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Osteoporosis

Osteoporosis is a systemic skeletal disease characterized by decreased bone mass and microarchitectural deterioration of bone tissue, which consequently increases bone fragility and susceptibility to osteoporosis, thin bones. In women, most cases of osteoporosis are caused by estrogen deficiency and aging. Osteopenia is defined as a bone mineral density between 1 and 2.5 standard deviations below the young-adult mean. Osteopenia is a precursor condition to osteoporosis.

Clinical Risk Factors for Osteoporosis

Low estrogen levels

• Many years of menopause

• Early menopause, natural or surgical

•Amenorrhea in premenopausal women (ie, eating disorders, athletes)

Positive family history of osteoporosis White or Asian race Small skeletal frame Sedentary lifestyle Cigarette smoking

Alcohol intake more than three standardized glasses per week

Medications such as glucocorticoids at doses greater than the equivalent of prednisone 10 mg/d

Clinical Risk Factors

An important clinical decision is determining which women should have a measurement of bone mineral density. Many authorities recommend that women with one or more clinical risk factors for osteoporosis should be offered a bone density measurement.

Prevention

The most effective approach to osteoporosis prevention is ensuring that each woman reaches her genetically endowed peak bone mass and minimizing the amount of bone loss during menopause. Interventions to prevent osteoporosis span the continuum of life and extend into menopause with the addition of estrogen.

Prevention of osteoporosis begins in childhood, and adequate calcium intake is important. Recommendations for daily calcium intake are presented in Table 33. Many children and adolescents do not consume enough calcium.

Sedentary lifestyle is associated with reduced bone mass. Weight-bearing exercise stimulates osteoblasts to form new bone. The benefits of exercise can be demonstrated into the ninth decade of life, but they persist only if the exercise is continued. 

Estrogen therapy is the mainstay of prevention and treatment of osteoporosis in perimenopausal and postmenopausal women. Estrogen inhibits osteoclast activity, reducing bone reabsorption. One clinical algorithm for the prevention and treatment of osteoporosis is presented in Figure 18.

Alendronate is a bisphosphonate that binds to bone surfaces and inhibits osteoclast activity. When an osteoclast binds to the bone surface and attempts to remove bone, the alendronate on the bone surface enters the osteoclast and impairs cell function. Alendronate is approved for the prevention and treatment.

Raloxifene, a nonsteroidal benzothiophene, has been approved by the Food and Drug Administration for the prevention of osteoporosis. Raloxifene is a selective estrogen receptor modulator that has estrogen agonist properties in bone (inhibiting osteoclast activity) and liver (decreasing low-density lipoprotein cholesterol). Because raloxifene has no estrogen agonist activity.

Treatment

Estrogen replacement therapy is the primary preventive and treatment modality for hypoestrogenic women with osteoporosis. All women with low estrogen levels and osteoporosis should be offered estrogen treatment as the first line of therapy. Estrogen treatment decreases osteoclast activity, increases bone mass, reduces the risk of fracture, and preserves height. Estrogen replacement initiated during perimenopause or soon after the onset of menopause prevents the early phase.

Prevention of Osteoporosis

A 1994 National Institutes of Health Consensus Conference made recommendations regarding calcium intake to help women reduce their risk of developing osteoporosis (Table 33). Dairy products are the major sources of calcium because of their content 

Vitamin D is essential to promote calcium absorption and metabolism. Exposure of the skin to sunshine is a major source of vitamin D for many U.S. women, even if only their faces and hands are exposed.

In menopausal women, estrogen treatment clearly improves bone density. However, the minimum dose for preventing and reducing bone loss has not yet been established. Recent studies suggest that there is a dose-response curve between estrogen.

As noted above, alendronate is approved for the treatment of osteoporosis. Alendronate and other bisphosphonates inhibit osteoclast activity, increase bone density, reduce the risk of fracture overall by approximately 50%, and reduce the risk of multiple vertebral fractures by 90%. One benefit of these risk reductions is that they help to preserve a woman's height. A problem with alendronate is that only 1% is absorbed from the gastrointestinal tract.

A potential advantage of alendronate treatment is that alendronate remains tightly bound to the bone surface for many years. This probably provides some protection against osteoclast resorption of bone for some time after discontinuation of therapy.