Osteoarthritis and Cartilage骨关节炎与软骨
Osteoarthritis and Cartilage(英文缩写 OSTEOARTHR CARTILAGE),ISSN 1063-4584,eISSN 1522-9653,中文译名:骨关节炎与软骨 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 7.507 | Q1 |
| 2022 | 7.000 | Q1 |
| 2023 | 7.200 | Q1 |
| 2024 | 9.000 | Q1 |
| 2025 | 9.200 | Q1 |
Osteoarthritis and Cartilage 最新收录文献
-
1. {"_":"Injury Causes Altered Metabolism including O Consumption in Bovine and Human Chondrocytes.","sub":["2"]}
PMID:日期:2026-10-02Traumatic joint injuries both disrupt chondrocyte metabolism and increase the risk for post-traumatic osteoarthritis. Yet the relationships between trauma, altered metabolism, and cartilage degradation remain unclear. This study compares the metabolic responses of bovine (normal) and osteoarthritic (OA) chondrocytes to physiological and injurious mechanical stimuli under normoxic (20% O) and hypoxic (5% O) conditions. Primary chondrocytes were encapsulated in agarose and subjected to physiological and injurious mechanical stimulation in normoxic and hypoxic conditions. Samples were analyzed for O saturation and metabolomic profiles of central carbon metabolites using LC-MS. We find that healthy bovine chondrocytes exhibit robust, time-dependent adaptation to mechanical stimuli, whereas OA chondrocytes display a blunted response, particularly under injury conditions. Injurious mechanical stimuli led to altered O consumption and glutamine accumulation, suggesting disrupted respiration and reduced protein synthesis hypothesized to be a result of altered mitochondrial metabolism in OA cells. These findings underscore the role of mechanical cues in chondrocyte metabolism and inform future studies aimed at identifying metabolic targets relevant to post-traumatic osteoarthritis progression.
-
2. Evaluating the C-score from weight-bearing CT as a quantitative imaging biomarker for worsening knee osteoarthritis structure and pain in the multicenter osteoarthritis study.
2. 在多中心骨关节炎研究中，将负重CT得出的C评分作为评估膝关节骨关节炎结构和疼痛恶化的定量影像生物标志物PMID:日期:2026-09-29Investigate a novel "C-score" metric of femoral bone shape, derived from weight-bearing-CT (WBCT), as an imaging biomarker for knee osteoarthritis (OA) structural progression and pain worsening in men and women with, and at increased risk for, symptomatic knee OA. Images were acquired for 649 knees (56.3% females, mean±SD age 63.8±9.6 years, BMI 28.5±5.0 kg/m²). Statistical shape models (SSM) were constructed from segmented distal femurs. C-score was the distance along the femur shape vector from KL0/1 to KL2/3 mean shapes, standardized to 1 SD of KL0/1 variation in the SSM. Generalized estimating equations, adjusted for sex, age, >1 knee per participant, and BMI, determined associations between 2-year-worsening of OARSI Joint-Space-Narrowing (JSN) grade in the medial-tibiofemoral compartment and baseline C-score or minimally clinically important worsening (MCIW) of pain (2 points on the WOMAC-pain-subscore). 70 knees had medial-tibiofemoral JSN worsening. In adjusted models, C-score was associated with JSN progression (OR: 1.43 (1.07, 1.92); p=0.01). Baseline C-score was also associated with 2-year MCIW pain (OR: 1.27 (1.00-1.62); p=0.047). The association of C-score with progression of JSN was more pronounced in men, and the association with pain progression was more pronounced in women, but these sex differences were not statistically significant (p >0.05). In individuals with or at risk of knee OA, higher C-scores are moderately associated with medial-tibiofemoral JSN progression and worsening knee pain over 2-year-follow-up. The C-score is a promising imaging biomarker for knee OA structural progression and pain worsening.
