CHAPTER 45
Osteoporosis
Maureen F. Cooney, DNP, FNP-BC
Osteoporosis is the most common metabolic bone disease in the United States and it is characterized by both diminished bone mineral density (BMD) and deterioration of the microarchitecture of remaining bone. Because bone strength is proportional to its density, the consequences of these changes are bone fragility and an increased rate of fractures.
Osteoporosis is a silent disease, usually asymptomatic until a fracture occurs. There are no early warning symptoms; when fractures occur, bone density has already been lost. Osteoporosis is often preventable through a lifelong commitment to proper nutrition, adequate and appropriate exercise, and early intervention for those at risk. However, when it occurs, it is commonly associated with physical, psychosocial, and economic consequences.
ANATOMY, PHYSIOLOGY, AND PATHOLOGY
The matrix of bone comprises organic and inorganic components. Collagen, proteins, and lipids constitute the organic portion of the bone matrix. The inorganic matrix, which represents 65% of bone’s total weight, is largely composed of calcium and phosphate, with smaller amounts of magnesium, sodium, and potassium. Hydroxyapatite is the principal mineral component of bone and is 40% calcium by weight. Histologically, bone can be subdivided into two types: cancellous (spongy) and cortical (compact). Cancellous bone has a large surface area, and its metabolic activity is much more rapid than that of cortical bone. Viewed microscopically, bone of normal strength and density has a honeycomb appearance, whereas osteoporotic bone appears less dense, with a weaker, more spindly structure.
Bone mass is the total quantity of bone tissue in the skeleton. Greater bone mass equals more bone, which indicates a stronger skeleton. Most diagnostic studies for osteoporosis measure bone density of a part of the skeleton, another indicator for osteoporosis because high density also is representative of bone strength. Although bone mass and density differ slightly in meaning, these terms are used interchangeably in this chapter.
Bone mass undergoes predictable changes throughout the life cycle. During the first several decades of life, active growth occurs, building toward peak bone mass, the maximal bone density a person achieves. Peak bone mass is usually achieved by age 30 years, and adequate nutrition and physical activity are important to achieving this peak. In women after this age, there is a plateau or very slow decline from peak bone mass until menopause. Declining ovarian function accelerates the loss of bone mass at a rate of approximately 2% to 4% per year; this loss is most rapid in the first 2 years after menopause and gradually subsides within 5 to 10 years. This decline in bone loss then slows, but bone mass continues to decrease over the years. Total loss of bone can approach 50%. For men, bone mass decreases gradually, particularly after the age of 50 years, as testosterone levels diminish, without the sharper dip associated with menopause. However, men with hypogonadism also experience an accelerated rate of bone loss. All adults after age 30 years are on a lifelong course of decreasing bone mass leading to senile osteoporosis, but women have the additional burden of postmenopausal osteoporosis from estrogen deficiency.
Osteoporosis may be etiologically divided into primary and secondary types. Primary osteoporosis is further subdivided into three types: postmenopausal (Type I), principally affecting cancellous bone; age-associated disease (Type II), a slower loss of cancellous and cortical bone seen in both sexes, especially past the age of 70 years; and idiopathic osteoporosis, in which bone loss occurs in young- and middle-aged men and premenopausal women. Secondary osteoporosis is the result of underlying conditions (Table 45.1).
Bone is continually replaced by a process called bone remodeling. Humans remodel their skeletons to a greater degree than most other mammals at a rate that increases with age. Each year, approximately 20% of the skeleton is remodeled. Bone remodeling can be divided into two processes: resorption and formation. During resorption, osteoclasts excavate the bone surface by dissolving the mineral component of the bone and hydrolyzing the organic matrix. Saucer-shaped cavities are produced on the surface of cancellous bone; tunnels are formed in cortical bone.
Causes of Secondary Osteoporosis |
Malignancy (especially multiple myeloma) Chronic liver or renal disease Malabsorption Inflammatory diseases Cushing’s syndrome Hyperthyroidism Hyperparathyroidism Hypogonadism (in men) Athletic amenorrhea Eating disorders Systemic mastocytosis Rheumatoid arthritis Osteogenesis imperfecta Hyperprolactinemia | Pharmacologic agents Glucocorticoids Thyroid hormone Anticonvulsants Heparin Lithium Chemotherapy drugs Some diuretics GnRH agonists Aluminum-containing antacids Parenteral nutrition Early oophorectomy Subtotal gastrectomy Major organ transplantation |
GnRH, gonadotropin-releasing hormone.
Cancellous bone is subject to more remodeling activity and quicker turnover than cortical bone because its large surface area provides a greater number of remodeling sites and its metabolic rate is more rapid. Menopause actually causes increased activation of these remodeling sites, intensifying resorption and producing deeper cavities in cancellous bone.
Formation is carried out by osteoblasts, which migrate to the pits and tunnels and begin to fill them in by secreting collagen fibrils to form the bone matrix. After this protein matrix is formed, it becomes mineralized through the deposition of calcium hydroxyapatite crystals. Adequate intake of vitamin D and calcium is required for mineralization. During both the resorption and formation phases of remodeling, biochemical markers reflective of these processes arc released into the bloodstream.
