Fig. 5
Cellular interactions between dendritic cells (DCs) and osteoclasts (OCs) in pathological conditions. Under inflammatory conditions, such as rheumatoid arthritis and periodontitis, DCs can directly transdifferentiate into OCs, contributing to inflammation-induced bone erosion. This process of DCs-OCs transdifferentiation is modulated through three major mechanisms: (1) In the presence of macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor kappa-Î’ ligand (RANKL), DCs differentiate into OCs efficiently, as shown in the yellow dashed box. This interaction is a key driver of osteoclastogenesis under inflammatory conditions; (2) RANKL, produced by Th1, Th2, and Treg cells, or IL-17, produced by Th17 cells, can enhance DC-mediated osteoclastogenesis in an inflammatory microenvironment, as illustrated in the blue dashed box; (3) DCs can promote osteoclastogenesis by secreting osteoclastogenic cytokines, such as IL-23 and IL-34, which facilitate OC differentiation, as shown in the green dashed box. HSPCs hematopoietic stem and progenitor cells, GMP granulocyte-macrophage progenitor, MDP myeloid progenitor cells, Mo monocyte, DDOC dendritic cell-derived osteoclast
