The growing demand for real-time, high-resolution motion monitoring in orthopaedic sports medicine is driving the development of flexible wearable pressure/strain sensors. These devices, which transduce mechanical stimuli into electrical signals via piezoresistive, capacitive, piezoelectric, electromagnetic, and triboelectric mechanisms, enable continuous biomechanical data acquisition in dynamic, real-world settings, thereby overcoming the limitations of traditional lab-based methods. This review provides a comprehensive overview of recent advances in wearable pressure/strain sensors, covering fundamental sensing mechanisms and innovative design strategies, including using elastomers, polymer thin films, electronic textiles, and hydrogels. The review also highlights key emerging trends, such as microstructured, bioinspired, multimodal, and machine-learning-enabled signal-processing designs, which have significantly enhanced sensor performance by addressing challenges such as limited sensitivity, narrow detection range, environmental interference, and long-term instability. These sensors are now integrated into wearable devices with diverse applications in orthopaedic sports medicine, including real-time motion tracking, gait analysis, injury prediction and diagnosis, rehabilitation assessment, and human-machine interaction. This review also deliberates on existing limitations and delineates future directions for translating wearable pressure/strain sensors into practical orthopaedic sports medicine applications. To address the limitations of traditional lab-bound motion monitoring, such as high costs and restricted environments, it is essential to leverage the progress in flexible wearable sensing technology. This review provides a comprehensive overview of recent advancements in wearable pressure/strain sensors, highlighting their role in capturing high-resolution biomechanical data in real-world settings. By enabling continuous motion monitoring and objective assessment, these advancements offer valuable insights to improve clinical outcomes in orthopaedic sports medicine, with significant translational potential.
The imbalance in the dietary ω-6/ω-3 polyunsaturated fatty acid (PUFA) ratio contributes to chronic low-grade inflammation, a key pathological basis for degenerative musculoskeletal conditions such as osteoporosis and osteoarthritis. While individual reviews have explored aspects of ω-3 PUFAs in bone or muscle, a comprehensive narrative review integrating their multidimensional mechanisms with translational evidence across orthopedics and sports medicine is less common. This review consolidates evidence from fundamental science, clinical trials, and translational research, employing an interdisciplinary approach to systematically elucidate their mechanisms and application values. ω-3 PUFAs exert multi-layered anti-inflammatory and pro-repair effects through mechanisms including cell membrane remodeling, reprogramming of lipid mediator profiles (promoting the generation of specialized pro-resolving mediators), and inhibition of key pathways such as NF-κB and the NLRP3 inflammasome. Clinical studies indicate that ω-3 PUFA supplementation can improve bone metabolic markers, alleviate pain in osteoarthritis, and reduce inflammation and muscle loss in the perioperative period. In sports medicine, ω-3 PUFAs enhance muscle anabolic metabolism, optimize energy utilization, promote recovery, and demonstrate neuroprotective potential. Their extended application value lies in regulating the "bone-muscle axis," providing targeted nutritional support for athletes, and serving as a nutritional countermeasure in extreme environment medicine. Statement of Significance: This review constructs an integrative framework linking molecular mechanisms to clinical translation, positioning ω-3 PUFAs as key physiological modulators for musculoskeletal health and delineating future directions for precision nutrition-based intervention strategies.
Self-assembled herbal bioactive materials (SAHBMs) represent a rapidly advancing frontier integrating phytochemistry, supramolecular chemistry, and biomedical engineering. By leveraging the intrinsic pharmacological activity and self-organization of herbal compounds, SAHBMs offer improved solubility, stability, and therapeutic efficacy. Despite growing interest, existing studies remain largely narrative and subjective. This study employs bibliometric mapping to provide a systematic, data-driven overview of the field. Publications related to SAHBMs (2000 to June 2025) were retrieved from the Web of Science Core Collection, yielding 1085 records. Analyses were conducted using VOSviewer, CiteSpace, Pajek, SCImago Graphica, and R-based visualizations to assess publication dynamics, institutional and national contributions, collaboration and citation networks, journal dissemination, keyword evolution, and disease associations. Annual publications increased markedly over time, with China contributing 57.1% of outputs, while France and Germany achieved higher citation impact. Collaboration networks highlighted active China-United States partnerships. Core institutions included the Chinese Academy of Sciences and China Agricultural University, while prolific authors such as Wang Penglong and Huang Xuemei shaped research trajectories. Thematic clustering revealed dual disciplinary cores in nanoscience/materials and pharmacology/medicine. Co-cited works emphasized antibacterial, anti-inflammatory, and oncological applications. Keyword bursts such as "wound healing", "drug delivery system", and "regenerative medicine" highlighted evolving thematic emphases and application-oriented research attention. This first bibliometric analysis of SAHBMs delineates global trajectories, intellectual anchors, and emerging frontiers. Challenges remain in stability, biokinetics, and the generation of evidence needed for further preclinical development. Future progress will depend on artificial intelligence-assisted molecular design, advanced preclinical modeling, and strengthened global collaboration. Bibliometric trends suggest that SAHBMs is evolving as a nanomaterials-oriented research field, with increasing attention to self-assembled nanostructures, self-assembly mechanisms, and functional biomedical applications such as carrier-free drug delivery and regenerative medicine.
