Whenever the plasma concentration of Ca2+ begins to fall, the parathyroid glands are stimulated to secrete increased amounts of parathyroid hormone (PTH), which acts to raise the blood Ca2+ back to normal levels. As might be predicted from this action of PTH, people who have their parathyroid glands removed (as may occur accidentally during surgical removal of the thyroid) will experience hypocalcemia. This can cause severe muscle tetany, for reasons previously discussed, and serves as a dramatic reminder of the importance of PTH.
Parathyroid hormone helps to raise the blood Ca2+ concentration primarily by stimulating the activity of osteoclasts to resorb bone. In addition, PTH stimulates the kidneys to reabsorb Ca2+ from the glomerular filtrate while inhibiting the reabsorption of PO43-. This raises blood Ca2+ levels without promoting the deposition of calcium phosphate crystals in bone. Finally, PTH promotes the formation of 1,25-dihydroxyvitamin D3 (as described in the next section), and so it also helps to raise the blood calcium levels indirectly through the effects of this other hormone.
Many cancers secrete a hormone known as parathyroid hormone-related protein. This molecule causes hypercalcemia by interacting with the PTH receptors, and thus increasing bone resorption, stimulating the renal reabsorption of Ca2+, and promoting the renal excretion of PO43-.
As mentioned in chapter 11, the thyroid gland secretes a hormone called calcitonin. Though its physiological significance in humans is questionable, its pharmacological action (as a drug) can be useful—it inhibits the resorption of bone. People with stress fractures of vertebrae due to osteoporosis (discussed in the next Clinical box), may be helped by injections or nasal sprays of calcitonin.
Another hormone needed for regulation of the skeletal system is estrogen. As may be recalled from chapter 11, estrogen is derived from androgen. For both men and women, estrogen produced within the epiphyseal discs (the cartilage "growth plates" in growing children) is needed for the discs to "seal" (become bone); this stops growth. Also, proper bone mineralization, and the prevention of osteoporosis, requires the production of estrogen within the bone. Men are less prone to osteoporosis than are
Regulation of Metabolism postmenopausal women, because men have higher blood levels of testosterone that can be converted by the bone into estrogen. Postmenopausal women, by contrast, have low blood concentrations of androgens (secreted from the adrenal cortex), and so cannot produce as much estrogen locally within the bones.
The most common bone disorder in elderly people is osteoporosis. Osteoporosis is characterized by parallel losses of mineral and organic matrix from bone, reducing bone mass and density (fig. 19.19) and increasing the risk of fractures. Although the causes of osteoporosis are not well understood, age-related bone loss occurs more rapidly in women than men (osteoporosis is almost ten times more common in women after menopause than in men at comparable ages), suggesting that the fall in estrogen secretion at menopause contributes to this condition. The withdrawal of sex steroids causes increased formation of osteoclasts, producing an imbalance between bone resorption and bone deposition. Premenopausal women who have a very low percentage of body fat and amenor-rhea can also have osteoporosis.
Physicians advise teenage girls, who are attaining their maximum bone mass, to eat such calcium-rich foods as milk and other dairy products. This may reduce the progression of osteoporosis when they get older. Additionally, calcium supplementation and other dietary changes are recommended for women prior to menopause. Estrogen replacement therapy for postmenopausal women is common because it helps to prevent bone loss and reduce other symptoms of menopause. Osteoporosis may also be treated with drugs that inhibit bone resorption, including calcitonin (generally derived from salmon) administered by injection or nasal spray.
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