Bone & Joint Research最新文献

{"title":"Orientin alleviates chondrocyte senescence and osteoarthritis by inhibiting PI3K/AKT pathway.","authors":"Haitao Chen, Siyi Liu, Junwei Xing, Yinxian Wen, Liaobin Chen","doi":"10.1302/2046-3758.143.BJR-2023-0383.R2","DOIUrl":"10.1302/2046-3758.143.BJR-2023-0383.R2","url":null,"abstract":"<p><strong>Aims: </strong>Osteoarthritis (OA) is a common degenerative disease that leads to pain, disability, and reduced quality of life. Orientin exhibits considerable anti-inflammatory and antioxidative properties, but its role in chondrocyte senescence and OA progress has not yet been fully characterized. The aim of this study was to evaluate the protective effects of orientin on OA.</p><p><strong>Methods: </strong>The role of orientin in extracellular matrix (ECM) degradation, mitochondrial homeostasis, and chondrocyte senescence was investigated in vitro. Meanwhile, we used molecular docking, small molecular inhibitors, and RNA interference to screen and validate candidate proteins regulated by orientin. In an anterior cruciate ligament transection (ACLT) rat model, radiograph, micro-CT, and various histological examinations were applied to evaluate the therapeutic effects of orientin on OA.</p><p><strong>Results: </strong>We found that orientin inhibited ECM degradation and senescence-associated secretory phenotype (SASP) factor expression in interleukin (IL)-1β-treated chondrocytes. Additionally, orientin reduced the level of reactive oxygen species (ROS) and improved mitochondrial homeostasis. Furthermore, orientin suppressed IL-1β-induced activation of the nuclear factor kappa B (NF-κB) signalling pathway. We also found that orientin bound to phosphoinositide 3-kinase (PI3K) and inhibited NF-κB cascades via the PI3K/AKT pathway. In vivo, we demonstrated that orientin improved cartilage wear and reduced synovial inflammation and osteophyte in an ACLT rat model.</p><p><strong>Conclusion: </strong>Orientin improves mitochondrial homeostasis, inhibits chondrocyte senescence, and alleviates OA progress via the PI3K/AKT/NF-κB axis, which suggests that orientin is a potential effective therapeutic agent for OA.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"245-258"},"PeriodicalIF":4.7,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of metaphyseal holes and interposition material on the longitudinal growth stimulation of long bones in a rabbit model.","authors":"Byoung K Park, Kyoung-Mi Lee, Kyeong-Hyeon Park, Hoon Park, Eun A Ko, Jin W Lee, Hyun W Kim, Kun-Bo Park","doi":"10.1302/2046-3758.143.BJR-2024-0321.R2","DOIUrl":"10.1302/2046-3758.143.BJR-2024-0321.R2","url":null,"abstract":"<p><strong>Aims: </strong>It remains unclear which factors influence overgrowth of the tibia, resulting from the metaphyseal hole created during anterior cruciate ligament (ACL) reconstruction in skeletally immature patients. This study aimed to investigate the effects of growth stimulation by creating a metaphyseal hole in a rabbit model, based on its distance from the physis and type of interposition material.</p><p><strong>Methods: </strong>In Experiment 1, 38 skeletally immature male New Zealand white rabbits were randomized into one of four groups: a metaphyseal hole created at 5, 10, or 15 mm distal to the physis of the left proximal tibia with the hole filled with bone wax, or a sham control group. In Experiment 2, after establishing the distance associated with the most overgrowth, a defect was created at 10 mm distal to the physis in 20 additional rabbits, which were randomly assigned to have the defect filled with Tisseel, or be left unfilled. The rabbits were euthanized six weeks postoperatively.</p><p><strong>Results: </strong>The length and rate of overgrowth were higher in the groups with holes drilled 5 and 10 mm distal to the physis compared to the sham group. A significant increase in new bone width was observed in the 10 mm distal hole group. Growth stimulation in both radiological and histological analyses was not significant in the unfilled and Tisseel groups. Valgus deformities were observed in all groups with metaphyseal holes compared to the sham group.</p><p><strong>Conclusion: </strong>Creating a metaphyseal hole 10 mm distal to the physis of the proximal tibia can significantly stimulate longitudinal growth and induce tibia valga in rabbits; however, the effect varies depending on the type of interposition material. Notably, overgrowth was significant only in the group with holes filled with bone wax. Based on this study, the location of the metaphyseal hole during ACL reconstruction or physeal bar excision could be optimized.