Osteoarthritis (OA) is a degenerative joint disease marked by degradation of joint cartilage and synovial inflammatory infiltration. This study aims to evaluate serum miR-215-5p as a diagnostic biomarker for OA and to investigate its regulatory mechanism in IL-1β-induced chondrocytes. 110 OA patients and 105 healthy controls were recruited. Serum miR-215-5p and EREG expression were determined by quantitative reverse transcription polymerase chain reaction. The diagnostic value of miR-215-5p for OA was assessed using a receiver operating characteristic curve. C28/I2 chondrocytes were stimulated with IL‑1β to construct an OA cell model. Cell viability, migration ability, and inflammatory cytokine levels were evaluated via Cell Counting Kit-8, Transwell assay, and an enzyme-linked immunosorbent assay (ELISA). The association between miR-215-5p and EREG was validated using a dual-luciferase reporter assay and an RNA immunoprecipitation (RIP) assay. In OA patients, serum miR-215-5p was upregulated, while EREG was downregulated. MiR-215-5p exhibited good diagnostic performance for OA (area under the curve, AUC = 0.883). In interleukin-1β (IL-1β)-treated C28/I2 cells, inhibition of miR-215-5p enhanced cell viability and migration, and attenuated IL-1β, IL-6, and tumor necrosis factor-α (TNF-α) levels. EREG was confirmed to be a direct target of miR-215-5p. Knockdown of EREG partially reversed the promoting effect of miR-215-5p downregulation on the viability and migration capacity of IL-1β-treated C28/I2 cells and attenuated its inhibitory effect on inflammatory factors. miR-215-5p contributes to OA pathogenesis by regulating EREG and represents a promising diagnostic biomarker and potential therapeutic target for OA.

Precision diagnosis and molecular subtyping of arthritis call for analytical tools capable of providing objective, dynamic, and multiparametric readouts of disease progression and severity. Current clinical assessments mainly depend on symptom evaluation, imaging, and nonspecific biochemical indicators, lacking highly specific biomarkers and suffering from subjective interpretation and inconsistent multiparameter integration. To address this challenge, we designed a dual-nanozyme activity sensor array using metal-oxide-functionalized porphyrinic metal-organic frameworks (MOFs) for simultaneous and parallel multibiomarker detection and molecular classification of osteoarthritis (OA). Three types of metal oxide@PCN-224 nanomaterials with distinct metal centers were synthesized, and their peroxidase (POD)- and laccase (LAC)-mimicking activities were systematically investigated. Leveraging their differential dual-mimic activities, a multichannel sensing array for the simultaneous and discriminative detection of key OA-related biomarkers including C-reactive protein (CRP), hyaluronidase (HAase), matrix metalloproteinase-13 (MMP-13), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and interleukin-17 (IL-17) was constructed. Each biomarker interacts with the nanozymes to generate unique catalytic activity modulation "fingerprints" due to the difference in the nanozyme-biomarker interaction. Depending on their size, charge, and functional groups, biomarkers may undergo adsorption on the surface or alter the steric hindrance, local charge distribution, or interfacial electron transfer, leading to either inhibition or promotion of the activity of nanozymes. Integrated with pattern recognition algorithms, this sensing array not only addresses the specificity shortfall of single biomarker analysis but also achieves high-accuracy classification of synovial fluid samples from clinically staged OA patients (mild and serious). By integrating three materials with dual-enzyme activities, the sensor array can generate more diverse and distinguishable "fingerprint" signals, significantly improving classification accuracy and robustness. By correlating clinical staging and multifactor molecular fingerprints, this work offers an innovative integrated sensing strategy for the objective diagnosis, dynamic monitoring, and precise management of OA.

Adult-onset Still's disease (AOSD) is a rare systemic autoinflammatory disorder characterized by fever, rash, arthritis, and hyperferritinemia, often presenting as a diagnostic challenge due to its nonspecific manifestations. We report the case of a 35-year-old previously healthy male who presented with a 20-day history of pruritic erythematous skin lesions, high-grade fever, severe odynophagia, and symmetric inflammatory polyarthritis. Laboratory evaluation revealed leukocytosis with neutrophilia, elevated acute-phase reactants, liver enzyme abnormalities, and hyperferritinemia (1,050 ng/mL). Infectious, autoimmune, and neoplastic causes were excluded. During hospitalization, the patient developed chest pain with electrocardiographic changes and elevated troponin levels, consistent with acute pericarditis. Skin biopsy demonstrated nonspecific inflammatory dermatitis. A diagnosis of AOSD was established based on clinical findings and Yamaguchi criteria. Initial treatment with systemic corticosteroids resulted in partial improvement; however, early relapse required escalation to tocilizumab, achieving complete clinical remission at two months. This case highlights the importance of considering AOSD in patients with fever of unknown origin and elevated inflammatory markers, as well as the role of early targeted therapy in improving outcomes.