M. Alnaeeli and Y. -T. A. Teng Pages 893 - 910 ( 18 )
Recent studies have suggested that the dys-regulated progressive immune responses in some inflammatory conditions can lead to significantly increased osteoclasts (OC) frequency and activity associated with active bone destruction; termed inflammation-induced bone loss. Among the inflammatory infiltrates, monocytes/macrophages (Mo/MQ), T and B cells, have been well studied and documented as central players in osteoimmunological interactions (osteoimmunology: is an interdisciplinary field linking the immune and skeletal systems). We and others investigated the role(s) of dendritic cells (DC) during inflammation-induced osteoclastogenesis and bone loss. In addition to their innate effector functions, DC are potent professional antigen-presenting cells (APC) involved in triggering and orchestrating adaptive immunity, thereby implicated as potential osteo-immune players. Herein, bone remodeling and DCs biology including their development and functions are reviewed along with the contribution of DC at the crossroad of the osteo-immune interface during the process of inflammation-induced osteoclastogenesis. Furthermore, we provide a summary of recent progress, and discuss a proposed alternative mechanism underlying inflammation-induced bone loss. Understanding the cellular and molecular mechanisms regulating DCs roles in inflammation-induced osteoclastogenesis and bone loss might benefit future treatment approaches, especially if targeting DC can be translated into therapeutic strategies to ameliorate both tissue inflammation and bone destruction during disease progression associated with inflammatory bone diseases.
CD11c+dendritic cells, osteoclasts, osteoclastogenesis and bone loss, dendritc cell-derived osteoclast (DDOC), RANKL-RANK signaling, osteo-immune interface, Innate and adaptive immunity
Lab. of Molecular Microbial Immunity, Div. of Periodontology, Dept. of Microbiology&Immunology, and Eastman Dental Center, 625 Elmwood Ave. Rochester, New York.