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Open Access Highly Accessed Research article

Circulating mediators of bone remodeling in psoriatic arthritis: implications for disordered osteoclastogenesis and bone erosion

Nicola Dalbeth12*, Bregina Pool1, Timothy Smith1, Karen E Callon1, Maria Lobo2, William J Taylor3, Peter B Jones4, Jillian Cornish1 and Fiona M McQueen25

Author Affiliations

1 Department of Medicine, University of Auckland, 85 Park Rd, Auckland 1010, New Zealand

2 Department of Rheumatology, Auckland District Health Board, Greenlane West, Auckland 1051, New Zealand

3 Department of Medicine, University of Otago, Wellington, Mein St, Wellington 6021, New Zealand

4 Waikato Clinical School, University of Auckland, Pembroke Street, Hamilton 3240, New Zealand

5 Department of Molecular Medicine and Pathology, University of Auckland, 85 Park Rd, Auckland 1010, New Zealand

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Arthritis Research & Therapy 2010, 12:R164  doi:10.1186/ar3123

Published: 26 August 2010

Abstract

Introduction

Diverse bone pathologies are observed in patients with psoriatic arthritis (PsA). Uncoupling of bone remodeling with disordered osteoclastogenesis has been implicated in the pathogenesis of PsA. The aim of this study was to examine the role of soluble mediators of bone remodeling within the circulation of patients with PsA.

Methods

Patients with PsA (n = 38), with psoriasis (n = 10), and healthy controls (n = 12) were studied. Serum was obtained for testing of Dikkopf-1 (Dkk-1), macrophage-colony stimulating factor (M-CSF), osteoprotegerin (OPG), and receptor activator of nuclear factor-κB ligand (RANKL) with ELISA. Patients with PsA also had bone densitometry, plain radiographs of the hands and feet, and assessment of peripheral blood osteoclast precursors. Radiographs were scored for erosion, joint-space narrowing, osteolysis, and new bone formation.

Results

Compared with those with psoriasis and healthy controls, patients with PsA had higher circulating concentrations of Dkk-1 and M-CSF. In patients with PsA, M-CSF and RANKL, but not Dkk-1, concentrations positively correlated with radiographic erosion, joint-space narrowing, and osteolysis scores. Mediators of bone remodeling did not correlate with the number of joints with new bone formation or with total hip-bone mineral density. Peripheral blood CD14+/CD11b+ cells, and the number of osteoclast-like cells and resorptive pits after culture with RANKL and M-CSF also correlated with radiographic damage scores. Circulating M-CSF concentrations correlated with the percentage of peripheral blood CD14+/CD11b+ cells.

Conclusions

Systemic expression of soluble factors that promote osteoclastogenesis is disordered in patients with PsA and may contribute to periarticular bone loss in this disease.