Fig. 1

The development of RA bone destruction. In the process of RA, RAFLS, Th17, and M1 type macrophages secrete inflammatory factors such as TNF-α, IL-1β, IL-6, and IL-17, which promote RANKL secretion. Up-regulated RANKL stimulates the differentiation of osteoclast precursor cells into mature osteoclasts. The excessive proliferation of osteoclasts disrupts the delicate balance between osteoclasts and osteoblasts, leading to an imbalance in the bone microenvironment homeostasis. This dysregulation ultimately results in bone destruction characteristic of RA