Mediators of inflammation and bone remodeling in rheumatic disease.
Mediators of inflammation and bone remodeling in rheumatic disease.
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DOI：
10.1016/j.semcdb.2015.10.013
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发表时间：
2016-01
影响因子：
7.3
通讯作者：
Gravallese EM
中科院分区：
文献类型：
--
作者：
Shaw AT;Gravallese EM
骨骼的重塑是一个贯穿一生的持续过程。在正常生理条件下，吸收骨的破骨细胞和形成骨的成骨细胞紧密耦合和调节，以确保适当的平衡，使骨量没有净变化。然而，炎症会扰乱正常的骨骼动态平衡。炎症对骨骼的影响取决于受影响的解剖部位、细胞类型、局部微环境中存在的因子和细胞因子以及局部机械力。细胞因子在炎症诱导性骨丢失的发病机制中处于核心地位，并导致破骨细胞介导骨吸收和成骨细胞介导骨形成的解偶联，从而破坏正常的骨重建。在这篇综述中，我们将讨论细胞因子在两种情况下对骨骼的影响，类风湿性关节炎(RA)和脊柱性关节炎(SpA)，这是一种包括强直性脊柱炎(AS)、银屑病(PSA)、反应性关节炎、炎症性肠病和幼年型脊柱关节病的疾病类别。在这些疾病的背景下，骨骼的结果截然不同，了解导致对骨骼的净影响的致病机制对于开发这些疾病的骨骼健康的新治疗方法至关重要。
Remodeling of bone is a continuous process that occurs throughout life. Under normal physiologic conditions, bone-resorbing osteoclasts and bone-forming osteoblasts are tightly coupled and regulated to ensure the proper balance, such that there is no net change in bone mass. However, inflammation perturbs normal bone homeostasis. The impact of inflammation on bone is dependent upon the anatomic site affected, cell types, factors and cytokines present in the local microenvironment, and local mechanical forces. Cytokines are central to the pathogenesis of inflammation-induced bone loss and contribute to the uncoupling of osteoclast-mediated bone resorption and osteoblast-mediated bone formation, thereby disrupting normal remodeling. In this review, we will discuss the effects of cytokines on bone in two settings, rheumatoid arthritis (RA) and spondyloarthritis (SpA), a disease category that includes ankylosing spondylitis (AS), psoriatic arthritis (PsA), reactive arthritis, inflammatory bowel disease, and juvenile onset spondyloarthropathy. The outcome for bone in these disease settings is quite different, and an understanding of the pathogenic mechanisms leading to the net impact on bone has been essential in developing new therapeutic approaches to bone health in these diseases.