Osteoarthritis (OA), the most ubiquitous degenerative disease affecting the entire joint, is characterized by cartilage degradation and synovial inflammation. Although the pathogenesis of OA remains poorly understood, synovial inflammation is known to play an important role in OA development. However, studies on OA pathophysiology have focused more on cartilage degeneration and osteophytes, rather than on the inflamed and thickened synovium. Fibroblast‐like synoviocytes (FLS) produce a series of pro‐inflammatory regulators, such as inflammatory cytokines, nitric oxide (NO) and prostaglandin E₂ (PGE₂). These regulators are positively associated with the clinical symptoms of OA, such as inflammatory pain, joint swelling and disease development. A better understanding of the inflammatory immune response in OA‐FLS could provide a novel approach to comprehensive treatment strategies for OA. Here, we have summarized recently published literatures referring to epigenetic modifications, activated signalling pathways and inflammation‐associated factors that are involved in OA‐FLS‐mediated inflammation. In addition, the current related clinical trials and future perspectives were also summarized.

中文翻译：

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成纤维样滑膜细胞介导的滑膜炎在骨关节炎中的新兴作用：更新。

骨关节炎（OA）是影响整个关节的最普遍的变性疾病，其特征是软骨退化和滑膜炎症。尽管对OA的发病机理仍然知之甚少，但已知滑膜炎症在OA的发展中起着重要作用。但是，OA病理生理学的研究更多地集中在软骨变性和骨赘上，而不是发炎和增厚的滑膜上。成纤维样滑膜细胞（FLS）产生一系列促炎性调节剂，例如炎性细胞因子，一氧化氮（NO）和前列腺素E ₂（PGE ₂）。这些调节剂与OA的临床症状如炎症性疼痛，关节肿胀和疾病发展呈正相关。对OA-FLS中炎性免疫反应的更好理解可以为OA的综合治疗策略提供一种新颖的方法。在这里，我们总结了最近发表的文献，这些文献涉及与OA-FLS介导的炎症有关的表观遗传修饰，激活的信号通路和炎症相关因子。此外，还总结了当前相关的临床试验和未来展望。