Bone mineral density and body composition of children and adolescents in health and disease

Osteoporosis is characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture risk. Osteoporosis is a major public health problem involving postmenopausal women and aging individuals. The lifetime risk of osteoporotic fractures of the vertebral bodies (symptomatic), hip, and distal radius is about 40 % for white women and 13 % for white men. At present, the best possibility to assess the fracture risk of an individual is the measurement of bone mass (g) or bone mineral density (BMD, glcm). Studies in postmenopausal women showed that for each standard deviation decrease in BMD there was a 2-3 fold increase in fracture risk. Bone mass later in life is determined by the peak bone mass acquired during adolescence and the subsequent rate of bone loss. Low peak bone mass results in a higher risk of osteoporosis. A high peak bone mass provides a larger reserve later in life. BMD increases during childhood until the peak bone mass is achieved, around the age of 18 to 20 years. Thereafter, bone mass stabilizes and then decreases progressively in both sexes after 35 to 40 years of age with a steeper decline in women after the menopause

Bone mineral density and body composition of children and adolescents in health and disease

Osteoporosis is characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture risk. Osteoporosis is a major public health problem involving postmenopausal women and aging individuals. The lifetime risk of osteoporotic fractures of the vertebral bodies (symptomatic), hip, and distal radius is about 40 % for white women and 13 % for white men. At present, the best possibility to assess the fracture risk of an individual is the measurement of bone mass (g) or bone mineral density (BMD, glcm). Studies in postmenopausal women showed that for each standard deviation decrease in BMD there was a 2-3 fold increase in fracture risk. Bone mass later in life is determined by the peak bone mass acquired during adolescence and the subsequent rate of bone loss. Low peak bone mass results in a higher risk of osteoporosis. A high peak bone mass provides a larger reserve later in life. BMD increases during childhood until the peak bone mass is achieved, around the age of 18 to 20 years. Thereafter, bone mass stabilizes and then decreases progressively in both sexes after 35 to 40 years of age with a steeper decline in women after the menopause

Metabolism of carveol and dihydrocarveol in Rhodococcus erythropolis DCL14

Rhodococcus erythropolis DCL14 assimilates all stereoisomers of carveol and dihydrocarveol as sole source of carbon and energy. Induction experiments with carveol- or dihydrocarveol-grown cells showed high oxygen consumption rates with these two compounds and with carvone and dihydrocarvone. (Dihydro)carveol-grown cells of R. erythropolis DCL14 contained the following enzymic activities involved in the carveol and dihydrocarveol degradation pathways of this micro-organism: (dihydro)carveol dehydrogenase (both NAD - and dichlorophenolindophenol-dependent activities), an unknown cofactor-dependent carvone reductase, (iso-)dihydrocarvone isomerase activity, NADPH-dependent dihydrocarvone monooxygenase (Baeyer–Villiger monooxygenase), -lactone hydrolase and an NAD -dependent 6-hydroxy-3-isopropenylheptanoate dehydrogenase. Product accumulation studies identified (4R)-carvone, (1R,4R)-dihydrocarvone, (4R,7R)-4-isopropenyl-7-methyl-2-oxo-oxepanone, (3R)-6-hydroxy-3-isopropenylheptanoate, (3R)-3-isopropenyl-6-oxoheptanoate, (3S,6R)-6-isopropenyl-3-methyl-2-oxo-oxepanone and (5R)-6-hydroxy-5-isopropenyl-2-methylhexanoate as intermediates in the (4R)-carveol degradation pathway. The opposite stereoisomers of these compounds were identified in the (4S)-carveol degradation pathway. With dihydrocarveol, the same intermediates are involved except that carvone was absent. These results show that R. erythropolis DCL14 metabolizes all four diastereomers of carveol via oxidation to carvone, which is subsequently stereospecifically reduced to (1R)-(iso-)dihydrocarvone. At this point also dihydrocarveol enters the pathway, and this compound is directly oxidized to (iso-)dihydrocarvone. Cell extracts contained both (1R)-(iso-)dihydrocarvone 1,2-monooxygenase and (1S)-(iso)-dihydrocarvone 2,3-monooxygenase activity, resulting in a branch point of the degradation pathway; (1R)-(iso-)dihydrocarvone was converted to 4-isopropenyl-7-methyl-2-oxo-oxepanone, while (1S)-(iso)-dihydrocarvone, which in vivo is isomerized to (1R)-(iso-)dihydrocarvone, was converted to 6-isopropenyl-3-methyl-2-oxo-oxepanone. 4-Isopropenyl-7-methyl-2-oxo-oxepanone is hydrolysed to 6-hydroxy-3-isopropenylheptanoate, which is subsequently oxidized to 3-isopropenyl-6-oxoheptanoate, thereby linking the (dihydro)carveol degradation pathways to the limonene degradation pathway of this micro-organism. 6-Isopropenyl-3-methyl-2-oxo-oxepanone is, in vitro, hydrolysed to 6-hydroxy-5-isopropenyl-2-methylhexanoate, which is thought to be a dead-end metabolite

