The skeletal system is sexually dimorphic, to being average larger and more robust in men compared to women. Sex hormones are considered key mediators of skeletal sexual dimorphism. Studies suggest that prepuberal androgen deficiency, possibly in early childhood, causes permanent defects in bone mineral density. Results from our laboratory show that disturbances of the hypothalamic-pituitary-gonadal axis results in changes in skeletal development and that these differences occur from time-dependent manner, with more profound physical changes in both sexes, gonadal arise when the failure is determined to around birth, critical phase of brain sexual differentiation in mice. There are few published studies evaluating the mechanisms of action of sex hormones during the neonatal stage on bone microarchitecture and modulation of the cellular and molecular activities during development. Understanding these mechanisms is required for the development of therapeutic strategies that exploit the benefits to bone health without unwanted side effects in other tissues. Thus, considering the paucity of studies in the literature investigating the cellular mechanisms by which neonatal castration and androgenization induces irreversible changes on skeletal development and bone biophysical properties, the objective of this study is to investigate the effects of androgen manipulation during the neonatal period on sexually dimorphic characteristics of bone tissue, evaluated by histomorphometric and immunohistochemical analyzes in animals prepubescent and pubescent young adult.
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