Abstract
Rheumatoid arthritis (RA) is an inflammatory disease characterized by a variety of symptoms and pathologies often presenting with polyarthritis. The primary symptom in the initial stage is joint swelling due to synovitis. With disease progression, cartilage and bone are affected to cause joint deformities. Advanced osteoarticular destruction and deformation can cause irreversible physical disabilities. Physical disabilities not only deteriorate patients’ quality of life but also have substantial medical economic effects on society. Therefore, prevention of the progression of osteoarticular destruction and deformation is an important task. Recent studies have progressively improved our understanding of the molecular mechanism by which synovitis caused by immune disorders results in activation of osteoclasts; activated osteoclasts in turn cause bone destruction and para-articular osteoporosis. In this paper, we review the mechanisms of bone metabolism under physiological and RA conditions, and we describe the effects of therapeutic intervention against RA on bone.
Highlights
Rheumatoid arthritis (RA) is a systemic autoimmune disease, occurring more commonly in women
The differentiation of osteoclast progenitors into osteoclasts is tightly regulated by osteoblasts [51] and osteocytes [41,42], which express RANKL and macrophage colony-stimulating factor (M-CSF) cytokines required for stimulating the differentiation of progenitor cells into osteoclasts
We reviewed bone metabolism under physiological and RA conditions, and described the effects of therapeutic intervention against RA on the bone
Summary
RA is a systemic autoimmune disease, occurring more commonly in women. It is prevalent in approximately 0.5–1% of the population [1–3]. The disease is characterized by persistent synovitis, which causes the destruction of cartilage and bone, and it eventually leads to the deformation of joints [4,5]. The goal of RA treatment is to achieve clinical, structural, and functional remission states. Even when pain and swelling are mitigated and clinical remission is achieved due to therapeutic intervention, the progression of articular destruction might still occur, resulting in functional deterioration in some cases. Recent studies have progressively improved our understanding of the molecular mechanism by which synovitis caused by immune disorders results in activation of osteoclasts; activated osteoclasts in turn cause bone destruction and para-articular osteoporosis. The molecular mechanisms of inflammatory cytokines on osteoblast differentiation have been studied, and their effects on bone metabolism are becoming clearer. Bone remodeling is controlled by osteoblasts, osteoclasts, and osteocytes [17,19–21] (Figure 1)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
