From bone biology to clinical outcome: state of the art and future perspectives

Schett, Georg; Saag, Kenneth G.; Bijlsma, J. W. J.

doi:10.1136/ard.2010.135061

Cited by 78 publications

(61 citation statements)

References 59 publications

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“…Inflammatory cytokines, such as interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF), activate osteoclasts and cause periarticular bone atrophy and destruction in patients with RA (1,2). In addition to periarticular osteoporosis, systemic osteoporosis is often associated with RA; several mechanisms have been proposed to underlie the increased risk for osteoporosis in patients with RA, including RA-related inflammation, glucocorticoid treatment, and immobility due to arthralgia or joint deformity.…”

Section: Introductionmentioning

confidence: 99%

Serum Fibroblast Growth Factor 23 (FGF23) in Patients with Rheumatoid Arthritis

et al. 2016

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Objective Rheumatoid arthritis (RA) is a chronic inflammatory disease accompanied by periarticular and systemic osteoporosis. Fibroblast growth factor 23 (FGF23), which is mainly produced by osteocytes, circulates to the kidneys and regulates bone metabolism. We herein assessed serum FGF23 and its relationship to inflammation and osteoporosis in patients with RA. Methods Sixty-one patients with RA were included. Serum concentrations of FGF23 were determined using a sandwich enzyme-linked immunosorbent assay. Results The mean (± standard deviation) serum FGF23 concentration was 34.9±9.2 (range, 21.0-61.0) pg/ mL. The serum FGF23 level was significantly and positively correlated with the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) levels, disease activity score-28 based on the ESR (DAS-28 ESR) and DAS-28 CRP (r=0.261, p=0.044, r=0.280, p=0.029, r=0.409, p=0.001 and r=0.421, p=0.001, respectively). The serum matrix metalloproteinase-3 level was also significantly and positively correlated with the serum FGF23 level (r=0.331, p=0.015). Concentrations of type I collagen cross-linked N-telopeptide in the serum was significantly correlated with the serum FGF23 level (r=0.272, p=0.034). Neither the bone mineral density in the femoral neck nor lumbar was significantly correlated with the serum FGF23 level. Serum phosphate, calcium, 25-hydroxy vitamin D, and intact parathyroid hormone were not related to the serum FGF23 level. Conclusion In patients with RA, serum FGF23 is correlated with inflammation, the disease activity of RA, and bone absorption markers. Serum FGF23 may be associated with abnormal bone absorption related to RA inflammation. Further studies are necessary to clarify the mechanism underlying this association.

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Section: Introductionmentioning

confidence: 99%

Serum Fibroblast Growth Factor 23 (FGF23) in Patients with Rheumatoid Arthritis

et al. 2016

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“…Under pathological conditions associated with arthritis, the process of osteoclastogenesis is markedly enhanced by various osteoclastogenic factors, including proinflammatory cytokines (interleukin (IL)-1, IL-6, IL-17, IL-18, tumor necrosis factor α (TNF-α)), chemokines (such as CC-chemokine ligand 2 (CCL2), CCL3, CCL4), and apoptotic mediators (Fas-ligand (FasL), TNF-related apoptosisinducing ligand, herpesvirus entry mediator ligand) [6,7]. It has been shown that even a small rise in the level of systemic inflammation can precipitate osteodestruction, leading to fractures and disabilities related to arthritis [2,8].…”

Section: Introductionmentioning

confidence: 99%

Association of systemic and intra-articular osteoclastogenic potential, pro-inflammatory mediators and disease activity with the form of inflammatory arthritis

Ikić¹,

Jajić²,

Lazić³

et al. 2013

International Orthopaedics (SICOT)

