Osteoporosis is a public health problem affecting more than 40 million people, one-third of postmenopausal women and a substantial portion of the elderly in the United States and almost as many in Europe and Japan. An additional 54% of postmenopausal women have low bone density measured at the hip, spine, or wrist. Osteoporosis results in more than 1,500,000 fractures annually in the United States alone. At least 90% of all hip and spine fractures among elderly women are a consequence of osteoporosis. The direct expenditures for osteoporotic fractures have increased during the past decade from $5 billion to almost $15 billion per year. Thus, family physicians and other primary care providers will (1) frequently care for patients with subclinical osteoporosis, (2) recognize the implications of those who present with osteoporosis-related fractures, and (3) determine when to implement prevention for younger people.

Of the 25 million women in the United States thought to have osteoporosis, 8 million have a documented fracture. The female-to-male fracture ratios are reported to be 7:1 for vertebral fractures, 1.5:1 for distal forearm fractures, and 2:1 for hip fractures. Approximately 30% of hip fractures in persons aged 65 years and older occur in men. Osteoporosis-related fractures in older men are associated with lower femoral neck bone mineral density (BMD), quadriceps weakness, higher body sway, lower body weight, and decreased stature. Osteoporotic fractures are more common in whites and Asians than in African Americans and Hispanics, and more common in women than in men. Little is known regarding the influence of ethnicity on bone turnover as a possible cause of the variance in bone density and fracture rates among different ethnic groups. Significant differences in bone turnover in premenopausal and early perimenopausal women can be documented. The bone turnover differences do not appear to parallel the patterns of BMD. Other factors, such as differences in bone accretion, are likely responsible for much of the ethnic variation in adult BMD.

Osteoporosis is characterized by microarchitectural deterioration of bone tissue that leads to decreased bone mass and bone fragility. The major processes responsible for osteoporosis are poor bone mass acquisition during adolescence and accelerated bone loss during the perimenopausal period (mid-50s to the sixth decade in women and the seventh decade in men) and beyond. Both processes are regulated by genetic and environmental factors. Reduced bone mass, in turn, is the result of varying combinations of hormone deficiencies, inadequate nutrition, decreased physical activity, comorbidity, and the effects of drugs used to treat various medical conditions.

Primary osteoporosis—deterioration of bone mass not associated with other chronic illness—is related to increasing age and decreasing gonadal function. Therefore, early menopause or premenopausal estrogen deficiency states may hasten its development. Prolonged periods of inadequate calcium intake, a sedentary lifestyle, and tobacco and alcohol abuse also contribute to primary osteoporosis.

Secondary osteoporosis results from chronic conditions that contribute significantly to accelerated bone loss. These include endogenous and exogenous thyroxine excess, hyperparathyroidism, cancer, gastrointestinal diseases, medications, renal failure, and connective tissue diseases. Secondary forms of osteoporosis are listed in Table 29-1. If secondary osteoporosis is suspected, appropriate diagnostic workup may identify a different management course.

Nutrition

Bone mineralization is dependent on adequate nutritional status in childhood and adolescence. Therefore, measures to prevent osteoporosis should begin with increasing the milk intake of adolescents to improve bone mineralization. Nutrients other than calcium are also essential for bone health. Adolescents must, therefore, maintain a balance in calcium intake, protein intake, other calorie sources, and phosphorus. Substituting phosphorus-laden soft drinks for calcium-rich dairy products and juices compromises calcium uptake by bone and promotes decreased bone mass.

Eating disorders are nutritional conditions that affect BMD. Inability to maintain normal body mass promotes bone loss. The body weight history of women with anorexia nervosa has been found to be the most important predictor of the presence of osteoporosis as well as the likelihood of recovery. The BMD of these patients does not increase to a normal range, even several years after recovery from the disorder, and all persons with a history of an eating disorder remain at high risk for osteoporosis in the future.

Major demands for calcium are placed on the mother by the fetus during pregnancy and lactation. The axial spine and hip show losses of BMD during the first 6 months of lactation, but this bone mineral loss appears to be completely restored 6-12 months after weaning. Risk factors for osteoporosis are summarized in Table 29-2.

Lifestyle

Sedentary lifestyle or immobility (being confined to bed or a wheelchair) increases the incidence of osteoporosis. Low body weight and cigarette smoking negatively influence bone mass. Excessive alcohol consumption has been shown to depress osteoblast function and, thus, to decrease bone formation. Those at risk for low BMD should avoid drugs that negatively affect BMD (see Table 29-1).

Behavioral Measures

Behavioral measures that decrease the risk of bone loss include eliminating tobacco use and excessive consumption of alcohol and caffeine. A balanced diet with adequate calcium and vitamin D intake and a regular exercise program (see below) retard bone loss. Medications, such as glucocorticoids, that decrease bone mass should be avoided if possible. The importance of maintaining estrogen levels in women should be emphasized. Measurement of bone density should be considered in the patient who presents with risk factors, but additional evidence is needed before instituting preventive measures.