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"236-244"},"PeriodicalIF":4.7,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11906220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum.","authors":"Yan Xiao, Zhang Yue, He Zijing, Zheng Yao, Mao Sui, Zeng Xuemin, Zhang Qiang, Yuan Xiao, Ren Dapeng","doi":"10.1302/2046-3758.143.BJR-2025-00003","DOIUrl":"10.1302/2046-3758.143.BJR-2025-00003","url":null,"abstract":"","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"223"},"PeriodicalIF":4.7,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11904850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and validation of transcriptome-wide association study-derived genes as potential druggable targets for osteoarthritis.","authors":"Xindie Zhou, Xinjian Ye, Jiapei Yao, Xiaolong Lin, Yiping Weng, Yong Huang, Yaojun Lu, JingJing Shang, Luming Nong","doi":"10.1302/2046-3758.143.BJR-2024-0251.R1","DOIUrl":"10.1302/2046-3758.143.BJR-2024-0251.R1","url":null,"abstract":"<p><strong>Aims: </strong>Osteoarthritis (OA) is a widespread chronic degenerative joint disease with an increasing global impact. The pathogenesis of OA involves complex interactions between genetic and environmental factors. Despite this, the specific genetic mechanisms underlying OA remain only partially understood, hindering the development of targeted therapeutic strategies.</p><p><strong>Methods: </strong>A transcriptome-wide association study (TWAS) was conducted for site-specific OA phenotypes using functional summary-based imputation (FUSION). High-confidence candidate genes were identified through rigorous quality control measures, including joint/conditional analysis, permutation tests, best model evaluation, and colocalization analysis. Co-expression network analysis was performed to elucidate the functional biology of these candidate genes. Druggable gene targets and their structural models were retrieved from the DrugBank and SWISS-MODEL databases. Finally, the enrichment of mitogen-activated protein kinase 3 (<i>MAPK3</i>) and <i>SMAD3</i> in OA was validated biochemically using in vitro and in vivo OA models, as well as human histological sections.</p><p><strong>Results: </strong>Utilizing the FUSION algorithm, TWAS identified 794 candidate genes for OA. After quality control, 14 genes were classified as high-confidence genes, with seven recognized as potential drug targets including <i>GCAT, MAPK3, MST1R, PFKM, RAD9A, SMAD3,</i> and <i>USAP8</i>. Co-expression analysis revealed a strong biological association between <i>SMAD3</i> and <i>MAPK3</i>. Both in vitro and in vivo experiments demonstrated high activity and enriched expression of these two genes in OA.</p><p><strong>Conclusion: </strong>The present study identified tissue-specific candidate genes and validated high-confidence druggable targets for OA, providing new insights into the genetic landscape and biological processes involved in OA. Further functional studies are warranted to confirm these findings.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"224-235"},"PeriodicalIF":4.7,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11904851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanical compression induces chondrocyte hypertrophy by regulating Runx2 O-GlcNAcylation during temporomandibular joint condyle degeneration.","authors":"Yan Xiao, Zhang Yue, He Zijing, Zheng Yao, Mao Sui, Zeng Xuemin, Zhang Qiang, Yuan Xiao, Ren Dapeng","doi":"10.1302/2046-3758.143.BJR-2024-0257.R1","DOIUrl":"10.1302/2046-3758.143.BJR-2024-0257.R1","url":null,"abstract":"<p><strong>Aims: </strong>Excessive chondrocyte hypertrophy is a common feature in cartilage degeneration which is susceptible to joint overloading, but the relationship between mechanical overloading and chondrocyte hypertrophy still remains elusive. The aim of our study was to explore the mechanism of mechanical compression-induced chondrocyte hypertrophy.</p><p><strong>Methods: </strong>In this study, the temporomandibular joint (TMJ) degeneration model was built through forced mandibular retrusion (FMR)-induced compression in TMJ. Chondrocytes were also mechanically compressed in vitro. The role of O-GlcNAcylation in mechanical compression-induced chondrocyte hypertrophy manifested through specific activator Thiamet G and inhibitor OSMI-1.</p><p><strong>Results: </strong>Both in vivo and in vitro data revealed that chondrocyte hypertrophic differentiation is promoted by compression. Immunofluorescent and immunoblotting results showed that protein pan-O-GlcNAcylation levels were elevated in these hypertrophic chondrocytes. Pharmacologically inhibiting protein pan-O-GlcNAcylation by OSMI-1 partially mitigated the compression-induced hypertrophic differentiation of chondrocytes. Specifically, runt-related transcription factor 2 (Runx2) and SRY-Box 9 transcription factor (Sox9) were subjected to modification of O-GlcNAcylation under mechanical compression, and pharmacological activation or inhibition of O-GlcNAcylation affected the transcriptional activity of Runx2 but not Sox9. Furthermore, compression-induced protein pan-O-GlcNAcylation in chondrocytes was induced by enhanced expression of glucose transporter 1 (GLUT1), and depletion of GLUT1 by WZB117 dampened the effect of compression on chondrocyte hypertrophy.