The mechanical environments endured by the human body profoundly influence life activities across different scales, from single molecules to complicated systems. Gaining insight into the mechanical factors and their biological implications is crucial for deciphering physiological and pathological processes and advancing innovations in drug development and therapeutic approaches for various diseases. Recently, we have witnessed rapid advances in biomechanics and mechanobiology, which, however, are not fully recognized by the clinical community and effectively integrated into medical decision-making, highlighting a translational gap between mechano-based discovery and therapeutic application. Here, we first provide a comprehensive review of research progress in biomechanics and mechanobiology, focusing on key areas such as the cardiovascular system, bone and joints, ocular tissues, liver, lung, the craniomandibular system, cancer, and immunology. We demonstrate how mechanical cues drive health and disease across biological levels, offering insights into complex physiological and pathological mechanisms. Further, we explore the diverse applications of biomechanics and mechanobiology in disease diagnosis, treatment, and rehabilitation. Mechanical insights fuel medical innovations through advanced diagnostic tools, novel therapies, and effective rehabilitation protocols, enhancing clinical outcomes. Looking ahead, we outline future directions of biomechanics and mechanobiology, emphasizing interdisciplinary integration, artificial intelligence, model development, and extreme environments, which hold the promise to deepen scientific understanding and propel technological innovations. This review highlights the transformative potential of biomechanics and mechanobiology in driving scientific and clinical advancements and helps bridge the long-standing gap between biomechanical research and clinical practice.
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a chronic, multisystemic disorder characterized by severe, persistent fatigue not alleviated by rest and worsened by minimal exertion, often accompanied by post-exertional malaise (PEM), unrefreshing sleep, cognitive dysfunction, and autonomic disturbances. Despite decades of research, its pathophysiology remains incompletely understood, and skeletal muscle involvement has only recently gained attention. This review aims to provide a historical and pathophysiological synthesis of ME/CFS, emphasizing the pivotal role of skeletal muscle in the onset and persistence of symptoms, and to integrate molecular, cellular, and pathophysiological evidence into a coherent explanatory framework. This is a narrative review of published literature (1990-2025) with critical integration of clinical, biochemical, and experimental data on oxidative stress, mitochondrial dysfunction, Excitation-Contraction (E-C coupling) dysregulation, and muscle secretome alterations in ME/CFS also in relation to post-viral syndromes (e.g., Long COVID). Evidence consistently points to mitochondrial oxidative stress, redox imbalance, impaired Ca2+ handling, and altered signaling pathways in skeletal muscle of patients with ME/CFS. Historical milestones show an evolution from psychogenic interpretations toward recognition of ME/CFS as a biological disorder with neuromuscular and metabolic underpinnings. ME/CFS can be interpreted as a skeletal muscle-metabolic disorder characterized by oxidative distress, mitochondrial dysfunction, and impaired energy regulation, leading to the clinical picture of exercise intolerance and post-exertional malaise. Integrating basic and clinical research through a translational approach provides the foundation for new diagnostic tools, targeted therapies, and biomarkers.
