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In bone, a major physiologic role of PTH appears to be to maintain normal Ca homeostasis by binding to PTH1R on cells of the osteoblast lineage and enhancing release of the cytokine, receptor activator of nuclear factor kB (NF-kB) ligand (RANKL) [30], which then binds to its receptor, RANK, on osteoclast precursors and osteoclasts, enhancing the formation of mature osteoclasts from precursors and augmenting the resorptive activity of existing osteoclasts, especially in cortical bone. PTH may also reduce the osteoblastic protein, osteoprotegerin, which binds to RANKL, forming an inactive complex, and preventing it from binding to RANK, thus reducing osteoclastic activity [31]. It has also been suggested that PTH can acutely release mineral at the bone surface in an osteoclast-independent manner by modifying its solubility [32]. PTH may also have anabolic effects via its action on osteoblastic cells, mainly on trabecular bone.

Vitamin D is essential for normal mineralization of bone via enhancing intestinal calcium and phosphate absorption and maintaining these ions within a range that facilitates hydroxyapatite deposition in bone matrix. A major direct function of 1,25(OH)₂D may also be to act directly on bone to enhance osteoclastic bone resorption by increasing the RANKL/OPG ratio in order to enhance the proliferation, differentiation, and activation of the osteoclastic system [33, 34]. High levels of 1,25(OH)₂D may also inhibit mineralization. Endogenous and exogenous 1,25(OH)₂D have also been reported to have an anabolic role in vivo [35, 36].