Abstract
Osteoclasts play a critical role in both normal bone metabolism and bone resorption in the joints of patients with rheumatoid arthritis. It has been reported that non-steroidal anti-inflammatory drugs (NSAIDs) inhibit murine osteoclastogenesis in vitro and murine arthritis models in vivo, but not the destruction of joints of patients with rheumatoid arthritis. In the current review article, we review the recent findings in the effect of NSAIDs on the formation and function of human and murine osteoclasts both in vitro and in vivo, underlining the importance of studies using human osteoclasts. Since 2009, we have suggested a novel term ‘human osteoclastology’.
Highlights
Many studies have investigated the hypothesis that activated T cells directly or indirectly modulate the formation and function of osteoclasts in bone resorption associated with rheumatoid arthritis (RA)since the receptor activator of nuclear factor κB (NF-κB) ligand (RANKL) was cloned as a factor inducing osteoclastogenesis in 1997–8
In 1999, we demonstrated that interleukin-17 (IL-17), which was Pharmaceuticals 2010, 3 first cloned in 1995, potently induces murine osteoclastogenesis via the expression of RANKL on murine osteoblasts, and that IL-17 is present in synovial fluid and tissues from patients with RA [4]
In 2009, we reported that, in human osteoclastogenesis induced by RANKL, T-cell leukemia translocationassociated gene (TCTA) protein is required for cellular fusion [21]
Summary
Many studies have investigated the hypothesis that activated T cells directly or indirectly modulate the formation and function of osteoclasts in bone resorption associated with rheumatoid arthritis (RA). Since the receptor activator of NF-κB ligand (RANKL) was cloned as a factor inducing osteoclastogenesis in 1997–8. These findings of RANKL were the breakthrough in the study of osteoclastogenesis. We and others have reported that activated T cells expressing RANKL induce osteoclastogenesis [1,2,3]. IL-1β or tumor necrosis factor α (TNF-α) induces RANKL on osteoblasts via the expression of PGE2. We first review the mechanism of osteoclastogenesis and the effects of non-steroidal anti-inflammatory drugs (NSAIDs) on the differentiation and activity of human and murine osteoclasts both in vitro and in vivo. NSAIDs should be more carefully used in patients with RA, osteoporosis, and bone fracture
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