Osteoarticular diseases, including degenerative, inflammatory, genetic, and metabolic subtypes, cause severe physical impairment, psychological distress, and substantial economic burden globally. Current therapies often fail to halt progression or carry significant side effects, highlighting the need for novel interventions. Luteolin, a natural flavonoid with a C6-C3-C6 skeleton and characteristic hydroxyl substitutions, exhibits diverse pharmacological activities, including antioxidant, anti-inflammatory, and anti-apoptotic effects. It modulates key signaling pathways (e.g., NF-κB, MAPK, Nrf2/ARE, PI3K/Akt) to suppress synovial inflammation, inhibit matrix metalloproteinase-driven cartilage degradation, protect chondrocytes from oxidative stress-induced apoptosis, and regulate immune-metabolic dysfunctions. Preclinical studies demonstrate its potential efficacy in major osteoarticular diseases such as osteoarthritis, rheumatoid arthritis, reheumatic arthritis, gouty arthritis, and traumatic arthritis, with therapeutic effects observed in cell and animal models but not yet validated in human subjects. However, translational challenges persist, including low oral bioavailability, poor aqueous solubility, and a severe lack of large-scale, well-designed clinical validation. Future research should focus on advanced delivery systems, rigorous clinical trials, and exploring understudied mechanisms to facilitate its clinical translation. This review summarizes luteolin's therapeutic potential and mechanisms in osteoarticular diseases, providing critical insights for developing natural therapeutics.
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Background: Μetabolic syndrome (MetS)-comprises central adiposity, elevated blood pressure, dyslipidaemia, and dysglycaemia, increasing the risk of type 2 diabetes and cardiovascular disease. Exercise training improves cardiorespiratory fitness and several MetS components, but real-world effectiveness is limited by poor adherence, restricted supervision, and insufficient personalisation. Objective: This scoping review mapped the clinical intervention evidence on technology-enhanced exercise and structured physical activity relevant to MetS, while distinguishing direct MetS evidence from translational evidence. Methods: In accordance with PRISMA-ScR, we searched PubMed and extended the search to Scopus and Web of Science; a supplementary IEEE Xplore search and a post hoc Embase check were also conducted. Eligible studies were interventions using web-based delivery, wearables, telemonitoring/mobile health (mHealth), artificial intelligence (AI) coaching, virtual reality (VR)/exergaming, or continuous glucose monitoring (CGM) alongside exercise training or structured physical activity. Results: Nineteen studies met the eligibility criteria. The evidence base was weighted toward wearable/app-based feedback and telemonitoring/mHealth/web-based approaches, with fewer studies on VR/exergaming, CGM-enabled exercise, and AI coaching. Most studies were randomised or cluster-randomised, but interventions were usually short term. Across categories, technology most consistently supported adherence, self-monitoring, accountability, remote supervision, and, in selected cases, physiology-informed personalisation. Direct MetS evidence was strongest for wearables with structured feedback, telemonitoring, mHealth, and web-based delivery, whereas AI coaching and CGM were supported by adjacent translational evidence. Conclusions: Technology-enhanced exercise and structured physical activity show promising but heterogeneous and still preliminary potential for MetS management. Key limitations include short follow-up, uneven representation across categories, inconsistent reporting of exercise dose/intensity fidelity and adverse events, and limited equity and implementation outcomes.
Tumour necrosis factor-α (TNF-α) is a central pro-inflammatory cytokine whose biogenesis, secretion, and signalling are tightly interconnected with cellular protein-quality control systems. Current evidence shows that TNF-α maturation, co-translational and post-modifications, ER-luminal folding and trimerisation, Golgi trafficking, and ectodomain shedding by ADAM17 are constrained by ER chaperones and ER-associated degradation (ERAD). Furthermore, TNF-α signalling reciprocally interfaces with the proteostasis network (PN) largely through inflammatory stress pathways such as NF-κB-dependent transcriptional control of chaperones, ubiquitin-proteasome components, and autophagy regulators. However, dysregulation of this bidirectional crosstalk mechanistically contributes to disease, including chronic inflammatory disorders, cancer, and degenerative diseases. In this study we provide a synthesis of the current literature on pathways related to protein homeostasis control that determines whether TNF-α exposure is adaptive or proteotoxic. We also discuss the translational implications this could have by including rational combinations of TNF-α targeted blockers with PN modulators (chemical chaperones, proteasome or autophagy modulators), which reduce the proteotoxic burden. Therefore, understanding the crosstalk between TNF-α signalling and components of the PN system promises new mechanistic insights and translational targets for TNF-α-driven diseases.
