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An in-depth report on the causes, diagnosis, treatment, and prevention of osteoporosis.
Because the patterns of reforming and resorbing bone often vary from patient to patient, experts believe several different factors account for this problem. Important chemicals (such as estrogen, parathyroid hormone, and vitamin D) and blood factors that affect cell growth are involved with this process. Changes in levels of any of these factors could play a role in the development of osteoporosis.
Although ordinarily associated with women, sex hormones play a role in osteoporosis in both genders, most likely by controlling the birth and duration of life of both osteoclasts (bone breakers) and osteoblasts (bone builders).
Women and Estrogen. Experts are still puzzled by the rapid decline in bone density after menopause, when a woman’s ovaries stop producing estrogen. Estrogen comes in several forms:
The ovaries produce most of the estrogen in the body, but it can also be formed in other tissues, such as body fat, skin, and muscle. After menopause, some amounts of estrogen continue to be manufactured in the peripheral body fat. Even though the ovaries have stopped producing estrogens directly, they continue to be a source of the male hormone testosterone, which converts into estradiol.
Estrogen may have an impact on bone density in various ways:
Men and Androgens and Estrogen. In men, the most important androgen (male hormone) is testosterone, which is produced in the testes. Other androgens are produced in the adrenal glands. Androgens are converted to estrogen in various parts of a man’s body, including bone.
Studies have suggested that the loss of estrogen as well as testosterone may contribute to bone loss in elderly men. In one study, elderly men were first given a drug that blocked their normal hormones and then were given estrogen and testosterone patches. When the estrogen patch was removed, the bone breakdown process accelerated. When both patches were removed, the number of the bone-building cells (the osteoblasts) decreased. In other words, both hormones appeared to be integral to bone function in men.
Low levels of vitamin D and high levels of parathyroid hormone (PTH) are associated with hip fracture in women after menopause:
Several studies on family members, including twins, have strongly suggested that genetic factors help determine bone density. Some examples include the following:
Corticosteroids. More than 30 million Americans have disorders that are commonly treated using corticosteroids (also called glucocorticoids or steroids). Oral corticosteroids are known to reduce bone mass in both men and women. Studies report a higher risk for bone loss in adults who take inhaled steroids regularly. The risk is higher with increasing doses, but is still lower than with oral steroids. (Children on inhaled steroids may have temporary impaired growth, but they do not appear to be at risk for bone loss.)
Other Medications . Anti-epileptic (also called anti-seizure) drugs increase the risk for bone loss (as does epilepsy itself). Other drugs that increase the risk for bone loss include heparin, progestin without estrogen (such as Depo-Provera or other progestin-based contraceptives), and hormonal drugs that suppress estrogen (such as gonadotropin-releasing hormone agonists). Diuretics (used to treat high blood pressure) have different effects on osteoporosis, depending on the type. Loop diuretics, which block sodium, have been associated with bone loss. Thiazide diuretics, on the other hand, confer protection against fracture during the time they are used.
Predisposing Medical Conditions . Osteoporosis can be secondary to several other conditions, including alcoholism, diabetes, hyperthyroidism, epilepsy, chronic liver or kidney disease, celiac disease, scurvy, rheumatoid arthritis, leukemia, cirrhosis, gastrointestinal diseases, vitamin D deficiency, hypogonadism (impaired development of reproductive organs), lymphoma, hyperparathyroidism, and rare genetic disorders such as Marfan’s and Ehlers-Danlos syndrome.
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