Pituitary hormone implicated in bone loss after menopause

the fine balance between bone formation and resorption. After menopause, resorption exceeds new bone formation, leading to a net bone loss that can be slowed by estrogen therapy through mechanisms that have remained somewhat murky, Zaidi said.

However, emerging evidence has begun to cast some doubt on whether estrogen deficiency can fully explain bone loss after menopause, he added. For example, mice without an intact pituitary gland become resistant to the effects of ovary loss on bone density. FSH levels also show a closer correlation than estrogen levels to the rate of bone turnover in postmenopausal women.

The researchers now show that mice lacking FSH or its receptor become resistant to bone loss despite severe loss of ovarian function. In mice with normal ovaries and approximately half the normal concentration of FSH, bone mass increased due to a decline in bone resorption by cells known as osteoclasts, which break down bone. Indeed, they report, FSH stimulates receptors found on the surface of bone-degrading osteoclasts and their precursors, leading to the bone cells' formation and function.

The study suggests that FSH plays a role in the normal process by which bone is mobilized by osteoclasts before it can be replaced, Zaidi said.

"As you run or walk throughout life, microcracks develop in bone," he explained. "Therefore, bone remodeling and replacement with new bone is required to maintain skeletal integrity. Osteoclasts essentially dig around those cracks to clear the way for repairs."

In combination with the research group's earlier finding that thyroid-stimulating hormone directly regulates the skeleton, the findings revise the understanding of how pituitary-derived hormones function, Zaidi added. Scientist had thought pituitary hormones acted primarily through their effects on other endocrine glands.

"This should change the textbook picture of pituitary hormone physiology," he said.


Contact: Heidi Hardman
Cell Press

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