YOU ARE NOW CONNECTED TO THE TOXLINE (1981 FORWARD, NON-ROYALTY) FILE. ==OSTEOPOROSIS IN CHILDREN== 6 AUTHOR Amagai H TITLE [Osteoporosis in young people] SOURCE Nippon Rinsho; VOL 52, ISS 9, 1994, P2395-9 (REF: 15) ABSTRACT Osteoporosis in young people is divided into idiopathic juvenile osteoporosis and secondary osteoporosis. Idiopathic juvenile osteoporosis is a rare, self-limited disease characterized by its recover after 3 or 4 years from the incidence. In severe type of idiopathic juvenile osteoporosis, the deformity of spine and extremities due to numerous vertebral and metaphyseal fractures and frequent long bone fractures makes a limitation of daily activities. On the treatment it is important to take care not to make deformity. Idiopathic juvenile osteoporosis is very rare in Japan and unknown cause, is necessary to make more researches in its cause. Many disease are known to cause secondary osteoporosis. And the patients number of secondary osteoporosis are much more than idiopathic juvenile osteoporosis. In secondary osteoporosis, of cause, it is most important to treat the original disease. The treatment of secondary osteoporosis is made a great difference by patient condition. Osteoporosis in young people makes deformity of spine and extremities and height loss, and influences the growth and development for serious disorder. It is necessary for treatment of these young people to take care to make the disorder to minimum. 28 AUTHOR Odell WD AUTHOR Heath H 3d TITLE Osteoporosis: pathophysiology, prevention, diagnosis, and treatment. SOURCE Dis Mon; VOL 39, ISS 11, 1993, P789-867 (REF: 369) ABSTRACT Bone is a living tissue; throughout life, new bone formation coexists with bone resorption. Although a large number of hormones and cytokines modulate osteoblast and osteoclast function, osteoporosis results from any disorder in which bone formation becomes uncoupled from bone resorption. Many disorders are associated with the uncoupling of bone formation and resorption. The most common is loss of gonadal steroid action on bone, as occurs in menopause or in male and female hypogonadism not associated with menopause. Other relatively common causes include primary hyperparathyroidism and endogenous or exogenous hypercortisolism and thyrotoxicosis. A large number of other, less frequent disorders also cause osteoporosis. Treatment of osteoporosis consists first of removing the cause if possible, for example, abolishing hypercortisolism, thyrotoxicosis, or hyperparathyroidism. In menopausal women or hypogonadal men or women, replacement of estrogens or androgens represents effective therapy. Estrogens and androgens given to hypogonadal subjects strikingly reduce bone resorption. For patients with established osteoporosis who either cannot take gonadal steroids or who are not hypogonadal, calcitonin decreases bone resorption and may stabilize bone mass. Estrogen replacement and calcitonin are approved by the Food and Drug Administration for treatment of osteoporosis. Experimental therapies presently include 1,25-dihydroxyvitamin D (calcitriol), bisphosphonates in intermittent treatment regimes, and fluoride in lower dosages than were used in previous studies. The use of fluoride is controversial, and to some extent it has fallen into disrepute. Effective use of any treatment is predicated on understanding the pathophysiology in any particular disease setting. 24 AUTHOR Fujita T TITLE Vitamin D in the treatment of osteoporosis revisited. SOURCE Proc Soc Exp Biol Med; VOL 212, ISS 2, 1996, P110-5 (REF: 76) ABSTRACT Interest in vitamin D treatment for osteoporosis has recently been revived because of the focus in various parts of the world on the elderly population, which is predominantly vitamin D deficient, in addition to postmenopausal osteoporosis due to estrogen withdrawal, which has been the central theme of osteoporosis research for many years. Combined use of other agents along with vitamin D has fortified the therapeutic armory against osteoporosis. The recent suggestion of a role of vitamin D receptor polymorphism in the development and progress of osteoporosis, possibly by interfering with its expected action, provoked intense discussions on the role of vitamin D in the pathogenesis and treatment of osteoporosis. Vitamin D receptor polymorphism may explain some of the racial differences in the incidence of osteoporosis and its complications. Responses to vitamin D treatment may also be predicted by vitamin D receptor allelic analysis, though the currently proposed allelic patterns are yet far from being widely accepted. The outlook for vitamin D treatment for osteoporosis may require insight into vitamin D receptor, not only for vitamin D's given form, but also for a possible future form designed to intervene at the genomic level.