Osteoarthritis is a major cause of disability worldwide, and understanding epidemiological trends in osteoarthritis is critical for public health planning and intervention strategies. This study analyzed the global, regional, and national burden on osteoarthritis utilizing the Global Burden of Disease Study 2021. Trends from 1990 to 2021 were primarily assessed, with projections to 2050 based on demographic changes and historical data. In 2021, 607 (95% UI: 538–671) million people worldwide suffered from osteoarthritis, including 46.6 (95% UI: 41.1–51.6) million new cases, and the DALYs was 21.3 (95% UI: 10.2–42.9) million. Age-standardized incidence, prevalence and DALYs rates increased to 535.00/100,000 (95% UI: 472.38–591.97), 6967.29/100,000 (95% UI: 6180.70–7686.06), and 244.50/100,000 (95% UI: 117.06–493.11), with knee osteoarthritis accounting for more than 56%. Age-standardized rates of osteoarthritis were higher in females than in males. East Asia, South Asia, and Western Europe were the regions and China, India, and the United States were the countries with the highest burdens. In addition, high body-mass index led to 4.43 (95% UI: -0.42–12.34) million DALYs, with an increase of 205.10%. Bayesian age-period cohort projections showed that the burden of osteoarthritis would continue to rise from 2021 to 2050. As an ageing population and rising obesity rates, the burden of osteoarthritis will continue to rise, with females and the middle-aged and older age groups being the current populations of concern. Awareness-raising, early detection, and effective management are essential to reduce the burden of osteoarthritis in the coming decades, especially among vulnerable groups.

Chondroitin sulphate captured an increasing amount of attention in the field of drug delivery systems. Nanoparticles and chondroitin sulphate were combined in different ways to form effective target nanocarriers. The study aimed to evaluate the biomedical application of chondroitin sulphate with nanoparticles in drug delivery systems. We searched PubMed, Google Scholar, and MEDLINE for studies that included data for the application of chondroitin sulphate and nanoparticles in targeting drug delivery published in English up to 25 February 2020. OHAT (Office of Health Assessment and Translation) Risk-of-Bias Tool was used to assessing the quality and risk of bias of each study. We performed a qualitative synthesis of findings from included studies. The toxicity of developed drugs has been evaluated using cell viability percentage and 50% inhibitory concentration of drugs. Twenty original articles reported the application of chondroitin sulphate on drug delivery systems were selected. Drug loading and encapsulation efficiency were from 2% to 16.1% and from 39.50% to 93.97%, respectively. The drug release was fast at start time and followed by a slow and sustain released stage. The risk of bias was rated as high in two out of twenty studies. Most of the studies presented baseline characteristics and outcomes appropriately.

Osteoarthritis (OA) is a prevalent and disabling joint disorder characterized by progressive cartilage degradation, subchondral bone changes, synovial inflammation, and chronic pain. While traditionally attributed to mechanical and age-related factors, increasing attention has been directed toward the role of nutritional components in disease modulation. This article critically examines the emerging role of three essential trace elements, zinc, copper, and selenium, in the pathophysiology of OA. These micronutrients are fundamental to antioxidant defense, immune modulation, and extracellular matrix (ECM) integrity. Altered systemic or local levels of zinc, copper, and selenium have been associated with oxidative stress, inflammation, and dysregulated cartilage metabolism in OA. Drawing on clinical studies, in vivo and in vitro experimental models, and population-based data, we synthesize evidence on trace element status in OA patients, mechanistic pathways, and therapeutic potential, including emerging nanomedicine strategies that enhance the targeted delivery and therapeutic efficacy of trace elements in joint tissues. This review highlights the need for integrated trace element profiling in OA research and clinical care and supports the exploration of targeted nutritional interventions in OA prevention and management.

Kashin-Beck disease (KBD) is an endemic, environmentally associated cartilage disease. Previous studies have shown that the environmental suspected pathogenic factors of KBD, T-2 toxin and low selenium, are involved in the regulation of inflammation, oxidative stress and autophagy in some tissues and organs. In cartilage diseases, the level of cellular autophagy determines the fate of the chondrocytes. However, whether autophagy is involved in KBD cartilage lesions, and the role of low selenium and T-2 toxins in KBD cartilage injury and autophagy are still unclear. This work took the classical AMPK/mTOR/ULK1 autophagy regulatory pathway as the entry point to clarify the relationship between the environmental suspected pathogenic factors and chondrocyte autophagy. Transmission electron microscopy was used to observe the autophagy of chondrocytes in KBD patients. qRT-PCR and western blot were used to analyze the expression of AMPK/mTOR/ULK1 pathway and autophagy markers. The rat model of KBD was established by low selenium and T-2 toxin, the autophagy in rat cartilage was detected after 4- and 12-week interventions. Chondrocyte autophagy was found in KBD, and the AMPK/mTOR/ULK1 pathway was down-regulated. In the rat model, the pathway showed an up-regulated trend when low selenium and T-2 toxin, were treated for a short time or low concentration, and autophagy level increased. However, when low selenium and T-2 toxin were treated for a long time or at high concentrations, the pathway showed a down-regulated trend, and the autophagy level was reduced and even defective. In conclusion, in the process of KBD cartilage lesion, chondrocyte autophagy level may increase in the early stage, and decrease in the late stage with the progression of lesion. Low selenium and T-2 toxins may affect autophagy by AMPK/mTOR/ULK1 pathway.