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Calcitonin is a hormone secreted by the thyroid in humans. Calcitonin decreases osteoclast activity, and decreases the formation of new osteoclasts, resulting in decreased resorption. [4] Calcitonin has a greater effect in young children than in adults, and plays a smaller role in bone remodeling than PTH. [4]
The calcitonin receptor (CT) is a G protein-coupled receptor that binds the peptide hormone calcitonin and is involved in maintenance of calcium homeostasis, [5] particularly with respect to bone formation and metabolism. [6] [7] [8]
Calcitonin lowers blood calcium and phosphorus mainly through its inhibition of osteoclasts. Osteoblasts do not have calcitonin receptors and are therefore not directly affected by calcitonin levels. However, since bone resorption and bone formation are coupled processes, eventually calcitonin's inhibition of osteoclastic activity leads to ...
An osteoclast is a large multinucleated cell and human osteoclasts on bone typically have four nuclei [5] and are 150–200 μm in diameter. When osteoclast-inducing cytokines are used to convert macrophages to osteoclasts, very large cells that may reach 100 μm in diameter occur. These may have dozens of nuclei, and typically express major ...
Parafollicular cells, also called C cells, are neuroendocrine cells in the thyroid. They are called C cells because the primary function of these cells is to secrete calcitonin. [1] They are located adjacent to the thyroid follicles and reside in the connective tissue. These cells are large and have a pale stain compared with the follicular cells.
Bone tissue is removed by osteoclasts, and then new bone tissue is formed by osteoblasts. Both processes utilize cytokine (TGF-β, IGF) signalling.In osteology, bone remodeling or bone metabolism is a lifelong process where mature bone tissue is removed from the skeleton (a process called bone resorption) and new bone tissue is formed (a process called ossification or new bone formation).
The role of calcitonin, a hormone generated by the thyroid that increases bone deposition, is less clear and probably not as significant as that of PTH. [36] The activation of osteoclasts is regulated by various molecular signals, of which RANKL (receptor activator of nuclear factor kappa-B ligand) is one of the best-studied. [100]
The cells also use paracrine signalling to control the activity of each other. [73] [74] For example, the rate at which osteoclasts resorb bone is inhibited by calcitonin and osteoprotegerin. Calcitonin is produced by parafollicular cells in the thyroid gland, and can bind to receptors on osteoclasts to directly inhibit osteoclast activity ...