In the pathogenesis of osteoporosis, the most important aspect of remodeling is the rate of formation relative to resorption. During childhood and early adulthood, as bone mass builds, the rate of formation exceeds that of resorption; it then plateaus until about the age of 40 years. Thereafter, resorption outpaces formation, and bone density continues to decrease.
Also significant is each person’s peak bone mass, which becomes the starting point for later loss. Slow decreases in mass in someone who achieved a relatively low peak may ultimately yield the same net bone mass as a more rapid decline in someone whose peak mass was high. This highlights the importance of proper nutrition and exercise during the years of active bone growth to attain maximal peak mass.
Osteoporotic changes are more significant at certain body sites. Because cancellous bone has greater remodeling activity than cortical bone, it is subject to a more rapid loss of density. The vertebral body, femoral neck, and distal radius are composed of cancellous bone, and they are therefore the most common sites of osteoporotic fractures. Other fracture sites are the pelvis, tibial plateau, proximal humerus, and ribs.
The fragility of porous bone predisposes not only to fractures from trauma but also to nonviolent fractures. Nonviolent fractures, caused by minimal trauma that would not result in fracture in a young adult, are responsible for 90% of hip and wrist fractures in the elderly. Overall, the spine is the most common site for osteoporotic fractures. Secondary to vertebral compression, spinal fractures may occur in the absence of recognizable trauma, triggered perhaps by a cough or sneeze. In fact, 50% of people with vertebral fractures from osteoporosis have no recollection of back pain, and only one third of persons with vertebral fractures are clinically diagnosed. Fractured vertebrae assume a wedge shape, narrowing anteriorly, causing kyphosis, height and waistline loss, and abdominal protrusion.
EPIDEMIOLOGY
Osteoporosis affects an estimated 25 million Americans, 80% of whom are women. Approximately 1.5 million osteoporotic fractures occur each year (Moyer, 2013). Fifty percent of women and one third of older men will experience an osteoporotic fracture during their lifetime (Hamdy et al., 2010). In America, the cost of osteoporosis-related fractures in 2005 was $19 billion, but this is expected to increase to more than $25 billion/year over the next 2 decades (Warriner & Saag, 2013).
The most common osteoporotic fracture is the vertebral crush fracture; approximately 500,000 of these occur per year in the United States. Mostly affecting women older than 55 years, vertebral fractures are often clinically silent. Whether clinically silent or apparent, they are major predictors of future fracture risk and are associated with increased morbidity and mortality. Complications include back pain, height loss, kyphosis, and balance difficulties. Over time, an increased number of vertebral fractures may lead to restrictive lung disease, increased risk of pneumonia, and altered abdominal anatomy. Spinal deformities such as dowager’s hump can result in changes in body image, loss of self-esteem, and increase in the risk of depression. Symptomatic vertebral fractures limit mobility and function and ultimately reduce quality of life and the ability to live independently. Although less debilitating in the long term, Colles’s fractures of the distal radius, occurring at a rate of 200,000 per year, may hinder the patient’s ability to function in the workplace.
Most significant in terms of complications, death, and cost is osteoporotic hip fracture. Each year in the United States, more than 7 million days of restricted activity, 3.4 million hospital bed days, and 60,000 nursing home admissions are attributable to hip fractures. Nearly 20% of patients with hip fractures require long-term care facility placement (U.S. Department of Health and Human Services, 2004). Hip fractures, which occur at a rate of approximately 250,000 per year, claim the lives of up to 25% of those affected within the first year after the fracture, with men having higher mortality rates than women. This death rate is attributable to peri- and postoperative complications, including pneumonia, deep vein thrombosis, and pulmonary embolism. Of those who survive, about 50% lose the ability to walk without assistance and 25% require an assisted living situation (Metcalfe, 2008). The vast majority suffer permanent disability, with compromised ability to perform activities of daily living.
Cultural Factors
Much of the variation in BMD and bone geometry is attributable to heredity. BMD tends to be higher in African American and Hispanic women and lower in Whites and Asians. The BMD of African American women is consistently higher than white women at every weight level. Whites have twice the incidence of hip fractures as African Americans. Hip geometry, which varies among races, may influence the risk for hip fracture. Longer hip-axis lengths, an example of hip geometry, are associated with an increased risk for hip fracture. Hip-axis lengths are longer in Whites compared to African Americans and Asians, even after adjustments for height. Overall, the risk for fracture is 49% higher among White women than among African American women (Cauley, 2011). Although being Asian is a risk factor for osteoporosis when compared to Whites, the Japanese have a lower incidence of hip and other nonspinal fractures. This finding was attributed to different hip geometry and a decreased rate of falls. Although low BMD and hip geometry are factors that contribute to the risk for fractures associated with osteoporosis, there are many other ethnic and racial factors that influence the development and progression of osteoporosis and fractures. For example, diet is a cultural factor that could enhance the risk of osteoporosis. A group that does not consume dairy products or other calcium sources would be unlikely to achieve maximal peak bone density.
