Multitargeted biological actions of polydatin in preventing pseudogout acute attack
Abstract format and assignment number: Oral presentation OP0131
Presenting author: F Oliviero (Italy)
Date: Thursday 12th June 2025, 10:30
Polydatin (PD), a polyphenol, prevents calcium pyrophosphate crystal-induced arthritis in mice by reducing inflammation, joint swelling and muscle damage. Using in vivo and in vitro models, the study shows PD modulates leukocyte migration, angiogenesis and cytokine production. Its anti-inflammatory effects are partly mediated through SIRT-1 activation and CCR-1 inhibition. These findings support PD as a promising candidate for treating crystal-induced arthropathies through multiple immunomodulatory mechanisms.
Development of allosteric activators of cystathionine γ-lyase (CSE) to augment hydrogen sulfide (H₂S) and inhibit pathologic cartilage calcification
Abstract format and assignment number: Oral presentation OP0127
Presenting author: S Nasi (Switzerland)
Date: Thursday 12th June 2025, 10:30
This study explores a novel therapeutic strategy for osteoarthritis by enhancing hydrogen sulfide (H₂S) production through CSE-positive allosteric modulators (CSE-PAMs). Using human and murine chondrocytes, CSE-PAMs significantly reduced calcium crystal deposition, oxidative stress, IL-6 secretion, and ALP activity—key drivers of cartilage calcification. These effects were dependent on CSE, as shown in knockout models. Transcriptomic analysis confirmed modulation of calcification-related genes. CSE-PAMs offer promising potential as disease-modifying agents in osteoarthritis by targeting pathological cartilage calcification through H₂S-mediated mechanisms.
Experimental study of targeting PAD4 to inhibit the formation of neutrophil extracellular trap network for the treatment of gout
Abstract format and assignment number: Oral presentation OP0130
Presenting author: Y Wang (China)
Date: Thursday 12th June 2025, 10:30
NETs, regulated by PAD4, play dual roles in gout inflammation. Using single-cell transcriptomics, this study identified PADI4 as a key gene in neutrophils from gout patients. A gout mouse model was treated with PAD4 inhibitors, reducing NET formation and joint inflammation. MSU crystals dose-dependently induced NETs, with gout patients’ neutrophils showing heightened NET response. PAD4 targeting may offer a novel therapeutic strategy for gout by modulating inflammatory NET activity.
A multimodal dissection of spatial tissue niches associated with severity in childhood arthritis
Abstract format and assignment number: Oral presentation OP0252
Presenting author: C Bolton (UK)
Date: Friday 13th June 2025, 10:30
To investigate the cellular mechanisms driving juvenile idiopathic arthritis (JIA), synovial tissue from early-stage patients was analysed using single-cell RNA sequencing, spatial transcriptomics and multiplexed immunofluorescence. The study identified spatial niches of inflammatory cells associated with disease severity, notably SPP1+ macrophages and fibrin-associated myeloid cells. While some pathogenic mechanisms were shared with adult arthritis, JIA tissue displayed unique features, including greater vascularity and TGFβ-activated stromal cells. These findings highlight age-specific inflammatory pathways and support precision therapies tailored to paediatric arthritis.
A cutting-edge three-dimensional stromal-immune microenvironment emulates interactions between synovial fibroblasts and macrophages in inflammatory arthropathies
Abstract format and assignment number: Oral presentation OP0251
Presenting author: S Giaglis (Switzerland)
Date: Friday 13th June 2025, 10:30
This study developed and validated a 3D human synovial organoid model using patient-derived cells to better replicate joint inflammation in arthritis. Traditional models fail to capture the complexity of the synovium and predict individual treatment responses. By combining synovial fibroblasts and macrophages into scaffold-free 3D structures, the model mimics native tissue interactions. Cytokine-driven inflammatory responses were confirmed, offering a scalable, reproducible tool for personalized therapeutic testing and addressing the limitations of current 2D in vitro and animal models.
ABCC6-deficient mice as a spontaneous model of osteoarthritis (OA) and calcific tendinopathy (CT)
Abstract format and assignment number: Poster POS1287
Presenting author: E Faure (Switzerland)
Date: Saturday 14th June 2025, 09:00
This study evaluated ABCC6-deficient mice as a model of joint and tendon calcification. Compared to wild-type, ABCC6-/- mice showed significantly increased crystal deposition in knee joints from 16 to 43 weeks, with associated cartilage degradation and synovial inflammation at 43 weeks. Achilles tendon calcification was also significantly higher. However, no changes in tibial subchondral bone parameters were observed. These findings support ABCC6-deficient mice as a spontaneous model of joint and tendon calcification resembling osteoarthritis and calcific tendinopathy.
Alejandro Gómez-Gómez
Alejandro is a rheumatologist at Hospital Vall d’Hebron in Barcelona. His research focuses on Sjögren’s disease and other immune-mediated diseases using multi-omics approaches. He is also interested in studying inflammatory uveitis and recently obtained his PhD with a thesis on the immunosuppressive treatment of non-infectious uveitis. He is a member of the Spanish Society of Rheumatology and the EMEUNET Visibility & Global Affairs Sub-committee.