Pain experienced during functional activities, referred to as movement-evoked pain (MEP), is a common and disabling symptom in individuals with knee osteoarthritis (KOA). Unlike pain at rest, MEP may better reflect the real-life burden of KOA and is increasingly recognised as a core outcome in musculoskeletal pain trials. However, its clinical utility remains limited by a lack of evidence on its measurement properties. This study aims to evaluate the test-retest reliability and validity of MEP assessments during functional tasks in individuals with KOA.

Most high-tech drugs and tissue engineering products based on human chondrocytes currently available on the market are aimed at restoring traumatic damage to cartilage tissue. However, in the presence of inflammation, their regenerative potential is significantly reduced, which limits their use in patients with osteoarthritis-one of the most common degenerative and inflammatory joint pathologies. The central element of the pathogenesis of osteoarthritis is inflammation-not classical acute inflammation, but rather chronic low-grade inflammation, primarily mediated by mechanisms of the innate immune response. Therefore, a key challenge is to enhance the anti-inflammatory effectiveness of cell-based drugs to broaden their indications to include degenerative diseases such as osteoarthritis and arthrosis. In recent years, cell-based drugs using stem cells, including mesenchymal stem cells (MSCs), hematopoietic stem cells (HSCs), and stromal vascular fraction (SVF) cells, have been actively studied. Despite their confirmed safety in inflammatory processes, meta-analyses of clinical trials show limited effectiveness in improving symptoms and MRI data in the treatment of osteoarthritis. A promising direction appears to be the development of combined cell-based drugs that combine MSCs with M2-polarized macrophages; however, data on their clinical effectiveness are still insufficient. This review explores key cellular effectors of inflammation and its molecular mechanisms, potential strategies for creating tissue engineering products that possess not only regenerative but also pronounced anti-inflammatory effects. The development of such products will expand their application in the treatment of inflammatory-degenerative joint diseases.

Periodontitis (PD) and rheumatoid arthritis (RA) are chronic inflammatory disorders that impose substantial individual and societal burdens worldwide. PD is characterized by progressive destruction of the periodontal ligament and alveolar bone, leading to tooth loss, impaired oral function, and sustained systemic inflammatory burden. RA, affecting approximately 0.5-1% of the population, is a chronic autoimmune disease marked by persistent synovial inflammation, progressive joint destruction, disability, and reduced quality of life. Increasing evidence indicates that these conditions are biologically and clinically interconnected. Both diseases share key pathogenic pathways, including microbial dysbiosis, immune dysregulation, chronic inflammation, genetic susceptibility, and aberrant autoantibody responses. Particular attention has focused on keystone periodontal pathogens such as Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, which may promote protein citrullination and the formation of anti-citrullinated protein antibodies (ACPA), thereby providing a plausible mechanistic bridge between periodontal infection and systemic autoimmunity. Shared genetic risk factors, including HLA-DRB1 susceptibility alleles, further support a common host predisposition. Clinical, epidemiological, and translational studies increasingly support a bidirectional association. Individuals with PD appear to have a higher risk of RA development, whereas patients with RA demonstrate greater prevalence, severity, and progression of periodontal disease. Interventional studies suggest that nonsurgical periodontal therapy may reduce local periodontal inflammation, circulating inflammatory biomarkers, and RA disease activity indices, while effective pharmacological control of RA may also improve periodontal outcomes. This narrative review critically evaluates the PD-RA relationship across four interconnected domains: (i) epidemiological and clinical associations between PD and RA, (ii) key mechanisms underlying RA pathogenesis, (iii) shared biological pathways linking both diseases, and (iv) the extent to which treatment of one condition influences the other. Particular emphasis is placed on major sources of heterogeneity and confounding-including smoking, metabolic comorbidities, disease stage, therapeutic exposure, and variable diagnostic definitions-that may explain inconsistencies across the literature. By integrating current mechanistic and clinical evidence, this review provides a structured synthesis that extends beyond a descriptive overview of association studies. A clearer understanding of the periodontal-rheumatologic axis may facilitate risk stratification, identify novel therapeutic targets, and support integrated multidisciplinary care. Targeting both oral and systemic inflammation may improve outcomes in patients with coexisting PD and RA and may potentially reduce the risk or severity of one condition in individuals already affected by the other.

