The physiologic effects of estrogen on bone are complicated and not completely understood; however, there are many theories as to the ways in which estrogen affects bone health: Stimulates bone formation by direct action on osteoblasts (bone-producing cells). Inhibits osteoclasts (bone-resorbing cells). Has direct action on osteoclasts by inhibiting their function and promoting apoptosis. Has direct effect on bone angiogenesis. After menopause, the loss of cancellous bone increases rapidly.This loss is mediated by a large increase in the number and activity of osteoclasts. Later, this results in progressive secondary hyperparathyroidism and slow bone loss. Estrogen deficiency is the most likely cause of changes in calcium homeostasis, resulting in decreased intestinal calcium absorption,
increased renal calcium wasting, and, perhaps also, effects on vitamin D metabolism.
See also calcium metabolism in the endocrine chapter. There you can find information about calcium and vitamin D suppletion.
The graphic below shows the normal action of osteoclasts. Osteoclast precursor cells are attracted to sites with bone damage (1). There they fuse to become multinucleated active osteoclasts (2). They resorb the damaged bone thereby liberating growth factors which recruit osteoblasts (3). Osteoblasts then create new bone (4).
The only anti-resorptive therapy for post-menopausal osteoporosis that also relieves certain hypoestrogenic symptoms is:
Extra info: Alendronate, calcium and calcitonin only have an effect on the bone metabolism and do not alter estrogen levels. Raloxifene reduces the risk of hormone-positive breast cancer.