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"Pain. Joints. Spine." 1 (21) 2016

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Male hypogonadism and bone mass

Authors: Mascarenhas M.R., Barbosa A.P. - Endocrinology and Metabolic Diseases, Faculty Medicine of Lisbon; Fracturary Osteoporosis Outpatient Clinic — Endocrinology, Diabetes and Metabolism Department, Santa University Maria Hospital-CHLN, EPE, Lisboa, Portugal; Duarte N., Poupino J., Faria C., Gomes A.C., Barbosa D., Silvestre C., Paixão R., Gomes V., Osório A.S., Sampaio F., Monteiro J. - Fracturary Osteoporosis Outpatient Clinic — Endocrinology, Diabetes and Metabolism Department, Santa University Maria Hospital-CHLN, EPE, Lisboa, Portugal

Categories: Rheumatology, Traumatology and orthopedics

Sections: Medical forums

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The article was published on p. 77


Normal sex steroids hormone levels are essential for optimizing peak bone mass and their deficiencies during adulthood may modify the bone mass, as it causes bone loss by increased bone resorption and can be associated with a low BMD, osteoporosis or/and fragility fractures risk. Sex steroid hormones affect the skeleton by direct and indirect mechanisms. Androgens affect osteoblast activity and probably stimulate directly the bone formation and may exert a moderate resorption of the trabecular bone, similar to estrogens effects on bone. In male hypogonadism there is not enough sex steroid hormone synthesis by the testes, sperm or both; hypogonadism is also characterized by the lack of estrogen and unequivocally androgen: the bone disease of men with hypogonadism is associated with the absence of estrogen actions. In adult men with primary or hypogonadotropic hypogonadism due to bilateral orchiectomy there is a BMD decrease detectable 1 to 3 years after orchiectomy. These men had a rapid loss of vertebral bone mass (about 7 % per year) progressing together with an increased osteoclast activity, which is inhibited by non-aromatisable androgens; the rapid bone mass loss and increased bone turnover are more intense in the years just after orchiectomy, with a consequent diminished bone loss phase, a process menopause-like. In prepubertal secondary or hypogonadotropic hypogonadism there is a reduced BMD at the cortical and cancellous bone. GnRH analogues therapy (inhibition of the pituitary gonadotropins production and secretion originating gonadal deficiency) in adults is also related with a marked bone mass loss and osteoporotic fractures. Chronic glucocorticoid therapy may reduce substantially testosterone levels and contribute also to the bone mass loss.

Our group detected a significant low BMD at several skeletal sites in hypogonadal men, as compared with a group with normal gonadal function. Studies in chronic male hypogonadism revealed decreased rates of bone formation, increase in average of bone remodeling rates, increased levels of osteocalcin, interaction between testosterone and vitamin D metabolism and a reduction in the trabeculae number. The BMD is correlated with free testosterone plasma levels in old men. In prepubertal hypogonadism and growth hormone deficiency, vertebrae sizes are small due to short stature and vertebral fractures (compression or wedge) are frequent. Hypogonadism may contribute to severe osteoporosis in about 15 % of men; androgen deficiency is associated with 30 % of the osteoporotic vertebral fractures and hip fractures that occur most often in old hypogonadal men with vitamin D deficiency.
Testosterone therapy inhibits osteoclast activity and increases bone formation. Therapy of adult males with hypogonadism showed positive effects on BMD in most osteoporotic patients but the BMD may not normalize even if the testosterone levels are already normal for one year. Our group observed a significant low BMD in a group of hypogonadal men treated during 7 years. Finally, no data were published about osteoporotic fractures risk and testosterone therapy for the different types of male hypogonadism. 

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