Trapeziometacarpal osteoarthritis (TMO) is among the most prevalent forms of upper extremity osteoarthritis. It is frequently associated with significant levels of pain and disability, particularly among ageing women. The typical care pathway for TMO relies on non-surgical approaches for up to 2 years, before surgery is considered. One of the most common non-surgical approaches is an intra-articular cortisone injection. However, these are not universally recommended due to their safety profile and unclear efficacy compared with saline injections. Recent evidence suggests that saline might be non-inferior to cortisone, but this remains to be clarified. This pilot trial aims to assess the feasibility of a trial examining the non-inferiority of saline compared with cortisone injections for TMO.

Spondyloarthritis (SpA) is a complex inflammatory disease involving multiple cytokine pathways, including tumor necrosis factor-α (TNF-α) and Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling. Despite advances in biologic and targeted synthetic therapies, up to 40% of patients with SpA remain refractory to monotherapy. This case series from a tertiary care center in India evaluated the efficacy and safety of dual-targeted therapy (DTT) combining tofacitinib, a JAK inhibitor, with TNF inhibitors in four patients with refractory SpA and psoriatic arthritis (PsA). All four patients had longstanding disease (mean duration 11.5 years) and had failed at least one prior biologic. Case 1 (PsA): Long-standing disease (24 years) failed optimized adalimumab; following DTT, disease activity in psoriatic arthritis (DAPSA) score improved from high disease activity (36) to low disease activity (8). Case 2 (SpA): Refractory to two TNF inhibitors; after adding tofacitinib, the Ankylosing Spondylitis Disease Activity Score incorporating C-reactive protein (ASDAS-CRP) score improved from very high activity (3.7) to low disease activity (1.7). Case 3 (SpA): Presented with very high ASDAS-CRP (3.8); rapid clinical response and laboratory remission (ASDAS-CRP, 1.6) were achieved within months of starting DTT. Case 4 (SpA): Failed adalimumab monotherapy; the addition of tofacitinib led to an improvement in ASDAS-CRP from 3.5 to 1.7. No serious adverse events or significant laboratory abnormalities were observed over 5-18 months. DTT combines extracellular TNF-α blockade with intracellular JAK-STAT inhibition. This addresses the pathway redundancy and compensatory mechanisms in refractory SpA. Our findings add to the emerging real-world evidence supporting DTT therapy as a promising option for patients with refractory SpA. Our real-world findings demonstrate improved disease control and safety when monotherapy fails. Future prospective studies are essential to optimize the selection, dosing, and long-term safety of DTT.

This study aimed to develop a brucine (Bru) hydrogel-forming microneedle (Bru-HFM) delivery system that could achieve long-term, programmed drug release, through adjusting degree of cross-linking in polyvinyl alcohol (PVA)/carbomer 934P (CP) hydrogel. A one-way orthogonal experiment and a Franz diffusion cell were employed to optimize the preparation process. The resulting Bru-HFM exhibited favorable appearance, mechanical strength, and swelling properties. The drug release performance of the different drug-carrying sites of HFMs was compared. The results illustrated that in vivo drug release rate over 144 h was significantly higher in the needle body-carrying group (95.32%) than in the whole-microneedle (51.85%) and back-lining groups (57.39%). The amount of residue in the back-lining group was obvious, in line with expectations. The burst release rate of 78.81% could meet the high-dose demand during the acute phase of inflammation, whereas continuous release through the cross-linking network over 48-144 h achieved a total release rate of 95.32%. This covered the maintenance phase of chronic inflammation treatment, and the microneedles remained structurally intact at the end of drug release, permitting their detachable. The general pharmacodynamic evaluation results demonstrated that the pathological state of the ankle joints of rats with collagen-induced arthritis was significantly improved in the needle body-carrying group, which also exhibited significantly reduced serum levels of IL-6, IL-17, and TNF-α (all P < 0.05), indicating a significant therapeutic effect on rheumatoid arthritis. This study provides a new strategy and theoretical basis for designing HFMs for programmed drug release and inflammatory disease treatment.

