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脊柱关节病患者的骨骼受累情况。

Bone Involvement in Patients with Spondyloarthropathies.

作者信息

Lems Willem, Miceli-Richard Corinne, Haschka Judith, Giusti Andrea, Chistensen Gitte Lund, Kocijan Roland, Rosine Nicolas, Jørgensen Niklas Rye, Bianchi Gerolamo, Roux Christian

机构信息

Amsterdam University Medical Center, Location VUmc, Amsterdam, the Netherlands.

INSERM U 1153, Université de Paris-APHP.Centre, Service de Rhumatologie, Hopital Cochin, Paris, France.

出版信息

Calcif Tissue Int. 2022 Apr;110(4):393-420. doi: 10.1007/s00223-021-00933-1. Epub 2022 Jan 23.

Abstract

Spondyloarthropathies (SpA) are common systemic inflammatory rheumatic diseases, in which, as in other rheumatic diseases, levels of markers of bone resorption are elevated, leading to bone loss and elevated risk of vertebral fractures. However, the diseases are also associated with new bone formation in the spine, the so-called syndesmophytes. We tried to unravel the pathogenesis of formation and growth of syndesmophytes and evaluated new diagnostic and treatment options. After a successful meeting of the Working Group on Rheumatic Diseases at the ECTS 2020, we (WL and CR) were excited about the quality of the speakers (CM, JH, AG, and GL) and their complimentary lectures. Given the relative lack of reviews on spondyloarthropathies and bone, we decided to work together on a comprehensive review that might be interesting for basic scientists and clinically relevant for clinicians. Radiographic progression in axSpA is linked to several risk factors, like male sex, smoking, HLA-B-27, increased levels of CRP, presence of syndesmophytes, and marked inflammation on MRI. The potential role of mechanical stress in the context of physically demanding jobs has been also suggested to promote structural damages. Different treatment options from NSAIDs to biologic agents like TNF inhibitors (TNFi) or IL-17inhibitors (IL-17i) result in a reduction of inflammation and symptoms. However, all these different treatment options failed to show clear and reproducible results on inhibition on syndesmophyte formation. The majority of data are available on TNFi, and some studies suggested an effect in subgroups of patients with ankylosing spondylitis. Less information is available on NSAIDs and IL-17i. Since IL-17i have been introduced quite recently, more studies are expected. IL-17 inhibitors (Il-17i) potently reduce signs and symptoms, but serum level of IL-17 is not elevated, therefore, IL-17 probably has mainly a local effect. The failure of anti-IL-23 in axSpA suggests that IL-17A production could be independent from IL-23. It may be upregulated by TNFα, resulting in lower expression of DKK1 and RANKL and an increase in osteogenesis. In active AS markers of bone resorption are increased, while bone formation markers can be increased or decreased. Bone Turnover markers and additional markers related to Wnt such as DKK1, sclerostin, and RANKL are valuable for elucidating bone metabolism on a group level and they are not (yet) able to predict individual patient outcomes. The gold standard for detection of structural lesions in clinical practice is the use of conventional radiographics. However, the resolution is low compared to the change over time and the interval for detecting changes are 2 years or more. Modern techniques offer substantial advantages such as the early detection of bone marrow edema with MRI, the fivefold increased detection rate of new or growing syndesmophytes with low-dose CT, and the decrease in 18F-fluoride uptake during treatment with TNFα-inhibitors (TNFi) in a pilot study in 12 AS patients. Detection of bone involvement by new techniques, such as low-dose CT, MRI and 18-Fluoride PET-scans, and bone turnover markers, in combination with focusing on high-risk groups such as patients with early disease, elevated CRP, syndesmophytes at baseline, male patients and patients with HLA-B27 + are promising options for the near future. However, for optimal prevention of formation of syndesmophytes we need more detailed insight in the pathogenesis of bone formation in axSpA and probably more targeted therapies.

摘要

脊柱关节炎(SpA)是常见的系统性炎性风湿性疾病,与其他风湿性疾病一样,其骨吸收标志物水平升高,导致骨质流失和椎体骨折风险增加。然而,这些疾病还与脊柱新骨形成有关,即所谓的骨桥形成。我们试图阐明骨桥形成和生长的发病机制,并评估新的诊断和治疗选择。在2020年欧洲风湿病防治联合会(ECTS)风湿病工作组成功召开会议后,我们(WL和CR)对演讲者(CM、JH、AG和GL)的水平及其精彩演讲感到兴奋。鉴于关于脊柱关节炎与骨的综述相对较少,我们决定共同撰写一篇全面的综述,这可能会引起基础科学家的兴趣,对临床医生也具有临床相关性。轴性脊柱关节炎(axSpA)的影像学进展与多个风险因素相关,如男性、吸烟、HLA - B27、CRP水平升高、骨桥形成以及MRI上的明显炎症。在体力要求较高的工作环境中,机械应力的潜在作用也被认为会促进结构损伤。从非甾体抗炎药(NSAIDs)到生物制剂如肿瘤坏死因子抑制剂(TNFi)或白细胞介素 - 17抑制剂(IL - 17i)等不同的治疗选择可减轻炎症和症状。然而,所有这些不同的治疗选择在抑制骨桥形成方面均未显示出明确且可重复的结果。关于TNFi的可用数据最多,一些研究表明其对强直性脊柱炎患者亚组有作用。关于NSAIDs和IL - 17i的信息较少。由于IL - 17i是最近才引入的,预计会有更多研究。白细胞介素 - 17抑制剂(Il - 17i)能有效减轻体征和症状,但IL - 17的血清水平并未升高,因此,IL - 17可能主要具有局部作用。axSpA中抗白细胞介素 - 23治疗的失败表明IL - 17A的产生可能独立于白细胞介素 - 23。它可能被肿瘤坏死因子α上调,导致DKK1和核因子κB受体活化因子配体(RANKL)表达降低以及骨生成增加。在活动期强直性脊柱炎中,骨吸收标志物增加,而骨形成标志物可能增加或减少。骨转换标志物以及与Wnt相关的其他标志物如DKK1、硬化蛋白和RANKL对于在群体水平阐明骨代谢很有价值,但它们(目前)尚无法预测个体患者的预后。临床实践中检测结构损伤的金标准是使用传统X线摄影。然而,与随时间的变化相比,其分辨率较低,检测变化的间隔为2年或更长时间。现代技术具有显著优势,如通过MRI早期检测骨髓水肿、通过低剂量CT使新的或正在生长的骨桥的检测率提高五倍,以及在一项针对12例强直性脊柱炎患者的初步研究中发现使用肿瘤坏死因子α抑制剂(TNFi)治疗期间18F - 氟化物摄取减少。通过低剂量CT、MRI和18F - 氟化物PET扫描等新技术以及骨转换标志物检测骨受累情况,并关注高危人群如早期疾病患者、CRP升高患者、基线存在骨桥患者、男性患者以及HLA - B27阳性患者,是近期很有前景的选择。然而,为了最佳地预防骨桥形成,我们需要更深入地了解axSpA中骨形成的发病机制,并可能需要更有针对性的治疗方法。

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