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Vitamin D, the major steroid hormone that controls mineral ion homeostasis, exerts its actions through the vitamin D receptor (VDR). The VDR is expressed in many tissues, including several tissues not thought to play a role in mineral metabolism. Studies in kindreds with VDR mutations (vitamin D-dependent rickets type II, VDDR II) have demonstrated hypocalcemia, hyperparathyroidism, rickets, and osteomalacia. Alopecia, which is not a feature of vitamin D deficiency, is seen in some kindreds. We have generated a mouse model of VDDR II by targeted ablation of the second zinc finger of the VDR DNA-binding domain. Despite known expression of the VDR in fetal life, homozygous mice are phenotypically normal at birth and demonstrate normal survival at least until 6 months. They become hypocalcemic at 21 days of age, at which time their parathyroid hormone (PTH) levels begin to rise. Hyperparathyroidism is accompanied by an increase in the size of the parathyroid gland as well as an increase in PTH mRNA levels. Rickets and osteomalacia are seen by day 35; however, as early as day 15, there is an expansion in the zone of hypertrophic chondrocytes in the growth plate. In contrast to animals made vitamin D deficient by dietary means, and like some patients with VDDR II, these mice develop progressive alopecia from the age of 4 weeks.

Broadly defined, phytoestrogens include isoflavones, coumestans, and lignans. A number of these compounds have been identified in fruits, vegetables, and whole grains commonly consumed by humans. Soybeans, clover and alfalfa sprouts, and oilseeds (such as flaxseed) are the most significant dietary sources of isoflavones, coumestans, and lignans, respectively. Studies in humans, animals, and cell culture systems suggest that dietary phytoestrogens play an important role in prevention of menopausal symptoms, osteoporosis, cancer, and heart disease. Proposed mechanisms include estrogenic and antiestrogenic effects, induction of cancer cell differentiation, inhibition of tyrosine kinase and DNA topoisomerase activities, suppression of angiogenesis, and antioxidant effects. Although there currently are no dietary recommendations for individual phytoestrogens, there may be great benefit in increased consumption of plant foods

Cadmium, lead, mercury, and aluminum are toxic metals that may interact metabolically with nutritionally essential metals. Iron deficiency increases absorption of cadmium, lead, and aluminum. Lead interacts with calcium in the nervous system to impair cognitive development. Cadmium and aluminum interact with calcium in the skeletal system to produce osteodystrophies. Lead replaces zinc on heme enzymes and cadmium replaces zinc on metallothionein. Selenium protects from mercury and methylmercury toxicity. Aluminum interacts with calcium in bone and kidneys, resulting in aluminum osteodystrophy. Calcium deficiency along with low dietary magnesium may contribute to aluminum-induced degenerative nervous disease

Background. Prolonged corticosteroid therapy increases the risk of osteoporosis and fracture. We studied whether corticosteroid-induced osteoporosis could be prevented by treatment with calcium, calcitriol (1,25-dihydroxyvitamin D3), and calcitonin. Methods. One hundred three patients starting long-term corticosteroid therapy were randomly assigned to receive 1000 mg of calcium per day orally and either calcitriol (0.5 to 1.0 micrograms per day orally) plus salmon calcitonin (400 IU per day intranasally), calcitriol plus a placebo nasal spray, or double placebo for one year. Data on treatment efficacy were available for 92 of these patients. Bone density was measured every four months for two years by photon absorptiometry. There were no significant differences between groups with respect to age, underlying disease, initial bone density, or corticosteroid dose during the first year. Results. Calcitriol (mean dose, 0.6 micrograms per day), with or without calcitonin, prevented more bone loss from the lumbar spine (mean rates of change, -0.2 and -1.3 percent per year, respectively) than calcium alone (-4.3 percent per year, P = 0.0035). Bone loss at the femoral neck and distal radius was not significantly affected by any treatment. In the second year, lumbar bone loss did not occur in the group previously treated with calcitonin plus calcitriol (+0.7 percent per year), but it did occur in the group given calcium alone (-2.3 percent per year). The calcitriol group also lost lumbar bone (-3.6 percent per year) but received more corticosteroid in the second year than the other two groups. Conclusions. Calcitriol and calcium, used prophylactically with or without calcitonin, prevent corticosteroid-induced bone loss in the lumbar spine

