Background: Delayed puberty means the absence of secondary sexual characters until the age of 16 or the lack of puberty development until the limit of +2DS regarding the age when the puberty normally begins at considered population. Considering the major ethiological factor implied in delayed puberty, three mechanisms can be distinguished: hypothalamic, hypophyseal and gonadal. Osteoporosis depends mainly on the deficiency of one or of all sexual hormones, arised during the ontogenesis process.
Methods: We enrolled 26 cases of delayed puberty, aged 1235, of which 14 cases (53.85%) of hypergonadotropic hypogonadism (female Turner syndrome 10 cases; Klinefelter four cases) and 12 cases (46.15%) of hypogonadotropic hypogonadism (hypophyseal dwarfism with sexual infantilism three cases; functional adipose-genital syndrome seven cases; tumor-like hypophyseal insufficiency two cases). Plasmatic level of the two markers of bone turnover (osteocalcine and CrossLap) was evaluated by ELISA method. Dual absorption with X-rays assesed bone mineral density.
Results: DEXA identified, 10 cases (38.46%) of osteoporosis, where the osteocalcine values (29.4112.96 ng/ml) and CrossLap (0.1971.768 ng/ml) were comparable with those of women in postmenopausal period, six cases (23.08%) of osteopenia, and 10 cases (38.46%) of T score value and biochemical markers in normal range.
Conclusions: Our study suggests two major objectives of therapy for existent osteoporosis/osteopenia at delayed puberty pacients: precocious diagnosis of gonadal insufficiency, in to apply some prophylaxis measures for bone modifications beginning from pre-puberty, thus insuring the stabilization or increasing bone mass corresponding to sex and age; therapy associates estro-progestative/ androgenic substitution and antiresorbtion or proformation medication.