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Abstract
The synovium exercises its main function in joint homeostasis through the secretion of factors (such as lubricin and hyaluronic acid) that are critical for the joint lubrication and function. The main synovium cell components are fibroblast-like synoviocytes, mesenchymal stromal/stem cells and macrophage-like synovial cells. In the synovium, cells of mesenchymal origin modulate local inflammation and fibrosis, and interact with different fibroblast subtypes and with resident macrophages. In pathologic conditions, such as rheumatoid arthritis, fibroblast-like synoviocytes proliferate abnormally, recruit mesenchymal stem cells from subchondral bone marrow, and influence immune cell activity through epigenetic and metabolic adaptations. The resulting synovial hyperplasia leads to secondary cartilage destruction, joint swelling, and pain. In the present review, we summarize recent findings on the molecular signature and the roles of stromal cells during synovial pannus formation and rheumatoid arthritis progression.
Highlights
The joint synovial lining is a thin membrane divided into two anatomical and functional compartments: the surface layer and the sub-lining layer
It is a thin membrane of two to three cell layers composed of fibroblast-like synoviocytes (FLS) and macrophage-like synovial cells
Rheumatoid arthritis (RA) is an example of chronic disease that is primarily defined by joint synovial lining inflammation, resulting in subchondral bone and cartilage destruction
Summary
The joint synovial lining is a thin membrane divided into two anatomical and functional compartments: the surface layer (intima) and the sub-lining layer (subintima). The intima is a superficial layer of cells that produce lubricious synovial fluid in the intra-articular cavity. In healthy subjects, it is a thin membrane of two to three cell layers composed of fibroblast-like synoviocytes (FLS) and macrophage-like synovial cells. RA prevalence is 1–2% in Western countries It is a multifactor autoimmune disease characterized by the presence of autoantibodies and genetic susceptibility [1,2]. The B and T cells that infiltrate the inflamed RA synovium, where they form aggregates, are qualitatively and quantitatively heterogeneous. We will describe recent findings on synovium stromal cell heterogeneity during synovial pannus formation and RA progression
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