Postmenopausal bone loss: A reverse manifestation of pubertal packing of mineral into the female skeleton

摘要

The prevailing unitary model of involutional osteoporosis suggests that the female postmenopausal bone loss consists of two separate phases: the accelerated, transient phase, which is most distinct over the subsequent decade after the menopause and accounts for 20-30% of the cancellous bone loss and 5-10% of the cortical bone loss (type I osteoporosis), and the following gradual, continuous bone loss (type II osteoporosis). Estrogen deficiency is currently quite unanimously accepted as the primary cause of the type T osteoporosis, as well as also a major determinant of the type II osteoporosis, and quite logically, the quest to uncover the origin of type I (and II) osteoporosis has focused on the estrogen withdrawal-related skeletal changes at and around the menopause. However, given that the cyclical secretion of estrogen begins normally in the early adolescence and continues over the entire fertile period (excluding the potential periods of pregnancy) until the eventual cessation of female reproductive capability at menopause, one could argue that this menopause-oriented approach is limited in scope. In this communication, some classic findings of the pubertal effects of estrogen on female bones are presented, findings that Fuller Albright actually already knew when he first described the disease called postmenopausal osteoporosis in 1940. When these findings are incorporated with the primary Junction of the axial skeleton and long bones-the locomotion-an alternative, novel evolution-based proposal for the origin of the accelerated phase of postmenopausal bone loss and accordingly, the pathogenesis of the postmenopausal bone loss is introduced: estrogen induces the packing of mechanically excess mineral into female skeleton at puberty, a bone stock that is an apparent evolutionary safety reservefor the needs of reproduction (fetal skeletogenesis and lactation). When the female reproductive function ceases at menopause, this deposit of mineral is removed as unnecessary, serving as the origin of the type I postmenopausal osteoporosis.