Synovial hyperplasia (an increase in cell number) is a typical feature of the autoimmune disease called rheumatoid arthritis (RA). During the progression of this disease the synovial membrane becomes a place where constant inflammatory processes take place, which can eventually lead to cartilage damage and joint destruction and deformation. Due to the changes in proliferative and apoptotic processes the total number of cells increases in the synovium, and significantly increases also the number of fibroblast-like synoviocytes  . These cells, together with other immune cells such as macrophages, lymphocytes, neutrophils, mast cells, dendritic cells and platelets, create an inflammatory environment in the synovium, attract more immune cells to the damaged place and thus contribute to the joint destruction. Fibroblast-like synoviocytes that are present in the synovium during rheumatoid arthritis display altered phenotype compared to the cells present in normal tissues. They lose the property called contact inhibition (cells arrest their growth in the case when more cells come into contact with each other), and they also lose the growth dependency on adhesive surfaces; both these phenomena contribute to the increase in the number of fibroblast-like synoviocytes in the inflammatory tissue and are also typical for example for the growth of cancerous cells. In addition, these cells can produce a number of pro-inflammatory signalling molecules, especially Il-6 and IL-8, prostanoids and matrix metalloproteinases (MMPs), which may directly affect other cells and also participate in the inflammation enhancement. These processes are influenced by microvesicles derived from platelets, which can contribute to the activation of fibroblast-like synoviocytes through secretion of IL-1   .
Synovial hyperplasia (an increase in cell number) is a typical feature of the autoimmune disease called rheumatoid arthritis (RA). During the progression of this disease the synovial membrane becomes a place where constant inflammatory processes take place, which can eventually lead to cartilage damage and joint destruction and deformation. Due to the changes in proliferative and apoptotic processes the total number of cells increases in the synovium, and significantly increases also the number of fibroblast-like synoviocytes (FLS) . These cells, together with other immune cells such as macrophages, lymphocytes, neutrophils, mast cells, dendritic cells and platelets, create an inflammatory environment in the synovium, attract more immune cells to the damaged place and thus contribute to the joint destruction. FLS that are present in the synovium during RA display altered phenotype compared to the cells present in normal tissues. They lose the property called contact inhibition (cells arrest their growth in the case when more cells come into contact with each other), and they also lose the growth dependency on adhesive surfaces; both these phenomena contribute to the increase in the number of FLS in the inflammatory tissue and are also typical for example for the growth of cancerous cells. In addition, these cells can produce a number of pro-inflammatory signalling molecules, especially Il-6 and IL-8, prostanoids and matrix metalloproteinases (MMPs), which may directly affect other cells and also participate in the inflammation enhancement. These processes are influenced by microvesicles derived from platelets, which can contribute to the activation of fibroblast-like synoviocytes through secretion of IL-1 . The aggressive phenotype of FLS in RA and the effect these cells have on their microenvironment can be summarized into hallmarks that distinguish them from healthy FLS. These hallmark features of FLS in RA are divided into 7 cell-intrinsic hallmarks and 4 cell-extrinsic hallmarks. The cell-intrinsic hallmarks are: reduced apoptosis, impaired contact inhibition, increased migratory invasive potential, changed epigenetic landscape, temporal and spatial heterogeneity, genomic instability and mutations, and reprogrammed cellular metabolism. The cell-extrinsic hallmarks of FLS in RA are: promotes osteoclastogenesis and bone erosion, contributes to cartilage degradation, induces synovial angiogenesis, and recruites and stimulates immune cells .
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Fibroblast-like synoviocytes
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rheumatoid arthritis
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fibroblast-like synoviocytes
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The aggressive phenotype of FLS in RA and the effect these cells have on their microenvironment can be summarized into hallmarks that distinguish them from healthy FLS. These hallmark features of FLS in RA are divided into 7 cell-intrinsic hallmarks and 4 cell-extrinsic hallmarks. The cell-intrinsic hallmarks are: reduced apoptosis, impaired contact inhibition, increased migratory invasive potential, changed epigenetic landscape, temporal and spatial heterogeneity, genomic instability and mutations, and reprogrammed cellular metabolism. The cell-extrinsic hallmarks of FLS in RA are: promotes osteoclastogenesis and bone erosion, contributes to cartilage degradation, induces synovial angiogenesis, and recruites and stimulates immune cells