Connective Tissue Research最新文献

{"title":"Spatial transcriptomic applications in orthopedics.","authors":"Thomas L Jenkins, Jasper H N Yik, Dominik R Haudenschild","doi":"10.1080/03008207.2025.2501703","DOIUrl":"https://doi.org/10.1080/03008207.2025.2501703","url":null,"abstract":"<p><strong>Purpose: </strong>This review highlights the transformative impact of spatial transcriptomics on orthopedic research, focusing on its application in deciphering intricate gene expression patterns within musculoskeletal tissues.</p><p><strong>Methods: </strong>The paper reviews literature for spatial transcriptomic methods, specifically 10X Visium, 10X Xenium, seqFISH+, MERFISH, NanoString GeoMx DSP, used on musculoskeletal tissues (cartilage, joints, bone, tendon, ligament, and synovium).</p><p><strong>Results: </strong>Searches identified 29 published manuscripts reporting spatial transcriptomic data in cartilage, bone, tendon, synovium, and intervertebral disc. Most publications of spatial transcriptomic data are from tendon and synovium. 10X Visium has been used in 22 of the 29 papers identified. Spatial transcriptomics has been used to identify novel cell populations and cell signaling pathways that regulate development and disease.</p><p><strong>Conclusions: </strong>Imaging-based spatial transcriptomic methods may be better for hypothesis testing as they generally have subcellular resolution but sequence fewer genes. Sequencing methods may be better for untargeted, shotgun approaches that can generate useful hypotheses from the spatial data from unimpaired tissue sections. Spatial transcriptomic methods could become useful for clinical diagnostics and precision medicine approaches.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"1-12"},"PeriodicalIF":2.8,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanical insights into fat pads: a comparative study of infrapatellar and suprapatellar fat pads in osteoarthritis.","authors":"Sofia Pettenuzzo, Alice Berardo, Elisa Belluzzi, Assunta Pozzuoli, Pietro Ruggieri, Emanuele Luigi Carniel, Chiara Giulia Fontanella","doi":"10.1080/03008207.2025.2502591","DOIUrl":"https://doi.org/10.1080/03008207.2025.2502591","url":null,"abstract":"<p><strong>Objective: </strong>Osteoarthritis (OA) is the most common musculoskeletal disorder, primarily affecting knee joints and causing pain and disability. The infrapatellar (IFP) and the suprapatellar (SFP) fat pad are knee adipose tissues that play essential mechanical roles during articular activity but are also sources of adipokines and cytokines, contributing to OA progression. For this reason, this work aims to provide new insights into IFP and SFP implications in knee OA.</p><p><strong>Materials and methods: </strong>IFP and SFP tissue mechanical properties were studied through compression, indentation and shear mechanical tests performed on samples collected from patients who underwent total knee arthroplasty surgery due to end-stage OA. The energy loss, peak stress, and initial and final elastic moduli were calculated from the unconfined compression tests. The time-dependent response, evaluated in terms of equilibrium relative stiffness, was computed from stress-relaxation loading conditions. Considering shear tests, they provided strain-energy dissipation density, peak shear stress, and the shear moduli.</p><p><strong>Results: </strong>Experimental results showed the typical adipose tissue mechanics features: non-linear stiffening with strain and time-dependent response. Experimental results showed that OA IFP is stiffer than OA SFP, indeed IFP final compression elastic modulus was greater than the SFP (84.43 kPa vs 35.54 kPa respectively) (<i>p</i> = 0.042). Regarding the viscoelastic properties they were comparable: the equilibrium relative stiffness was reported as 0.13 for IFP and 0.11 for SFP (<i>p</i> = 0.026).</p><p><strong>Conclusions: </strong>These outcomes provide new insights into the OA influence on knee mechanics and lay the basis for developing computational tools to improve knee prosthesis design.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"1-12"},"PeriodicalIF":2.8,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cross-regulation of inflammation and <i>metabolic</i> m<i>echanisms in</i> o<i>steoarthritis: recent advances bridging the gap to novel treatments</i>.","authors":"Yousef Abu-Amer","doi":"10.1080/03008207.2025.2500530","DOIUrl":"https://doi.org/10.1080/03008207.2025.2500530","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a debilitating degenerative disease of the joints and one of the most prevalent joint disorders affecting millions of individuals worldwide. This disease is highlighted by significant morbidity owing to encumbering joint pain and functional impairment. OA ensues following disruption of normal homeostasis in the joint resulting from aging, metabolic changes, or as a consequence of joint injury (referred to as post-traumatic OA). These processes are largely driven by low-grade inflammation that gradually compromises the anabolic and protective activities of joint resident cells including chondrocytes, synovial fibroblasts (SFs) and immune cells. Ample research suggests that the process of cartilage deterioration is the endpoint of complex pathologic processes culminating with synovitis, subchondral bone sclerosis, osteophyte formation, aberrant remodeling, and ultimately articular cartilage degradation. There remains a great need for identifying early markers and a \"window of opportunity\" to enable timely interventions in OA. However, this effort is hampered by the complex nature of the disease and its comorbidities. Joint holistic approaches using recent unbiased multi-omic tools are currently at the forefront promising better understanding of OA development. Currently, there are no meaningful disease-modifying drugs to treat OA, with surgical procedures as the ultimate effective intervention for end stage OA patients. The disability, pain, and surgical costs associated with OA management position this disease among the costliest and onerous for our society. This mini review will highlight advances in the last two decades and major obstacles limiting progress in OA research with particular emphasis on metabolic and inflammatory comorbidities.