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- W2110901553 endingPage "251" @default.
- W2110901553 startingPage "228" @default.
- W2110901553 abstract "Summary: Rheumatoid arthritis, juvenile idiopathic arthritis, the seronegative spondyloarthropathies including psoriatic arthritis, and systemic lupus erythematosus are all examples of rheumatic diseases in which inflammation is associated with skeletal pathology. Although some of the mechanisms of skeletal remodeling are shared among these diseases, each disease has a unique impact on articular bone or on the axial or appendicular skeleton. Studies in human disease and in animal models of arthritis have identified the osteoclast as the predominant cell type mediating bone loss in arthritis. Many of the cytokines and growth factors implicated in the inflammatory processes in rheumatic diseases have also been demonstrated to impact osteoclast differentiation and function either directly, by acting on cells of the osteoclast‐lineage, or indirectly, by acting on other cell types to modulate expression of the key osteoclastogenic factor receptor activator of nuclear factor (NF) κB ligand (RANKL) and/or its inhibitor osteoprotegerin (OPG). Further elucidation of the mechanisms responsible for inflammation‐induced bone loss will potentially lead to the identification of novel therapeutic strategies for the prevention of bone loss in these diseases. In this review, we provide an overview of the cell types, inflammatory mediators, and mechanisms that are implicated in bone loss and new bone formation in inflammatory joint diseases." @default.
- W2110901553 created "2016-06-24" @default.
- W2110901553 creator A5018214967 @default.
- W2110901553 creator A5024038808 @default.
- W2110901553 creator A5070137364 @default.
- W2110901553 creator A5080984126 @default.
- W2110901553 date "2005-11-22" @default.
- W2110901553 modified "2023-10-15" @default.
- W2110901553 title "Rheumatic diseases: the effects of inflammation on bone" @default.
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