The primary concern for patients with osteoporosis is the increased risk for fractures. Osteoporosis-associated fractures most commonly involve the hip, spine, or wrist. More than 1.5 million osteoporotic fractures occur in the United States yearly.³ It is estimated that the annual incidence of hip fractures in the United States will exceed 6.3 million cases by the year 2050.⁴ Osteoporosis-related fractures can result in significant disability. Only a third of patients regain their premorbid level of function after a hip fracture, and a third require placement in a nursing home within 1 year of the fracture.⁵^–⁷ Twenty percent of patients are no longer living 1 year after a hip fracture.^5,⁸ Besides functional disability and chronic pain, osteoporotic fractures can result in significant anxiety, depression, emotional distress, decreased quality of life, and impaired social well-being.

The increased risk for vertebral compression fractures (VCFs) in patients with osteoporosis is of particular concern to spine care providers. Approximately half of all osteoporotic fractures are spine related.⁹ VCFs are responsible for 150,000 hospital admissions, 161,000 doctors visits, and more than 5 million days of restricted activity annually.¹⁰ It is estimated that 25% of women older than 50 years will suffer a symptomatic VCF during their lifetime.⁹ Although many VCFs are essentially asymptomatic or cause limited symptoms, they can also carry significant morbidity, with chronic pain related to the injury developing in up to a third of patients.¹¹ In addition, VCFs can lead to progressive sagittal-plane deformity with concomitant reduced lung capacity. Kyphosis caused by severe or multilevel fractures can also alter the biomechanical stress at other segments and lead to increased risk for additional fractures.¹²^–¹⁴ This disease is associated with 23% higher mortality in women older than 65 years than in age-matched controls, with additional fractures contributing to increasing mortality.¹⁵

Osteoporosis also places a significant burden on national health care expenditures. The estimated health care cost for osteoporosis-associated fractures was $13.8 billion in 1995 and increased to $17 billion in 2001.^2,¹⁶ This figure includes hospital and nursing home expenses, but the majority of the cost is for inpatient medical care. The projected national health care expenditure for osteoporosis is predicted to rise to $50 billion by the year 2040.²

Pathophysiology

Pathophysiology of Osteoporosis

The National Institutes of Health Consensus Conference defined osteoporosis as a skeletal disorder characterized by compromised bone strength, as reflected in the integration of bone density and bone quality, that predisposes to an increased risk for fracture.¹ Bone density is determined primarily by two factors: one’s peak bone mass and the degree of bone loss throughout one’s lifetime. Bone quality is multifactorial and is dependent on one’s bony architecture, mineralization, ratio of bone formation to resorption, and accumulation of damage. Fractures are defined as mechanical failure as a result of a force or load applied to bone. Pathophysiologically, osteoporosis is a disease of decreased bone mass in the absence of a mineralization defect. Therefore, overall bone mass decreases while the remaining bone maintains normal calcification. Bone loss occurs when the rate of bone resorption is greater than that of new bone formation. With aging, osteoclastic resorption exceeds osteoblastic activity. The net effect is progressive loss of skeletal bone mass, which generally begins by the fourth decade.

Osteoporosis that occurs as a result of aging is termed primary osteoporosis. Primary osteoporosis is characterized by a slow phase and an accelerated phase. In the slow phase, the rate of resorption begins to exceed the rate formation, with 0.3% to 0.5% of bone mass being lost per year. The slow phase occurs in both men and women in older age groups and is hypothesized to be due to impaired vitamin D metabolism by the kidneys. The accelerated phase occurs only in postmenopausal women and is probably related to the loss of estrogen, which results in increased bone resorption. In the accelerated phase, bone mass decreases at a rate of 2% to 3% per year and the decrease continues for up to 10 years. Bone loss generally affects cancellous bone earlier and to a greater extent than cortical bone.

Several factors are protective against primary osteoporosis. Higher peak bone mass attained early in life provides a greater reserve to counteract the eventual increase in bone resorption later in life. Peak bone mass demonstrates linear growth until shortly after adolescence, at which time it consolidates for about 5 to 15 years. A balanced diet with sufficient calories, calcium supplementation, and vitamin D also reduces the risk for the development of osteoporosis. Regular impact loading and resistance exercises contribute to greater peak bone mass. Gonadal hormones are also protective against osteoporosis. Estrogen appears to be particularly important in maintaining bone mass in women. Estrogen suppresses resorption of cancellous bone and maintains balanced turnover between osteoblastic and osteoclastic activity. Administration of estrogen to postmenopausal women decreases bone loss, whereas estrogen deficiency results in increased bone resorption. In adolescents, gonadal hormones contribute to the development of maximal peak bone mass.

Several factors increase the risk for the development of osteoporosis. Late menarche or premature menopause, which results in decreased overall lifetime exposure to estrogen, increases one’s likelihood of becoming osteoporotic. Inadequate dietary intake of calcium through either poor nutrition or eating disorders can also lead to increased bone loss. A sedentary lifestyle or the absence of regular exercise likewise increases the risk for osteoporosis. Tobacco and excessive alcohol use also contribute to bone loss.

Ethnicity appears to be related to risk for the development of osteoporosis. White women have the greatest risk for osteoporosis, and this segment of the population also has a greater risk for vertebral and nonvertebral fractures than African American, Native American, and Asian women.^17,¹⁸ African American women have higher overall bone mineral density (BMD) than white women throughout their lifetime. This discrepancy is reflected in a lower lifetime risk for hip fracture in African American women than in white women (6% for African American women versus 14% for white women).¹

Secondary osteoporosis is a pathologic loss of bone density that occurs in the presence of an underlying medical condition. Common endocrinologic causes include hypogonadal states and hyperthyroidism. Gastrointestinal causes include malabsorptive diseases such as celiac sprue and inflammatory bowel disease. Hematologic disease and bone marrow dysplasia can also result in secondary osteoporosis. Chronic nutritional deficiencies can likewise lead to progressive bone loss. Various medications are associated with secondary osteoporosis, of which corticosteroids are the most commonly encountered. Corticosteroids, often used for immune suppression and treatment of asthma and rheumatoid arthritis, suppress bone formation and inhibit calcium absorption.