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"1-6"},"PeriodicalIF":2.8,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143969217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fatigue loading and volumetric microscopy demonstrate changes to the mouse cervix throughout and after pregnancy.","authors":"Jeremy D Eekhoff, Jaime A Santillan, Chet S Friday, Carrie E Barnum, Stephanie N Weiss, Snehal Shetye, Lauren Anton, Michal A Elovitz, Louis J Soslowsky","doi":"10.1080/03008207.2025.2499173","DOIUrl":"https://doi.org/10.1080/03008207.2025.2499173","url":null,"abstract":"<p><strong>Introduction: </strong>The cervix plays important mechanical roles in pregnancy and regulating the timing of parturition. Dysfunction of the cervix is implicated in disorders of parturition including spontaneous preterm birth, failed induction of labor and post term pregnancies. To address these disorders, it is imperative to first understand the function of the cervix throughout a normal pregnancy. However, current knowledge on the response of the cervix to mechanical fatigue and the underlying microstructural changes throughout a pregnancy is lacking.</p><p><strong>Methods: </strong>In this study, mechanical fatigue properties were measured at different stages of pregnancy using uniaxial fatigue testing that simulated circumferential hoop stresses in the cervix. Collagen microstructure was quantified using second harmonic generation imaging and three-dimensional orientation analysis.</p><p><strong>Results: </strong>The stiffness and modulus of the cervix during fatigue testing were dramatically reduced in all stages of pregnancy, and pregnant samples experienced greater peak strain before failure. All mechanical properties recovered postpartum despite persistent changes in cervix size. Microstructural analysis demonstrated increased local collagen alignment in postpartum samples, which may indicate a mechanism that serves to improve material properties after childbirth.</p><p><strong>Discussion: </strong>Altogether, conclusions from this study enhance our understanding of how properties of the cervix change with pregnancy and lay the foundation for future work investigating how alterations from this healthy function can lead to spontaneous preterm birth and other reproductive complications.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"1-9"},"PeriodicalIF":2.8,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bone marrow mesenchymal stem cells (BMSCs)-derived exosomal METTL3 regulates the m6A methylation of SMAD5 to promote osteogenic differentiation of osteoblasts.","authors":"Zhenhua Li, Yifei Liu, Xiulan Zhao, Guohua Xu","doi":"10.1080/03008207.2025.2496832","DOIUrl":"https://doi.org/10.1080/03008207.2025.2496832","url":null,"abstract":"<p><strong>Background: </strong>Methyltransferase-like 3 (METTL3) is implicated in human diseases, including osteoporosis (OP). In this study, we aimed to explore the functions and mechanisms of METTL3 in OP using bone marrow mesenchymal stem cells (BMSCs).</p><p><strong>Methods: </strong>The identification of BMSCs-derived exosomes was conducted by transmission electron microscope (TEM), Nanoparticle Tracking Analysis (NTA) and western blot. The osteogenic differentiation of osteoblasts (hFOB1.19) was analyzed by Alizarin red staining assay, Alkaline phosphatase (ALP) staining assay and western blot. The relationship between METTL3 and SMAD family member 5 (SMAD5) was analyzed by Methylated RNA Immunoprecipitation (MeRIP) assay and dual-luciferase reporter assay.</p><p><strong>Results: </strong>BMSCs-derived exosomes (BMSC-Exos) promoted the osteogenic differentiation and elevated METTL3 expression in hFOB1.19 cells. Exosomal METTL3 knockdown repressed the osteogenic differentiation in hFOB1.19 cells. METTL3 could stabilize and regulate SMAD5 expression by N6-methyladenosine (m6A) modification. Moreover, SMAD5 overexpression restored exosomal METTL3 knockdown-mediated effect on the osteogenic differentiation in hFOB1.19 cells.</p><p><strong>Conclusion: </strong>BMSCs-derived exosomal METTL3 mediated the m6A methylation of SMAD5 to facilitate osteogenic differentiation of hFOB1.19 cells.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"1-12"},"PeriodicalIF":2.8,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"\"The role of mitogen-activated protein kinase signaling pathway in bone formation during mid-palatal suture expansion\".","authors":"Xiaoyue Xiao, Shujuan Zou, Zhiai Hu, Jianwei Chen","doi":"10.1080/03008207.2025.2498509","DOIUrl":"https://doi.org/10.1080/03008207.2025.2498509","url":null,"abstract":"<p><strong>Purpose: </strong>Orthodontic interventions such as maxillary expansion are pivotal in correcting malocclusions; however, the intracellular mechanisms of bone remodeling during this process are not well understood. This study investigated the role of the mitogen-activated protein kinase (MAPK) pathway in bone remodeling during maxillary expansion and relapse in rats.