Anandarajah Allen P, Schwarz Edward M
Clinical Immunology Research Center, Rochester, New York 14642, USA.
Adv Exp Med Biol. 2009;649:85-99. doi: 10.1007/978-1-4419-0298-6_6.
Bone loss is a common finding in the spondyloarthropathies. It may be localized and present as erosions or be generalized and cause osteoporosis. The pathogenesis of bone loss in the spondyloarthropathies is yet to be fully understood. There is however increasing evidence to support a role for the osteoclasts in bone erosions. Similarly a balance between the receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) levels is thought to regulate osteoclastic activity and therefore bone loss in the inflammatory arthritides. In this chapter we will review the recent literature on the role of osteoclasts and the RANKL/OPG system in the various spondyloarthropathies and try to formulate a hypothesis for the possible mechanism of bone loss in this group of inflammatory rheumatic disease.
骨质流失是脊柱关节炎中的常见表现。它可能是局限性的,表现为骨侵蚀,也可能是全身性的,导致骨质疏松。脊柱关节炎中骨质流失的发病机制尚未完全明确。然而,越来越多的证据支持破骨细胞在骨侵蚀中起作用。同样,核因子κB受体活化因子配体(RANKL)和骨保护素(OPG)水平之间的平衡被认为可调节破骨细胞活性,进而调节炎性关节炎中的骨质流失。在本章中,我们将回顾关于破骨细胞以及RANKL/OPG系统在各种脊柱关节炎中作用的最新文献,并尝试就这组炎性风湿性疾病中骨质流失的可能机制提出一个假说。