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The endocrine role of estrogens on human male skeleton.

Rochira V, Kara E, Carani C - Int J Endocrinol (2015)

Bottom Line: At puberty, epiphyseal closure and growth arrest occur when a critical number of estrogens is reached.This threshold should be better identified in-between the ranges of 15 and 25 pg/mL.Future basic and clinical research will optimize strategies for the management of bone diseases related to estrogen deficiency in men.

View Article: PubMed Central - PubMed

Affiliation: Unit of Endocrinology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via P. Giardini 1355, 41126 Modena, Italy ; Azienda USL di Modena, Nuovo Ospedale Civile Sant'Agostino Estense (NOCSAE), Via P. Giardini 1355, 41126 Modena, Italy.

ABSTRACT
Before the characterization of human and animal models of estrogen deficiency, estrogen action was confined in the context of the female bone. These interesting models uncovered a wide spectrum of unexpected estrogen actions on bone in males, allowing the formulation of an estrogen-centric theory useful to explain how sex steroids act on bone in men. Most of the principal physiological events that take place in the developing and mature male bone are now considered to be under the control of estrogen. Estrogen determines the acceleration of bone elongation at puberty, epiphyseal closure, harmonic skeletal proportions, the achievement of peak bone mass, and the maintenance of bone mass. Furthermore, it seems to crosstalk with androgen even in the determination of bone size, a more androgen-dependent phenomenon. At puberty, epiphyseal closure and growth arrest occur when a critical number of estrogens is reached. The same mechanism based on a critical threshold of serum estradiol seems to operate in men during adulthood for bone mass maintenance via the modulation of bone formation and resorption in men. This threshold should be better identified in-between the ranges of 15 and 25 pg/mL. Future basic and clinical research will optimize strategies for the management of bone diseases related to estrogen deficiency in men.

No MeSH data available.


Related in: MedlinePlus

Proposed range for a critical serum estradiol threshold above which both skeletal maturation and mineralization can proceed in an optimal way. E2: estradiol; BioE2: Bioavailable estradiol.
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Related In: Results  -  Collection


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fig2: Proposed range for a critical serum estradiol threshold above which both skeletal maturation and mineralization can proceed in an optimal way. E2: estradiol; BioE2: Bioavailable estradiol.

Mentions: Based on the poor compliance of an aromatase-deficient man, we tried to develop a dose-response relationship between serum E2 and radiological changes of the long bones in terms of bone age [45]. Due to patient's poor compliance, serum E2 remained below 20 pg/mL for a long time without any change of bone age and growth plate appearance at X-ray [45]. The closure of the epiphyses was obtained only several months later when E2 rose above 20 pg/mL and the patient was taking the right dose of transdermal E2 [45]. This suggests that serum E2 above 20 pg/mL is necessary for epiphyseal cartilage fusion [45] and that only in the case of severe estrogen deficiency the epiphyses remain still open despite the advancement of the chronological age (Figure 2). The same results can be deduced from a recent study comparing sex steroids, pubertal stage, and skeletal maturation between obese and lean boys [17]. If boys at the end of puberty (with a genital Tanner stage 5) are considered, bone age (of about 18 years on average) was greatly advanced and consistent with fused epiphyses in obese boys with a mean serum E2 clearly above 20 pg/mL (median 34.8 pg/mL, min–max: 25.6–41.1 pg/mL), while bone age (of about 16 years on average) was less advanced and consistent with still unfused epiphyses in lean boys with a mean serum E2 below 20 pg/mL (median 15.7 pg/mL, min–max: 13.2–21.0 pg/mL) [17].


The endocrine role of estrogens on human male skeleton.

Rochira V, Kara E, Carani C - Int J Endocrinol (2015)

Proposed range for a critical serum estradiol threshold above which both skeletal maturation and mineralization can proceed in an optimal way. E2: estradiol; BioE2: Bioavailable estradiol.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4383300&req=5

fig2: Proposed range for a critical serum estradiol threshold above which both skeletal maturation and mineralization can proceed in an optimal way. E2: estradiol; BioE2: Bioavailable estradiol.
Mentions: Based on the poor compliance of an aromatase-deficient man, we tried to develop a dose-response relationship between serum E2 and radiological changes of the long bones in terms of bone age [45]. Due to patient's poor compliance, serum E2 remained below 20 pg/mL for a long time without any change of bone age and growth plate appearance at X-ray [45]. The closure of the epiphyses was obtained only several months later when E2 rose above 20 pg/mL and the patient was taking the right dose of transdermal E2 [45]. This suggests that serum E2 above 20 pg/mL is necessary for epiphyseal cartilage fusion [45] and that only in the case of severe estrogen deficiency the epiphyses remain still open despite the advancement of the chronological age (Figure 2). The same results can be deduced from a recent study comparing sex steroids, pubertal stage, and skeletal maturation between obese and lean boys [17]. If boys at the end of puberty (with a genital Tanner stage 5) are considered, bone age (of about 18 years on average) was greatly advanced and consistent with fused epiphyses in obese boys with a mean serum E2 clearly above 20 pg/mL (median 34.8 pg/mL, min–max: 25.6–41.1 pg/mL), while bone age (of about 16 years on average) was less advanced and consistent with still unfused epiphyses in lean boys with a mean serum E2 below 20 pg/mL (median 15.7 pg/mL, min–max: 13.2–21.0 pg/mL) [17].

Bottom Line: At puberty, epiphyseal closure and growth arrest occur when a critical number of estrogens is reached.This threshold should be better identified in-between the ranges of 15 and 25 pg/mL.Future basic and clinical research will optimize strategies for the management of bone diseases related to estrogen deficiency in men.

View Article: PubMed Central - PubMed

Affiliation: Unit of Endocrinology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via P. Giardini 1355, 41126 Modena, Italy ; Azienda USL di Modena, Nuovo Ospedale Civile Sant'Agostino Estense (NOCSAE), Via P. Giardini 1355, 41126 Modena, Italy.

ABSTRACT
Before the characterization of human and animal models of estrogen deficiency, estrogen action was confined in the context of the female bone. These interesting models uncovered a wide spectrum of unexpected estrogen actions on bone in males, allowing the formulation of an estrogen-centric theory useful to explain how sex steroids act on bone in men. Most of the principal physiological events that take place in the developing and mature male bone are now considered to be under the control of estrogen. Estrogen determines the acceleration of bone elongation at puberty, epiphyseal closure, harmonic skeletal proportions, the achievement of peak bone mass, and the maintenance of bone mass. Furthermore, it seems to crosstalk with androgen even in the determination of bone size, a more androgen-dependent phenomenon. At puberty, epiphyseal closure and growth arrest occur when a critical number of estrogens is reached. The same mechanism based on a critical threshold of serum estradiol seems to operate in men during adulthood for bone mass maintenance via the modulation of bone formation and resorption in men. This threshold should be better identified in-between the ranges of 15 and 25 pg/mL. Future basic and clinical research will optimize strategies for the management of bone diseases related to estrogen deficiency in men.

No MeSH data available.


Related in: MedlinePlus