Bone mineral density in girls and boys at different pubertal stages: relation with gonadal steroids, bone formation markers, and growth parameters

Yılmaz, Dilek; Ersoy, Betül; Bilgin, Elvan; Gümüşer, Gül; Onur, Ece; Pinar, Erbay Dundar

doi:10.1007/s00774-005-0631-6

Cited by 148 publications

(132 citation statements)

References 39 publications

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“…This is similar to other studies in healthy children that showed significant correlations between bone mass and BTMs [20][21][22][23]. A study by Jürimäe et al [21] showed significantly negative associations between BTMs and lumbar spine BMD, which remained significant after adjustment for age and pubertal stages.…”

Section: Discussionsupporting

confidence: 89%

Biochemical markers of bone turnover in children with clinical bone fragility

Bowden

Akusoba

Hayes

et al. 2016

Journal of Pediatric Endocrinology and Metabolism

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Background: The role of biochemical bone turnover markers (BTMs) in assessing low bone mass and monitoring bisphosphonate treatment in pediatric patients with clinical bone fragility is not well established. The aim of the study was to examine the correlations of BTMs and the bone mineral density (BMD), and evaluate the effects of bisphosphonates therapy on BTMs in children with clinical bone fragility. Methods: Clinical data of 115 patients with clinical bone fragility (mean age 9.7±5.8 years), 102 of whom received bisphosphonates, were studied. Serum alkaline phosphatase (ALP), osteocalcin (OC), urine pyridinoline (PD) and deoxypyridinoline (DPD), BMD at baseline and subsequent years were analyzed. Results: There was a significant negative correlation between urine PD and lumbar BMD (slope = -0.29, p < 0.001). There were no correlations between BTMs and lumbar BMD Z-score. There was a significant positive correlation between serum OC and serum ALP, urine PD and DPD (p < 0.001). Serum OC, urine PD and DPD index, as expressed as measured value/upper limit of normal value for age, decreased during the first 3 years of bisphosphonate therapy. Conclusions: In children with clinical bone fragility, BTMs correlated with each other, but not with lumbar BMD Z-score. While they were not reliable predictors of degree of low BMD, the bone markers showed suppression during bisphosphonate therapy and may be helpful in monitoring the response to therapy.

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Section: Discussionsupporting

confidence: 89%

Biochemical markers of bone turnover in children with clinical bone fragility

Bowden

Akusoba

Hayes

et al. 2016

Journal of Pediatric Endocrinology and Metabolism

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“…Recruitment should thus be restricted to children in pubertal stages II to IV according to established Tanner stages [174][175][176]. Notably, statistically significant differences were found in changes of LS-aBMD z-scores when comparing prepubertal (Tanner stage I) to pubertal children (Tanner stages II-V) in our study (p=0.02).…”

Section: Strengths and Limitationsmentioning

confidence: 72%

Effect of high-dose vitamin D supplementation on bone density in youth with osteogenesis imperfecta: A randomized controlled trial

Plante

Veilleux

Glorieux

et al. 2016

Bone

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Background Osteogenesis imperfecta (OI) is a genetic disease characterized by fragile bones and short stature. Recently, a positive association was found between serum 25‐hydroxyvitamin D (25OHD) concentrations and lumbar spine areal bone mineral density (LS‐aBMD) z‐scores in this population. Objectives: To assess whether high‐dose vitamin D supplementation (2000 IU) will result in significantly higher LS‐aBMD z‐scores after one‐year; and to evaluate the effect of vitamin D supplementation on lower limb muscle power. Results: At baseline, average serum 25OHD concentration was 65.6 nmol/L (SD 20.4) with no difference seen between treatment groups (p=0.77). Deficient serum 25OHD concentrations (<50 nmol/L) were measured in only 21% of patients at baseline. Supplementation resulted in higher serum 25OHD concentrations in almost all participants (90%) with significantly higher increases seen with 2000 IU (mean [95% C.I.] = 30.5 nmol/L [21.3; 39.6] vs 15.2 nmol/L [6.4; 24.1], p= 0.02). No significant changes were detected in BMD measurements or in lower limb muscle power between treatment groups from baseline to final visit. Conclusions Supplementation with either 400 or 2000 IU of vitamin D translates into significant increases in serum 25OHD concentrations in children with OI. However, increases in baseline serum 25OHD concentrations already within a healthy range (蠅50 nmol/L) do not translate into increases in BMD z‐scores in children with OI. This research was supported by the Shriners Hospital for Children as well as by The Network for Oral and Bone Health Research.

