n-3 PUFA, including ALA, EPA and DHA, are widely found in plant oils and marine organisms. These fatty acids demonstrate significant biological effects, and their adequate intake is essential for maintaining health. However, modern diets often lack sufficient n-3 PUFA, especially among populations that consume little fish or seafood, leading to a growing interest in n-3 PUFA supplementation in nutrition and health research. In recent decades, the role of n-3 PUFA in preventing and treating various diseases has gained increasing attention, particularly in cardiovascular, neurological, ophthalmic, allergic, hepatic and oncological fields. In orthopaedics, n-3 PUFA exert beneficial effects through several mechanisms, including modulation of inflammatory responses, enhancement of cartilage repair and regulation of bone metabolism. These effects demonstrate potential for the treatment of conditions such as osteoarthritis, rheumatoid arthritis, gout, osteoporosis, fractures, sarcopenia and spinal degenerative diseases. This review summarises the clinical applications of n-3 PUFA, with a focus on their research progress in the field of orthopaedics, and explores their potential in the treatment of orthopaedic diseases.

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic inflammation of the synovial membrane, leading to cartilage destruction and bone erosion. Due to the complex pathogenesis of RA and the limitations of current therapies, increasing research attention has been directed towards novel strategies targeting fibroblast-like synoviocytes (FLS), which are key cellular components of the hyperplastic pannus. Recent studies have highlighted the pivotal role of FLS in the initiation and progression of RA, driven by their tumour-like transformation and the secretion of pro-inflammatory mediators, including cytokines, chemokines and matrix metalloproteinases. The aggressive phenotype of RA-FLS is marked by excessive proliferation, resistance to apoptosis, and enhanced migratory and invasive capacities. Consequently, FLS-targeted therapies represent a promising avenue for the development of next-generation RA treatments. The efficacy of such strategies – particularly those aimed at modulating FLS signalling pathways – has been demonstrated in both preclinical and clinical settings, underscoring their therapeutic potential. This review provides an updated overview of the pathogenic mechanisms and functional roles of FLS in RA, with a focus on critical signalling pathways under investigation, including Janus kinase/signal transducer and activator of transcription (JAK/STAT), mitogen-activated protein kinase (MAPK), nuclear factor kappa B (NF-κB), Notch and interleukin-1 receptor-associated kinase 4 (IRAK4). In addition, we discuss the emerging understanding of FLS-subset-specific contributions to immunometabolism and explore how computational biology is shaping novel targeted therapeutic strategies. A deeper understanding of the molecular and functional heterogeneity of FLS may pave the way for more effective and precise therapeutic interventions in RA.

Many people with rheumatoid arthritis (RA) believe that certain foods may influence disease activity. Elimination reintroduction diets and oral food challenges are dietary strategies used to identify foods that may exacerbate symptoms. This review summarises and appraises the literature on elimination diet interventions that include food reintroductions or oral food challenges in adults with RA. It describes study design, measures used to assess the effects of food exclusion and challenge, foods identified that may affect RA symptoms, and the measures used to assess the outcome of excluding those foods. A search of five databases, two thesis repositories and Open Grey was conducted to identify records published from inception to January 2025, using terms related to RA, elimination diets and food sensitivity. Eligible records were screened independently by two reviewers, and data extraction followed Joanna Briggs Institute guidelines. Data are presented using a narrative synthesis approach with descriptive data analysis. In total, forty-eight records met inclusion criteria comprising twenty intervention studies (sample sizes 4–94) and seventeen case studies, conducted across twelve countries (1949–2024). Interventions included single-food exclusions, few-food diets, low-allergen meal replacements and fasting protocols. Reintroduction methods varied from a single-food challenge to multiple reintroductions, with five studies using blinded challenges. Outcome measures included physician- or participant-observed symptom changes, clinical assessments and laboratory measures, though these were heterogeneous. Findings reveal a lack of standardised protocols, dated methodologies and limited contemporary research. Controlled studies are needed to establish evidence-based protocols, investigate mechanisms, and guide dietary strategies as adjuncts to RA pharmacological treatment.

Rheumatoid arthritis (RA) is characterised by chronic inflammation in joints. Obesity, stress, being women and dietary pattern are important in pathogenesis. The joint damage in RA is accelerated by oxidative stress. The aim of this study was to examine the serum total antioxidant level, nutritional status and Mediterranean diet adherence of adult women with RA. Thirty-five adult women RA patients and thirty-five healthy control participated in this study (45·4 ± 11·61 and 42·5 ± 8·50 years, respectively). Nutritional status, physical activity levels and adherence to the Mediterranean diet were questioned. Physicians assessed the disease activity score of patients with RA. Serum total antioxidant and oxidant status were analysed. The serum total antioxidant status of the control group was higher, whereas the oxidative stress index and total oxidant status were lower than that of the RA group. Dietary protein, fibre, EPA, retinol, Fe, Zn and total antioxidant intake in the RA group were lower than in the control group (P < 0·05). Individuals with higher fibre intake showed a significantly lower risk for RA after adjusting for potential confounding factors (OR = 0·845, 95 % CI = 0·773–0·923, P < 0·001). The mean physical activity level of the control group was higher than that of the RA group (1·59 ± 0·10 and 1·53 ± 0·13, respectively) (P = 0·01). In conclusion, serum antioxidant parameters and dietary antioxidant intake are decreased in patients with RA. Therefore, medical treatment for these patients should be supplemented with medical nutrition therapy to achieve optimal nutritional status.