This study investigated whether the accuracy of 3D-guided osteotomies is influenced by surgeon experience. Two types of experience were assessed: (1) general surgical experience, defined as self-reported years in practice as an orthopaedic trauma surgeon, and (2) prior use of patient-specific guides (PSGs). Secondary aim was to evaluate whether accuracy varies by anatomical location. 24 orthopaedic-trauma surgeons performed 75 corrective osteotomies on cadaveric long-bones (43 single-cut, 32 double-cut; 107 cuts in total). Each osteotomy was preoperatively planned on CT-derived 3D-reconstructions, and PSGs were manufactured to guide the cuts. Postoperative CT-scans were used to compare planned and executed osteotomy planes. Surgeons completed a questionnaire reporting years of practice and annual PSG usage. A Spearman’s rank-order correlation was used to test differences in accuracy versus experience, a Kruskal-Wallis test was performed to explore differences across anatomical locations. General surgical experience ranged from 0 to 25 years (median 9), and PSG-usage from 0 to 20 cases annually (median 2). No association was found between general surgical experience and osteotomy accuracy (p = 0.406 and p = 0.548). In contrast, PSG-experience correlated with improved accuracy for angular and translational deviation of the osteotomy plane (p = 0.027 and p = 0.029). In addition, midshaft osteotomies of the lower extremity showed smaller angular deviations but larger translational errors compared with metaphyseal (p < 0.001 and p = 0.003). Experience with PSGs, rather than general surgical experience, improves accuracy in 3D-guided osteotomies, highlighting the need for training and repeated use. In contrast to metaphyseal, midshaft lower-extremity osteotomies are executed less accurately because fewer anatomical reference points are available. The online version contains supplementary material available at 10.1007/s00068-026-03179-4.
Exercise-induced muscular stress triggers a complex cascade of adaptive responses, including micro-injury, inflammation, activation of satellite cells, mitochondrial remodeling, and myofibrillar repair. The efficiency of recovery processes is crucial for athletic performance, especially among elite athletes, where rapid restoration of muscle function, reduction of inflammation, and improved sleep quality influence training results. Beyond traditional recovery methods, EVs and, more recently, plant-derived exosome-like nanovesicles (PELNs) have emerged as promising bioactive mediators of intercellular communication and tissue regeneration. PELNs contain various biomolecules such as lipids, proteins, small RNAs, and plant-specific metabolites that may affect oxidative stress, inflammatory signaling, and cellular repair pathways. While most research has focused on mammalian or cell-line sources, growing evidence indicates that PELNs may improve muscle regeneration and recovery through cellular modulation and enhanced sleep-related recovery. Notably, PELNs represent a multi-target strategy that may simultaneously modulate neuroendocrine pathways involved in sleep regulation and metabolic-inflammatory mechanisms governing skeletal muscle repair. By influencing circadian rhythm signaling, mitochondrial dynamics, and redox homeostasis, PELNs may bridge the sleep-muscle recovery axis, an emerging concept in exercise physiology. This dual regulatory capacity distinguishes PELNs from conventional recovery interventions and highlights their innovative and translational potential in sports science. This review aims to compile current evidence linking PELNs to exercise-induced muscle recovery, highlighting potential mechanisms, including the regulation of inflammatory and redox balance, microRNA-driven signaling, and neurometabolic adaptation. By combining insights from exercise physiology and molecular regenerative biology, we propose that PELNs offer a natural approach to enhancing recovery and performance in athletes.
