Department of Medicine, University of Auckland, Auckland 1010, New Zealand.
Arthritis Res Ther. 2010;12(4):R164. doi: 10.1186/ar3123. Epub 2010 Aug 26.
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.
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.
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.
Systemic expression of soluble factors that promote osteoclastogenesis is disordered in patients with PsA and may contribute to periarticular bone loss in this disease.
在患有银屑病关节炎（PsA）的患者中观察到多种骨骼病理学。破骨细胞生成紊乱导致的骨重塑脱耦联与 PsA 的发病机制有关。本研究旨在探讨循环中骨重塑的可溶性介质在 PsA 患者中的作用。
研究了 38 例 PsA 患者、10 例银屑病患者和 12 例健康对照者。通过 ELISA 检测血清中 Dickkopf-1（Dkk-1）、巨噬细胞集落刺激因子（M-CSF）、骨保护素（OPG）和核因子-κB 受体激活剂配体（RANKL）的浓度。PsA 患者还进行了骨密度测定、手和脚的普通 X 线片检查以及外周血破骨细胞前体的评估。X 线片用于评估侵蚀、关节间隙变窄、骨溶解和新骨形成。
与银屑病患者和健康对照组相比，PsA 患者的循环 Dkk-1 和 M-CSF 浓度更高。在 PsA 患者中，M-CSF 和 RANKL 浓度与 X 线侵蚀、关节间隙狭窄和骨溶解评分呈正相关，但 Dkk-1 浓度则不然。骨重塑的介质与新骨形成的关节数或总髋骨矿物质密度均无相关性。与 RANKL 和 M-CSF 培养后的外周血 CD14+/CD11b+细胞数以及破骨样细胞数和吸收陷窝数也与放射学损伤评分相关。循环 M-CSF 浓度与外周血 CD14+/CD11b+细胞的百分比相关。
PsA 患者体内促破骨细胞生成的可溶性因子表达紊乱，可能导致该疾病的关节周围骨丢失。
