Effects of disease-modifying antirheumatic drugs and antiinflammatory cytokines on human osteoclastogenesis through interaction with receptor activator of nuclear factor κB, osteoprotegerin, and receptor activator of nuclear factor κB ligand.

Lee, Chang‐Keun; Lee, Eun Young; Chung, Son Mi; Mun, Se Hwan; Yoo, Bin; Moon, Hee‐Bom

doi:10.1002/art.20637

Cited by 137Bone Metabolism and DiseasesRheumatoid Arthritis Research and TherapiesNatural Compounds in Disease Treatment

Effects of disease-modifying antirheumatic drugs and antiinflammatory cytokines on human osteoclastogenesis through interaction with receptor activator of nuclear factor κB, osteoprotegerin, and receptor activator of nuclear factor κB ligand.

Lee, Chang‐Keun, Lee, Eun Young, Chung, Son Mi, Mun, Se Hwan, Yoo, Bin, Moon, Hee‐Bom·2004·Arthritis & Rheumatism

DOI 10.1002/art.20637

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Abstract

Objective: To demonstrate the effects of disease‐modifying antirheumatic drugs and antiinflammatory cytokines on human osteoclastogenesis through their effects on receptor activator of nuclear factor κB (RANK), osteoprotegerin (OPG), and RANK ligand (RANKL). Methods: Peripheral blood mononuclear cells (PBMCs) and rheumatoid arthritis (RA) fibroblast‐like synoviocytes (FLS) were cocultured in the presence of macrophage colony‐stimulating factor, 1,25‐dihydroxyvitamin D 3, and various concentrations of methotrexate (MTX), sulfasalazine (SSZ), hydroxychloroquine (HCQ), anti–tumor necrosis factor α monoclonal antibody (infliximab), interleukin‐4 (IL‐4), and IL‐10. Osteoclast formation was assayed by counting cells after staining for tartrate‐resistant acid phosphatase. RANKL expression in RA FLS and RANK expression in PBMCs were assayed by Western blotting, reverse transcription–polymerase chain reaction (RT‐PCR), and real‐time PCR. OPG expression was measured by enzyme‐linked immunosorbent assay, RT‐PCR, and real‐time PCR in cultures of RA FLS. Results: MTX, SSZ, infliximab, and IL‐4, but not IL‐10 and HCQ, each inhibited osteoclast formation in a dose‐dependent manner. We observed no evidence of synergistic inhibition of osteoclast formation by IL‐4 and IL‐10. High doses of infliximab suppressed the expression of RANK in PBMCs. MTX, SSZ, infliximab, and IL‐4 each inhibited the expression of RANKL in RA FLS in a dose‐dependent manner, and also increased the secretion of OPG in RA FLS supernatants. Conclusion: MTX, SSZ, infliximab, and IL‐4 inhibit human osteoclastogenesis by modulating the interaction of RANKL, RANK, and OPG. These results are indicative of the underlying mechanisms of the antiresorptive effects of these 4 agents.

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In vitro, infliximab decreases RANK expression in peripheral blood mononuclear cells; infliximab, methotrexate, sulfasalazine, or hydroxychloroquine inhibit RANKL expression and increase OPG secretion in cultured synovial cells.
“This agrees with in vitro cell culture studies showing a decrease in RANK expression in peripheral blood mononuclear cells treated with infliximab and inhibition of RANKL expression and increase in OPG secretion in cultured synovial cells treated with infliximab, methotrexate, sulfasalazine, or hydroxychloroquine (429).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [429]

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Authors: Lee, C., Lee, E. Y., Chung, S. M., Mun, S. H., Yoo, B., & Moon, H.
Affiliations: Asan Medical Center (KR)
ORCID: Lee, Chang‐Keun
Mun, Se Hwan
Yoo, Bin
Moon, Hee‐Bom
Venue: Arthritis & Rheumatism
Publisher: Wiley
Published: 2004-12
Volume: 50
Issue: 12
Pages: 3831-3843
ISSN: 0004-3591 (ISSN-L)
1529-0131
DOI: 10.1002/art.20637
OpenAlex: W2125895268
Cited by: 137
References: 35
Citations by year: 2026: 2 · 2025: 5 · 2024: 1 · 2023: 4 · 2022: 5 · 2021: 2 · 2020: 6 · 2019: 4 · 2018: 7 · 2017: 6 · 2016: 7 · 2015: 9 · 2014: 9 · 2013: 12 · 2012: 8
FWCI: 2.85
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 7 d)
Locations: Arthritis & Rheumatism (publishedVersion)
PubMed (publishedVersion)
Seoul National University Open Repository (Seoul National University) (submittedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
Health Sciences › Medicine › Complementary and alternative medicine › Natural Compounds in Disease Treatment
Keywords: osteoclastogenesis, rheumatoid arthritis, disease-modifying antirheumatic drugs, anti-TNF therapy, infliximab, methotrexate, sulfasalazine, hydroxychloroquine, IL-4, IL-10, RANK, RANKL, osteoprotegerin, synovial fibroblasts, bone resorption
MeSH terms: Tartrate-Resistant Acid Phosphatase, Acid Phosphatase, Arthritis, Rheumatoid, Carrier Proteins, Cell Survival, Dose-Response Relationship, Drug, Fibroblasts, Glycoproteins, Humans, Isoenzymes, Leukocytes, Mononuclear, Membrane Glycoproteins, Osteoclasts, Osteogenesis, RNA, Messenger, Synovial Membrane, Blotting, Western, Cytokines, Receptors, Tumor Necrosis Factor, Receptors, Cytoplasmic and Nuclear, Antirheumatic Agents, Coculture Techniques, Reverse Transcriptase Polymerase Chain Reaction, Osteoprotegerin, RANK Ligand, Receptor Activator of Nuclear Factor-kappa B

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Effects of disease-modifying antirheumatic drugs and antiinflammatory cytokines on human osteoclastogenesis through interaction with receptor activator of nuclear factor κB, osteoprotegerin, and receptor activator of nuclear factor κB ligand.

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