Current guidelines discourage sports participation for athletes with arrhythmogenic cardiomyopathy (ACM). However, the evidence that exercise is a disease-accelerator is most compelling for PKP2-mediated ACM. This study aims to examine management, return-to-play (RTP) decisions, outcomes, and phenotype evolution among athletes with genotype-positive ACM. A retrospective review of electronic medical record of 1,229 patients in our Arrhythmogenic/Dilated Cardiomyopathy Registry was used to identify self-identified athletes. They were evaluated, risk stratified, and treated at Mayo Clinic Windland Smith Rice Genetic Heart Rhythm Clinic between July 2000 and February 2025. A total of 138 genotype-positive athletes with ACM were identified (58 women [42%], mean age of 31 ± 19 years, plakophilin [PKP2]-ACM [n = 61; 44%], desmoplakin [DSP]-ACM [n = 32; 23%]). After diagnosis of ACM, 34 athletes (25%) experienced at least 1 breakthrough cardiac event (BCE), accounting for a total of 68 events, and 6 patients experienced 14 BCEs following physician-approved RTP. During a median follow-up of 25 months (IQR: 6-71), the overall event rate for the entire cohort was 7.9 BCEs per 100 patient-years (95 % CI: 5.8-10.5), and the event rate after physician-approved RTP was 14.6 per 100 patient-years (95% CI: 7.8-24.9). During RTP period, one-half of these BCEs occurred during sports participation, whereas the remainder occurred at rest or unknown context. This is the first single-center cohort of patients with ACM being empowered to RTP and remain athletes. These athletes have exhibited higher rates of BCEs and disease conversion/progression than our athletes with a variety of other genetic heart diseases. Further studies are needed to determine how to further guide safe sports participation in genetically mediated ACM.
Sarcopenia and osteoarthritis are two common musculoskeletal disorders that often coexist, posing significant challenges in clinical management. These conditions share underlying mechanisms such as chronic inflammation, metabolic dysfunction, and biomechanical stress, which accelerate musculoskeletal degeneration. Sarcopenia, characterized by muscle loss and weakness, and osteoarthritis, marked by cartilage degradation and joint dysfunction, frequently overlap, leading to increased disability and reduced quality of life. The presence of both conditions creates a detrimental cycle where muscle weakness exacerbates joint pain, and joint dysfunction further weakens muscles. This comorbidity complicates treatment, requiring integrated strategies that address both muscle and joint pathology. Advances in personalized therapies, driven by multi-omics technologies, are crucial in targeting these interconnected conditions more effectively. Precision medicine, using genetic, metabolic, and physiological data, can help tailor treatments and improve patient outcomes. Furthermore, the integration of adaptive interventions, digital twin models, and real-time feedback systems will play key roles in refining individualized treatment plans. Multi-omics integration and real-world evidence are also transforming how clinical trials are designed and how we assess disease progression, moving away from structural markers to functional and patient-centered outcomes. Effective interventions must involve early detection, personalized approaches, and interdisciplinary care, aiming to break the cycle of degeneration and improve patients' functional independence and quality of life. This review identifies the biomechanical, metabolic, and epigenetic "vicious cycles" that drive the comorbidity of sarcopenia and osteoarthritis. By integrating multi-omics data, digital twin modeling, and real-time biomechanical feedback, this work provides a framework for clinical precision medicine. The clinical significance lies in identifying a "mechanical window of opportunity" for early intervention-using personalized exercise and nutritional strategies to restore joint homeostasis and prevent irreversible functional decline.
Total hip arthroplasty (THA) is a cornerstone of geriatric medicine, yet the selection of optimal fixation strategies and surgical approaches remains a subject of intense clinical debate. As global demographics shift toward an aging population, the demand for THA is projected to rise exponentially, necessitating a thorough evaluation of perioperative outcomes and long-term survivorship. This review critically analyzes recent 2024-2025 evidence regarding the biomechanical stability and clinical efficacy of cemented versus cementless fixation in patients aged 70 years or older. Current literature suggests that while cementless technology dominates younger cohorts, cemented fixation provides superior initial rotational stability in the osteoporotic environment, significantly reducing the risk of intraoperative periprosthetic fractures. Furthermore, this report examines the impact of the Direct Anterior Approach (DAA) compared to the Posterior Approach (PA) within the framework of Enhanced Recovery After Surgery (ERAS), highlighting the DAA's benefits in minimizing soft-tissue trauma and reducing hospital length of stay. Finally, we synthesize modifiable and non-modifiable risk factors for periprosthetic joint infection (PJI) and fracture progression. Understanding these multifaceted factors is essential for tailoring personalized surgical interventions and improving functional recovery in the geriatric population.
