Expression of osteoclast differentiation factor in rheumatoid arthritis

Shigeyama, Yukio; Pap, Thomas; Künzler, Peter; Simmen, Beat R.; Gay, Renate E.; Gay, Steffen

doi:10.1002/1529-0131(200011)43:11<2523::aid-anr20>3.0.co;2-z

Cited by 219 publications

(143 citation statements)

References 24 publications

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“…Since the RANKL/RANK/ OPG system has been shown to be important in inflammation-induced bone resorption, including that in rheumatoid arthritis (27)(28)(29)46) and in periodontal disease (4,31), we focused on these molecules. Since RANKL mRNA expression in the MG-63 cells was scarce, we used neonatal mouse calvarial bones for these experiments, the rationale being that activation of BK receptors synergistically potentiates IL-1-induced bone resorption in the calvarial bones (11).…”

Section: Discussionmentioning

confidence: 99%

“…Mice deficient in OPG exhibit abundant osteoclasts and an osteoporotic phenotype. RANKL is expressed in synovial tissue from patients with rheumatoid arthritis (27)(28)(29) and has been found to be crucial for osteoclast formation and bone loss in experimentally induced arthritis in mice (30). RANKL is also expressed in gingival tissue from patients with periodontal disease (31,32), and increased RANKL/OPG is associated with bone loss in periodontitis (4,31).…”

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confidence: 99%

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Bradykinin potentiates cytokine‐induced prostaglandin biosynthesis in osteoblasts by enhanced expression of cyclooxygenase 2, resulting in increased RANKL expression

Brechter¹,

Lerner²

2007

Arthritis & Rheumatism

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Objective. Bradykinin (BK) stimulates bone resorption in vitro and synergistically potentiates interleukin-1 (IL-1)-induced bone resorption and prostaglandin (PG) formation, suggesting that kinins are important in inflammation-induced bone loss. The present study was undertaken to study 1) the role of the kinin B1 and B2 receptors in the synergistic interaction with IL-1 and tumor necrosis factor ␣ (TNF␣), 2) the molecular mechanisms involved in synergistic enhancement of PG formation, and 3) the effects of kinins on cytokine-induced expression of RANKL, RANK, and osteoprotegerin (OPG) (the latter being crucial molecules in osteoclast differentiation).Methods. Formation of PGs, expression of enzymes involved in arachidonic acid metabolism, and expression of RANKL, RANK, and OPG were assessed in the human osteoblastic cell line MG-63 and in mouse calvarial bones.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Bradykinin potentiates cytokine‐induced prostaglandin biosynthesis in osteoblasts by enhanced expression of cyclooxygenase 2, resulting in increased RANKL expression

Brechter¹,

Lerner²

2007

Arthritis & Rheumatism

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“…In contrast, RANKL is not expressed in normal synovium, suggesting a link between the expression of RANKL mRNA and development of synovial lesions in RA (7). RANKL is expressed by lymphocytes, macrophages, and, in RA, also by synovial fibroblasts (57). RA synovial fibroblasts therefore appear to be additional sources for RANKL (18).…”

Section: Rank/rankl/opg and Ramentioning

confidence: 95%

“…In this regard, it has been shown that the induction of TRAP-positive multinucleated osteoclasts derived from peripheral blood mononuclear cells depends on the level of RANKL produced by cultured RA synovial fibroblasts (57). Moreover, expression of RANKL at sites of bone destruction has been found to be strongest in both osteoclasts and synovial fibroblasts (57,58).…”

Section: Rank/rankl/opg and Ramentioning

confidence: 99%

The RANK/RANKL/osteoprotegerin system in rheumatoid arthritis: New insights from animal models

Neumann

Müller‐Ladner

2005

Arthritis & Rheumatism

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“…Tumor necrosis factor (TNF) is a key cytokine in RA (6), and selective overexpression of TNF in mice is sufficient for the development of destructive arthritis (7). Of note, synovial fibroblasts and lymphocytes drive the differentiation of osteoclasts from monocyte precursor cells via the expression of RANKL (8)(9)(10)(11). Osteoclasts are cells that are specifically designed to resorb bone (12).…”

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confidence: 99%

Tenosynovitis and osteoclast formation as the initial preclinical changes in a murine model of inflammatory arthritis

Hayer¹,

Redlich²,

Korb³

et al. 2007

Arthritis & Rheumatism

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Objective. To determine the nature of the initial changes of joint inflammation occurring before, at the time of, and shortly after onset of clinically apparent arthritis.Methods. Human tumor necrosis factor (TNF)-transgenic mice were assessed for clinical, histologic, immunophenotypic, serologic, and molecular changes at the preclinical phase of arthritis, at the onset of disease, and at the stage of early clinical disease. In addition, the effects of a genetic osteoclast deficiency and pharmacologic inhibition of TNF were studied in these initial phases of disease.Results. Initial articular changes were observed even before the start of clinical symptoms. Infiltration of the tendon sheaths by granulocytes and macrophages as well as formation of osteoclasts next to the inflamed tendon sheaths were the first pathologic events. Tenosynovitis rapidly led to remodeling of the sheaths into pannus-like tissue, which formed osteoclasts that invaded the adjacent mineralized cartilage. Early lesions were associated with up-regulation of interleukin-1 (IL-1) and IL-6 as well as activation of p38 MAPK and ERK. In contrast, absence of osteoclasts led to uncoupling of tenosynovitis from invasion into cartilage and bone. TNF blockade also attenuated the pathologic changes associated with tenosynovitis.Conclusion. Structural damage begins even before the onset of clinical symptoms of arthritis and involves the tendon sheaths as well as adjacent cartilage and bone. These results suggest that tenosynovitis is an initiating feature of arthritis and that joint destruction starts right from the onset of disease. Our findings thus underscore the importance of immediate initiation of an effective therapy in patients with rheumatoid arthritis.

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Expression of osteoclast differentiation factor in rheumatoid arthritis

Abstract: The present results suggest that activated RASF, by expressing ODF, play an important role in rheumatoid bone destruction. Moreover, the data provide evidence that RASF not only activate osteoclasts, but also contribute directly to osteoclastogenesis.

Cited by 219 publications

References 24 publications

Bradykinin potentiates cytokine‐induced prostaglandin biosynthesis in osteoblasts by enhanced expression of cyclooxygenase 2, resulting in increased RANKL expression

Bradykinin potentiates cytokine‐induced prostaglandin biosynthesis in osteoblasts by enhanced expression of cyclooxygenase 2, resulting in increased RANKL expression

The RANK/RANKL/osteoprotegerin system in rheumatoid arthritis: New insights from animal models

Tenosynovitis and osteoclast formation as the initial preclinical changes in a murine model of inflammatory arthritis

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