The molecular triad OPG/RANK/RANKL: involvement in the orchestration of pathophysiological bone remodeling.

By S. Théoleyre, Y. Wittrant, S. K. Tat, Y. Fortun, F. Redini, D. Heymann. Cytokine & growth factor reviews, 2004

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Receptor activator of nuclear factor kappaB ligand and osteoprotegerin regulation of bone remodeling in health and disease. (2008, neutral): “1,25-dihydroxyvitamin D 12 1 1 28, 103, 318 Hormones Estrogen 1 2/— 46, 76, 84, 104–108 Testosterone 12 — 106, 219 Glucocorticoid 2 1 254, 258, 259 PTH 2 1 86, 88 PTHrP 2 1 101 Cytokines IL-1 12 1 1 28, 98, 99 IL-4 2/— 109 IL-7 1 100 IL-13 1 2 — 52 IL-17 2 1 — 52 TNF 1 28, 52, 98 Interferon 1 1 1 52”
Osteoblast-Osteoclast Communication and Bone Homeostasis (2020, background): “OPG is considered to function as a decoy receptor binding to RANKL, negatively regulating osteoclast differentiation and activation by blocking the RANKL-RANK interaction [6,57].”
Osteoblast-Osteoclast Interactions (2017, background): “sion in osteoblasts is regulated by amount of hormones, cytokines and growth factors (14), such as estrogen, 1, 25(OH)2D3 and tumor necrosis factor(TNF).”
Denosumab and bisphosphonates: different mechanisms of action and effects. (2011, background): “The link between these local factors and the endocrine regulation of skeletal homeostasis through bone resorption and remodeling is, however, established by the fact that both RANKL and OPG expression and secretion are regulated by several calciumregulating hormones, such as sex hormones, parathyroi”