Rheumatoid arthritis (RA) is a prevalent autoimmune disease, and there is growing evidence suggesting a potential correlation between dietary factors and the pathogenesis of this condition. In order to investigate the causal relationship between diet and RA, we conducted a two-sample Mendelian randomisation (MR) analysis to examine the causal associations between twenty-two dietary factors and RA. Summary data from genome-wide association studies (GWAS) of RA were obtained from large GWAS meta-analyses. GWAS summary data for twenty-two dietary factors were obtained from UK Biobank. Random-effects inverse variance weighted was used as the primary method for assessing causality, and analyses of heterogeneity and horizontal pleiotropy were performed to ensure the accuracy of the results. Research indicates a negative genetic causal relationship between cereal intake (OR = 0·64, 95 % CI: 0·41, 0·99, P = 0·048) and oily fish intake (OR = 0·70, 95 % CI: 0·52, 0·95, P = 0·020) with the risk of RA. Other dietary factors were not causally related to RA. Sensitivity analysis shows that our results are reliable. This study provides genetic evidence suggesting that cereal intake and oily fish intake are protective factors for RA, indicating that RA patients and individuals at high risk should make appropriate dietary adjustments.

Sjögren's syndrome (SS) is a chronic autoimmune disease caused by immune system disorders. The main clinical manifestations of SS are dry mouth and eyes caused by the destruction of exocrine glands, such as the salivary and lacrimal glands, and systemic manifestations, such as interstitial pneumonia, interstitial nephritis and vasculitis. The pathogenesis of this condition is complex. However, this has not been fully elucidated. Treatment mainly consists of glucocorticoids, disease-modifying antirheumatic drugs and biological agents, which can only control inflammation but not repair the tissue. Therefore, identifying methods to regulate immune disorders and repair damaged tissues is imperative. Cell therapy involves the transplantation of autologous or allogeneic normal or bioengineered cells into the body of a patient to replace damaged cells or achieve a stronger immunomodulatory capacity to cure diseases, mainly including stem cell therapy and immune cell therapy. Cell therapy can reduce inflammation, relieve symptoms and promote tissue repair and regeneration of exocrine glands such as the salivary glands. It has broad application prospects and may become a new treatment strategy for patients with SS. However, there are various challenges in cell preparation, culture, storage and transportation. This article reviews the research status and prospects of cell therapies for SS.

An anti-inflammatory diet is characterised by incorporating foods with potential anti-inflammatory properties, including fruits, vegetables, whole grains, nuts, legumes, spices, herbs and plant-based protein. Concurrently, pro-inflammatory red and processed meat, refined carbohydrates and saturated fats are limited. This article explores the effects of an anti-inflammatory diet on non-communicable diseases (NCD), concentrating on the underlying mechanisms that connect systemic chronic inflammation, dietary choices and disease outcomes. Chronic inflammation is a pivotal contributor to the initiation and progression of NCD. This review provides an overview of the intricate pathways through which chronic inflammation influences the pathogenesis of conditions including obesity, type II diabetes mellitus, CVD, autoinflammatory diseases, cancer and cognitive disorders. Through a comprehensive synthesis of existing research, we aim to identify some bioactive compounds present in foods deemed anti-inflammatory, explore their capacity to modulate inflammatory pathways and, consequently, to prevent or manage NCD. The findings demonstrated herein contribute to an understanding of the interplay between nutrition, inflammation and chronic diseases, paving a way for future dietary recommendations and research regarding preventive or therapeutic strategies.

Immunity activation and inflammation are the main characteristics of rheumatoid arthritis and clonal hematopoiesis. However, it remains unclear whether rheumatoid arthritis increase the risk of clonal hematopoiesis. Here, a Mendelian randomization (MR) analysis was conduct to explore the causal effects of rheumatoid arthritis on clonal hematopoiesis. Summary statistics data of rheumatoid arthritis (13,838 cases and 33,742 controls) and clonal hematopoiesis (10,203 cases and 173,918 controls) derived from a genomewide association study were selected to analyze. We selected inverse-variance weighted, MR-Egger, weighted median, simple mode, and weighted mode to evaluate the causal effect of rheumatoid arthritis on clonal hematopoiesis. The two-sample MR analysis suggested a strong causal relationship between rheumatoid arthritis and clonal hematopoiesis by inverse-variance weighted (OR = 1.002311673, 95% CI [1.000110757, 1.004517433], p = .039706) and weighted median (OR = 1.002311673, 95% CI [1.000110757, 1.004517433], p = .039518447) methods. No significant pleiotropy or heterogeneity was found in the sensitivity analysis. These results supported a potentially causal relationship between rheumatoid arthritis and clonal hematopoiesis, and the exposure of rheumatoid arthritis increased the risks of clonal hematopoiesis. Our findings highlight the importance of how chronic inflammation and immune activation induced rheumatoid arthritis enhances the risks of clonal hematopoiesis, and that early intervention with rheumatoid arthritis patients might reduce the clonal hematopoiesis risks in rheumatoid arthritis patients. Moreover, our study provides clues for prediction of risk factors and potential mechanisms of clonal hematopoiesis.