</p><p><strong>Materials and methods: </strong>Thirty male Wistar rats were randomly divided into three groups: Control (Ctrl), Expansion only (EO), and Expansion with MEK inhibitor U0126 (EO  +  INH). Customized expanders applied 100 g force for seven days, followed by natural relapse. Tissue changes within the mid-palatal suture were assessed via micro-computed tomography, histology, and immunohistochemistry. In vitro, primary bone marrow mesenchymal stem cells (BMSCs) were exposed to cyclic tensile stress with or without MAPK inhibition, followed by evaluation of protein expression, alkaline phosphatase activity, and Alizarin red staining.</p><p><strong>Results: </strong>The EO group showed a significant increase in maxillary arch width compared to the EO  +  INH group, a difference that remained significant after relapse. This group also had higher levels of phosphorylated mitogen-extracellular kinase (p-MEK), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), and phosphorylated Ets-like transcription factor 1 (p-ELK1), along with increased osteoblast markers and bone resorption. Conversely, MAPK inhibition impeded bone remodeling, indicated by decreased osteogenic markers and fewer TRAP-positive cells. In vitro, tensile stress enhanced osteogenic differentiation, which was attenuated with MAPK inhibition.</p><p><strong>Conclusions: </strong>Mechanical activation of MEK-ERK1/2-ELK1 pathway is essential for effective maxillary expansion. Thus, inhibiting this pathway significantly impairs bone remodeling, underscoring its potential as a therapeutic target to enhance bone formation in orthodontic treatments.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"1-11"},"PeriodicalIF":2.8,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical and molecular landscape of post-traumatic osteoarthritis.","authors":"Kyohei Takase, Patrick C McCulloch, Jasper H N Yik, Dominik R Haudenschild","doi":"10.1080/03008207.2025.2490797","DOIUrl":"https://doi.org/10.1080/03008207.2025.2490797","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage breakdown, chronic pain, and disability. Post-traumatic osteoarthritis (PTOA), a secondary form of OA, arises from joint injuries and consistently accounts for a proportion of symptomatic cases. Unlike primary OA, PTOA has a well-defined initiation point, presenting an opportunity for early intervention. Over the past two decades, research has shifted from a cartilage-centric view to a broader understanding of OA as a multifaceted disease involving inflammation, oxidative stress, and complex molecular crosstalk between chondrocytes, synoviocytes, osteocytes, and immune cells. Key inflammatory mediators, such as IL-1β, IL-6, TNF-α, and Wnt/β-catenin signaling, drive disease progression. Advances in imaging, biomarker discovery, and animal models have provided insights into early disease mechanisms. However, gaps remain in understanding the molecular events that trigger PTOA onset, the interplay between joint tissues, and the identification of reliable early biomarkers. Delayed diagnosis, lack of disease-modifying therapies, and OA's complexity remain critical barriers. Future directions should focus on precision medicine integrating biomarkers, imaging, and artificial intelligence for early diagnosis and risk stratification. Emerging regenerative and gene therapies, while promising, would benefit from moving beyond single-pathway targeting, as OA's multifaceted nature makes a combination approach desirable to simultaneously address inflammation, oxidative stress, cartilage matrix degradation, and tissue repair. Multidisciplinary collaborations between clinicians, molecular biologists, and bioengineers are essential to translating discoveries into effective interventions. A paradigm shift toward early, personalized treatment strategies is necessary to improve long-term outcomes in PTOA and OA management.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"1-7"},"PeriodicalIF":2.8,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143961864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of anterior cruciate ligament injury-induced disruption of joint homeostasis and onset of osteoarthritis.","authors":"Robert H Brophy, Richard M Silverman, Muhammad Farooq Rai","doi":"10.1080/03008207.2025.2490097","DOIUrl":"https://doi.org/10.1080/03008207.2025.2490097","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a progressive joint disorder that leads to pain and disability for millions of people worldwide. Post-traumatic OA (PTOA), a form of OA, arises secondary to joint injury and often impacts younger individuals. Among the most common joint injuries leading to disrupted joint homeostasis and PTOA is anterior cruciate ligament (ACL) rupture. Even with successful surgical stabilization, the risk of developing PTOA persists due to several factors, including altered biology that contributes to disease progression. Recent research into the biology of ACL injuries has advanced our understanding of the mechanisms by which PTOA develops, including the inflammatory pathways involved, the expression of biomarkers specific to ACL injuries, and their interaction with factors such as the chronicity of the injury. Evidence suggests that homeostatic