Different hormonal disorders can influence bone metabolism and cause secondary osteoporosis. In childhood, pituitary disorders hamper gaining of proper peak bone mass and skeletal size, later on in the adult life they can increase bone loss. The consequence of diminished bone strength is significant increase of fracture risk. Among pituitary disorders such effects are possible in patients with GH, prolactin, gonadotropins secretion disturbances, and GH and ACTH excess, while hypopituitarism, hyperprolactinemia, Cushings disease and acromegaly. In hypopituitarism, thyroid hormones and GH deficiency (GHD) cause bone metabolism disturbances and impairs skeletal growth, later on disturbances in GH and gonadotropins secretion lead to osteopenia or osteoporosis. There is an increased fracture risk in GHD patients. Sometimes, additional effect of secondary hypogonadism, hyperprolactinemia and GHD is observed while hypopituitarism due to pituitary tumor. Hyperprolactinemia increases bone resorption and BMD loss, there is increased fracture risk in patients with prolactinoma. Hypercortisolism due to Cushings disease (ACTH-dependent Cushings syndrome) diminishes formation and increases resorption of bone, causing trabecular bone loss and increased fracture risk. Moreover, there are decreased calcium absorption and disturbances in sex steroids secretion. In acromegaly, GH excess stimulates bone formation, but concomitant hyperpolactinemia and hypogonadism caused by pituitary macroadenoma lead to the increase of bone resorption and spinal fractures.