Autoimmune diseases are pathological autoimmune reactions in the body caused by various factors, which can lead to tissue damage and organ dysfunction. They can be divided into organ-specific and systemic autoimmune diseases. These diseases usually involve various body systems, including the blood, muscles, bones, joints and soft tissues. The transient receptor potential (TRP) and PIEZO receptors, which resulted in David Julius and Ardem Patapoutian winning the Nobel Prize in Physiology or Medicine in 2021, attracted people's attention. Most current studies on TRP and PIEZO receptors in autoimmune diseases have been carried out on animal model, only few clinical studies have been conducted. Therefore, this study aimed to review existing studies on TRP and PIEZO to understand the roles of these receptors in autoimmune diseases, which may help elucidate novel treatment strategies.

This study was designed to assess the relationship between dietary insulin index (DII) and dietary insulin load (DIL) and rheumatoid arthritis (RA) risk in a case–control study. This study enrolled ninety-five newly diagnosed RA patients and 200 age- and sex-matched healthy controls. Dietary intakes were assessed using a validated 168-item semi-quantitative FFQ. DII and DIL were calculated using food insulin index values from previously published data. In the unadjusted model, individuals in the highest DIL tertile had the significantly higher odds of RA than those in the lowest tertile of the DIL scores (OR = 1·32, 95 % CI (1·15, 1·78), Pfor trend = 0·009). After adjusting for confounders, the risk of RA was 2·73 times higher for participants in the highest tertile of DIL than for those in the lowest tertile (OR = 2·73, 95 % CI (1·22, 3·95), Pfor trend < 0·001). In addition, patients in the highest DII tertile had higher risk of RA than those in the first tertile (OR = 2·22, 95 % CI (1·48, 3·95), Pfor trend = 0·008). This association persisted after adjusting for potential confounders (OR = 3·75, 95 % CI (3·18, 6·78), Pfor trend = 0·002). Our findings suggest that diets high in DII and DIL may increase the risk of developing RA, independent of other potential confounders. These findings can be verified by more research, particularly with a prospective design.

Emerging evidence suggests that preterm-born individuals (<37 weeks gestation) are at increased risk of developing chronic health conditions in adulthood. This study compared the prevalence, co-occurrence, and cumulative prevalence of three female predominant chronic health conditions – hypertension, rheumatoid arthritis [RA], and hypothyroidism – alone and concurrently. Of 82,514 U.S. women aged 50–79 years enrolled in the Women’s Health Initiative, 2,303 self-reported being born preterm. Logistic regression was used to analyze the prevalence of each condition at enrollment with birth status (preterm, full term). Multinomial logistic regression models analyzed the association between birth status and each condition alone and concurrently. Outcome variables using the 3 conditions were created to give 8 categories ranging from no disease, each condition alone, two-way combinations, to having all three conditions. The models adjusted for age, race/ethnicity, and sociodemographic, lifestyle, and other health-related risk factors. Women born preterm were significantly more likely to have any one or a combination of the selected conditions. In fully adjusted models for individual conditions, the adjusted odds ratios (aORs) were 1.14 (95% CI, 1.04, 1.26) for hypertension, 1.28 (1.12, 1.47) for RA, and 1.12 (1.01, 1.24) for hypothyroidism. Hypothyroidism and RA were the strongest coexisting conditions [aOR 1.69, 95% CI (1.14, 2.51)], followed by hypertension and RA [aOR 1.48, 95% CI (1.20, 1.82)]. The aOR for all three conditions was 1.69 (1.22, 2.35). Perinatal history is pertinent across the life course. Preventive measures and early identification of risk factors and disease in preterm-born individuals are essential to mitigating adverse health outcomes in adulthood.

Rheumatoid arthritis (RA) is a heterogeneous autoimmune disorder that leads to severe joint deformities, negatively affecting the patient's quality of life. Extracellular vesicles (EVs), which include exosomes and ectosomes, act as intercellular communication mediators in several physiological and pathological processes in various diseases including RA. In contrast, EVs secreted by mesenchymal stem cells perform an immunomodulatory function and stimulate cartilage repair, showing promising therapeutic results in animal models of RA. EVs from other sources, including dendritic cells, neutrophils and myeloid-derived suppressor cells, also influence the biological function of immune and joint cells. This review describes the role of EVs in the pathogenesis of RA and presents evidence supporting future studies on the therapeutic potential of EVs from different sources. This information will contribute to a better understanding of RA development, as well as a starting point for exploring cell-free-based therapies for RA.