RANKL/OPG; Critical role in bone physiology

Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation.

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Effect of Parathyroid Hormone (1-34) on Fractures and Bone Mineral Density in Postmenopausal Women with Osteoporosis

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Osteoclast differentiation factor is a ligand for osteoprotegerin/osteoclastogenesis-inhibitory factor and is identical to TRANCE/RANKL

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OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph node organogenesis.

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Induction and Activation of the Transcription Factor NFATc1 (NFAT2) Integrate RANKL Signaling in Terminal Differentiation of Osteoclasts

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Osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification.

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Modulation of Osteoclast Differentiation and Function by the New Members of the Tumor Necrosis Factor Receptor and Ligand Families

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A homologue of the TNF receptor and its ligand enhance T-cell growth and dendritic-cell function.

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Evidence for osteocyte regulation of bone homeostasis through RANKL expression

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RANK is essential for osteoclast and lymph node development.

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Matrix-embedded cells control osteoclast formation

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c-Fos: a Key Regulator of Osteoclast-Macrophage Lineage Determination and Bone Remodeling

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TRAF6 deficiency results in osteopetrosis and defective interleukin-1, CD40, and LPS signalingPreprint

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Denosumab in postmenopausal women with low bone mineral density.

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Modulation of Osteoclast Differentiation

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Role of osteoblasts in hormonal control of bone resorption—A hypothesis

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OSTEOBLASTIC CELLS ARE INVOLVED IN OSTEOCLAST FORMATION

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Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis

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Isolation of a novel cytokine from human fibroblasts that specifically inhibits osteoclastogenesis.

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Severe osteoporosis in mice lacking osteoclastogenesis inhibitory factor/osteoprotegerin.

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Osteoclast-Like Cell Formation and its Regulation by Osteotropic Hormones in Mouse Bone Marrow Cultures*

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RANKL maintains bone homeostasis through c-Fos-dependent induction of interferon-β

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Coupling the activities of bone formation and resorption: a multitude of signals within the basic multicellular unit

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Osteoclast-derived activity in the coupling of bone formation to resorption

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Severe osteopetrosis, defective interleukin‐1 signalling and lymph node organogenesis in TRAF6‐deficient mice

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Wnt5a-Ror2 signaling between osteoblast-lineage cells and osteoclast precursors enhances osteoclastogenesis

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Tumor necrosis factors alpha and beta induce osteoblastic cells to stimulate osteoclastic bone resorption.

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The Bone Marrow-Derived Stromal Cell Lines MC3T3-G2/PA6 and ST2 Support Osteoclast-Like Cell Differentiation in Cocultures with Mouse Spleen Cells

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Mutations in TNFRSF11A, affecting the signal peptide of RANK, cause familial expansile osteolysis

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Cells of bone: proliferation, differentiation, and hormonal regulation

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Catabolic effects of continuous human PTH (1-38) in vivo is associated with sustained stimulation of RANKL and inhibition of osteoprotegerin and gene-associated bone formation.

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Activated T Lymphocytes Support Osteoclast Formation in Vitro

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Osteoprotegerin Produced by Osteoblasts Is an Important Regulator in Osteoclast Development and Function

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Activation of NF-κB by RANK Requires Tumor Necrosis Factor Receptor-associated Factor (TRAF) 6 and NF-κB-inducing Kinase

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Cancellous Bone Remodeling Occurs in Specialized Compartments Lined by Cells Expressing Osteoblastic Markers

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Biochemical Characterization with Parathormone and Calcitonin of Isolated Bone Cells: Provisional Identification of Osteoclasts and Osteoblasts

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Osteoblasts mediate interleukin 1 stimulation of bone resorption by rat osteoclasts.

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Randomized active-controlled phase II study of denosumab efficacy and safety in patients with breast cancer-related bone metastases.

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Normocalcemia is maintained in mice under conditions of calcium malabsorption by vitamin D–induced inhibition of bone mineralization

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Osteoblast-derived WNT16 represses osteoclastogenesis and prevents cortical bone fragility fractures

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Bone Resorption Restored in Osteopetrotic Mice by Transplants of Normal Bone Marrow and Spleen Cells

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Osteoblast-Like Cells in the Presence of Parathyroid Hormone Release Soluble Factor that Stimulates Osteoclastic Bone Resorption*

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Oncostatin M promotes bone formation independently of resorption when signaling through leukemia inhibitory factor receptor in mice

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WNT16 Influences Bone Mineral Density, Cortical Bone Thickness, Bone Strength, and Osteoporotic Fracture Risk

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Transforming Growth Factor β Affects Osteoclast Differentiation via Direct and Indirect Actions

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Activation of resorption in fatigue-loaded bone involves both apoptosis and active pro-osteoclastogenic signaling by distinct osteocyte populations

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Monocytes Induce STAT3 Activation in Human Mesenchymal Stem Cells to Promote Osteoblast Formation

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Osteoprotegerin regulates bone formation through a coupling mechanism with bone resorption.

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A TNF receptor loop peptide mimic blocks RANK ligand-induced signaling, bone resorption, and bone loss.

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EphrinB2/EphB4 inhibition in the osteoblast lineage modifies the anabolic response to parathyroid hormone

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