Bone mineral density and body composition before and during treatment with gonadotropin-releasing hormone agonist in children with central precocious and early puberty

Major changes in bone mineral density (BMD) and body composition occur during puberty. In the present longitudinal study, we evaluated BMD and calculated volumetric BMD [bone mineral apparent density (BMAD)], bone metabolism, and body composition of children (32 girls and 2 boys) with central precocious and early puberty before and during treatment with GnRH agonist (GnRH). Patients were studied at baseline and during treatment for 6 months (n = 34), 1 yr (n = 33), and 2 yr (n = 16). Lumbar spine and total body BMD and body composition were measured with dual-energy x-ray absorptiometry. The variables were compared with age- and sex-matched reference values of the same population and expressed as SD score (SDS). Bone age was assessed. Serum calcium, phosphate, alkaline phosphatase, osteocalcin, the carboxyterminal propeptide of type I collagen (PICP), cross-linked telopeptide of collagen I (ICTP), 1,25 dihydroxyvitamin D and urinary hydroxyproline/creatinine, and calcium/ creatinine ratios were measured. Mean lumbar spine BMD SDS was significantly higher than zero at baseline (P < 0.02) and did not differ from normal, after 2 yr of treatment. Mean spinal BMAD SDS and total body BMD SDS were not significantly different from zero at baseline and had not changed significantly after 2 yr of treatment. During therapy, fat mass and percentage body fat SDS increased, whereas lean tissue mass SDS decreased. Mean lumbar spine BMD and BMAD and total body BMD SDS, calculated for bone age, were all lower than zero at baseline (BMD P < 0.001 and BMAD P < 0.05) and also after 2 yr treatment (respectively, P < 0.001, P < 0.05, and P < 0.01). Biochemical bone parameters were significantly higher than prepubertal values at baseline, and they decreased during treatment. In conclusion, patients with central precocious and early puberty had normal BMD for chronological age but low BMD for bone age, after 2 yr of treatment with GnRH. Bone turnover decreased during treatment. Changes in body composition resembled those seen in patients with GH deficiency

Bone mineral density in children and adolescents: relation to puberty, calcium intake, and physical activity

The association of height, weight, pubertal stage, calcium intake, and physical activity with bone mineral density (BMD) was evaluated in 500 children and adolescents (205 boys and 295 girls), aged 4-20 yr. The BMD (grams per cm2) of lumbar spine and total body was measured with dual energy x-ray absorptiometry. Lumbar spine volumetric BMD was calculated to correct for bone size. BMD and volumetric BMD increased with age. During puberty, the age-dependent increment was higher. After adjustment for age, the Tanner stage was significantly associated with all three BMD variables in girls and with spinal BMD in boys. In boys, positive correlations were found between BMD and both calcium intake and physical activity after adjustment for age. Stepwise regression analysis with weight, height, Tanner stage, calcium intake, and physical activity as determinants with adjustment for age resulted in a model with Tanner stage in girls and weight in boys for all three BMD variables. The major independent determinant of BMD was the Tanner stage in girls and weight in boys

Changes in bone mineral density, body composition, and lipid metabolism during growth hormone (GH) treatment in children with GH deficiency

