Current Rheumatology Reports ( IF 5.7 ) Pub Date : 2022-10-29 , DOI: 10.1007/s11926-022-01092-4
Mauro Fatica 1 , Arianna D'Antonio 1 , Lucia Novelli 2 , Paola Triggianese 1 , Paola Conigliaro 1 , Elisabetta Greco 1 , Alberto Bergamini 1 , Carlo Perricone 3 , Maria Sole Chimenti 1
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Purpose
This review aims at investigating pathophysiological mechanisms in spondyloarthritis (SpA). Analysis of genetic factors, immunological pathways, and abnormalities of bone metabolism lay the foundations for a better understanding of development of the axial clinical manifestations in patients, allowing physician to choose the most appropriate therapeutic strategy in a more targeted manner.
Recent Findings
In addition to the contribution of MHC system, findings emerged about the role of non-HLA genes (as ERAP1 and 2, whose inhibition could represent a new therapeutic approach) and of epigenetic mechanisms that regulate the expression of genes involved in SpA pathogenesis. Increasing evidence of bone metabolism abnormalities secondary to the activation of immunological pathways suggests the development of various bone anomalies that are present in axSpA patients.
Summary
SpA are a group of inflammatory diseases with a multifactorial origin, whose pathogenesis is linked to the genetic predisposition, the action of environmental risk factors, and the activation of immune response. It is now well known how bone metabolism leads to long-term structural damage via increased bone turnover, bone loss and osteoporosis, osteitis, erosions, osteosclerosis, and osteoproliferation. These effects can exist in the same patient over time or even simultaneously. Evidence suggests a cross relationship among innate immunity, autoimmunity, and bone remodeling in SpA, making treatment approach a challenge for rheumatologists. Specifically, treatment targets are consistently increasing as new drugs are upcoming. Both biological and targeted synthetic drugs are promising in terms of their efficacy and safety profile in patients affected by SpA.
中文翻译：
分子生物学如何增强我们对 axSpA 的承诺及其管理
目的
本综述旨在调查脊柱关节炎（SpA）的病理生理机制。对遗传因素、免疫通路、骨代谢异常等的分析，为更好地了解患者中轴临床表现的发展奠定了基础，使医生能够更有针对性地选择最合适的治疗策略。
最近的发现
除了 MHC 系统的贡献之外，还发现了非 HLA 基因（如 ERAP1 和 2，其抑制可能代表一种新的治疗方法）的作用以及调节 SpA 发病机制相关基因表达的表观遗传机制的作用。越来越多的证据表明，继发于免疫途径激活的骨代谢异常表明 axSpA 患者中存在各种骨异常。
概括
SpA是一组多因素起源的炎症性疾病，其发病机制与遗传易感性、环境危险因素的作用以及免疫反应的激活有关。现在众所周知，骨代谢如何通过增加骨转换、骨质流失和骨质疏松、骨炎、侵蚀、骨硬化和骨质增生而导致长期结构损伤。这些效应可能会随着时间的推移甚至同时存在于同一患者身上。有证据表明 SpA 的先天免疫、自身免疫和骨重塑之间存在交叉关系，这使得治疗方法对风湿病学家来说是一个挑战。具体来说，随着新药的推出，治疗目标不断增加。生物药物和靶向合成药物在治疗 SpA 患者中的疗效和安全性方面都具有前景。
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