DIAGNOSTIC CRITERIA
Definitive diagnostic criteria are:
Dual-energy x-ray absorptiometry (DXA) bone density reading at the spine, hip, or wrist is more than 2.5 standard deviations below the young, healthy adult mean (Management of osteoporosis in postmenopausal women: 2010 position statement of the North American Menopause Society, 2010)
Quantitative ultrasonography of the calcaneus has been shown to be equivalent to DXA for prediction of fractures, but the measurements are not interchangeable with DXA; thus, cutoff diagnostic criteria for osteoporosis have not been established (U.S. Preventive Services Task Force, 2011)
Suggestive diagnostic criteria are:
Fragility fractures (fractures that occur with minor trauma, such as a fall from standing height or less) or no known trauma (Warriner & Saag, 2013)
History of hip or vertebral fracture (Warriner & Saag, 2013).
HISTORY AND PHYSICAL EXAMINATION
Historical findings related to osteoporosis differ based on whether the patient is presenting before or after an osteoporotic fracture. Those evaluated before the fracture stage are likely to be asymptomatic; the history, therefore, is directed at risk factor evaluation. Those who have had osteoporotic fractures are more likely to have related complaints, although they, too, may be asymptomatic. Table 45.2 lists pertinent historical data for the assessment of osteoporosis.
The physical examination should include measurement of height and careful inspection of the posture and spinal curves. Low body mass index (BMI; <20) is a strong independent risk factor for osteoporosis and fracture; weight of <127 pounds, associated with small bones, is also a risk factor. Kyphosis and loss of space between the inferior portion of the anterior rib cage and the iliac crests are indicators of collapse of the vertebral bodies. A protuberant abdomen may also be noted. Mild to moderate scoliosis may appear, particularly if there have been fractures of vertebrae between T2 and T11. A complete musculoskeletal examination should be performed, including palpation of the spine, paravertebral muscles, and other involved areas for tenderness or deformity, range of motion, and assessment of gait. Assessments of muscle mass, strength, and balance help identify deficits that may be correctable. The examiner should also look for physical manifestations of diseases that could cause secondary osteoporosis (see Table 45.1).
Historical Data for Assessment of Osteoporosis |
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The most reliable diagnostic tool for osteoporosis is DXA, a measure of BMD. BMD is the strongest indicator of future fracture risk. DXA provides a high-resolution, highly reproducible image of the lumbar spine and intertrochanteric regions of the hip. Radiation exposure from DXA is <3 mrem, one tenth that of a routine chest x-ray. DXA is less costly than quantitative computed tomography, which exposes the patient to 100 to more than 1,000 mrem. Other positive attributes of BMD measurement are ease and noninvasiveness, reproducibility for reliable follow-up measurements, a strong correlation between bone density and bone strength, and evidence of treatment response through BMD readings. Although not a perfect predictor of fracture risk, DXA of the femoral neck is considered the best predictor of hip fracture and compared well with DXA of the forearm for predicting other fracture sites. The accuracy of DXA for women has been demonstrated in previous studies, and in recent years, DXA has shown comparable results in men. A limitation of DXA is that changes in bone density significant enough to show on DXA (variations of at least 2%–4%), may not be evident for at least a year. This limits the utility of DXA in terms of assessing immediate- or short-term response to treatment.
Interpretation of BMD readings is based on comparison to expected values for young healthy adults between ages 30 and 40 years. Table 45.3 depicts the bone density states depending on the number of standard deviations from the mean of the healthy comparison group. A 1.5-fold to twofold increase in fracture risk is associated with each drop of one standard deviation of bone density.
Another method of interpreting DXA results is the use of T-scores and Z-scores. T-score is applied to postmenopausal women and men older than 50 years and is determined by the number of standard deviations above or below the mean BMD for healthy adults aged 20 to 29 years of the same race and gender (see Table 45.3). The Z-score is used for persons younger than 50 years and is determined by the number of standard deviations above or below the expected BMD for each age and gender category. A Z-score below –2.0 is considered low BMD for that particular group, whereas Z-score at or above –2.0 is considered within the expected range for that age group.
There are no universal guidelines for the use of DXA in the assessment of osteoporosis. Expense is a limiting factor. The National Osteoporosis Foundation (2013) recommends BMD measurements for all women aged 65 years or older and for all men aged 70 years or older. It also recommends BMD measurements for postmenopausal women younger than 65 years of age and men aged 50 to 69 years based on osteoporosis risk factors. BMD studies may be recommended for those with several risk factors for osteoporosis, for establishment of a pretreatment baseline, and for those who have had prior osteoporotic fractures. DXA measurements may help when treatment decisions, such as whether to begin estrogen replacement therapy (ERT), have to be made. Follow-up measurements at appropriate intervals (no more frequently than every 14–18 months) can gauge response to treatment.