-
3. Cell-based and tissue engineering therapies for cartilage repair and osteoarthritis.
3. 基于细胞和组织的工程疗法用于软骨修复和骨关节炎PMID:日期:2026-09-29The repair of damaged articular cartilage remains a significant challenge, despite extensive research conducted since the 1970s. This is primarily due to the avascular nature and complex zonal architecture of cartilage and its intricate biomechanics. At present, no pharmacological treatments effectively halt the progression of cartilage breakdown in osteoarthritis. Cell-based and tissue engineering approaches offer innovative solutions for possible life-long cartilage repair. Here, we provide a comprehensive narrative review of the diverse methods for cartilage repair that have been developed and investigated over the years, emphasizing both the successes achieved and the limitations encountered in these approaches. Relevant publications from 1970 to 2026 were identified using PubMed searches. Given the vast quantity of literature, we focused on cell-based and tissue engineering interventions that were evaluated in vivo. Additionally, clinical trials were reviewed using data from clinicaltrials.gov. Autologous chondrocyte implantation has been a pioneering technique for the repair of articular cartilage defects. Numerous strategies have since been investigated, including the use of various cells, sophisticated scaffolds, substrates, bioactive molecules, and different combinations thereof. Cell sources utilized include cultured chondrocytes, mesenchymal stromal cells, and induced pluripotent stem cells. Scaffolds and substrates are increasingly advanced, with gradient designs to better mimic natural tissue. Choosing optimal techniques and cell sources remains challenging and context-dependent. Advances in the understanding of developmental and regenerative biology are guiding more informed approaches to cartilage tissue engineering. Insights into joint-resident stem and progenitor cells present new opportunities to activate intrinsic repair processes. Regenerative interventions for cartilage repair have the potential to deliver substantial long-term benefits to patients. A wide array of innovative approaches have been explored in recent years. The challenge lies in effectively translating these advances into clinical applications. A one-fits-all solution is unrealistic, and identifying patients who are likely to respond to a specific treatment will enhance success. The repair of joint surface defects in an osteoarthritic joint may require more complex strategies.
-
4. Fundamentals of osteoarthritis: Surgical therapy in osteoarthritis.
4. 骨关节炎基础：骨关节炎的外科治疗PMID:日期:2026-09-24To deliver an updated, evidence-based overview of the different surgical therapies for osteoarthritis (OA). This narrative review reports on principles of surgical therapies for severe, end stage OA and of options addressing pre-osteoarthritic deformities, aiming to possibly delay OA development. It focuses primarily on joint arthroplasty and other surgical approaches for the knee, hip and other major joints affected by OA. Surgical therapy in end-stage OA aims to reduce pain and restore joint function, allowing patients to regain their regular activities. Usually, this involves total joint arthroplasty (TJA), by far the most common surgical procedure addressing severe hip and knee OA, with a high evidence supported by randomized controlled trials and registry data. Evidence for osteotomies around the knee to delay TJA is fair. High-quality evidence supporting other surgical therapies addressing pre-osteoarthritic deformities to possibly delay OA progression and for other joints affected by OA is weaker compared to TJA. Surgical therapy is an important part of the continuum of care when conservative methods fail to provide adequate pain relief, classically indicated in cases of end-stage OA in older patients. Total knee and hip arthroplasty are the gold standard procedures, providing significant pain relief and improved function. Future studies need to confirm the long-term potential of other surgical therapies addressing pre-osteoarthritic deformities to possibly delay OA progression.
-
5. Osteoarthritis service delivery model: Regional care networks.
5. 骨关节炎服务提供模式：区域护理网络PMID:日期:2026-09-22该文献暂无摘要。
-
6. Can Obesity Pharmacotherapy Modify Osteoarthritis? Interpreting Pain Relief, Weight-Loss Quality, and Structural Outcomes.
6. 肥胖药物治疗能否改善骨关节炎？解读疼痛缓解、减重质量与结构结局PMID:日期:2026-09-21To evaluate the emerging role of obesity pharmacotherapies, particularly glucagon-like peptide-1 (GLP-1) receptor agonists and multi-agonists, in osteoarthritis (OA) management, by examining the interpretation of pain outcomes, potential structural joint effects, the importance of weight-loss quality, implications for time to total joint replacement (TJR), and the patient populations most likely to benefit from current obesity pharmacotherapies. We conducted a narrative review of clinical and basic science literature examining the relationships between obesity, OA, and weight loss, with a particular focus on GLP-1 therapies and emerging obesity medications. Evidence from randomized controlled trials, observational studies, translational investigations, and regulatory guidance documents was reviewed with emphasis on pain outcomes, structural joint effects, and factors influencing progression to TJR. Recent randomized controlled trials, primarily involving patients with OA and class III obesity (body mass index >40), demonstrate substantial pain reduction following obesity pharmacotherapy. However, interpretation of these benefits is complicated by obesity-associated pain, multimorbidity, and limitations of patient-reported outcomes such as WOMAC. Current evidence supports symptomatic improvement associated with weight loss, but whether obesity pharmacotherapies directly modify OA-related pain pathways or slow structural progression remains unknown. Moreover, the quality of weight loss may be important, as reductions in fat mass may be accompanied by bone loss and reduced muscle mass. Patients at heightened risk of structural deterioration, such as sarcopenia or elevated bone resorption, may be particularly vulnerable to these effects. Emerging concepts such as clinical obesity further highlight the biological heterogeneity of OA populations and suggest that treatment responses may differ considerably between patients. In the absence of evidence demonstrating direct joint structural modification, obesity pharmacotherapies cannot currently be considered disease-modifying OA treatments. Nonetheless, they may set a new benchmark for pain management in selected OA patients living with obesity. Because weight loss may not necessarily translate to structural benefit despite symptomatic improvement, pain should not serve as a stand-alone outcome in OA-obesity trials. Future studies should evaluate structural outcomes, weight-loss quality, and patient heterogeneity to ensure that obesity therapies deliver sustained symptomatic benefits in OA without compromising musculoskeletal health.
