Castrated Men Exhibit Bone Loss: Effect of Calcitonin Treatment on Biochemical Indices of Bone Remodeling*

Štěpán, J; Lachman, M; Zvěřina, Jan; Pacovský, V; Baylink, David J.

doi:10.1210/jcem-69-3-523

Cited by 391 publications

(22 citation statements)

References 24 publications

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“…Additionally, the loss of testicular function also underlies bone loss in men. Although osteoporosis more commonly affects women, the loss of androgens in males following castration or a decrease in androgen levels related to aging has the same dramatic effect on the skeleton (Stepan et al 1989, Riggs et al 2002, Vanderschueren et al 2004, Kaufman & Vermeulen 2005.…”

Section: Sex Steroid Hormones Maintain Skeletal Integritymentioning

confidence: 99%

The mutual dependence between bone and gonads

Karsenty¹

2012

Journal of Endocrinology

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It has long been known that sex steroid hormones regulate bone mass accrual. This observation raises the testable hypothesis that bone may in turn regulate the synthesis and secretion of sex steroid hormones in one or both genders. This hypothesis is comprised within a more general hypothesis that bone mass, energy metabolism, and reproduction are regulated coordinately. The identification of osteocalcin as an osteoblast-specific secreted molecule allows us to address this question in molecular terms. This review details how the regulation of male fertility by osteocalcin was unraveled, and how osteocalcin signaling in Leydig cells of the testis occurs. It also discusses the implication of this novel mode of regulation of testosterone synthesis observed in males but not in females.

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Section: Sex Steroid Hormones Maintain Skeletal Integritymentioning

confidence: 99%

The mutual dependence between bone and gonads

Karsenty¹

2012

Journal of Endocrinology

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“…In healthy men, testosterone (T) secretion only marginally declines with age [1]. Androgen suppression, however, leads to reductions in both lean tissue mass (LTM) and bone mineral density (BMD) and to increased bone turnover [2]. This hormonal change could increase the risk of osteoporosis [3, 4], which is associated with bone fracture and higher morbidity [3].…”

Section: Introductionmentioning

confidence: 99%

Testosterone Is Significantly Reduced in Endurance Athletes without Impact on Bone Mineral Density

Maı̈moun¹,

Lumbroso²,

Manetta

et al. 2003

Horm Res Paediatr

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Aims: To compare the basal plasma reproductive hormonal profile in three groups of athletes involved in different training programs, and to define the relationship between androgen level and bone mineral density (BMD) in male athletes. Methods: Basal serum total testosterone (TT), free androgen index (FAI), sex hormone-binding globulin (SHBG), cortisol, cortisol to TT ratio, luteinizing hormone (LH), estrogen and BMD were evaluated in cyclists (CY; n = 11), triathletes (TR; n = 14) and swimmers (SW; n = 13) and compared with less active controls (n = 10). Results: TT and FAI levels were lower (p < 0.05) in CY and TR, whereas the ratio of cortisol to TT was increased in CY only (p < 0.05). No alteration in serum LH, SHBG, estrogen or cortisol concentration was observed. BMD was higher in the proximal femur in TR (p < 0.05). No BMD or hormonal differences were found in SW. Conclusion: Only the endurance training of CY and TR induced androgen deficiency without apparent alteration of BMD.

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“…Loss of androgens in later life is associated with increased bone resorption and loss of trabecular bone, but cortical bone mass is not greatly affected [11,12]. In a study of 12 men who had undergone judicial castration for ''sexual delinquency'' [13], bone turnover was increased and lumbar spine BMD fell significantly, with evidence of the most rapid loss in the first 5 years after castration. Rates of bone loss were as high as 7% per year, comparable to loss rates seen in early postmenopausal women.…”

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confidence: 99%

Sex Hormones and Osteoporosis in Men

et al. 1998

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Osteoporosis in men is a common disorder, the incidence of which is increasing. Bone is lost with advancing age in men as well as in women, leading to an increased risk of fracture after minimal trauma. Recent epidemiological data from North America suggests a lifetime risk of fracture of the hip, spine, or forearm of 13.1% in white men aged 50 [1]. Despite the considerable public health burden attributable to these fractures, our understanding of their pathogenesis is incomplete and there is no established treatment for osteoporosis in men.Androgen deficiency is thought to play an important role in many cases of male osteoporosis. Biochemical evidence of hypogonadism is found in about 20% of men with vertebral fractures [2] and up to 50% of men with hip fractures [3,4], often without other clinical features of gonadal failure. In cell culture studies using human osteoblastlike cells from both men and women [5][6][7], specific androgen receptors can be identified by nuclear and cytosolic binding assays (Table 1). Similarly, osteoblasts obtained from fresh femoral bone specimens can also metabolize the circulating androgen androstenedione to testosterone and 5␣-dihydrotestosterone (DHT) in both men and women [8] at rates dependent mainly on androstenedione concentration. Cells of osteoclast lineage may also have these properties, though this is less well established. Androgen receptors have also been directly demonstrated in osteoblasts and osteocytes around the growth plate [9]. Androgens may promote proliferation and differentiation of osteoblasts, inhibit osteoclast recruitment or affect osteoblast-to-osteoclast signaling.Animal studies have mostly been performed in orchiectomized (orch) male rats, though there are reservations about the appropriateness of this model because the rat skeleton grows throughout life. Replacement therapy with either testosterone or 5␣-DHT results in enhanced bone mass, though this remains lower than in control rats [10].In male humans, androgens have a marked effect on bone growth and peak bone mass via the growth hormone/ IGF-I axis; accordingly, androgen deficiency before puberty leads to lower bone mineral density (BMD) in both cortical and trabecular bone. Loss of androgens in later life is associated with increased bone resorption and loss of trabecular bone, but cortical bone mass is not greatly affected [11,12]. In a study of 12 men who had undergone judicial castration for ''sexual delinquency'' [13], bone turnover was increased and lumbar spine BMD fell significantly, with evidence of the most rapid loss in the first 5 years after castration. Rates of bone loss were as high as 7% per year, comparable to loss rates seen in early postmenopausal women. In this study, calcitonin therapy was effective in reducing bone loss, and low calcitonin levels have been reported in another group of young hypogonadal men who had not undergone surgery [14]. Others have found low plasma 1,25 dihydroxyvitamin D levels and impaired calcium absorption in hypogonadal men [15].This combination o...

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Castrated Men Exhibit Bone Loss: Effect of Calcitonin Treatment on Biochemical Indices of Bone Remodeling*

Cited by 391 publications

References 24 publications

The mutual dependence between bone and gonads

The mutual dependence between bone and gonads

Testosterone Is Significantly Reduced in Endurance Athletes without Impact on Bone Mineral Density

Sex Hormones and Osteoporosis in Men

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