Pituitary-bone connection in skeletal regulation

Abstract

Pituitary hormones have traditionally been thought to exert specific, but limited function on target tissues. More recently, the discovery of these hormones and their receptors in organs such as the skeleton suggests that pituitary hormones have more ubiquitous functions. Here, we discuss the interaction of growth hormone (GH), follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH), adrenocorticotrophic hormone (ACTH), prolactin, oxytocin and arginine vasopressin (AVP) with bone. The direct skeletal action of pituitary hormones therefore provides new insights and therapeutic opportunities for metabolic bone diseases, prominently osteoporosis.

What Is Breast in the Bone?

“…PRL may be responsible for bone loss at lactation [94,95,96], consistent with evidence [97,98,99] that demonstrates a direct effect of PRL on osteoblasts, which express the PRLR. These results are consistent with the phenotype of hyperprolactinemia patients, who experience bone loss [100], thought to be either due to the indirect effect of PRL that results in hypogonadism, and therefore, low estrogen, or alternatively by the direct action of PRL on osteoblasts [99,101]. PRL-PRLR directly increases bone turnover by raising the RANKL/OPG ratio [99,102].…”

Crosstalk of Brain and Bone—Clinical Observations and Their Molecular Bases

“…Besides these direct effects, hyperprolactinemia is also proposed to negatively act on bone in an indirect manner, involving hypogonadism, hypercalcemia and an enhanced secretion of parathyroid hormone-related peptide (PTHrP) [ 188 ]. As PRL treatment however showed a positive effect on bone formation in infant rats [ 193 ] and a decreased RANKL/OPG ratio in human fetal osteoblasts [ 192 ], the effect of PRL on bone is proposed to be dependent on the developmental stage [ 194 ] and warrants further mechanistic understanding.…”

“…Adrenocorticotrophic hormone (ACTH), the key mediator of corticosteroid-release from the adrenal gland, represents an important co-regulator of immune responses, vascular tone, central metabolism and bone turnover [ 194 , 195 ]. Chronically elevated levels of glucocorticoids are a well-established cause for osteoporosis and presumbly osteonecrosis due to their inhibitory impact on bone-forming osteoblasts [ 47 , 196 ].…”

“…Chronically elevated levels of glucocorticoids are a well-established cause for osteoporosis and presumbly osteonecrosis due to their inhibitory impact on bone-forming osteoblasts [ 47 , 196 ]. Zaidi et al propose that ACTH in interaction with VEGF supports the prevention of glucocorticoid-induced osteonecrosis [ 170 , 194 , 195 ]. Additional studies described the expression of ACTH by monocytes/macrophages [ 197 ], which acts cortisol-independent on melanocortin 2 receptors (MC2R) expressed by osteoblastic cells [ 195 ].…”

Evaluation of bone texture imaging parameters on panoramic radiographs of patients with Sheehan’s syndrome: a STROBE-compliant case-control study

“…1 Pituitary hormones play an important connection with skeleton-related bone metabolism because bone cells usually express hormone receptors for growth hormone, follicle stimulating hormone, thyroid stimulating hormone, adrenocorticotrophic hormone, prolactin, oxytocin and vasopressin, and their role are evident especially in several diseases. 2,3 Among the disturbances that can affect the pituitary gland, Sheehan's syndrome (SSH) is a disease that affects the secretion of adenohypophyseal hormones. This condition is known as postpartum pituitary necrosis, and it is a rare condition that was firstly reported in 1937 by HL Sheehan and co-authors that described 12 cases of gland necrosis and pituitary failure following obstetric complications.…”