The emerging role of fibroblast-like synoviocytes-mediated synovitis in osteoarthritis: An update

Osteoarthritis (OA), the most ubiquitous degenerative disease affecting the entire joint, is characterized by cartilage degradation and synovial inflammation. Although the pathogenesis of OA remains poorly understood, synovial inflammation is known to play an important role in OA development. However, studies on OA pathophysiology have focused more on cartilage degeneration and osteophytes, rather than on the inflamed and thickened synovium. Fibroblast-like synoviocytes (FLS) produce a series of pro-inflammatory regulators, such as inflammatory cytokines, nitric oxide (NO) and prostaglandin E₂ (PGE₂ ). These regulators are positively associated with the clinical symptoms of OA, such as inflammatory pain, joint swelling and disease development. A better understanding of the inflammatory immune response in OA-FLS could provide a novel approach to comprehensive treatment strategies for OA. Here, we have summarized recently published literatures referring to epigenetic modifications, activated signalling pathways and inflammation-associated factors that are involved in OA-FLS-mediated inflammation. In addition, the current related clinical trials and future perspectives were also summarized.