Abstract
Purpose: Arthritis is the leading cause of years lived with disability for millions of people worldwide. Osteoarthritis (OA) and rheumatoid arthritis (RA) are the most prevalent forms of arthritis. Among these inflammatory joint diseases, fibroblast-like synoviocytes (FLS), which maintain the structural and dynamic integrity of joints physiologically, have been identified as key drivers of cartilage degradation. FLS can be divided into two major populations: THY1- and THY1+ FLS. The destructive phenotype which is restricted to the THY1- FLS of the synovial lining stimulates osteoclastogenesis via RANKL secretion, thereby promoting bone erosion, while THY1+ FLS of the sublining layer are classified as invasive cells with immune effector function driving synovitis.
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