The proinflammatory cytokine interleukin‐1β (IL‐1β) is produced as inactive proIL‐1β and then processed by caspase‐1 to become active. In 2002, it was demonstrated that the intracellular multiprotein complex known as the inflammasome functions as a molecular platform to trigger activation of caspase‐1. Inflammasomes are known to function as intracellular sensors for a broad spectrum of various pathogen‐associated and damage‐associated molecular patterns. In 1985, it was demonstrated that Porphyromonas gingivalis, a representative bacterium causing chronic periodontitis, induces IL‐1 production by murine peritoneal macrophages. Since then, many studies have suggested that IL‐1, particularly IL‐1β plays key roles in the pathogenesis of periodontal diseases. However, the term “inflammasome” was not used until the involvement of inflammasomes in periodontal disease was suggested in 2009. Several subsequent studies on the roles of the inflammasome in the pathogenesis of periodontal diseases have been published. Interestingly, two contradictory reports on the modulation of inflammasomes by P. gingivalis have been published. Some papers have described how P. gingivalis activates the inflammasome to produce IL‐1β whereas some stated that P. gingivalis inhibits inflammasome activation to subvert immune responses. Several lines of evidence have suggested that the inflammasome activation is modulated by periodontopathic bacteria other than P. gingivalis. Hence, studies on the roles of inflammasomes in the pathogenesis of periodontal diseases began only 8 years ago and many pathological roles of inflammasomes remain to be clarified.

中文翻译：

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炎性体在牙周疾病发病机理中作用的研究的历史方面。

促炎性细胞因子白介素-1β（IL-1β）以非活性的proIL-1β的形式产生，然后被caspase-1处理成为活性的。2002年，证明了称为炎症小体的细胞内多蛋白复合物可作为触发caspase-1活化的分子平台。炎症小体可作为细胞内传感器，用于各种病原体相关和损伤相关分子模式的广泛范围。1985年，证明牙龈卟啉单胞菌引起慢性牙周炎的代表性细菌，可诱导鼠腹膜巨噬细胞产生IL-1。从那以后，许多研究表明IL-1，尤其是IL-1β在牙周疾病的发病机理中起着关键作用。但是，直到2009年建议炎症小体参与牙周疾病时，才使用“炎症小体”一词。随后有关炎症小体在牙周病发病机理中的作用的几项后续研究已经发表。有趣的是，关于牙龈卟啉单胞菌调节炎症小体的两个矛盾报道已经发表。一些论文描述了牙龈卟啉单胞菌如何激活炎性体产生IL-1β，而另一些则指出牙龈卟啉单胞菌。抑制炎症小体激活以破坏免疫反应。几条证据表明炎性体的活化是由牙龈卟啉菌外的牙周病细菌调节的。因此，关于炎性小体在牙周疾病发病机理中的作用的研究仅在八年前就开始了，炎性小体的许多病理学作用仍有待澄清。