破骨细胞形成过多、骨吸收过强是导致骨质疏松的重要原因。适量活性氧自由基（ROS）参与破骨细胞分化，其中硫氧还蛋白Trx和硫氧还蛋白结合蛋白TBP-2是重要的ROS调控蛋白。我们前期发现，抑制TBP-2表达可抑制破骨分化；破骨细胞特异性TBP-2敲除小鼠呈骨量升高表型，破骨细胞减少；RANKL诱导破骨细胞内ROS，促进TBP-2与NLRP3结合，诱导NLRP3炎症小体形成。结合文献及前期数据，提出“RANKL增加破骨细胞内ROS，TBP-2与Trx分离，转而与NLRP3结合，激活炎症小体，促进破骨分化导致骨质疏松”假说。本研究拟从分子、细胞、动物和人体水平，探讨氧化还原与炎症小体交互作用促进骨质疏松发生的作用，为治疗骨质疏松提供新思路。

Excessive osteoclast formation and bone resorption cause osteoporosis.An appropriate amount of reactive oxygen species (ROS) is required for osteoclastogenesis. Thioredoxin (Trx) and thioredoxin binding protein (TBP-2) are crucial redox proteins in ROS regulation.We previous data found that the inhibition of TBP-2 can inhibit osteoclast differentiation.Osteoclastic specific TBP-2 knockout mice showed increased bone mass and decreased osteoclasts.In addition, RANKL induced intracellular expression of ROS, promoting TBP-2 binding to NLRP3, and subsequently inducing the formation of NLRP3 inflammasomes in osteoclast. According to the literature and previous data, the hypothesis was proposed that "RANKL increases intracellular ROS levels, which promotes TBP-2 separating from Trx and binding to NLRP3, activating inflammasomes and promoting osteoclast differentiation, finally leading to osteoporosis".This study aims to explore the pathophysiology of osteoporosis by demonstrating the interaction between redox reaction and inflammasomes in osteoclasts on molecular, cellular, animal and human levels, providing new ideas for the treatment of osteoporosis.