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Bone erosion in rheumatoid arthritis: mechanisms, diagnosis and treatment
Open accessAbstract
Bone erosion is a central feature of rheumatoid arthritis and is associated with disease severity and poor functional outcome. Erosion of periarticular cortical bone, the typical feature observed on plain radiographs in patients with rheumatoid arthritis, results from excessive local bone resorption and inadequate bone formation. The main triggers of articular bone erosion are synovitis, including the production of proinflammatory cytokines and receptor activator of nuclear factor κB ligand (RANKL), as well as antibodies directed against citrullinated proteins. Indeed, both cytokines and autoantibodies stimulate the differentiation of bone-resorbing osteoclasts, thereby stimulating local bone resorption. Although current antirheumatic therapy inhibits both bone erosion and inflammation, repair of existing bone lesions, albeit physiologically feasible, occurs rarely. Lack of repair is due, at least in part, to active suppression of bone formation by proinflammatory cytokines. This Review summarizes the substantial progress that has been made in understanding the pathophysiology of bone erosions and discusses the improvements in the diagnosis, monitoring and treatment of such lesions.
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“TNF-α can also indirectly increase RANKL expression and affect osteoclast differentiation by activating osteoblasts, B cells, and T cells [88].”
From Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literature (2024) · cites this paper as [88]
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“RANKL-dependent pathways activated by pro-inflammatory cytokines can induce osteoclast formation, therefore, enhancing osteoclast activity [87, 88].”
From Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literature (2024) · cites this paper as [88]
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Self-citation
Metadata
- Authors
- Schett, G., & Gravallese, E.
- Affiliations
- Friedrich-Alexander-Universität Erlangen-Nürnberg (DE)
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Schett, Georg
- Venue
- Nature Reviews Rheumatology
- Published
- 2012-09-25
- Volume
- 8
- Issue
- 11
- Pages
- 656-664
- ISSN
- 1759-4790 (ISSN-L)
- 1759-4804
- PMC
- PMC4096779
- OpenAlex
- W2032362610
- Cited by
- 947
- References
- 124
- Citations by year
- 2026: 72 · 2025: 72 · 2024: 89 · 2023: 75 · 2022: 82 · 2021: 89 · 2020: 80 · 2019: 75 · 2018: 73 · 2017: 74 · 2016: 53 · 2015: 52 · 2014: 35 · 2013: 26
- FWCI
- 5.39
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Rheumatology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- Funders
- American College of Rheumatology Research and Education Foundation
- Rheumatology Research Foundation
- European Commission
- Deutsche Forschungsgemeinschaft
- Bundesministerium für Bildung und Forschung
- National Institutes of Health (5r01ar055952-05)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01-AR055952)
- Topics
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Keywords
- bone erosion, rheumatoid arthritis, bone resorption, osteoclasts, synovitis, inflammatory cytokines, RANKL, anti-citrullinated protein antibodies, bone formation, bone regeneration, radiographic erosions, antirheumatic therapy
- MeSH terms
- Animals, Arthritis, Rheumatoid, Bone Resorption, Cell Differentiation, Humans, Osteoclasts, Cytokines
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