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Journal ArticleDOI

Sex Steroids and Bone

Juliet E. Compston
- 01 Jan 2001 - 
- Vol. 81, Iss: 1, pp 419-447
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TLDR
Further elucidation of the mechanisms by which sex steroids affect bone has the potential to improve the clinical management not only of osteoporosis, both in men and women, but also of a number of other diseases related to sex hormone status.
Abstract
Sex steroids are essential for skeletal development and the maintenance of bone health throughout adult life, and estrogen deficiency at menopause is a major pathogenetic factor in the development of osteoporosis in postmenopausal women. The mechanisms by which the skeletal effects of sex steroids are mediated remain incompletely understood, but in recent years there have been considerable advances in our knowledge of how estrogens and, to a lesser extent androgens, influence bone modeling and remodeling in health and disease. New insights into estrogen receptor structure and function, recent discoveries about the development and activity of osteoclasts, and lessons learned from human and animal genetic mutations have all contributed to increased understanding of the skeletal effects of estrogen, both in males and females. Studies of untreated and treated osteoporosis in postmenopausal women have also contributed to this knowledge and have provided unequivocal evidence for the potential of high-dose estrogen therapy to have anabolic skeletal effects. The development of selective estrogen receptor modulators has provided a new approach to the prevention of osteoporosis and other major diseases of menopause and has implications for the therapeutic use of other steroid hormones, including androgens. Further elucidation of the mechanisms by which sex steroids affect bone thus has the potential to improve the clinical management not only of osteoporosis, both in men and women, but also of a number of other diseases related to sex hormone status.

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Journal ArticleDOI

Androgens and bone

TL;DR: Observations in androgen-resistant animals clearly demonstrated that the sexual dimorphism of bone depends on the presence of a functional androgen receptor, and optimal peak bone mass seems related to an appropriately timed androgen secretion.
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Skeletal changes in rats given daily subcutaneous injections of recombinant human parathyroid hormone (1-34) for 2 years and relevance to human safety.

TL;DR: The data suggest that the increased incidence of bone neoplasia in rats treated for 2 years is likely not predictive of an increased risk of bone cancer in skeletally mature adult humans being given PTH(1-34) for a limited period of time in the treatment of osteoporosis.
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Dose-response relationships between energy availability and bone turnover in young exercising women.

TL;DR: Bone formation was impaired by less severe restrictions than that which increased bone resorption and military servicewomen and others may need to improve their nutrition to avoid these effects.
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Evidence of estrogen receptors in normal human osteoblast-like cells

TL;DR: The data suggest that estrogen acts directly on human bone cells through a classical estrogen receptor-mediated mechanism, indicating an induction of functional progesterone receptors.
References
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Journal ArticleDOI

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Journal ArticleDOI

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Journal ArticleDOI

Targeted Disruption of Cbfa1 Results in a Complete Lack of Bone Formation owing to Maturational Arrest of Osteoblasts

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