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Current Concepts of Bone Metabolism

LEO LUTWAK, M.D., Ph.D.; FREDERICK R. SINGER, M.D.; and MARSHALL R. URIST, M.D.
[+] Article and Author Information

▸Requests for reprints should be addressed to Leo Lutwak, M.D., Endocrinology Section, Veterans Administration Hospital, 16111 Plummer St., Sepulveda, CA 91343.


Los Angeles, California


Ann Intern Med. 1974;80(5):630-644. doi:10.7326/0003-4819-80-5-630
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Bone morphogenesis is a function of biochemical components of the organic matrix of bone, which consists of a noncollagenous protein resistant to solution, a solid support fibrous protein (collagen), and a neutral proteinase that degrades the noncollagenous protein. The proteinase functions in association with inhibitors that retard destruction of the protein and account for survival of morphogenetic activity in bone matrix. Calcitonin mediates another control mechanism for bone formation; it produces a decrease in osteoclasts, a delayed increase in osteoblasts, and significantly lowers plasma calcium and hydroxyproline concentrations in patients with increased bone turnover. Although calcitonin administration does not have a significant hypocalcemic effect in normal persons, the urinary excretion of dializable and nondializable peptides containing hydroxyproline is decreased. Chronic dietary insufficiency of calcium or excess of phosphate, or both, may lead to secondary nutritional hyperparathyroidism in animals and man, manifested primarily by increased resorption of trabecular bone. Osteoporosis of the jaw, leading to periodontal disease, is suggested as the precursor of the systemic osteoporosis seen in older patients.

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