ECM2028, 12-14 June 2028, Copenhagen, DenmarkFibroblast Activity and Tissue Destruction in Rheumatology: Understanding Tissue Activity and Its Implications for Drug Development
Fibrogenesis, fibroblast activity and tissue destruction and its relevance in autoimmunity, PsA, RA, SSc and lupus
September 30, 2026
The body continuously regenerates, which inherently means that tissue is constantly being broken down and formed. In rheumatic diseases we usually focus on inflammation and immune activity, but inflammation is what starts the process, not what causes the lasting harm. The damage comes when that balance tips, fibroblasts become activated, and cartilage, bone, and connective tissue are broken down faster than the body can repair them.
Join us to explore how evaluating tissue activity reveals what is actively happening in the disease biology, whether a treatment is truly working, and how these insights can support the development of better therapies in autoimmunity, PsA, RA, SSc and lupus.
Agenda
- Welcome and introduction
- Fibroid and synovial pathotypes in rheumatoid arthritis
- Tissue destruction and regulation of fibrogenesis in rheumatology
- And more!
- Questions from the chat
Scientific topics
Rheumatic diseases are commonly viewed through the lens of inflammation and immune activity. However, inflammation represents only part of the underlying disease biology. Fibroblast activation, extracellular matrix remodeling, and ongoing tissue destruction can provide complementary information about what is happening within affected tissues and how disease activity changes during treatment.
In psoriatic arthritis, tissue turnover biomarkers offer a way to investigate structural and connective tissue activity alongside traditional measures of inflammation. Understanding these processes may help distinguish different aspects of disease activity, monitor the biological effects of treatment, and provide additional insight into therapeutic response.
Rheumatoid arthritis is likewise characterized by substantial heterogeneity within the synovium. Distinct synovial pathotypes, including fibroblast-rich or fibroid phenotypes, point to disease mechanisms that may not be adequately described by inflammatory activity alone. Emerging research into fibroblast states, synovial organization, and the regulation of fibrogenesis is therefore changing how we understand persistent disease and differences in treatment response.
Across systemic sclerosis, lupus, and autoimmunity more broadly, the same principle applies. Many different disease pathways end up driving the same core process: the breakdown and rebuilding of tissue. This means disease activity can be understood as the balance between how much tissue is being destroyed and how much is being formed. The protein fragments released when tissue breaks down give us the most direct way to measure that balance.
By bringing together perspectives on biomarkers, synovial pathobiology, and fibrogenesis, this webinar will examine how measuring tissue activity—not only inflammation—could improve patient characterization, pharmacodynamic assessment, and ultimately drug development in rheumatology.
Registration is freeSpeaker information coming soon!
The ECM Pharmacology Symposium Series is a close collaboration with our industry sponsor Nordic Bioscience.
