The CAMAC brings together investigators focused on the mechanisms of bone loss and bone erosions in inflammatory diseases such as rheumatoid arthritis.  The monocyte/macrophage origin of osteoclasts and the influence of the immune system and chronic inflammation on bone biology are now well recognized.  Reflecting a long-standing interest in immune activation and rheumatoid arthritis, innovative models of pathways leading to RA-associated bone erosion are being explored in the Center in multiple cell types, including Th17 cells as well as the development of these lesions in murine models (Mountz).  This perspective in “osteoimmunology” leverages the work of multiple CAMAC investigators on the Th17 axis, the gut and microbiota (Weaver); and through the encouragement of the CAMAC, the scope extends to the role of TLRs in inflammatory bone loss (Feng).  The role of the primary cilium in skeletal integrity (Serra, Yoder), represents an exciting new innovation in our understanding of cartilage and skeletal development (Javed, MacDougall).  Coupled with the recruitment of Yi-Ping Li and his work in gene transfer, promising new insights into the biology of these tissues and strategies to prevent or treat bone and cartilage injury (Zayzafoon, Nagy, Ponnashagan, Sanderson) are anticipated.