Regulation of bone destruction in rheumatoid arthritis through RANKL-RANK pathways

Abstract

Recent studies have demonstrated that osteoclasts, the primary cells responsible for bone resorption, are mainly involved in bone and joint destruction in rheumatoid arthritis (RA) patients. Recent progress in bone cell biology has revealed the molecular mechanism of osteoclast differentiation and bone resorption by mature osteoclasts. We highlight here the potential role of the receptor activator of nuclear factor κB ligand (RANKL)-RANK pathways in bone destruction in RA and review recent clinical trials treating RA by targeting RANKL.

Human CD56bright NK Cells: An Update

“…Furthermore, the NK cell-monocyte contact induces the differentiation of monocytes into osteoclasts (86). This is important because in RA, bone destruction results from a process of osteoclast differentiation that is associated with a pathway involving the receptor activator of NF-kB and its ligand (RANKL-RANK) (87,88). Because RANKL is primarily expressed on the CD56 bright subset (86), these cells have a high potential to induce osteoclast formation in the SF and to lead indirectly to the consequent bone destruction.…”

Positive Correlation of RANK Expression on Human Monocytes with Age: RANK Expressed on Human Monocytes may play a Role in Senile Osteoporosis

“…The RANK-RANKL system involves both osteoclastogenesis and the immune system [12][13][14]. High-level expression of RANK on CD14 + cells, shown in a previous study, may induce osteoclastogenesis via activated T cells expressing RANKL.…”

Effect of polygonimitin C on bone formation and resorption in human osteoblast-like MG63 cells

“…Osteoclasts differentiation and maturity are enhanced by the combination of RANKL produced by osteoblasts and RANK [24]. The OPG produced by osteoblasts is a decoy receptor for RANKL and inhibits combination of RANKL and RANK [25].…”