These findings justify the need to assure adequate vitamin D intake in patients being treated with anticonvulsants, independently of the treatment, age, sex, and activity status, in order to prevent osteomalacia.

The effect of silicon (Si) supplement on preventing bone mass loss induced by ovariectomy (OVX) in rats was investigated. Three groups of 15, 100-day-old female Wistar rats each, with a mean initial weight of approximately 260 g per animal, were selected for the present study. One of the experimental group consisting of 15 OVX rats was fed a diet supplemented with 500 mg of Si per kg of feed (Si + OVX). The other two groups consisting of 15 OVX and 15 sham-OVX rats did not receive these supplements. Morphometric (weight and length) and densitometric studies with dual-energy X-ray absorptiometry were performed on the whole femur and 5th lumbar vertebra of each animal 30 days after the experiment. The Si + OVX rats did not show a loss of bone mass induced by OVX at axial level (5th lumbar vertebra) or periphery (femur). Nonetheless, a significant increase (ANOVA with Bonferroni/Dunn post hocs test) of longitudinal development of the femur (P < 0.0001) was patent. These results, obtained through the measurements of axial and peripheral bones, warrant closer scrutiny in connection with the Si inhibitory effect on bone mass loss as well as the stimulatory effect on bone formation. Both actions, namely, inhibition of resorption and stimulation of formation, infer that Si may have a potential therapeutic application in the treatment of involutive osteoporosis.

The mechanism underlying diabetic osteopenia is still unclear and may involve osteoblastic activity and/or the deficit of insulin's anabolic action. Bone gla protein (BGP) is synthesized by the osteoblast and its synthesis increases with 1,25(OH)2D3 and fluoride. Because 1,25(OH)2D3 also stimulates insulin secretion, sodium fluoride administration can be used to investigate deficient osteoblastic activity in diabetics, as reflected by BGP levels. BGP was determined before and after administering sodium fluoride at a dosage of 50 mg/day/15 days to three groups: 14 patients with insulin-dependent diabetes, 16 diabetics on oral antidiabetic treatment, and 25 controls, all of similar age, sex, and characteristics. Basal BGP values (mean +/- SD) were low in diabetics on insulin treatment (4.3 +/- 1.1 ng/ml) and in diabetics on oral antidiabetics (5.8 +/- 1.2 ng/ml) as compared with controls (6.5 +/- 0.7 ng/ml) (P less than 0.001 and less than 0.05, respectively). After giving fluoride, BGP values did not change in the two diabetic groups but did vary in controls (8.1 +/- 0.6 ng/ml, P less than 0.001). These results suggest that deficient osteoblast function could be responsible for osteopenia in diabetics.

The effect of exposure to lead on the longitudinal development of bone and on bone mass was studied in rats. A group of 35, 50-day-old female Wistar rats was divided into a control group of 15 rats and an experimental group of 20 rats fed a diet supplemented with 17 mg of lead acetate per kg feed for 50 days. Total body bone densitometry (TBBMC) was performed the day before ending the 50-day experiment. On day 50, all rats were killed and their right femur and 5th lumbar vertebra were dissected. The bones were cleaned of soft tissue and femoral length and vertebral length were measured with a caliper and all bones were weighed on a precision scale. Final body weight (P < 0.05), TBBMC (P < 0.005), and femur weight (P < 0.005) were significantly lower in the control group. Femur length did not differ between groups, but the length of the 5th lumbar vertebra was greater in the control group (P < 0.05). Histomorphometry of the femur showed that Cn-BV/TV, Tb-N, Tb-Th were lower (P < 0.05 in all) and Tb-Sp was higher (P < 0.05) in the group given the lead-supplemented diet. These findings suggested lead-induced inhibition of axial bone development and a histomorphometric decrease in bone mass, produced mainly by enhanced resorption, and a densitometric increase in bone mass, produced by lead accumulation in bone.

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Weight and gonadal status are the main determinants of bone mass in women. Because of this it is important to study which influences it more. The effect of weight (expressed as body mass index, BMI) and gonadal status of women on total-body bone mineral content (TBBMC) and regional bone mineral content (BMC) was investigated. A total of 373 normal women (mean age 48.9 +/- 13.4 years) were studied: 171 postmenopausal women (mean age 59.3 +/- 9.5 years; years since menopause 11.3 +/- 6.7 years); 76 perimenopausal women (mean age 48.9 +/- 2.2 years); and 126 premenopausal women (mean age 34.7 +/- 7.4 years). In all the women, TBBMC and regional BMC were determined by dual-energy X-ray absorptiometry. Also biochemical markers of bone metabolism (total alkaline phosphatase and tartrate-resistant acid phosphatase) and serum estrone and estradiol were determined. When the women were stratified by gonadal status and BMI, thin women (BMI <20 kg/m2) had significantly lower TBBMC and regional BMC, lower gonadal steroid concentration and higher levels of biochemical markers than overweight (BMI 25-30 kg/m2) and obese (BMI >30 kg/m2) women, regardless of gonadal status. Overweight and obese women had findings suggestive of increased parathyroid activity, but greater bone mass. Weight rather than gonadal steroid concentration is the main determinant of bone mass in women regardless of gonadal status.