OPGL is a key regulator of osteoclastogenesis and bone morphogenesis

Summary form only received as follows: Morphogenesis and remodeling of bone is a physiologically controlled process that involves the synthesis of bone matrix by osteoblasts and the coordinate resorption of bone by osteoclasts. Imbalances between osteoclast and osteoblast activities can arise from a wide variety of hormonal changes or perturbations of inflammatory and growth factors, resulting in skeletal abnormalities characterized by decreased (osteoporosis) or increased (osteopetrosis) bone mass. The TNF-family molecule osteoprotegerin-ligand (OPGL) has been identified as a potential osteoclast differentiation factor and regulator of T cell/dendritic cell interactions. The author reports that mice with a disrupted opgl gene have severe osteopetrosis, a defect in tooth eruption, and completely lack osteoclasts due to an inability of osteoblasts to support osteoclastogenesis. opgl^--/ mice had defects in early thymocyte differentiation, and impaired antigen receptor-mediated proliferation and cytokine production in T cells. Surprisingly, opgl^-$/mice lacked all lymph nodes, but displayed normal splenic structure and Peyer´s patches. These data show that OPGL is required for lymph node organogenesis and T cell activation, and that OPGL is an essential regulator of osteoclast development. Here, the author discusses novel findings on the role of OPGL in osteoporosis, lymphoid functions and arthritis. Moreover, the role of OPGL and T cells on the biomechanical properties of bones is shown