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“…In support of these assumptions, several studies demonstrate a positive correlation between serum estrogen and BMD during puberty in females (16,49,57,59), thus concluding that estrogen must be a major stimulator of bone development during this period of rapid growth. Although several studies make this conclusion, there is no direct evidence that estrogen is the key molecule responsible for the increased bone accretion and increased GH during puberty.…”

mentioning

confidence: 82%

“…In terms of the potential messenger molecules that regulate the surge in the GH/IGF axis, it is well accepted that the pubertal surge in estrogen is responsible for increased GH, which in turn stimulates IGF-I and thus bone growth. Several studies demonstrate increased growth and GH with estrogen treatment during puberty or a positive correlation between bone development and increased pubertal growth, which are associated with increased estrogen (7,19,28,32,37,47,57). If estrogen is indeed the major factor involved in regulating the pubertal surge in GH/IGF axis and increased bone accretion, then we would expect OVX prior to the pubertal growth period to result in decreased rise in IGF-I levels, bone size, and bone mass; however, this was not the case.…”

Section: Estrogen Is Not a Key Mediator Of The Gh/igf Surge During Pumentioning

confidence: 99%

Prepubertal OVX increases IGF-I expression and bone accretion in C57BL/6J mice

Govoni

Wergedal²,

Chadwick³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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It is generally well accepted that the pubertal surge in estrogen is responsible for the rapid bone accretion that occurs during puberty and that this effect is mediated by an estrogen-induced increase in growth hormone (GH)/insulin-like growth factor (IGF) action. To test the cause and effect relationship between estrogen and GH/IGF, we evaluated the consequence of ovariectomy (OVX) in prepubertal mice (C57BL/6J mice at 3 wk of age) on skeletal changes and the GH/IGF axis during puberty. Contrary to our expectations, OVX increased body weight (12-18%), bone mineral content (11%), bone length (4%), bone size (3%), and serum, liver, and bone IGF-I (30 -50%) and decreased total body fat (18%) at 3 wk postsurgery. To determine whether estrogen is the key ovarian factor responsible for these changes, we performed a second experiment in which OVX mice were treated with placebo or estrogen implants. In addition to observing similar results compared with our first experiment, estrogen treatment partially rescued the increased body weight and bone size and completely rescued body fat and IGF-I levels. The increased bone accretion in OVX mice was due to increased bone formation rate (as determined by bone histomorphometry) and increased serum procollagen peptide. In conclusion, contrary to the known estrogen effect as an initiator of GH/IGF surge and thereby pubertal growth spurt, our findings demonstrate that loss of estrogen and/or other hormones during the prepubertal growth period effect leads to an increase in IGF-I production and bone accretion in mice. osteoporosis; estrogen; puberty; bone size; bone mineral density OSTEOPOROSIS IS A MAJOR HEALTH concern in humans, and this disease is characterized by a low bone mineral density (BMD), which leads to increased bone fragility and risk of fractures. BMD is an important determinant of bone strength, and low BMD is the result of increased bone resorption and decreased bone formation. It has been well established that the pubertal growth period is a critical period in time when rapid increase in bone accretion takes place. We and others (19,32,48) have demonstrated in both humans and mice that 40 -50% of bone accretion occurs during puberty. Understanding the mechanisms involved in regulating bone accretion during this period of rapid growth is of considerable importance in the prevention and treatment of osteoporosis.In terms of the potential messenger molecules that contribute to rapid skeletal growth during puberty, it has been suggested that the growth hormone (GH)/insulin-like growth factor (IGF) axis is a key regulator of early bone development (34, 55). Recent studies using transgenic mouse models lacking IGF-I or GH have provided convincing evidence for a key role for GH/IGF axis in the regulation of skeletal growth that occurs during puberty (28). It is well accepted that increased IGF-I during sexual maturation is regulated by increased GH production and/or action as demonstrated by reduced IGF-I and bone density in mice lacking GH (28). In addition, we and ot...

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Bone mineral density in girls and boys at different pubertal stages: relation with gonadal steroids, bone formation markers, and growth parameters

Cited by 148 publications

References 39 publications

Biochemical markers of bone turnover in children with clinical bone fragility

Biochemical markers of bone turnover in children with clinical bone fragility

Effect of high-dose vitamin D supplementation on bone density in youth with osteogenesis imperfecta: A randomized controlled trial

Prepubertal OVX increases IGF-I expression and bone accretion in C57BL/6J mice

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