balance of anabolic and catabolic processes in the knee is disturbed after ACL tears, triggering a catabolic and degenerative phenotype, ultimately leading to premature joint degeneration, pain, and disability. Several key knowledge gaps exist, such as the determinants of the transition from acute to chronic inflammation, inter-patient variability in inflammatory responses, and influence of systemic factors on disease development. PTOA research faces numerous challenges, including protracted nature of the disease, the complexity of joint biology, and difficulties in translating molecular discoveries into clinical practice. Future research should prioritize improving biomarker precision for early detection, developing targeted therapies, and leveraging emerging technologies like machine learning to personalize treatment. This approach will enhance our understanding of the biological basis of PTOA resulting from ACL injuries and identify opportunities to mitigate the long-term consequences of these injuries.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"1-7"},"PeriodicalIF":2.8,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Application of knee joint distraction: challenges and opportunities.","authors":"M P Jansen, S C Mastbergen","doi":"10.1080/03008207.2025.2490796","DOIUrl":"https://doi.org/10.1080/03008207.2025.2490796","url":null,"abstract":"<p><p>Knee osteoarthritis (OA) is a debilitating condition with limited treatment options beyond symptom management or total knee arthroplasty (TKA). For younger patients, TKA presents challenges, including higher failure rates and revision surgeries. Knee joint distraction (KJD) has emerged as a promising joint-preserving alternative for end-stage knee OA, demonstrating significant improvements in pain, function, and quality of life in clinical trials and clinical practice. Almost 20 years of research has highlighted KJD's capacity to delay or prevent TKA by promoting cartilage and subchondral bone repair through whole-joint remodeling. Recent studies, including a multicenter trial with a purpose-built distraction device, confirm the treatment's efficacy and durability, with benefits lasting up to 10 years. However, long-term outcomes remain limited, and variability in patient response underscores the need for refined predictive tools. Challenges include the high incidence of pin tract infections during treatment and integrating KJD into routine clinical practice, as highlighted by limited trial enrollment in the UK KARDS trial and variability in healthcare system compatibility. Future research should focus on minimizing complications, improving patient selection through advanced imaging and biomarker analyses, and further understanding the mechanisms underlying KJD-induced joint remodeling. Large-scale trials like the ongoing Dutch GODIVA study are poised to provide robust evidence for KJD's broader adoption, implementation, and reimbursement in healthcare systems. With continued advancements, KJD holds the potential to transform the management of knee OA, offering a viable alternative to TKA for younger patients and addressing a critical unmet need in OA care.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"1-7"},"PeriodicalIF":2.8,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological impact of meniscus injury on post-traumatic osteoarthritis.","authors":"Nathan H Varady, Scott A Rodeo","doi":"10.1080/03008207.2025.2487916","DOIUrl":"https://doi.org/10.1080/03008207.2025.2487916","url":null,"abstract":"<p><p>Post-traumatic osteoarthritis (PTOA) is a common and debilitating problem following meniscal injury, which may lead to pain, loss of function, and early joint failure. Over the past 25 years, clinical, laboratory, and translational studies have greatly improved our understanding of PTOA pathogenesis and prevention. Clinical studies have established the benefit of meniscal preservation in preventing PTOA, leading to a significant increase in meniscus repair. Similarly, improved understanding of the biomechanical importance of the meniscal root attachment has increased focus on the detection and treatment of meniscal root injuries. Laboratory studies have demonstrated a preliminary mechanistic pathway of PTOA development following meniscal injury, whereby injury and altered joint loading stimulate a pro-inflammatory response that leads to both articular cartilage breakdown and impaired meniscal healing. In vitro evidence suggests that mechanical loading of the meniscus may ameliorate this catabolic response, with implications for treatment and rehabilitation protocols. Numerous animal models have emerged, allowing for in vivo assessment of PTOA initiation and offering a platform to test potential therapeutic targets. Despite these advances, meniscal repair remains imperfect and is not always possible, and investigations translating laboratory findings to the human setting have been limited. Future directions include further characterizing the immune and cellular responses to meniscal injury, investigating therapies to target the pro-inflammatory cascade and enhance meniscal healing, and developing new models to better distinguish PTOA pathogenesis in human subjects. Continued laboratory, translational, and clinical research efforts are required to identify treatment strategies to reduce the burden of PTOA after meniscal injury.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"1-6"},"PeriodicalIF":2.8,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}