title: [RANKL and OPG regulation on bone remodeling].
abstract: Bone remodeling is a spatially coordinated lifelong process whereby old bone is absorbed by osteoclasts and replaced by bone-forming osteoblasts. Postmenopausal osteoporosis and other conditions are associated with an increased rate of bone remodeling, which leads to accelerated bone loss and increased risk of fracture. Bone resorption is dependent on a cytokine known as RANKL (receptor activator of NF-κB ligand). The catabolic effects of RANKL are prevented by osteoprotegerin (OPG) that binds RANKL and thereby prevents activation of its single cognate receptor called RANK. Evidence in numerous disease models and settings suggests that the ratio of RANKL:OPG represents an important role on bone resorption and remodeling.
authors.affiliation: Department of Prosthodontics, School and Hospital of Stomatology, Wuhan University, Wuhan 430079, Hubei Province, China. zhao-yi-@163.com
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhao
authors.forename: Yu
authors.initials: Y
authors.lastname: Cai
authors.forename: Yi-ning
authors.initials: YN
authors.lastname: Wang
mesh_terms: D016723:Bone Remodeling; D001862:Bone Resorption; D006801:Humans; D010006:Osteoblasts; D010010:Osteoclasts; D053244:Osteoprotegerin; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B
chemical_list: D053244:Osteoprotegerin; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B