Adults with childhood onset GH deficiency (GHD) have reduced bone mass, increased fat mass, and disorders of lipid metabolism. The aim of the present study was to evaluate bone mineral density (BMD), bone metabolism, body composition, and lipid metabolism in GHD children before and during 2-3 yr of GH treatment (GHRx). Forty children with GHD, mean age 7.9 yr, participated in the study of bone metabolism and body composition; and an additional group of 17 GHD children, in the study of lipid metabolism. Lumbar spine BMD, total body BMD, and body composition were measured with dual-energy x-ray absorptiometry. Volumetric BMD (bone mineral apparent density, BMAD) was calculated to correct for bone size. BMD, BMAD, lean tissue mass, bone mineral content, fat mass, and percentage body fat were expressed as SD scores (SDS), in comparison with normative data of the same population. Lumbar spine BMD and BMAD and total body BMD were all decreased at baseline. All BMD variables increased significantly during GHRx, lumbar spine BMD SDS, already after 6 months of treatment. Lean tissue mass SDS increased continuously. Bone mineral content SDS started to increase after 6 months GHRx. Fat mass SDS decreased during the first 6 months of GHRx and remained stable thereafter. Biochemical parameters of bone formation and bone resorption did not differ from normal at baseline and increased during the first 6 months of GHRx. Serum 1,25 dihydroxyvitamin D increased continuously during GHRx, whereas PTH and serum calcium remained stable. Lipid profile was normal at baseline: Atherogenic index had decreased and apolipoprotein A1(Apo-A1) had increased after 3 yr of treatment. In conclusion, children with GHD have decreased bone mass. BMD, together with height and lean tissue mass, increased during GHRx. GHRx had a beneficial effect on lipid metabolism

Longitudinal follow-up of bone density and body composition in children with precocious or early puberty before, during and after cessation of GnRH agonist therapy

We studied bone mineral density (BMD), bone metabolism, and body composition in 47 children with central precocious puberty (n = 36) or early puberty (n = 11) before, during, and after cessation of GnRH agonist. Bone density and body composition were measured with dual energy x-ray absorptiometry and expressed as SD scores. Bone age and biochemical parameters of bone turnover were assessed. Measurements were performed at baseline, after 6 months, and on a year

Indices from flow-volume curves in relation to cephalometric, ENT- and sleep-O2 saturation variables in snorers with and without obstructive sleep-apnoea

In a group of 37 heavy snorers with obstructive sleep apnoea (OSA, Group 1) and a group of 23 heavy snorers without OSA (Group 2) cephalometric indices, ENT indices related to upper airway collapsibility, and nocturnal O2 desaturation indices were related to variables from maximal expiratory and inspiratory flow-volume (MEFV and MIFV) curves. The cephalometric indices used were the length and diameter of the soft palate (spl and spd), the shortest distance between the mandibular plane and the hyoid bone (mph) and the posterior airway space (pas). Collapsibility of the upper airways was observed at the level of the tongue base and soft palate by fibroscopy during a Muller manoeuvre (mtb and msp) and ranked on a five point scale. Sleep indices measured were the mean number of oxygen desaturations of more than 3% per hour preceded by an apnoea or hypopnoea of more than 10 s (desaturation index), maximal sleep oxygen desaturation, baseline arterial oxygen saturation (Sa,O2) and, in the OSA group, percentage of sleep time with Sa,O2 < 90%. The variables obtained from the flow-volume curves were the forced vital capacity (FVC), forced expiratory and inspiratory volume in 1 s (FEV1 and FIV1), peak expiratory and peak inspiratory flows (PEF and PIF), and maximal flow after expiring 50% of the FVC (MEF50). The mean of the flow-volume variables, influenced by upper airway aperture (PEF, FIV1) was significantly greater than predicted.(ABSTRACT TRUNCATED AT 250 WORDS

Obesity is underestimated using body mass index and waist-hip ratio in long-term adult survivors of childhood cancer

Objective: Obesity, represented by high body mass index (BMI), is a major complication after treatment for childhood cancer. However, it has been shown that high total fat percentage and low lean body mass are more reliable predictors of cardio