</p><p><strong>Conclusion: </strong>Our study proposes a novel function of GLUT1-mediated protein O-GlcNAcylation in driving compression-induced hypertrophic differentiation of chondrocytes by O-GlcNAc modification of Runx2, which promoted its transcriptional activity and strengthened the expressions of downstream hypertrophic marker.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"209-222"},"PeriodicalIF":4.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890221/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum.","authors":"Yayuan Guo, Xueliang Peng, Bin Cao, Qian Liu, Shen Li, Fulin Chen, Dalong Zhi, Shequn Zhang, Zhuoyue Chen","doi":"10.1302/2046-3758.143.BJR-2025-00002","DOIUrl":"10.1302/2046-3758.143.BJR-2025-00002","url":null,"abstract":"","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"208"},"PeriodicalIF":4.7,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aberrant anabolism hinders constructive metabolism of chondrocytes by pharmacotherapy in osteoarthritis.","authors":"Raquel Largo, Aranzazu Mediero, Cristina Villa-Gomez, Ismael Bermejo-Alvarez, Gabriel Herrero-Beaumont","doi":"10.1302/2046-3758.143.BJR-2024-0241.R1","DOIUrl":"10.1302/2046-3758.143.BJR-2024-0241.R1","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a highly prevalent and disabling disease with an unmet therapeutic need. The characteristic cartilage loss and alteration of other joint structures result from a complex interaction of multiple risk factors, with mechanical overload consistently playing a central role. This overload generates an inflammatory response in the cartilage due to the activation of the innate immune response in chondrocytes, which occurs through various cellular mechanisms. Moreover, risk factors associated with obesity, being overweight, and metabolic syndrome enhance the inflammatory response both locally and systemically. OA chondrocytes, the only cells present in articular cartilage, are therefore inflamed and initiate an anabolic process in an attempt to repair the damaged tissue, which ultimately results in an aberrant and dysfunctional process. Under these circumstances, where the cartilage continues to be subjected to chronic mechanical stress, proposing a treatment that stimulates the chondrocytes' anabolic response to restore tissue structure does not appear to be a therapeutic target with a high likelihood of success. In fact, anabolic drugs proposed for the treatment of OA have yet to demonstrate efficacy. By contrast, multiple therapeutic strategies focused on pharmacologically managing the inflammatory component, both at the joint and systemic levels, have shown promise. Therefore, prioritizing the control of chronic innate pro-inflammatory pathways presents the most viable and promising therapeutic strategy for the effective management of OA. As research continues, this approach may offer the best opportunity to alleviate the burden of this incapacitating disease.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"199-207"},"PeriodicalIF":4.7,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881514/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of AGEs in muscle ageing and sarcopenia.","authors":"Zhaojing Guo, Hengzhen Li, Shide Jiang, Masoud Rahmati, Jingyue Su, Shengwu Yang, Yuxiang Wu, Yusheng Li, Zhenhan Deng","doi":"10.1302/2046-3758.143.BJR-2024-0252.R1","DOIUrl":"10.1302/2046-3758.143.BJR-2024-0252.R1","url":null,"abstract":"<p><p>Sarcopenia is an ageing-related disease featured by the loss of skeletal muscle quality and function. Advanced glycation end-products (AGEs) are a complex set of modified proteins or lipids by non-enzymatic glycosylation and oxidation. The formation of AGEs is irreversible, and they accumulate in tissues with increasing age. Currently, AGEs, as a biomarker of ageing, are viewed as a risk factor for sarcopenia. AGE accumulation could cause harmful effects in the human body such as elevated inflammation levels, enhanced oxidative stress, and targeted glycosylation of proteins inside and outside the cells. Several studies have illustrated the pathogenic role of AGEs in sarcopenia, which includes promoting skeletal muscle atrophy, impairing muscle regeneration, disrupting the normal structure of skeletal muscle extracellular matrix, and contributing to neuromuscular junction lesion and vascular disorders. This article reviews studies focused on the pathogenic role of AGEs in sarcopenia and the potential mechanisms of the detrimental effects, aiming to provide new insights into the pathogenesis of sarcopenia and develop novel methods for the prevention and therapy of sarcopenia.