Ultra-endurance sports like running over several hours or days exhibit great physical, psychological and metabolic strain on the respective athlete. Although the impact of ultramarathon running on the inflammatory/immunological system gained interest in the last years, there is no study that examined the effect of different running distances on inflammatory/immune system responses. During a non-stop ultramarathon, blood and saliva samples were collected before (Pre) and after the race (Post), and analyzed for changes in blood cell variables (immune cells leukocytes/thrombocytes), cytokine response (pro- and anti-inflammation: IL-6/IL-10/IL-1ra/IL1-beta/TNF-alpha), and stress-related parameters (CRP as acute phase protein; uric acid for oxidative stress; cortisol/kynurenine for general stress and energy metabolism). Biomarkers were supplemented by a stress-related questionnaire and 1) analyzed for the whole group of finishers (N = 43; 16f/27m) and 2) compared between the respective running distances (100/160.9/230 km). Leukocyte and thrombocyte count increased Post in all runners, with a more pronounced leukocyte response observed in 100 km vs. 160.9 km. IL-6/IL-10/IL-1ra increased Post in all sub-groups, whereas IL1-beta decreased only in the whole group. Stress/immune response showed an increase of salivary cortisol and CRP in all runners. Sub-group analysis revealed highest cortisol and CRP concentrations in 230 km Post race. Ultramarathons differ in the physiological strain they impose, with running distance being an important factor. Especially 100 km (faster pace, shorter duration) and 230 km (slower pace, longer duration) runners exhibited distinct inflammatory/immunological responses. Thus, broad generalizations regarding the impact of a given ultramarathon on the immune system and potential post-race infection risk are unwarranted, and individualized guidance is currently more effective.
Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by multifactorial pathological mechanisms, and remains a significant clinical challenge. Exosome therapy represents a future direction for delaying OA progression, yet its efficacy is often compromised by inflammatory microenvironment within the joints. To overcome these limitations, we present a novel combinatorial therapeutic platform that alleviates OA through a multi-targeted strategy, including the scavenging of reactive oxygen species (ROS), suppression of macrophage-driven inflammation, and inhibition of chondrocyte ferroptosis. This platform combines dental pulp stem cells-derived exosomes (Exo) with hollow mesoporous cerium oxide nanozymes, which were first loaded with curcumin and subsequently coated with hyaluronic acid, termed HA@Cur@CeO2. In vitro, this combination reduced intracellular ROS and promoted macrophage polarization toward the anti-inflammatory M2 phenotype, thereby remodeling the OA microenvironment and halting the inflammatory cascade. Additionally, Exo and HA@Cur@CeO2 nanozymes complementarily modulated ALOX12-and GPX4-dependent ferroptosis pathways in chondrocytes, with the combined approach yielding superior anti-ferroptotic effects. For in vivo assessment, Exo and HA@Cur@CeO2 were encapsulated within a chitosan/β-glycerophosphate hydrogel to achieve sustained release (Exo/HA@Cur@CeO2/Gel). This formulation significantly reduced inflammation, chondrocyte ferroptosis, cartilage degeneration, and subchondral bone remodeling, ultimately slowing OA progression. With excellent biocompatibility, this innovative combinatorial therapeutic strategy represents a comprehensive approach for enhancing Exo efficacy in OA treatment with promising translational potential.
Human transglutaminases (hTGs) are Ca2+-dependent enzymes that catalyze protein crosslinking, deamidation and other post-translational modifications, thus acting as key stabilizers of tissue architecture and modulators of protein function across diverse physiological contexts. This family comprises eight catalytically active members, TG1-7, the blood coagulation factor FXIII, and the inactive structural protein Band 4.2 of the erythrocyte membrane. Recent structural and biochemical advances have refined our understanding of the molecular principles governing transglutaminase function. Thus, current evidence reveals how domain organization and catalytic architecture integrate calcium binding, nucleotide-dependent regulation in TG2 and proteolytic activation in selected isoforms to control enzymatic activity. In this review, we provide an updated and comprehensive overview of the active hTGs, combining structural, biochemical and functional data to explain how closely related enzymes achieve isoform-specific regulation and distinct biological roles. We further examine how disruption of these mechanisms contributes to human pathology, highlighting representative examples in autoimmunity, inherited disorders and complex diseases. By integrating recent biochemical and structural findings with disease-associated evidence, we aim to offer a coherent framework for understanding how TG regulation underlies their diverse biological functions and clinical relevance.
