| Theme |
The multifaced role of bone for multisystem illness |
| Title |
Bone metabolism and rheumatoid arthritis |
| Author |
Yoshiya Tanaka |
The First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan |
| [ Summary ] |
Rheumatoid arthritis (RA) is a systemic inflammatory disease characterized by chronic synovitis and bone damage. Bone homeostasis is maintained by a balance between bone resorption by osteoclasts and bone formation by osteoblasts. It is also regulated by the immune system. Imbalances often result in pathological processes such as secondary osteoporosis. Th 1 and Th 17 are involved in activation of the immune system and also induce maturation of monocytes to osteoclasts, leading to osteoporosis, whereas regulatory T cells suppress both immune function and osteoclast differentiation. Proinflammatory cytokines such as TNF and IL-6 cause an imbalance in bone metabolism via direct and/or indirect effects on osteoclasts. As a result, inflammatory signals originate in the immune system, resulting in secondary osteoporosis and bone destruction. Based on an improved understanding of immune signals, investigation of the suppression of cell functions may lead to improved understanding and better treatment of bone destruction and osteoporosis. |