Sacroiliac joint (SIJ) anatomical variants are common on MRI and may complicate interpretation by mimicking inflammatory sacroiliitis; however, their relationship with inflammatory back pain (IBP)-like symptom patterns is not well defined in patients without axial spondyloarthritis (axSpA). To characterize inflammatory back pain (IBP)-like symptom patterns and accompanying MRI findings that may mimic sacroiliitis in patients with chronic low back pain (CLBP) and sacroiliac joint (SIJ) anatomical variants who did not fulfill classification criteria for axial spondyloarthritis (axSpA). In this cross-sectional study, consecutive patients younger than 45 years at the time of SIJ MRI/clinical evaluation, with chronic low back pain lasting at least 3 months, who underwent SIJ MRI between September 2023 and September 2025 were retrospectively screened for predefined SIJ anatomical variants and lumbosacral transitional anomalies. Patients with lumbosacral transitional anomalies were excluded at the screening stage. Those with at least one SIJ anatomical variant were invited for a standardized clinical assessment in which IBP features were captured using a single questionnaire covering the Calin, Rudwaleit (Berlin), and ASAS IBP criteria. All participants were systematically assessed against the ASAS classification criteria for axial spondyloarthritis (axSpA), and those who fulfilled these criteria were excluded from the final analysis. SIJ MRIs were read independently by two radiologists blinded to clinical data; agreement for variant detection was almost perfect (κ = 0.90). Bone marrow edema (BME) was evaluated according to the ASAS/OMERACT definition of MRI findings highly suggestive of active sacroiliitis, and structural changes were also recorded. Of 260 screened patients with CLBP, SIJ anatomical variants were identified in 108/260 (41.5%). After exclusions (n = 20), 88 patients were included in the final analysis; 75/88 (85.2%) were female, with a median age of 36 years (Q1-Q3: 28-39) and a median symptom duration of 3.0 years (Q1-Q3: 1.6-9.8). IBP positivity varied by criteria set: 51.1% (Calin), 34.1% (Berlin), and 27.3% (ASAS). Variants were predominantly bilateral (76/88, 86.4%). Among 98 recorded variant findings, accessory joint (n = 27) and iliosacral complex (n = 25) were the most frequent. ASAS/OMERACT-positive BME was present in 10/88 patients (11.4%); structural lesions included sclerosis in 22/88 (25.0%), erosions in 7/88 (8.0%), and fat metaplasia in 5/88 (5.7%). HLA-B27 positivity was observed in 4/69 tested patients (5.8%), and median CRP was 3.2 mg/L (Q1-Q3: 1.0-7.0). In a non-axSpA, variant-positive cohort, IBP-like symptom patterns were common, whereas ASAS/OMERACT-positive BME was infrequent. SIJ variants may therefore complicate clinical judgment because of symptom overlap in young patients within the typical age range for axSpA onset. Although infrequent, imaging features that mimic inflammatory disease highlight the need for careful clinical correlation to avoid misclassification as axSpA.

Rheumatoid arthritis (RA) is a chronic, inflammatory autoimmune disease characterized by progressive joint involvement. The disease is associated with reduced health-related quality of life, functional ability, work productivity, and daily activity, in addition to pain, fatigue, and inflammation-induced structural damage. RA emerges through a complex interplay of multiple factors, including the release of inflammatory cytokines. One such cytokine is tumor necrosis factor (TNF), which is inhibited by golimumab, an approved treatment for the disease. Golimumab is produced using a recombinant cell line that originated from genetically modified mice immunized with human TNF. This narrative review presents the efficacy and safety outcomes from the golimumab pivotal randomized controlled trials (RCTs) that evaluated the subcutaneous and intravenous formulations. Across the RCTs, treatment was associated with an American College of Rheumatology ≥ 20% improvement. A majority of participants reported at least one AE and the most frequent were upper respiratory infection, nasopharyngitis, and bronchitis. The review also presents data from post hoc analyses and real-world studies, which demonstrated benefits that included improvements in health-related quality of life and daily productivity, prolonged drug survival, and reduced fatigue, pain, disease activity, and structural damage. Lastly, data from meta-analyses, including RCTs and real-world studies, demonstrated that golimumab had an adverse event pattern similar to other TNF inhibitors. Collectively, these studies demonstrated that golimumab is an effective and safe treatment for RA when used according to the approved indication.