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Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation, local and systemic bone loss and a lack of compensatory bone repair. Fibroblast-like synoviocytes (FLS) are the most abundant cells of the stroma and a key population in autoimmune diseases such as RA. An increasing body of evidence suggests that these cells play not only an important role in chronic inflammation and synovial hyperplasia, but also impact bone remodelling. Under inflammatory conditions FLS release inflammatory cytokines, regulate bone destruction and formation and communicate with immune cells to control bone homeostasis. Other stromal cells, such as osteoblasts and terminally differentiated osteoblasts, termed osteocytes, are also involved in the regulation of bone homeostasis and are dysregulated during inflammation. This review highlights our current understanding of how stromal cells influence the balance between bone formation and bone destruction. Increasing our understanding of these processes is critical to enable the development of novel therapeutic strategies with which to treat bone loss in RA.

Original publication




Journal article


Clin Exp Immunol

Publication Date





1 - 11


RA, RA-FLS, bone remodelling, inflammatory cytokines, stromal cells, Arthritis, Rheumatoid, Bone Remodeling, Bone Resorption, Bone and Bones, Cytokines, Humans, Hyperplasia, Inflammation, Osteocytes, Stromal Cells, Synoviocytes, Wnt Signaling Pathway