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Aim: To investigate the relationship of forearm length (FL) or height to bone parameters of the forearm of a normal pediatric population in comparison to individuals with osteogenesis imperfecta (OI). Methods: Data on FL, height and peripheral quantitative computed tomography measurements of the forearm were collected from participants of the DONALD study (140 males and 156 females; age 5–19 years) and from 73 patients with OI (53 males; mean age ± SD: 11.7 ± 3.3 years). Bone mineral content (BMC) was transformed into standard deviation score (SDS) according to height or FL. Results: Height and Tanner stages significantly predicted FL in males (R2adjusted = 0.960) and females (R2adjusted = 0.934). Height was a stronger predictor of FL than Tanner stages. Compared to controls, patients with OI were characterized by lower BMC-SDSFL and lower BMC-SDSheight (–0.37 ± 1.77 vs. 0.00 ± 0.97, p = 0.002, and –0.15 ± 5.0 vs. –0.02 ± 1.01, p = 0.011, respectively). BMC-SDSFL was not significantly lower than BMC-SDSheight in controls, and also not lower in patients with OI (p = 0.865 and p = 0.809). The height/FL ratio was significantly decreased in patients with OI (mean ± SD: 6.34 ± 0.38 vs. 6.45 ± 0.21, p = 0.001) compared with controls. Conclusion: Because of disproportional growth, BMC may be overestimated in OI patients. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Objective: To assess bone mineral content (BMC) and body composition in adolescents and young adults with congenital adrenal hyperplasia. Methods: BMC, anteroposterior-projected bone area (BA), bone mineral density, and fat mass percentage were determined by dual-energy X-ray absorptiometry in 18 patients aged 18–33 years (8 females and 10 males) with 21-hydroxylase deficiency using a Hologic QDR 1000/W densitometer. Results: BMC and bone mineral density for age were significantly reduced at –1.2 standard deviation scores (SDS; range from –2.8 to +4.1) and –1.1 SDS (range from –3.2 to +2.6), respectively. The BA for height was significantly increased at +1.7 SDS (range from –0.5 to +4.8), and the BMC for BA was normal at 0.3 SDS (range from –2.0 to +3.6). The median final height was significantly reduced at –1.6 SDS (range from –5.6 to +0.3), and the fat mass percentage was significantly increased at +1.5 SDS (range from –1.0 to +5.0). Conclusion: Our study population of young adults with 21-hydroxylase deficiency had a short stature and broad bones with a normal BMC and had an increased fat mass percentage. Copyright © 2004 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Objectives: To compute the annual changes in total bone mineral content (BMCt), lean tissue mass and fat mass (LTM and FM) during growth. Methods: Whole body DXA data were used to calculate the annual changes of the parameter P (P = BMCt, LTM or FM), as a percentage, as ΔP% = 100 × (P[sub i+1] – P[sub i] ) / Pi; with P[sub i] and P[sub i+1] the values for P at age i and age (i+1). Smoothed curves were then obtained from ΔP% values plotted against age. Results: Changes in FM were different in males and females. A peak velocity was marked for the three tissues at age 6.5 in boys, and at age 6.5–7.5 in girls; a pubertal peak spurt appeared at age 12 in girls and between age 13 and 14 in boys. This latter peak was followed by an exponential decrease, and no significant changes were found for the three components after age 20 in girls and age 21–22 in boys. Conclusion: Changes in tissue accretion during growth are easy to follow when expressed in percentages. Fat changes, especially, should be around 17% in girls and 15% in boys at the age of puberty.Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Growth hormone (GH) and insulin-like growth factor-I have major effects on growth plate chondrocytes and all bone cells. Untreated childhood-onset GH deficiency (GHD) markedly impairs linear growth as well as three-dimensional bone size. Adult peak bone mass is therefore about 50% that of adults with normal height. This is mainly an effect on bone volume, whereas true bone mineral density (BMD; g/cm[sup 3] ) is virtually normal, as demonstrated in a large cohort of untreated Russian adults with childhood-onset GHD. The prevalence of fractures in these untreated childhood-onset GHD adults was, however, markedly and significantly increased in comparison with normal Russian adults. This clearly indicates that bone mass and bone size matter more than true bone density. Adequate treatment with GH can largely correct bone size and in several studies also bone mass, but it usually requires more than 5 years of continuous treatment. Adult-onset GHD decreases bone turnover and results in a mild deficit, generally between –0.5 and –1.0 z-score, in bone mineral content and BMD of the lumbar spine, radius and femoral neck. Cross-sectional surveys and the KIMS data suggest an increased incidence of fractures. GH replacement therapy increases bone turnover. The three controlled studies with follow-up periods of 18 and 24 months demonstrated a modest increase in BMD of the lumbar spine and femoral neck in male adults with adult-onset GHD, whereas no significant changes in BMD were observed in women. GHD, whether childhood- or adult-onset, impairs bone mass and strength. Appropriate substitution therapy can largely correct these deficiencies if given over a prolonged period. GH therapy for other bone disorders not associated with primary GHD needs further study but may well be beneficial because of its positive effects on the bone remodelling cycle. Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

To detect early abnormalities in bone mineralization, the lumbar spine bone mineral density (BMD) of diabetic children with a diabetes onset of less than 5 years and treated with a similar insulin treatment scheme was measured at the level of the lumbar spine by dual-energy X-ray absorptiometry (DEXA), a most sensitive technique for detecting osteopenia in children. Fifteen male and 8 female children and adolescents (mean age ± SD: 12.5±3.7 years), 1–5 years after the clinical onset of their diabetes, were studied. Measurements of the lumbar spine (L[sub 1] –L[sub 4] ) BMD, expressed in gHA/cm[sup 2] and as a z-score for age, were performed with a commercial DEXA apparatus (Hologic QDR 1000 W, Hologic Inc., Waltham, USA). Calcium-phosphorus metabolism was studied by measuring the circulating levels of calcium, phosphorus, alkaline phosphatase, osteocalcin, 25-OH-vitamin D and parathyroid hormone and the urinary excretion of calcium and phosphorus. The mean BMD of the studied group was 0.75 (0.16) gHA/cm[sup 2] giving a mean z-score of –0.31±0.95. Only 1 of the patients had a BMD lower than –2 SD. No sex difference in BMD z-score existed. BMD SD was positively correlated with height SD (R = 0.56, p < 0.005), but not with the age of the patients, the duration of the disease, the degree of metabolic control or the studied parameters of the calcium-phosphorus metabolism. In conclusion, diabetic children have a normal lumbar spine BMD during the first years of the disease, when a good metabolic control and no abnormalities in the calcium-phosphorus metabolism are present. As in normal children, areal BMD by DEXA is highly dependent on the body height, necessitating corrections if abnormalities in skeletal growth or pubertal development exist. [ABSTRACT FROM AUTHOR]

Osteoporosis is a common and serious complication of glucocorticoid therapy, resulting in increased risk of fragility fractures. Recent studies indicate that fracture risk is increased even at low doses of glucocorticoids and that this increased risk is seen soon after the commencement of glucocorticoid therapy. Both increased bone resorption and reduced bone formation contribute to bone loss, which affects cortical and cancellous sites. A number of interventions have been shown to prevent glucocorticoid-induced bone loss, although the strongest evidence exists for the bisphosphonates etidronate, alendronate and risedronate. Primary prevention of bone loss should be considered in all high-risk individuals taking oral glucocorticoids for 3 months or more, for example those aged 65 years or over or those with a previous fragility fracture. In other glucocorticoid-treated individuals, the decision to treat should be based on bone densitometry. Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]