-
7. Immuno-spin trapping after intraarticular procedures shows coordination between radical production, iron metabolism, and mitochondria in articular chondrocytes.
7. 关节内操作后的免疫自旋捕获显示关节软骨细胞中自由基产生、铁代谢与线粒体之间存在协调关系PMID:日期:2026-09-18Prior examinations of pathological effects of surgery have focused on inflammation. We sought to capture the effect of surgical injury on joint redox status. Endpoints were assessed in C57B6J mice 24 h after destabilization of the medial meniscus (DMM) using markers of protein oxidation alongside a non-biased measure of oxidative stress independent of individual reactive oxygen species. DMPO mean intensity, a marker of radical production, was analyzed using generalized linear mixed models with FDR-adjusted pairwise comparisons of marginal means between DMM and paired CC limbs. Potential differences between paired DMM and CC limbs in percentage DMPO-positive cells were analyzed with Wilcoxon signed-rank tests. The remaining redox and mitochondrial markers were compared between independent samples using Kruskal-Wallis tests with FDR-adjusted post hoc Wilcoxon rank sum tests. The highest basal radical production (DMPO mean intensity) in CC limbs was seen in synovium (mean (95% confidence interval) 35.8(26.8-48.0)AU, followed by cartilage (57.2(48.8-67)AU, p=0.008) then meniscus (6.5(3.9-10.9)AU, p<0.001) tissue. Paired DMM limbs had similar values for both synovium (38.8(31.1-48.4)AU), p=0.655) and meniscus (8.3(6.0-11.7)AU, p=0.493) but lower values for cartilage tissue (43.4(36.4-41.7), p=0.037) compared with CC limbs. DMM decreased chondrocyte radicals with minimal impact elsewhere. Intraarticular injections of prospective treatment vehicles constructed with xanthan gum (XG+DMM) or hyaluronic acid (HA+DMM) were examined. Compared to DMM, XG+DMM had greater protein nitration (median[IQR] XG+DMM 53.6[33.2-69.7] vs DMM=32.0[25.2-38.1], p=0.064) and oxidative stress (XG+DMM 37.0[33.5-51.8] vs DMM 26.0[25.1-27.3], p=0.009), but decreased synovial integrity (XG+DMM 41.7[32.2-46.4] vs DMM 67.6[54.1-75.6], p<0.001). In contrast, HA pretreatment was protective of cartilage oxidative function, preserving radical production (CC 58.4[55.4-63.9]; DMM 40.9[33.3-48.3]; HA+DMM 62.4[34.6-64.1], p=0.113 for DMM vs HADMM), protein nitration (CC 38[37-43]; DMM 8.0[7.0-12.0]; HA+DMM 44.0[7.0-65.0], p=0.071 for DMM vs HADMM), iron metabolism (CC 35[29.8-39.5]; DMM 4.5[1.0-29.0]; HA+DMM 73.5[34.0-85.5], p=0.024 for DMM vs HA+DMM), and mitochondrial staining (CC 20.5[17.8-23.9]; DMM 6.9 [3.2-11.5]; HA+DMM 32.4[17.9-35.0], p=0.024) for DMM vs HA+DMM. Redox effects from surgery in mice are more nuanced than might be expected, with decreases in chondrocyte oxidative metabolism the most apparent outcome. We propose perioperative HA treatment might blunt the negative effects intraarticular surgery.
-
8. M1-like macrophages accelerate cartilage endplate remodelling and low back pain partially through TRADD-mediated necroptosis.
