Hosted by Cardiff University's School of Medicine
- Physiologic mechanisms coupling bone resorption and formation
- Rheumatoid arthritis (RA) as a disease of bone loss
- Mechanisms of bone loss and inhibition of bone formation in RA
- Spondylarthritis (SpA) as a disease of bone formation
- Contrasting mechanisms of the impact on bone in RA and SpA
Prof. Gravallese is the Theodore Bevier Bayles Professor of Medicine at Harvard Medical School and Chief of Rheumatology, Inflammation, and Immunity at the Brigham and Women’s Hospital.
Her career interest in research has focused the fundamental mechanisms of inflammation and joint destruction in inflammatory arthritis. She has identified key pathways by which inflammation impacts bone in the rheumatic diseases. Her laboratory identified osteoclasts as the cell type responsible for bone destruction in RA and demonstrated that RANKL is a critical cytokine produced by cells within RA synovial tissues that drives osteoclastogenesis. Her laboratory has also identified the production in RA synovial tissue of inhibitors of osteoblast function that prevent “healing” of bone. These inhibitors are currently being explored as novel therapeutic targets to promote bone formation. Her work helped to launch a new field, “Osteoimmunology”, leading to other major contributions to our understanding of the impact of inflammation on bone. Her current studies focus on innate immune pathways in inflammation and bone remodeling in rheumatic disease, including the STING and AIM2 cytosolic DNA sensing pathways.
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