Fig. 2

Pathological bone remodeling phenotypes (a) Synovial inflammation, pannus formation and immune cell infiltration is associated with increased release of osteoclastogenic cytokines which drives osteoclast recruitment and differentiation resulting in aberrant bone erosive processes. b In OA increased subchondral remodeling is lead inflammatory changes or mechanical alterations cause infiltration of bone cells from the marrow and vascularization into the subchondral bone area leading to increased bone remodeling and instances of subchondral thinning. In RA, osteopenia localizes in the periarticular regions. A combination of increased cytokine signaling and inflammation from the bone marrow may activate osteoclastogenesis. At the same time osteoblast mediated bone formation is inhibited by anti-osteogenic factors such as DKK1 and SOST. c In OA, bone sclerosis occurs in response to increased mechanical loading, resulting in excessive bone formation, thickening of the subchondral bone plate and calcified cartilage, tidemark duplication and reduced mineralization of the bone