The inflammasomes are intracellular protein complexes that are assembled in response to a variety of perturbations including infections and injuries. Failure of the inflammasomes to rapidly clear the insults or restore tissue homeostasis can result in chronic inflammation. Recurring inflammation is also provoked by mutations that cause the constitutive assembly of the components of these protein platforms. Evidence suggests that chronic inflammation is a shared mechanism in bone loss associated with aging, dysregulated metabolism, autoinflammatory, and autoimmune diseases. Mechanistically, inflammatory mediators promote bone resorption while suppressing bone formation, an imbalance which over time leads to bone loss and increased fracture risk. Thus, while acute inflammation is important for the maintenance of bone integrity, its chronic state damages this tissue. In this review, we discuss the role of the inflammasomes in inflammation-induced osteolysis.

中文翻译：

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炎性骨疾病中不存在炎性体活动。

炎性小体是细胞内蛋白质复合物，可对多种干扰（包括感染和伤害）进行组装。炎性小体未能迅速清除损伤或无法恢复组织稳态可导致慢性炎症。引起这些蛋白质平台组分组成性装配的突变也引起了反复发炎。有证据表明，慢性炎症是与衰老，新陈代谢失调，自身炎症和自身免疫性疾病相关的骨质流失的共同机制。从机理上讲，炎症介质在抑制骨形成的同时促进了骨吸收，这种不平衡随着时间的流逝导致骨质流失和骨折风险增加。因此，尽管急性炎症对于维持骨骼完整性很重要，它的慢性状态会破坏该组织。在这篇综述中，我们讨论了炎症小体在炎症诱导的骨溶解中的作用。