Abstract Research into the bone destruction associated with rheumatoid arthritis has highlighted the importance of the interplay of the immune and skeletal systems. Arthritic bone destruction is attributable to the defective control of osteoclastogenesis by T cells. We revealed that excessive expression of receptor activator of NF-κB ligand (RANKL) and a paucity of interferon-γ underlie the enhanced osteoclastogenesis in arthritis. The interdisciplinary research field called osteoimmunology has attracted further attention after identification of a number of unexpected bone phenotypes in mice lacking immunomodulatory molecules. Accumulating evidence suggests that the immune and skeletal systems share not only cytokines but also various signaling molecules, transcription factors, and membrane receptors. Thus, bone turns out to be a dynamic tissue that is constantly renewed, where the immune system participates to a hitherto unexpected extent. This emerging field will be of great importance for a better understanding and treatment of rheumatic diseases.