Research progress on the effects and mechanisms of different cell types on osteoclast differentiation in bone metabolism in rheumatoid arthritis
Key Points
Osteoclast differentiation leads to bone metabolism imbalance in rheumatoid arthritis, impacting joint health.
Different cell types like T cells, B cells, and macrophages activate osteoclasts and disrupt bone homeostasis.
This research utilizes a systematic review approach to assess the influence of cell types on osteoclasts in RA.
Findings may guide precise treatments and interventions for bone metabolism disorders in RA patients.
Abstract
Rheumatoid arthritis is a systemic autoimmune disease characterized by chronic synovial inflammation, autoantibody production and progressive joint destruction. One of the main pathological features is irreversible damage and dysfunction of bone and joints, and the core pathological link is osteoclast-mediated imbalance of bone metabolism. With the advances in immunology, molecular biology and cytology, different types of cells, including T cells, B cells, macrophages, natural killer cells, synovial fibroblasts and vascular endothelial cells, activate osteoclasts in rheumatoid arthritis, leading to bone metabolism imbalance in RA and causing bone and joint damage. In this paper, we will systematically summarize the effects and mechanisms of different cell types on osteoclast differentiation in rheumatoid arthritis bone metabolism, which will provide theoretical basis and practical guidance for the precise treatment and targeted intervention of RA bone metabolism abnormalities.
Research progress on the effects and mechanisms of different cell types on osteoclast differentiation in bone metabolism in rheumatoid arthritis | Synapse
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Erratum for Research Article “Synovial fibroblast-neutrophil interactions promote pathogenic adaptive immunity in rheumatoid arthritis” by C. Carmona-Rivera, P. M. Carlucci, E. Moore, N. Lingampalli, H. Uchtenhagen, E. James, Y. Liu, K. L. Bicker, H. Wahamma, V. Hoffman, A. I. Catrina, P. Thompson, J. H. Buckner, W. H. Robinson, D. A. Fox, M. J. Kaplan2020 · 7 citations