Calcium channels: the potential therapeutic targets for inflammatory bone destruction of rheumatoid arthritis

Abstract

Inflammatory bone resorption causes progressive joint destruction which ultimately leads to functional disability in rheumatoid arthritis (RA). The primary cell responsible for bone resorption is the osteoclast, which means it is a potential therapeutic target against bone destruction. In fact, experimental and clinical findings suggest that blockade of osteoclast differentiation and function is highly effective in inhibiting bone destruction in RA. In this report, we show several lines of experimental evidence which suggest that a variety of Ca2+ channels are essential in osteoclast differentiation and function, and present a hypothesis that modulation of Ca2+ channels is a highly effective therapeutic strategy in preventing osteoclast-induced structural damage in RA.