Background and Methods. Osteoporosis is a common problem whose management is controversial. To evaluate the efficacy and safety of calcitriol (1,25-dihydroxyvitamin D3) in the treatment of postmenopausal osteoporosis, we conducted a three-year prospective, multicenter, single-blind study in 622 women who had one or more vertebral compression fractures. The women were randomly assigned to receive treatment with calcitriol (0.25 micrograms twice a day) or supplemental calcium (1 g of elemental calcium daily) for three years. New vertebral fractures were detected by means of lateral roentgenography of the spine each year, and calcium absorption was measured in 392 of the women. Results. The women who received calcitriol had a significant reduction in the rate of new vertebral fractures during the second and third years of treatment, as compared with the women who received calcium (second year, 9.3 vs. 25.0 fractures per 100 patient-years; third year, 9.9 vs. 31.5 fractures per 100 patient-years; P0.001). This effect was evident only in women who had five or fewer vertebral fractures at base line (second year, 5.2 vs. 25.3 fractures per 100 patient-years; third year, 4.2 vs. 31.0 fractures per 100 patient-years; P0.0001). The groups also differed significantly in the number of peripheral fractures; 11 such fractures occurred in 11 women in the calcitriol group, whereas 24 occurred in 22 women in the calcium group (P0.05). There was no significant difference between the groups in the incidence of side effects requiring withdrawal of treatment (8.6 percent in the calcitriol group vs. 6.5 percent in the calcium group). Conclusions. Continuous treatment of postmenopausal osteoporosis with calcitriol for three years is safe and significantly reduces the rate of new vertebral fractures in women with this disorder

The effect of fluoride treatment on the fracture rate in osteoporosis was studied. In a four-year prospective clinical trial, 202 postmenopausal women with osteoporosis and vertebral fractures were randomly assigned to receive sodium fluoride or placebo. The authors concluded that fluoride therapy increases cancellous bone mass but decreases cortical bone mineral density and increases skeletal fragility. Side effects of the treatment were gastrointestinal symptoms and lower-extremity pain

A technical report explores the potential roles in the development of osteoporosis of local and systemic factors that regulate bone growth and turnover. Attention is given to: the role of calcium-regulating, growth-regulating, and sex hormones; local regulation of bone metabolism; the role of prostaglandins and osteoclast-activating factors; bone-derived growth factors; the constitutive proteins of bone; and various other factors. It is postulated that, while no single factor is implicated, osteoporosis may be in part due to abnormalities of local factors that influence bone-cell function.(wz)

Among other things, magnesium regulates active calcium transport. As a result, there has been a growing interest in the role of magnesium (Mg) in bone metabolism. A group of menopausal women were given magnesium hydroxide to assess the effects of magnesium on bone density. At the end of the 2-year study, magnesium therapy appears to have prevented fractures and resulted in a significant increase in bone density

L'ostéodystrophie héréditaire d'Albright est une pathologie rare, associée à des troubles du bilan phosphocalcique liés à une résistance périphérique à la parathormone. Il s'agit d'une affection héréditaire, transmise sur le mode autosomique dominant et qui résulte d'une anomalie du gène GNAS1. Elle associe un morphotype particulier, des calcifications sous cutanées et une résistance osseuse et rénale à la parathormone. Nous rapportons un nouveau cas d'ostéodystrophie héréditaire d'Albright chez un nourrisson de 9 mois, suivi pour hypocalcémie profonde depuis j10 de vie. A travers ce cas, nous rappelons les différents aspects de cette affection sur les plans clinique, biologique, génétique ainsi que thérapeutique.

Osteoporosis is a metabolic bone disease characterized by low bone mass and deterioration of bone tissue that leads to bone fragility and an increase in fracture risk. It is a disease with a complex etiology that includes genetic and environmental contributors. Environmental factors that influence bone density include dietary factors--such as intakes of calcium, alcohol, and caffeine--and lifestyle factors--such as exercise and smoking. Ethnic differences in the propensity to nontraumatic bone fracture suggest that genetic factors are important. Recently, common allelic variations in the vitamin D receptor gene have been found to be associated with bone mineral density in racially diverse population groups, as well as in prepubertal girls, young adult and postmenopausal women, and men. However, many studies have not been able to find this association. Additional approaches, such as sib-pair analysis, will probably be necessary in the future to identify the important genetic determinants of osteoporosis