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"185-198"},"PeriodicalIF":4.7,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a novel rat long-bone nonunion model and efficacy evaluation of a prostaglandin EP4 selective agonist (AKDS001) combined with iliac bone grafting.","authors":"Daisuke Tateiwa, Masahiro Nishida, Joe Kodama, Hiromasa Hirai, Shinichi Nakagawa, Yuichiro Ukon, Kazuhiro Takeyama, Natsumi Yamamori, Kyoko Hirano, Masato Ikuta, Takayuki Kitahara, Takuya Furuichi, Masayuki Bun, Seiji Okada, Takashi Kaito","doi":"10.1302/2046-3758.143.BJR-2024-0220.R1","DOIUrl":"10.1302/2046-3758.143.BJR-2024-0220.R1","url":null,"abstract":"<p><strong>Aims: </strong>Nonunion occurs when a fracture fails to heal permanently, often necessitating surgical intervention to stimulate the bone healing response. Current animal models of long-bone nonunion do not adequately replicate human pathological conditions. This study was intended as a preliminary investigation of a novel rat nonunion model using a two-stage surgical intervention, and to evaluate the efficacy of a selective prostaglandin E2 receptor 4 agonist (AKDS001) as a novel nonunion therapeutic agent compared with existing treatments.</p><p><strong>Methods: </strong>Initially, Sprague-Dawley rats underwent intramedullary Kirschner wire (K-wire) fixation of a femoral fracture with the interposition of a 2 mm-thick silicon disc. After three weeks, the silicon disc was removed, and the intramedullary K-wire was replaced with plate fixation while maintaining the 2 mm defect. Contrary to the control group (1) that received no treatment, the following therapeutic interventions were performed at injury sites after freshening: (2) freshening group: no grafting; (3) iliac bone (IB) group: IB grafting; (4) AKDS group: AKDS001-loaded microspheres (MS) combined with IB (0.75 mg/ml); and (5) bone morphogenetic protein (BMP) group: grafting of a BMP-2-loaded collagen sponge (10 μg; 0.10 mg/ml). After six weeks, micro-CT (μCT) and histological analysis was performed.</p><p><strong>Results: </strong>In the control group, the radiological union rate was 0%, and histological findings showed that fracture sites comprised fibrous scar tissue, resembling the histology of human nonunion. The union rates in the freshening, IB, AKDS, and BMP groups were 16.7%, 0%, 62.5%, and 50.0%, respectively. The AKDS group demonstrated a significantly higher union rate than the IB group (p = 0.026). μCT and histological analysis indicated that the quality of newly formed bone was superior in the AKDS group than in the BMP group.</p><p><strong>Conclusion: </strong>We developed a novel long-bone nonunion model. The co-therapy of AKDS001-MS and IB grafting presents a promising new treatment for nonunion.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"166-175"},"PeriodicalIF":4.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11873957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rapid multiplex micro-ELISA assay for simultaneous measurement of synovial biomarkers : a potential aid in diagnosing periprosthetic joint infection?","authors":"Martina Maritati, Michael Vogl, Max Sonnleitner, Andrej Trampuz","doi":"10.1302/2046-3758.143.BJR-2024-0100.R1","DOIUrl":"10.1302/2046-3758.143.BJR-2024-0100.R1","url":null,"abstract":"<p><strong>Aims: </strong>The diagnosis of periprosthetic joint infection (PJI) remains a challenge, as no single diagnostic test shows high diagnostic accuracy. Recently, the measurement of synovial biomarkers has shown promising results. The aim of this study was to present a novel multiplex micro-enzyme-linked immunosorbent assay (ELISA) method for the rapid and simultaneous measurement of alpha-defensin, interleukin (IL)-6, and calprotectin developed in a model buffer system and human spiked synovial fluid.</p><p><strong>Methods: </strong>A microfluidics- and chemiluminescence-based multiplex micro-ELISA point-of-care testing system was employed for the rapid and simultaneous measurement of alpha-defensin, calprotectin, and IL-6 developed in a model buffer system and spiked human synovial fluid. Cut-off values of 1.56 µg/ml for alpha-defensin, 50 µg/ml for calprotectin, and 0.031 µg/ml for IL-6 were extracted from the literature as optimal cut-off values for the diagnosis of PJI, and were used for comparison.</p><p><strong>Results: </strong>Limit of detection (LoD) was determined for each individual biomarker by means of calibration curves with serial dilutions in a model buffer system. LoDs of 0.008, 0.002, and 0.00014 µg/ml were determined for alpha-defensin, calprotectin, and IL-6, respectively. The spiked synovial fluid assay determined LoDs of 0.08, 0.31, and 0.004 µg/ml for alpha-defensin, calprotectin, and IL-6, respectively.</p><p><strong>Conclusion: </strong>These findings highlight the proposed platform's unique features, including simultaneous measurement of three key synovial biomarkers, minimal sample volume requirements (5 to 50 µl), lower LoDs compared to conventional tests, and a short processing turnaround time of 22 minutes. Further validation studies are necessary to confirm its clinical utility.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"176-184"},"PeriodicalIF":4.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11874355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}