Suppression of bone turnover by B-cell depletion in patients with rheumatoid arthritis

Wheater, Gillian; Hogan, Vanessa; Teng, Y K Onno; Tekstra, Janneke; Lafeber, F.P.; Huizinga, Tom W J; Bijlsma, J. W. J.; Francis, Roger M.; Tuck, Stephen; Datta, Harish K.; Laar, Jacob M van

doi:10.1007/s00198-011-1607-0

Cited by 42 publications

(36 citation statements)

References 28 publications

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“…Consistent with our results, previous studies have shown that serum levels of osteocalcin are negatively correlated with disease activity in RA patients 46 47. Of note, one other study in 46 RA patients did not demonstrate a change in osteocalcin 6 months after rituximab treatment;48 the reason for this discrepancy is at present unclear. The fact that serum NTx did not change can perhaps be explained by the long disease duration of our cohort, as previous studies have shown that carboxy terminal telopeptide (a comparable bone resorption marker) levels are decreased in RA patients with a disease duration of more than 10 years.…”

Section: Discussionsupporting

confidence: 87%

Rituximab abrogates joint destruction in rheumatoid arthritis by inhibiting osteoclastogenesis

et al. 2011

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Section: Discussionsupporting

confidence: 87%

Rituximab abrogates joint destruction in rheumatoid arthritis by inhibiting osteoclastogenesis

et al. 2011

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“…A recent article showed that mice lacking RANKL in B cells were partially protected from ovariectomy-induced loss of cancerous bone [29]. The role of B lymphocytes has also been evaluated in diseases characterized by focal bone loss, such as periodontal inflammation [14, 30, 31] and rheumatoid arthritis [16, 32]. In rheumatoid arthritis, a recent study showed that B cell depletion ameliorates suppressed bone turnover [29].…”

Section: Discussionmentioning

confidence: 99%

Dysregulated systemic lymphocytes affect the balance of osteogenic/adipogenic differentiation of bone mesenchymal stem cells after local irradiation

Zhou

et al. 2017

Stem Cell Res Ther

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BackgroundWhile it is known that irradiation can induce local and systemic bone loss over time, how focal irradiation induces systemic bone complications remains unclear. Immune cells are thought to be crucial to bone homeostasis, and abnormal immune cells lead to serious disruption of bone homeostasis, such as in acute lymphoblastic leukaemia. This disruption primarily occurs due to inhibition of the osteogenic differentiation of bone mesenchymal stem cells (BMSCs).MethodsIn this study, we detected local and systemic bone loss in trabecular bone by micro-computed tomography (micro-CT) and measurement of peroxisome proliferator-activated receptor gamma (PPARγ) and runt-related transcription factor 2 (RUNX2) expression in BMSCs using real-time polymerase chain reaction and western blotting. Additionally, changes in lymphocytes (B cells and CD4+ and CD8+ T cells) in the peripheral blood and bone marrow were analysed by flow cytometry. BMSC-derived osteoblasts and adipocytes, cultured in osteogenic or adipogenic media or co-cultured with lymphocytes, were detected by BCIP/NBT, Alizarin Red S and Oil Red O staining.ResultsFocal irradiation induced local and systemic bone loss in trabecular bone. Increased PPARγ expression and decreased RUNX2 expression were observed, accompanied by upregulated adipogenesis and downregulated osteogenesis of BMSCs. B cells and CD8+ T lymphocytes were increased in the blood and bone marrow after irradiation, while CD4+ T lymphocytes were decreased in the blood. Inhibition of RUNX2 expression and reduction of alkaline phosphatase activity and mineralization deposits were observed in lymphocyte-co-cultured BMSCs, accompanied by an increase in PPARγ expression and in the number of lipid droplets.ConclusionsFocal irradiation induced local and systemic bone loss in trabecular bone. Increased B cells and CD8+ T lymphocytes led to systemic bone loss by decreasing BMSC osteogenesis.

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“…Nevertheless, changes in several B lymphocyte populations in patients affected by postmenopausal osteoporosis regardless of their estrogen status have been shown. 51 The role of B cells in the control of bone turnover has been studied in other diseases that affect bone, such as RA 48,52 and periodontal inflammation. 53 These studies suggest that B cells may be involved in the control of bone turnover in humans as well, mainly by the production of cytokines such as OPG and RANKL.…”

Section: Inflammatory Diseases Immune System and Bonementioning

confidence: 99%

Osteoimmunology: from mice to humans

Sassi¹

2016

Bonekey Reports

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The immune system has been recognized as one of the most important regulators of bone turnover and its deregulation is implicated in several bone diseases such as postmenopausal osteoporosis and inflammatory bone loss; recently it has been suggested that the gut microbiota may influence bone turnover by modulation of the immune system. The study of the relationship between the immune system and bone metabolism is generally indicated under the term 'osteoimmunology'. The vast majority of these studies have been performed in animal models; however, several data have been confirmed in humans as well: this review summarizes recent data on the relationship between the immune system and bone with particular regard to the data confirmed in humans.

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Suppression of bone turnover by B-cell depletion in patients with rheumatoid arthritis

Abstract: In conclusion, we have found that B-cell depletion increases bone formation and decreases bone resorption in RA patients; this may be a direct effect on osteoblasts and osteoclasts, respectively, and be at least partially explained by the decreased inflammation and disease activity.

Cited by 42 publications

References 28 publications

Rituximab abrogates joint destruction in rheumatoid arthritis by inhibiting osteoclastogenesis

Rituximab abrogates joint destruction in rheumatoid arthritis by inhibiting osteoclastogenesis

Dysregulated systemic lymphocytes affect the balance of osteogenic/adipogenic differentiation of bone mesenchymal stem cells after local irradiation

Osteoimmunology: from mice to humans

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