osteoporosis (redirected from post-traumatic osteoporosis)

osteoporosis (ŏs'tēō'pərō`sĭs), disorder in which the normal replenishment of old bone tissue is severely disrupted, resulting in weakened bones and increased risk of fracture; osteopenia results when bone-mass loss is significant but not as severe as in osteoporosis. Although osteoporosis can occur in anyone, it is most common in thin white women after menopause.

Bone mass is typically at its greatest during a person's mid-twenties; after that point there is a gradual reduction in bone mass as bone is not replenished as quickly as it is resorbed. In postmenopausal women the production of estrogen, a hormone that helps maintain the levels of calcium and other minerals necessary for normal bone regeneration, drops off dramatically, resulting in an accelerated loss of bone mass of up to 3% per year over a period of five to seven years. Smoking, excessive alcohol consumption, and a sedentary lifestyle increase the risk of bone-mass loss; a diet high in protein and sodium also speed calcium loss. The disorder also has a genetic component. A vitamin D receptor gene that affects calcium uptake and bone density has been identified, and the different forms of this gene appear to correlate with differences in levels of bone density among osteoporosis patients.

Osteoporosis has no early symptoms and is usually not diagnosed until a fracture occurs, typically in the hip, spine, or wrist. A diagnostic bone density test is thus recommended as a preventive measure for women at high risk. Treatment can slow the process or prevent further bone loss. Estrogen replacement therapy for postmenopausal women is effective but has potential side effects. Calcitonin, a thyroid hormone, is administered in some cases. Nonhormonal drugs for the treatment of osteoporosis include alendronate (Fosamax) and risedronate (Actonel), bisphosphonates that decrease bone resorption, and raloxifene (Evista), a selective estrogen receptor modulator that can increase bone mineral density. Teriparatide (Forteo), which consists of the biologically active region of human parathyroid hormone, stimulates the activity of osteoblasts, the specialized cells that form new bone. Dietary and supplemental calcium and vitamin D are usually recommended for people at risk, but a seven-year study of more than 36,000 women over 50 that was released in 2006 found that supplements conferred little benefit. Exercise, including weight training, has been found to strengthen bones directly and to improve muscle strength and balance and thus minimize the chance of falls.

Bibliography

See M. Hegsted, Advances in Nutrition Research, Vol. 9: Nutrition and Osteoporosis (1994).

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osteoporosis

Generalized loss of bone density, causing skeletal weakness. Around age 40, the rate of bone resorption in humans starts to exceed the rate of bone formation. Women experience accelerated bone loss after menopause, when the estrogen level decreases. When the amount of bone falls below a certain threshold, fractures occur with little or no trauma. Prevention begins with adequate calcium intake in youth, when bone mass is built, and then throughout life. Weight-bearing exercise and vitamin D are important at all ages. Medications can inhibit bone resorption or prevent bone loss in patients who are at risk for developing osteoporosis.