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Reactive oxygen species (ROS) play distinct but important roles in physiological and pathophysiological processes. Recent studies on osteoarthritis (OA) have suggested that ROS plays a crucial role in its development and progression, serving as key mediators in the degradation of the extracellular matrix, mitochondrial dysfunction, chondrocyte apoptosis, and OA progression. With the continuous development of nanomaterial technology, the ROS-scavenging ability and antioxidant effects of nanomaterials are being explored, with promising results already achieved in OA treatment. However, current research on nanomaterials as ROS scavengers for OA is relatively non-uniform and includes both inorganic and functionalized organic nanomaterials. Although the therapeutic efficacy of nanomaterials has been reported to be conclusive, there is still no uniformity in the timing and potential of their use in clinical practice. This paper reviews the nanomaterials currently used as ROS scavengers for OA treatment, along with their mechanisms of action, with the aim of providing a reference and direction for similar studies, and ultimately promoting the early clinical use of nanomaterials for OA treatment. Reactive oxygen species (ROS) play an important role in the pathogenesis of osteoarthritis (OA). Nanomaterials serving as promising ROS scavengers have gained increasing attention in recent years. This review provides a comprehensive overview of ROS production and regulation, as well as their role in OA pathogenesis. Furthermore, this review highlights the applications of various types of nanomaterials as ROS scavengers in OA treatment and their mechanisms of action. Finally, the challenges and future prospects of nanomaterial-based ROS scavengers in OA therapy are discussed. [Display omitted] [ABSTRACT FROM AUTHOR]

We examined the correlation between acetabular prostheses and sagittal anatomical parameters of the pelvis for the preoperative evaluation of total hip arthroplasty in 29 patients with ankylosing spondylitis between April 2004 and November 2011. No implant dislocation or subsidence was observed at 4.18 years. The relationship between sagittal parameters conformed to the equation Pelvic incidence (PI)=Pelvic tilt (PT)+Sacral slope (SS). Better outcomes were achieved in the SS>PT group, postoperative function was positively correlated with SS/PI. Functional abduction and anteversion were positively correlated with PT but negatively correlated with SS. Due to the compensatory changes in the pelvis and spine of patients with AS, the preoperative assessment of sagittal parameters plays pivotal roles in placing acetabular prostheses in optimal positions and preventing postoperative impingement and dislocation. [ABSTRACT FROM AUTHOR]

• Developing a semi-unsupervised learning system for streaming cell image segmentation. • Capturing the ambiguous images of platelet activation at sub-micron resolutions. • Segmenting 45 million platelets at minutes instead of 40 years of manual annotations. We developed a fast and accurate deep learning approach employing a semi-unsupervised learning system (SULS) for capturing the real-time noisy, sparse, and ambiguous images of platelet activation. Outperforming several leading supervised learning methods when applied to segment various platelet morphologies, the SULS detects their complex boundaries at submicron resolutions and it massively decreases to only a few hours for segmenting streaming images of 45 million platelets that would have taken 40 years to annotate manually. For the first time, the fast dynamics of pseudopod formation and platelet morphological changes including membrane tethers and transient tethering to vessels are accurately captured. [ABSTRACT FROM AUTHOR]