Exercise

Regular physical exercise can reduce the risk of osteoporosis and delay the physiologic decrease of BMD. Short- and long-term exercise training (measured up to 12 months; eg, walking, jogging, stair climbing) in healthy, sedentary, postmenopausal women results in improved bone mineral content. Bone mineral content increases more than 5% above baseline after short-term, weight-bearing exercise training. With reduced weight-bearing exercise, bone mass reverts to baseline levels. Similar increases in BMD have been seen in women who participate in strength training. In the elderly, progressive strength training has been demonstrated to be a safe and effective form of exercise that reduces risk factors for falling and may also enhance BMD.

Estrogen deficiency results in diminished bone density in younger women as well as in older women. Athletes who exercise much more intensely and consistently than the average person usually have above-average bone mass. However, the positive effect of exercise on the bones of young women is dependent on normal levels of endogenous estrogen. The low estrogen state of exercise-induced amenorrhea outweighs the positive effects of exercise and results in diminished bone density. When mechanical stress or gravitational force on the skeleton is removed, as in bed rest, space flight, immobilization of limbs, or paralysis, bone loss is rapid and extensive. Weight-bearing exercise can significantly increase the BMD of menopausal women. Furthermore, weight-bearing exercise and estrogen replacement therapy have independent and additive effects on the BMD of the limb, spine, and Ward triangle (hip).

There have been no randomized prospective studies systematically comparing the effect of various activities on bone mass. Recommended activities include walking and jogging, weight training, aerobics, stair climbing, field sports, racquet sports, court sports, and dancing. Swimming is of questionable value to bone density (because it is not a weight-bearing activity) and there are no data on cycling, skating, or skiing. It should be kept in mind that any increase in physical activity may have a positive effect on bone mass for women who have been very sedentary. To be beneficial, the duration of exercise should be between 30 and 60 minutes and the frequency should be three times per week.

Symptoms and Signs

The history and physical examination are neither sensitive enough nor sufficient for diagnosing primary osteoporosis. However, they are important in screening for secondary forms of osteoporosis and directing the evaluation. The goals of the evaluation should be (1) to establish the diagnosis of osteoporosis by assessing bone mass, (2) to determine fracture risk, and (3) to determine whether intervention is needed. A medical history provides valuable clues to the presence of chronic conditions, behaviors, physical fitness, and the use of long-term medications that could influence bone density. Those already affected by complications of osteoporosis may complain of upper or midthoracic back pain associated with activity, aggravated by long periods of sitting or standing, and easily relieved by rest in a recumbent position. The history should also assess the likelihood of fracture. Other indicators of increased fracture risk are low bone density, a propensity to fall, taller stature, and the presence of prior fractures.

The physical examination should be thorough for the same reasons. For example, lid lag and enlargement or nodularity of the thyroid suggest hyperthyroidism. Moon facies, thin skin, and a buffalo hump suggest hypercortisolism. Cachexia mandates screening for an eating disorder or cancer. A pelvic examination is one aspect of the total evaluation of hormonal status in women and a necessary part of the physical examination in women. Osteoporotic fractures are a late physical manifestation. Common fracture sites are the vertebrae, forearm, femoral neck, and proximal humerus. The presence of a “Dowager hump” in elderly patients indicates multiple vertebral fractures and decreased bone volume.

Because the true value of an assessment of bone density is to prevent injury, recent studies completed under the auspices of the World Health Organization Collaborating Centre for Metabolic Bone Diseases used a 10-year probability model to develop a more accurate assessment of fracture risk. A fracture risk assessment tool (FRAX) was developed to identify and account for clinical risk factors for fracture—age, low body mass index, parental history of hip fracture, current smoking, alcohol intake greater than 3 units daily, rheumatoid arthritis or other secondary causes of osteoporosis, oral glucocorticoids, and previous fragility fracture—Primary data were used from nine large patient cohorts in North America, Europe, Asia, and Australia representing over 1 million patient-years. The primary data are used to accurately evaluate the interaction of each risk factor, rather than being limited to the potential bias of published data. Additional secondary causes of osteoporosis include untreated hypogonadism, inflammatory bowel disease, prolonged immobility, organ transplantation, type 1 diabetes, thyroid disorders, and chronic obstructive pulmonary disease. This tool estimates the 10-year, patient-specific absolute risk of hip or major osteoporotic fracture (hip, spine, shoulder, or wrist), taking account of death from all causes and death hazards (eg, smoking). The tool may be used alone using individual clinical risk factors, with or without BMD.

Laboratory Findings

Basic chemical analysis of serum is indicated when the history suggests other clinical conditions influencing bone density. The tests presented in Tables 29-3 and 29-4 are appropriate for excluding secondary causes of osteoporosis. These tests provide clues to serious illnesses that may otherwise have gone undetected and that, if treated, could result in resolution or modification of the bone loss. Specific biochemical markers (human osteocalcin, bone alkaline phosphatase, immunoassays for pyridinoline cross-links and type 1 collagen–related peptides in urine) that reflect the overall rate of bone formation and bone resorption are now available. These markers are primarily of research interest and are not recommended as part of the basic workup for osteoporosis. They suffer from substantial biological variability and diurnal variation and do not differentiate causes of altered bone metabolism. For example, measures of bone turnover increase and remain elevated after menopause but do not necessarily provide information that can direct management.