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Purpose We aimed to assess osteoclastogenic potential of peripheral blood mononuclear cells (PBMC) and synovial fluid-derived mononuclear cells (SFMC) in different forms of arthritis and to correlate it with inflammatory mediators within intra-articular and circulatory compartments. Methods Paired PBMC and SFMC samples of patients with rheumatoid arthritis (RA; n =10) and psoriatic arthritis (PsA; n =10), and PBMC of healthy controls were cultured to assess osteoclastogenic potential by the number of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts (OCs) and expression of OC-related genes (receptor activator of nuclear factor-κΒ (RANK), cFMS, and TRAP). Osteoclastogenesis was correlated with the arthritis-related inflammatory indicators in serum and synovial fluid (SF). Results Number of OCs differentiated from PBMC was significantly higher in RA and PsA compared with control, with RA having more OCs compared with PsA. There was no difference in SFMC OC number between arthritic patients, but RANK expression in OCs differentiated from SFMC was higher in PsA compared with RA. SF of PsA patients more potently induced OC differentiation from control CD3 + PBMC compared with RA, paralleled with higher RANK-ligand expression in PsA SFMC. Positive correlations of OC number with erythrocyte sedimentation rate, serum level of CCL2, and PBMC gene expression of interleukin-18 and Fas-ligand were observed. Conclusion Osteoclastogenic potential is systemically enhanced in patients with RA, paralleled by disordered systemic and local expression of proinflammatory mediators, whereas PsA involves specific deregulation in RANKL/RANK axis. Our study reveals arthritis-specific mediators associated with the form of arthritis, indicating clinical relevance for diagnosis and treatment.

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“…These mediators induce expression of RANKL and macrophage colonystimulating factor, both of which are important for the differentiation and activation of osteoclasts. Also, the increased level of TNF␣ could induce Dkk-1, a Wnt antagonist, to inhibit the differentiation of osteoblast formation (19). Therefore, high disease activity could contribute to bone loss through 2 pathways.…”

Section: Introductionmentioning

confidence: 99%

Changes in hand bone mineral density and the association with the level of disease activity in patients with rheumatoid arthritis: Bone mineral density measurements in a multicenter randomized clinical trial

Dirven

Güler‐Yüksel

Beus

et al. 2011

Arthritis Care & Research

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Objective. To determine if metacarpal bone mineral density (mBMD) gain occurs in patients with rheumatoid arthritis (RA). If mBMD loss is driven by inflammation, we expect to find mBMD gain in patients who are in remission. Methods. mBMD was measured by digital x-ray radiogrammetry in consecutive radiographs of 145 patients with RA with either continuous high disease activity (HDA; Disease Activity Score [DAS] >2.4), low disease activity (LDA; 1.6 > DAS < 2.4), or continuous clinical remission (CR; DAS <1.6) during a 1-year observation period. The association of mBMD changes with disease activity was investigated with multinomial regression analysis. Next, clinical variables associated with mBMD gain were identified. Results. Mean change in mBMD in CR patients was ؊0.03%, compared to ؊3.13% and ؊2.03% in HDA and LDA patients, respectively (overall, P < 0.001). Of the patients in CR, 32% had mBMD loss (less than or equal to ؊4.6 mg/cm 2 /year), compared to 62% and 66% of the patients with HDA or LDA, respectively, whereas 26% of the patients in CR had mBMD gain (>4.6 mg/cm 2 /year), compared to 2% of the patients with HDA and 5% of the patients with LDA. Patients in CR had a higher chance of having mBMD gain, compared with LDA and HDA (relative risk [RR] 14.9, 95% confidence interval [95% CI] 3.0 -18.7 and RR 4.7, 95% CI 1.2-6.3, respectively). CR, hormone replacement therapy, and lower age were significant independent predictors of mBMD gain. Conclusion. In RA, mBMD gain occurs primarily in patients in continuous (>1 year) CR and rarely in patients with continuous HDA or LDA. This suggests that mBMD loss is driven by inflammation.

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From bone biology to clinical outcome: state of the art and future perspectives

Cited by 78 publications

References 59 publications

Serum Fibroblast Growth Factor 23 (FGF23) in Patients with Rheumatoid Arthritis

Serum Fibroblast Growth Factor 23 (FGF23) in Patients with Rheumatoid Arthritis

Association of systemic and intra-articular osteoclastogenic potential, pro-inflammatory mediators and disease activity with the form of inflammatory arthritis

Changes in hand bone mineral density and the association with the level of disease activity in patients with rheumatoid arthritis: Bone mineral density measurements in a multicenter randomized clinical trial

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