User:Jaimeafreire

Osteoblasts respond to stimuli, producing macrophage colony stimulating factor M-CSF and RANKL, these are necesary for osteoclastogenesis. Others factors like Parathyroid hormone, Vitamin D, estrogen, Tumor Necrosis Factor Alfa and interleukins can regulate this process. The RANK receptor interacts with its ligand (RANKL) this receptor is present in their precursors. The interaction between ligand and recepptor induced osteoclast differentiation and activation and prevents osteoclast cell death. The RANK-RANKL signaling is regulate by citokine receptor osteoprogestin. The osteoprogestin pathway mediated the osteoclast production inhibiting the osteoclasts differentiation precursors that are derived from immunological system. OPG binding to RANKL on stromal cells, blocks the RANKL-RANK interaction between osteoblast/stromal cells and osteoclast precursors. This has the effect of inhibiting the differentiation of the osteoclast precursor into a mature osteoclast. However, estrogen can ihnibit RANKL expression interacting with transforming growth factor beta.