Osteoclasts are type of bone cell that removes bone tissue by removing its mineralize matrix and breaking up the organic bone. This process is known as bone resorption.
- Since calcitonin is released from parafollicular cells in direct relation to circulating levels of Ca2+. It is suggested that calcitonin function to prevent elevated Ca2+ i.e., it prevents "postprandial hypercalcemia" i.e., absorption of Ca2+ from food during meal. Thus, calcitonin lower blood Ca2+ levels by inhibiting the osteoclast activity in bones.
- Ca2+ exchange is regulated by hormones, the most important of which is the parathyroid hormone (PTH), secreted by parathyroid gland. This hormone increases blood Ca2+ level. A major target tissue of PTH is bone, specifically stromal osteoblast cells of the bone marrow. In response of PTH, these osteoblast cells secrete one/more cytokines that then stimulate osteoclastic activity leading to the resorption of bone. In this way, demineralization of bone results in elevated levels of Ca2+.
- Hypocalcemia is stimulatory to PTH secretion from the parathyroid. PTH stimulates renal cortical 1-alpha-OHase activity and 1,25 (OH)2 D3 biosynthesis. 1,25 (OH)2 D3 stimulates Ca2+ reabsorption from the gut, increase release of Ca2+ reabsorption from the kidney. Vitamin D causes demineralization to provide Ca2+ and possibly PO43-, to maintain the critical plasma levels of these ions. However, Ca2+ and PO43- are provided for accretion of new bone.
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