Department of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Department of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Semin Arthritis Rheum. 2024 Oct;68:152527. doi: 10.1016/j.semarthrit.2024.152527. Epub 2024 Aug 3.
To summarize current insights on the immune pathology of bursitis caused by rheumatic inflammatory diseases, degenerative conditions, or mechanical stress and identify knowledge gaps in this field. Data on tenosynovitis pathology was included for comparison.
We performed a systematic review encompassing an electronic database search of all published literatures in PubMed/MEDLINE from inception to February 13, 2023, investigating the immunological changes occurring in the bursa of patients with inflammatory rheumatic diseases, degenerative conditions or mechanical stress (e.g., impingement syndrome).
Thirty-two articles provided data on the immune pathology of bursal tissue inflammation were identified. Histological and immunological perturbations included alterations of tissue morphology, infiltration of macrophages and some T cells, and enhanced expression of proinflammatory cytokines, such as interleukin (IL)-6, IL-1β and tumor necrosis factor alpha (TNF-α). These changes were described for all three underlying causes, although studies on bursitis associated with rheumatic inflammatory diseases were rare. Fibrosis was only reported in subacromial bursitis caused by mechanical stress within our included studies.
Current insights on bursitis were outdated and studies on bursitis associated with rheumatic inflammatory diseases are particularly lacking. Substantial overlap of enhanced expression of IL-6, IL-1β, TNF-α and infiltrating macrophages were found in bursitis irrespective of the underlying cause. In depth investigation on bursitis such as high throughput multi-omics are urgently needed to guide disease-specific therapeutic management.
总结风湿性炎症性疾病、退行性疾病或机械性应激引起的滑囊炎的免疫病理学的最新认识,并确定该领域的知识空白。纳入肌腱滑膜炎病理数据进行比较。
我们进行了一项系统综述,对从开始到 2023 年 2 月 13 日在 PubMed/MEDLINE 上发表的所有文献进行了电子数据库检索,调查了炎症性风湿性疾病、退行性疾病或机械性应激(如撞击综合征)患者滑囊中发生的免疫学变化。
确定了 32 篇提供滑囊组织炎症免疫病理学数据的文章。组织学和免疫学改变包括组织形态改变、巨噬细胞和一些 T 细胞浸润以及促炎细胞因子(如白细胞介素(IL)-6、IL-1β和肿瘤坏死因子-α(TNF-α))表达增强。这些变化在所有三种潜在病因中均有描述,尽管关于与风湿性炎症性疾病相关的滑囊炎的研究很少。在我们纳入的研究中,只有机械性应激引起的肩峰下滑囊炎报告了纤维化。
目前对滑囊炎的认识已经过时,特别是缺乏与风湿性炎症性疾病相关的滑囊炎研究。在滑囊炎中,IL-6、IL-1β、TNF-α 和浸润的巨噬细胞表达增强有很大的重叠,无论其潜在病因如何。迫切需要对滑囊炎进行深入研究,如高通量多组学,以指导针对特定疾病的治疗管理。