ENDOCRINE CAUSES OF BONE-DISEASE

被引:9
作者
GUPTA, KL
ROLLA, AR
机构
[1] NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215
[2] HARVARD UNIV,SCH MED,BOSTON,MA
[3] TUFTS UNIV,SCH MED,BOSTON,MA 02111
[4] NEW YORK MED COLL,DEPT MED,DIV GERONTOL & GERIATR MED,VALHALLA,NY 10595
关键词
D O I
10.1016/S0889-8529(18)30045-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Circulating hormones and growth factors and many paracrinic factors normally regulate skeletal metabolism. The right hormones and growth factors in the right amount and at the right times are very important for the development, growth, and maintenance of the skeleton. Growth factors arrive at the bone from the circulation or are produced locally by a variety of cells present in bone. Skeletal cells synthesize insulinlike growth factors I and II (IGF-1 and IGF-II), transforming growth factors-beta 1, 2, and 3, bone morphogenetic proteins (BMP), fibroblasts growth factors, platelet-derived growth factors, prostaglandins, and a variety of cytokines of the immune system.(6) Circulating hormones interact with these local paracrine factors in the regulation of bone remodeling. Hormonal deficiencies or excesses may thus affect the achievement of peak bone mass, its maintenance during maturity, and the rate of bone loss that accompanies aging. Most of these endocrine effects on bone become clinically apparent only after many years of hypersecretion or deficiency of the respective hormones. Elderly persons are at a particular disadvantage because, superimposed on postmenopausal and senile osteoporosis, the endocrine osteopathies accelerate the rate of bone loss. Many endocrinopathies have only a transient deleterious effect on the skeleton. Once the endocrinopathy is cured or improved, there is increased bone formation in an effort to recover the mineral density lost. Unfortunately, the recovery is frequently incomplete, and bone density does not return entirely to normal. This lack of full recovery is even more marked in elderly persons.
引用
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页码:373 / 393
页数:21
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