Bone Cell Regulation in Chronic Inflammatory Diseases
The long-term goal is to investigate the influence of chronic inflammation on bone cell function. We use mouse models of inflammatory arthritis and focus on TNF/RANKL/NF-κB signaling pathways. We demonstrated increased osteoclasts and osteoclast precursors and decreased osteoblasts and mesenchymal stem cells (MSCs) from mice and patients with rheumatoid arthritis (RA), indicating inadequate coupling between osteoblastic bone formation and osteoclastic bone resorption in chronic inflammatory bone disease. Recently, we have been studying the mechanisms whereby increased Notch activation limits MSC-osteoblast differentiation and bone formation in chronic inflammatory bone disease and the regulation of Notch by non-canonical NF-κB signaling. We are also interested how Notch signal regulates macrophage polarization and its role in the pathogenesis of RA.
