In:
Osteologie, Georg Thieme Verlag KG, Vol. 30, No. 04 ( 2021-11), p. 304-310
Abstract:
Rheumatoid arthritis (RA) is an immune mediated inflammatory disease (IMID),
characterized by chronic inflammation and irreversible bone loss. Studies have shown that fibroblast-like synoviocytes (FLS), a key cell population in the
pathogenesis of RA, have an impact on balancing bone-forming osteoblasts and bone-destroying osteoclasts towards joint damage. Once activated, RA-FLS are
able to destroy cartilage and subchondral bone through the release of RANKL, members of the metalloproteinase family and many more cytokines, chemokines and
growth factors. Additionally, RA-FLS are responsible for the perpetuation and chronicity of the disease due the interaction with immune cells supporting the
influx of T and B lymphocytes, monocytes, macrophages neutrophils and dendritic cells from the blood stream into the inflamed synovial tissue. In this review we
highlight the direct and indirect impact of synovial fibroblasts in RA on joint damage and disease progression. Moreover, we describe mechanisms of synovitis
and regulators of bone homeostasis in further inflammatory joint diseases such as ankylosing spondylitis (AS) and psoriatic arthritis (PsA) and compare them to
RA.
Type of Medium:
Online Resource
ISSN:
1019-1291
,
2567-5818
Language:
English
Publisher:
Georg Thieme Verlag KG
Publication Date:
2021
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