8. M1型巨噬细胞部分通过TRADD介导的坏死性凋亡加速软骨终板重塑和腰痛PMID:日期:2026-09-17This study aimed to investigate the role of M1-polarized macrophages in cartilage endplate (CEP) remodelling and low back pain (LBP). Human intervertebral disc samples were collected from patients with (n = 52) and without LBP (n = 5). Macrophage mTORC1 activation and M1-like polarization were analysed. Mice with myeloid lineage-specific TSC1 deletion (Tsc1cKO mice), which exhibit enhanced M1 macrophage polarization, were generated and subjected to surgery to induce LBP. CEP cells (CEPCs) were co-cultured with conditioned medium derived from macrophages of Tsc1cKO mice. CEP damage and LBP were assessed using histological scoring, immunostaining, spinal hypersensitivity, and radiographic analyses. Mice and CEPCs were treated with the TRADD inhibitor apostatin-1 to investigate the role of TRADD in CEP remodelling and LBP. Macrophage mTORC1 activation was increased in M1-polarized macrophages in CEPs during LBP. Tsc1cKO mice displayed a higher proportion of M1-like macrophages in the CEP (mean difference 9.9% [7.24%-12.56%], P < 0.001), with severe CEP remodelling and LBP. Rapamycin inhibited M1-polarized macrophage accumulation in the CEP (mean difference -14.7% [-18.92- -10.48%], P < 0.001) and ameliorated CEP remodelling and LBP. Using bioinformatics analyses, we found that TRADD-mediated CEPC necroptosis was a potential mediator of M1-polarized macrophages in LBP. Finally, apostatin-1 treatment attenujated CEP remodelling and LBP in mouse LBP and cell co-culture models. These findings highlight the role of mTORC1-dependent M1-polarized macrophages and TRADD-mediated necroptosis in CEP remodelling and LBP. Targeting these pathways may offer therapeutic strategies for the treatment of LBP.
-
9. Alcohol consumption and incident osteoarthritis: A nationwide population-based longitudinal study.
9. 饮酒与骨关节炎发病：一项基于全国人群的纵向研究PMID:日期:2026-09-15To examine the association between alcohol consumption and incident osteoarthritis (OA) and whether it persists after restriction for liver-related and weight-related factors. We analyzed South Korean National Health Insurance Service data for adults aged ≥40 years who underwent health screening in 2009-2011 and had no recorded OA at baseline. Alcohol consumption was assessed by self-reported drinking frequency and estimated daily ethanol intake. Participants were followed until first claims-based OA diagnosis (ICD-10 M15-M19, excluding traumatic OA), death, or December 31, 2023. Multivariable Cox models estimated adjusted hazard ratios (HRs). Prespecified restricted analyses were conducted in participants with normal liver function and no liver disease history and in participants with normal weight and no obesity history. Among 1,233,179 participants with drinking-amount data (mean age, 50.8 years), the mean follow-up period was 9.9 years, during which 571,077 cases of OA occurred. Compared with non-drinkers, the light-drinking group had an adjusted HR of 1.037 (95% CI, 1.030-1.045), the moderate-drinking group had an adjusted HR of 1.081 (95% CI, 1.072-1.091), and the heavy-drinking group had an adjusted HR of 1.186 (95% CI, 1.174-1.197). A similar dose-response pattern was observed for drinking frequency and across sensitivity analyses. The pattern also persisted in the normal liver function and normal weight cohorts, and women showed elevated OA risk at lower levels of alcohol consumption than men. Alcohol consumption was associated with incident OA in a dose-dependent manner that persisted after liver-related and weight-related restrictions, suggesting that this association is unlikely to be explained solely by hepatic dysfunction or obesity. These findings identify alcohol consumption as a factor associated with incident OA, warranting further investigation as a potentially modifiable contributor to OA risk.
-
10. Osteoarthritis year in review 2026: Genetics, genomics and epigenetics.
10. 2026年骨关节炎年度回顾：遗传学、基因组学与表观遗传学PMID:日期:2026-09-10The purpose of this narrative review is to highlight advances made over the past 12 months in the field of osteoarthritis (OA) genetics, genomics and epigenomics. PubMed and Europe PMC were searched to identify studies relevant to OA genetics, genomics and epigenomics published between 1st March 2025 and 30th April 2026. Searches used combinations of terms relating to genetics, genomics, epigenomics, functional genomics, molecular quantitative trait loci, chromatin accessibility and enhancer biology. Studies were limited to human subjects and English-language publications, with additional articles identified through expert knowledge of the field. Over the past year, the field has continued to transition from large-scale locus discovery towards biological interpretation of OA genetic risk. Major advances included the largest OA genome-wide association study to date, further development of polygenic risk score approaches, and increasing integration of molecular quantitative trait loci, chromatin accessibility, and enhancer biology datasets to prioritise effector genes and elucidate regulatory mechanisms. Several studies highlighted the highly context-dependent nature of OA genetic risk mechanisms, demonstrating that distinct tissues, cell types, and regulatory layers can identify different candidate effector genes at the same locus. Additional developments included increasing application of single-cell and multi-omic technologies to study OA-relevant tissues. Recent advances in OA genetics have shifted the field from locus discovery towards mechanistic interpretation. Emerging evidence demonstrates that the biological consequences of genetic variation are highly dependent upon tissue, cell state and disease context, with different functional genomic approaches prioritising distinct candidate genes and regulatory mechanisms at the same susceptibility locus. Together, these findings suggest that OA risk loci should increasingly be viewed as dynamic regulatory systems rather than simple variant-to-gene relationships, providing a framework for future studies aimed at resolving causal mechanisms, defining disease endotypes, and identifying therapeutic targets.