Wuorela M, Granfors K
National Public Health Institute, Department in Turku, Finland.
Am J Med Sci. 1998 Oct;316(4):264-70. doi: 10.1097/00000441-199810000-00007.
Reactive arthritis was originally defined as a sterile joint inflammation after infection elsewhere in the body, but this view has been challenged in the past decade since different antigens and DNA and RNA of various triggering microbes have been shown to exist at the sites of inflammation in the joints. It has been suggested that microbial antigens, or intact pathogens, are important for the pathogenesis of reactive arthritis, at least in the early phase of the disease, but the exact mechanism of how the pathogens contribute to the development of this usually self-limiting polyarthritis has not been discovered. This article reviews the theories on the role of infectious agents as triggers of reactive arthritis.
反应性关节炎最初被定义为身体其他部位感染后出现的无菌性关节炎症，但在过去十年中，这一观点受到了挑战，因为已证实在关节炎症部位存在各种触发微生物的不同抗原以及DNA和RNA。有人提出，微生物抗原或完整病原体对反应性关节炎的发病机制很重要，至少在疾病的早期阶段如此，但病原体如何导致这种通常为自限性的多关节炎的具体机制尚未被发现。本文综述了关于感染因子作为反应性关节炎触发因素作用的相关理论。
