Local and systemic control of the osteoblast
Abstract
The role of parathyroid hormone (PTH) as a protector of extracellular calcium levels requires that, in response to the challenge of hypocalcemia, the hormone activate a mechanism for the release of calcium from bone, its principal body storehouse. PTH does so not by a direct action on the bone-resorbing cell, the osteoclast, but by an indirect effect mediated by PTH receptors on bone stromal cells, including the mature bone-forming cell, the osteoblast. Regarded from the perspective of calcium homeostasis, the entrainment of osteoblasts and their stromal precursors by PTH could serve the straightforward function of linking new bone formation to bone resorption, thus restoring bone sacrificed to the demands of hypocalcemia. For example, primary hyperparathyroidism is an osteoporotic state, but most of the bone loss occurs from the cortical compartment, which is impoverished of osteoblasts. The cancellous or trabecular compartment of bone, which presents a large surface area to osteoblastic new bone formation, is relatively preserved in primary hyperparathyroidism and may actually be increased (1).
However, the anabolic effect of PTH is markedly accentuated when the hormone is administered once daily, an ancient observation (2) that has now led to the introduction of therapy using synthetic PTH fragments for the treatment of osteoporosis. Daily subcutaneous administration of PTH induces rapid, dramatic effects in cancellous bone mass (3), and a preliminary report indicates a…
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