Pituitary hormone-driven mechanism for skeletal loss

A single specific function has been traditionally ascribed to each anterior and posterior pituitary glycoprotein hormone. However, it has become clear over the past decade that these hormones and their receptors have more ubiquitous functions. Organs, such as the skeleton, are regulated by and respond to pituitary hormones, particularly when circulating levels are perturbed in disease. Additionally, certain pituitary hormones are also expressed in bone cells, underscoring paracrine regulation. The function of pituitary glycoprotein receptors in skeletal control appears evolutionarily more distant than effects on primary endocrine tissues (Blair et al. 2011). Growth hormone (GH), follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), adrenocorticotrophic hormone (ACTH), prolactin, oxytocin, and vasopressin all affect bone, and in mice, the haploinsufficiency of either the ligand and/or receptor yields a skeletal phenotype with the primary target organ remaining unaffected. Recognition and in-depth analysis of the mechanism of action of each pituitary hormone has improved our understanding of bone pathophysiology and opens new avenues for therapy. Here we discuss the interaction of each pituitary hormone with bone and the potential it holds in understanding and treating osteoporosis.