여성에서 골 성장과 보존
Development and Conservation of the Female Skeleton
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Estrogen is the key hormone for maintaining bone mass and estrogen deficiency is the major cause of age related bone loss in female. Estrogen together with growth hormone and IGF-1 initiate a 3- to 4- pubertal growth spurt that doubles skeletal mass and is also required for the attainment of maximal peak bone mass. Aging women undergo two phases of bone loss. The menopause initiates an accelerated phase of predominantly cancellous bone loss that declines rapidly over 4~8 yr to become asymptotic with a subsequent slow phase that continues indefinitely. The accelerated phase results from the loss of the direct restraining effects of estrogen on bone turnover, an action mediated by estrogen receptors in both osteoblasts and osteoclasts. In ensuing slow phase, the rate of cancellous bone loss is reduced, but the rate of cortical bone loss is unchanged or increased. This phase is mediated largely by secondary hyperparathyroidism that result from the loss of estrogen actions on extraskeletal calcium metabolism. Impaired osteoblast function due to estrogen deficiency, aging, or both also contributes to the slow phase of bone loss.
Abstract
Estrogen is the key hormone for maintaining bone mass and estrogen deficiency is the major cause of age related bone loss in female. Estrogen together with growth hormone and IGF-1 initiate a 3- to 4- pubertal growth spurt that doubles skeletal mass and is also required for the attainment of maximal peak bone mass. Aging women undergo two phases of bone loss. The menopause initiates an accelerated phase of predominantly cancellous bone loss that declines rapidly over 4~8 yr to become asymptotic with a subsequent slow phase that continues indefinitely. The accelerated phase results from the loss of the direct restraining effects of estrogen on bone turnover, an action mediated by estrogen receptors in both osteoblasts and osteoclasts. In ensuing slow phase, the rate of cancellous bone loss is reduced, but the rate of cortical bone loss is unchanged or increased. This phase is mediated largely by secondary hyperparathyroidism that result from the loss of estrogen actions on extraskeletal calcium metabolism. Impaired osteoblast function due to estrogen deficiency, aging, or both also contributes to the slow phase of bone loss.
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