Repetitive head impacts (RHI) from contact sports may cause a unique pattern of white matter hyperintensities (WMH) on T2-weighted fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI), termed RHI-associated WMH (RHI-WMH). These lesions are punctate, circular, and located at the gray-white matter boundary, an area vulnerable to trauma-related damage. We investigated the association of RHI with these lesions in two aging cohorts: (1) former American football players versus asymptomatic unexposed men and (2) individuals with RHI from various contact sports versus non-RHI participants. RHI-WMH were assessed using visual ratings and a novel automated quantification pipeline. Individuals with RHI had greater RHI-WMH by both detection methods in both cohorts. RHI-WMH were associated with plasma neurofilament light and p-tau231, and flortaucipir positron emission tomography (PET) uptake. RHI-WMH may represent a new supportive biomarker for the detection of RHI-related neuropathologies later in life.
This study employs bibliometric methods to systematically analyze the research trajectory and frontier trends in the application of chondroitin sulfate (CS) for the treatment of osteoarthritis (OA) from 2005 to 2025. Through a visual analysis of 2004 relevant articles from the Web of Science core collection, the field is revealed to have evolved through three distinct stages: from early pharmacological treatment and fundamental research, to the integration of tissue engineering and biomaterials, culminating in the current focus on intelligent therapeutic strategies centered on precision drug delivery systems. The findings indicate a global research landscape characterized by a "dual-core dominance of China and the United States." While China leads in publication output, its academic influence, as measured by citation metrics, lags behind that of European and American countries. Keyword analysis identifies "inflammation" and "drug delivery systems" as recent research hotspots, with targeted delivery systems based on biomaterials such as hydrogels and nanoparticles emerging as the technological frontier. The study also highlights persistent challenges in the clinical translation of CS, including issues related to delivery efficiency, material properties, large-scale manufacturing, and interdisciplinary collaboration. Looking forward, by integrating smart responsive materials, multimodal synergistic therapies, and strengthening international cooperation, CS-based strategies show promise in shifting the OA treatment paradigm from symptomatic relief to structural repair. By bridging macro-level literature analysis with micro-level materials chemistry insights, this work provides a comprehensive framework that integrates quantitative research mapping with mechanistic understanding of CS-based biomaterial design. This dual perspective aims to inform not only research planning and translational pathways, but also the rational design of CS derivatives with tailored physicochemical properties for specific OA therapeutic applications.
Osteoarthritis (OA) and osteoporosis (OP) are prevalent musculoskeletal disorders with substantial global health and economic burdens. Imaging is central to their diagnosis and monitoring, yet manual interpretation is vulnerable to inter-reader variability and workload-related fatigue. Artificial intelligence (AI), including machine learning (ML) and deep learning (DL), provides data-driven approaches to enhance the accuracy, efficiency, and objectivity of image interpretation. This review summarizes AI-assisted imaging advances for OA and OP over the past decade and discusses translational opportunities and challenges. A literature search was conducted in Web of Science, PubMed, and Scopus for English-language studies published between January 2015 and August 2025. Search terms included osteoarthritis, osteoporosis, X-ray, computed tomography (CT), magnetic resonance imaging (MRI), machine learning, deep learning, detection, classification, and diagnosis. Titles and abstracts were screened, and selected full texts were reviewed to summarize advances and diagnostic performance across modalities. Across X-ray, CT, and MRI, ML/DL approaches enable more objective quantification of OA- and OP-related abnormalities. Using public and cohort-based datasets, studies have evolved from radiomics-based ML pipelines to end-to-end DL frameworks for screening, classification, and grading. For OA, radiographs dominate Kellgren-Lawrence (KL) grading and large-scale screening, complemented by MRI for early tissue biomarkers and CT for quantifying subchondral bone remodeling. For OP, X-ray/CT captures bone texture and trabecular microarchitecture to support detection and classification, with MRI mainly used to assess marrow- and soft-tissue-related markers. Overall, DL typically improves automation and representation learning, while ML remains interpretable and competitive in smaller datasets. Emerging studies suggest that multimodal fusion and longitudinal modeling for progression assessment and prediction may further improve performance. AI-assisted imaging is reshaping OA and OP assessment by enabling earlier detection and more objective longitudinal monitoring. However, clinical translation is hindered by limited interpretability of many DL models and substantial data heterogeneity. Future research should prioritize standardized multicenter datasets and explainable AI frameworks. Prospective clinical studies and rigorous external validation are needed to bridge the gap between research and practice and to advance personalized musculoskeletal care.