PTH has two levels of action in bone. First, in response to acute decreases in serum calcium, PTH stimulates surface osteocytes to increase the outward flux of calcium ion from bone to rapidly restore serum calcium. Thus, during brief periods of hypocalcemia, PTH release results in mobilization of calcium from labile areas of bone that lie adjacent to osteoclasts. This effect is not associated with any significant increase in plasma phosphate or bone resorption. Second, PTH induces transformation of osteoprogenitor cells into osteoclasts, which increase bone formation. Thus, PTH has anabolic action on bone formation at physiological levels, and it is this action that allows it to be used pharmacologically to treat osteoporosis. However, in conditions that result in chronic calcium deficiency or prolonged hypocalcemia (e.g., renal osteodystrophy, vitamin D deficiency, or malabsorption syndromes), PTH mobilizes deep os-teocytes in perilacunar bone and can result in significant bone resorption and eventual osteopenia as it attempts to maintain normal concentrations of ionic or free plasma calcium.
In the kidney, PTH stimulates the conversion of 25-(OH)D3 into 1,25-(OH)2D3. Intrarenal 1,25-(OH)2 D3 causes an amplification of the PTH-induced calcium reabsorption and phosphate diuresis. 1,25-(OH)2D3 enhances PTH action in bone also. Once again, PTH does not directly affect intestinal calcium absorption, but it does so indirectly through induction of 1,25-(OH)2 D3 synthesis and enhanced enterocyte absorption.
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