Neerinckx Barbara, Lories Rik J
Laboratory of Tissue Homeostasis and Disease, Skeletal Biology and Engineering Research Center, Department of Development and Regeneration, KU Leuven & Division of Rheumatology, University Hospitals Leuven, Leuven, Belgium.
Curr Rheumatol Rep. 2017 Mar;19(3):14. doi: 10.1007/s11926-017-0639-7.
Progressive ankylosis is a feared consequence of long-standing axial spondyloarthritis. We aim to critically review current insights into the effect of therapy, the molecular pathways involved in this process, and to present a model explaining the sequence of events.
Long-term follow-up data suggest that successful control of inflammation may slow down radiographic progression of disease in axial spondyloarthritis. Structural effects of new therapies such as interleukin-17 targeting need to be further studied. Bone loss and architectural changes could act as driver for the tissue remodeling process trying to maintain spinal stability in the presence of inflammation. Despite some progress, the nature and mechanisms of new bone formation in axial spondyloarthritis still remain incompletely understood. However, long-term control of inflammation appears critical to avoid progressive disability due to structural damage.
进行性关节强硬是长期轴性脊柱关节炎令人担忧的后果。我们旨在批判性地回顾当前关于治疗效果、该过程中涉及的分子途径的见解,并提出一个解释事件序列的模型。
长期随访数据表明,成功控制炎症可能会减缓轴性脊柱关节炎疾病的影像学进展。针对白细胞介素-17等新疗法的结构效应需要进一步研究。骨质流失和结构变化可能是在炎症存在的情况下试图维持脊柱稳定性的组织重塑过程的驱动因素。尽管取得了一些进展,但轴性脊柱关节炎中新骨形成的性质和机制仍未完全了解。然而,长期控制炎症对于避免因结构损伤导致的进行性残疾似乎至关重要。