Female reproductive system and bone

The female reproductive system plays a major role in regulating the acquisition and loss of bone by the skeleton from menarche through senescence. Onset of gonadal sex steroid secretion at puberty is the major factor responsible for skeletal longitudinal and radial growth, as well as significant gain in bone density, until peak bone density is achieved in third decade of life. Gonadal sex steroids then help maintain peak bone density until menopause, including during the transient changes in skeletal mineral content associated with pregnancy and lactation. At menopause, decreased gonadal sex steroid production normally leads to rapid bone loss. The most rapid bone loss associated with decreased estrogen levels occurs in the first 8–10 years after menopause, with slower age-related bone loss occurring during later life. Age-related bone loss in women after the early menopausal phase of bone loss is caused by ongoing gonadal sex steroid deficiency, vitamin D deficiency, and secondary hyperparathyroidism. Other factors also contribute to age-related bone loss, including intrinsic defects in osteoblast function, impairment of the GH/IGF axis, reduced peak bone mass, age-associated sarcopenia, and various sporadic secondary causes. Further understanding of the relative contributions of the female reproductive system and each of the other factors to development and maintenance of the female skeleton, bone loss, and fracture risk will lead to improved approaches for prevention and treatment of osteoporosis.

Research highlights
► The female reproductive system regulates acquisition and loss of bone by the skeleton from menarche through old age.
► Onset of gonadal sex steroid secretion at puberty is the major factor responsible for skeletal growth and increased bone density.
► Gonadal sex steroids help maintain bone density during pregnancy and lactation.
► Rapid early postmenopausal bone loss in women results predominantly from gonadal sex steroid deficiency.
► Age-related bone loss in later life results from continued gonadal sex steroid deficiency, vitamin D deficiency, secondary hyperparathyroidism, and other factors.