• Osteoarthritis (OA) is the most common form of age-related arthritis and is characterized by low-grade inflammation and metabolic dysfunction. • Aberrant chondrocyte metabolism is a response to changes in the inflammatory microenvironment and may play a key role in cartilage degeneration and OA progression. • Under conditions of environmental stress, chondrocytes shift from oxidative phosphorylation to glycolysis, a process regulated by the AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR) pathways. • Metabolic changes in chondrocytes and other cells in the synovial joint could be a target for future therapeutic interventions. • Future research should place greater emphasis on immunometabolism and altered metabolic pathways as a means to understand the pathophysiology of aging and OA. Osteoarthritis (OA) is a degenerative joint disease characterized by low-grade inflammation and high levels of clinical heterogeneity. Aberrant chondrocyte metabolism is a response to changes in the inflammatory microenvironment and may play a key role in cartilage degeneration and OA progression. Under conditions of environmental stress, chondrocytes tend to adapt their metabolism to microenvironmental changes by shifting from one metabolic pathway to another, for example from oxidative phosphorylation to glycolysis. Similar changes occur in other joint cells, including synoviocytes. Switching between these pathways is implicated in metabolic alterations that involve mitochondrial dysfunction, enhanced anaerobic glycolysis, and altered lipid and amino acid metabolism. The shift between oxidative phosphorylation and glycolysis is mainly regulated by the AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR) pathways. Chondrocyte metabolic changes are likely to be a feature of different OA phenotypes. Determining the role of chondrocyte metabolism in OA has revealed key features of disease pathogenesis. Future research should place greater emphasis on immunometabolism and altered metabolic pathways as a means to understand the pathophysiology of age-related OA. This knowledge will advance the development of new drugs against therapeutic targets of metabolic significance. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is a leading cause of deformity in aging people. Emerging evidence suggests that microRNAs and Wnt signaling pathway are associated with its pathogenesis. We aimed to determine whether microRNA-320c inhibits the development of osteoarthritis by suppressing Wnt signaling pathway. MiR-320c and β-catenin expression was assessed in human adipose derived stem cells (hADSCs) model of chondrogenesis and in normal and OA primary human chondrocytes. OA chondrocytes were transfected with miR-320c or its antisense inhibitor and β-catenin siRNA respectively. Direct interaction between miR-320c and β-catenin mRNA as well as activity of β-catenin/TCF complex were confirmed by luciferase reporter assay. Mmu-miR-320-3p agomir was intra-articularly injected in collagenase-induced OA mouse model. OA progression was evaluated histologically and immunohistochemically. MiR-320c was decreased and β-catenin was increased in OA chondrocytes and late stage of hADSCs chondrogenesis. Overexpression of miR-320c and knockdown of β-catenin had similar effects that the cartilage-specific genes were elevated and hypertrophy-related genes were down-regulated in OA chondrocytes. Luciferase reporter assay confirm that miR-320c regulated the expression of β-catenin by directly targeting 3′UTR of β-catenin mRNA and decreased the relative transcriptional activity of the β-catenin/TCF complex. Injection of mmu-miR-320-3p attenuated OA progression in the OA mouse model. Our results supports that miR-320c can inhibits the degeneration of osteoarthritis chondrocytes via suppressing the canonical Wnt signaling pathway and indicates the potential of miR-320c as a novel therapeutic agent for osteoarthritis treatment. [ABSTRACT FROM AUTHOR]

Histone acetylation regulated by class I histone deacetylases (HDACs) plays a pivotal role in matrix-specific gene transcription and cartilage development. While we previously demonstrated that microRNA (miR)-455-3p is upregulated during chondrogenesis and can enhance early chondrogenesis, the mechanism underlying this process remains largely unclear. In this study, we characterized the effect of miR-455-3p on histone H3 acetylation and its role during cartilage development and degeneration. We observed that miR-455-3p was highly expressed in proliferating and pre-hypertrophic chondrocytes, while HDAC2 and HDAC8 were primarily expressed in hypertrophic chondrocytes. Meanwhile, miR-455-3p suppressed the activity of reporter constructs containing the 3′-untranslated regions of HDAC2/8 , inhibited HDAC2/8 expression and promoted histone H3 acetylation at the collagen 2 ( COL2A1 ) promoter in human SW1353 chondrocyte-like cells. Treatment with the HDAC inhibitor trichostatin A (TSA) resulted in increased expression of cartilage-specific genes and promoted glycosaminoglycan deposition. Moreover, TSA inhibited matrix metalloproteinase 13 ( Mmp13 ) expression and promoted nuclear translocation of SOX9 in interleukin-1-treated primary mouse chondrocytes. Lastly, knockdown of HDAC2/3/8 increased SRY (sex-determining region Y)-box 9 (SOX9) and decreased Runt-related transcription factor 2 (RUNX2) expression. Taken together, these findings suggest that miR-455-3p plays a critical role during chondrogenesis by directly targeting HDAC2/8 and promoting histone H3 acetylation, which raises possibilities of using miR-455-3p to influence chondrogenesis and cartilage degeneration. [ABSTRACT FROM AUTHOR]

