Rheumatoid arthritis is a chronic disease that affects multiple joints. It is considered to be an autoimmune disease in which a T helper (Th)-1 type response has been implicated to play an important pathogenetic role. As osteoclasts, cells that resorb bone, play a crucial part in the bone destruction that occurs in RA, we and others have investigated the pathophysiology of these cells. The findings that interferon (IFN)-gamma strongly inhibits osteoclastogenesis and that interleukin (IL)-17 has the ability to enhance osteoclast differentiation have cast doubt on the hypothesis that RA is a Th1 disease. In this review, I describe the relationship between Th cells, the so-called "commander" of the immune response, and RA, mainly from the viewpoint of the environments Th cells create for the excessive differentiation and function of osteoclasts, resulting in the destruction of bone.