The association of coffee and tea consumption with osteoporosis is highly controversial, and few studies have focused on the combined effects of the two beverages. This study aimed to investigate the independent and combined associations of coffee and tea consumption with osteoporosis risk. A prospective cohort study involving 487,594 participants aged 38–73 years from the UK Biobank was conducted. Participants with reported coffee and tea consumption and without osteoporosis at baseline were included. Coffee and tea consumption were assessed via a touch-screen questionnaire at baseline. Newly diagnosed osteoporosis during the follow-up period, defined based on ICD-10 codes (M80-M82), was the primary outcome. Cox regression analyses were utilized to calculate hazard ratios (HRs) and 95 % confidence intervals (CIs). Dose-effect associations were assessed using restricted cubic spline analysis. During a median follow-up of 12.8 years, 15,211 cases of osteoporosis were identified. Compared to individuals without coffee or tea consumption, drinking coffee was associated with an HR of 0.93 (95 % CI: 0.89–0.96), and tea consumption with an HR of 0.86 (95 % CI: 0.83–0.90). Continuous trends were significant for both coffee and tea consumption, showing non-linear associations with osteoporosis incidence. Moderate consumption, such as 1–2 cups of coffee or 3–4 cups of tea per day, was associated with a lower incidence of osteoporosis, with HRs of 0.9 (95 % CI: 0.86–0.94) and 0.85 (95 % CI: 0.81–0.90), respectively. Additionally, combined coffee and tea consumption displayed a U-shaped association with osteoporosis risk, with the lowest risk observed in individuals who consumed 1–2 cups of both beverages daily, with an HR of 0.68 (95 % CI: 0.61–0.75). Our findings highlight the potential benefits of moderate coffee and tea consumption in reducing the risk of osteoporosis. • Consumption of coffee and tea correlates with reduced osteoporosis risk. • Combined consumption of coffee and tea further lowers osteoporosis risk, exhibiting a dose-dependent relationship akin to a U-shaped curve. • Ground coffee shows the strongest association with reduced risk, while decaffeinated coffee does not. • Men tend to experience greater benefits from coffee and tea consumption in relation to osteoporosis risk. [ABSTRACT FROM AUTHOR]

[Display omitted] • Pioneered use of intra-articular injection of D-α-Tocopherol polyethylene glycol 1000 succinate (TPGS) to treat osteoarthritis. • Applied a hybrid hydrogel incorporated with TPGS (TPGS@CS-hydrogel) to repair cartilage defect. • TPGS@CS-hydrogel resulted in excellent cartilage repair outcomes. • The chondrogenic capacity of mesenchymal stem cell improved in TPGS@CS-hydorgel. Osteoarthritis (OA) is a progressive and degenerative disease associated with articular cartilage injury. Current conservative or surgical treatments cannot effectively terminate the progress of OA, usually leading to total joint replacement at the end stage. Also, it is still challenging to treat cartilage defect for it demands a dual-pronged approach which simultaneously addresses both cartilage repair and the relief of osteochondral inflammation. In this study, we embarked on a pioneering exploration of D-α-Tocopherol polyethylene glycol 1000 succinate (TPGS), an FDA-approved, water-soluble derivative of natural vitamin E. TPGS was found to effectively relieve inflammation both in vitro and in vivo. We further extended the application of TPGS by establishing an injectable collagen-chondroitin sulfate (CS) hydrogel incorporated with TPGS (TPGS@CS-hydrogel), and achieved excellent cartilage repair. RNA-seq showed that the anti-inflammatory effect of TPGS@CS-hydrogel were related to the interruption of interplay of oxidative stress and inflammation, thus promoting cartilage regeneration. In conclusion, both TPGS and TPGS@CS-hydrogel provided new insights for the prevention and treatment of articular inflammation and cartilage lesion. [ABSTRACT FROM AUTHOR]