1 Introduction

Osteoporosis is the most common bone disease of older adults and is a major public health problem worldwide. Osteoporosis is characterized by low bone mass, deterioration of bone microstructure, and compromised bone strength resulting in an increased risk of fracture. Typically, patients with osteoporosis experience no symptoms until they sustain a fracture, making diagnosis and primary fracture prevention challenging.

2 Epidemiology and economic impact

The World Health Organization (WHO) defines osteoporosis as a bone mineral density (BMD) at the spine or hip of ≤ 2.5 standard deviations (SDs) below the mean BMD of a young woman, as measured by dual-energy x-ray absorptiometry (DEXA) ( Table 1.10-1 ). A BMD between 2.5 and 1 SDs below the mean represents osteopenia.

A T-score of -1.0 represents a BMD 1 SD below the mean BMD for a young adult reference population.

The presence of a fragility fracture is diagnostic of osteoporosis even in the absence of a measurable decrease in BMD.

In the US, 10.2 million adults over 50 years of age are estimated to have osteoporosis and 43.4 million to have osteopenia [1]. These numbers will rise in the coming decades as the population ages, with 14 million older adults projected to have osteoporosis and 47 million to have osteopenia by 2020 [2].

The presence of osteoporosis or osteopenia increases the risk of fragility fractures which are defined as fractures secondary to a fall from standing or lower height and at a site associated with decreased BMD, including the hip, spine, and wrist. Such fractures increase in incidence after the age of 50 years [3].

There is a strong correlation between BMD and fragility fracture risk. In a 1993 study, each decrease of 1 SD in bone density at the femoral neck increased the risk of hip fracture by a factor of 2.5, and women in the lowest quartile of BMD had an 8.5-fold greater risk of hip fracture compared to women in the highest quartile [4]. However, more fragility fractures occur in patients with osteopenia than in those with osteoporosis because of the greater prevalence of osteopenia.

At the age of 50 years, the lifetime risk of sustaining any fragility fracture is estimated at 40% for women and 13% for men in the US; 46% and 22%, respectively, in Sweden, and 42% overall in Australia [3]. The risk of hip fracture for a 50-year-old Caucasian American woman is 17% [5]; the corresponding risk is 23% in Sweden and 17% in Australia [3].

This risk increases with aging. For each decade after age 50, the risk of hip fracture doubles, and a 90-year-old woman has approximately a 30% chance of sustaining a hip fracture in her remaining lifetime [6]. As the population ages, the worldwide incidence of hip fracture is projected to increase from 1.7 million in 1990 to 6.3 million in 2050 [7], with the largest increase expected in Asia and Latin America. Currently, age- and gender-adjusted 10-year rates of hip fracture are highest in Scandinavia [8]. The shifting demographics of aging will decrease the worldwide proportion of hip fractures that occur in North America and Europe from 50% in 2005 to 25% by 2050 [3].

Hip fractures comprise only about 14% of fragility fractures, and vertebral and wrist fractures also have significant sequelae. At age 50, a Caucasian American woman has a 32% risk of sustaining a clinical or radiographic vertebral fracture and a 15% chance of sustaining a wrist fracture during her lifetime. A Swedish woman′s risk is 15% and 21%, respectively; an Australian woman′s risk is 10% and 13%, respectively [3]. As with hip fractures, the incidence of vertebral and wrist fractures increase with age.

Fragility fractures result in significant healthcare expenditures. In the US, osteoporosis contributes to 2 million fractures per year, resulting in about 430,000 hospital admissions, 2.5 million office visits, and 180,000 nursing home admissions and incurring costs of USD 18 billion per year. Despite comprising a minority of fragility fractures, hip fractures make up 72% of fracture cost; in 2002, a single hip fracture was estimated to cost USD 34,000–43,000 according to 2005 US governmental data [9]. By 2025, the annual cost of fracture care in the US is projected to be USD 25.3 billion [9]. Worldwide, the cost of hip fractures alone is estimated to rise to USD 131.5 billion by 2050 [10].

3 Clinical impact

Osteoporosis and fragility fractures carry significant morbidity and mortality:

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  At 1 year more than 50% of patients with hip fractures continue to have significant functional limitations, with more than half of previously independent patients unable to walk one block, climb five stairs, get in and out of the shower, sit on the toilet, or rise from an armless seated position unassisted [11].

  
  
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  About 30% of hip fracture sufferers require long-term nursing home care [12], and only 40% fully regain their prior level of functioning [2].

  
  
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  Vertebral fractures can cause chronic pain; difficulty bending and reaching overhead; kyphosis and subsequent decreases in pulmonary function; and alterations in abdominal anatomy with resulting constipation, early satiety, and decreased oral intake.

  
  
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  All fractures increase the risk of depression and cognitive impairment.

  
  
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  A patient who sustains any type of fragility fracture is 50–100% more likely to sustain another, and fracture patients often develop a fear of falling, which in itself increases fracture risk.

  
  
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  Fractures are also associated with increased mortality.

  
  
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  Hip fracture surgery carries an overall mortality of 4%.

Twenty percent of hip fracture patients die within 1 year of the fracture event; hip fractures confer a five- to eightfold increase in all-cause mortality in the first 3 months following the event, and this risk is higher for men. Vertebral fractures have been shown to have similar mortality to hip fractures [5]. This mortality risk is likely both a cause and a consequence of the fragility fracture. Functionally failing patients are likely to have fragility fracture as part of their terminal decline.

4 Practical considerations for the perioperative period

5 Basics of bone metabolism and pathophysiology of age-associated bone loss

Bone remodeling is the normal homeostatic process by which old bone is resorbed and replaced by new bone in order to maintain a healthy skeleton. This process occurs in several stages:

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  Activation—osteoclast precursors arrive at the surface of formed bone.

  
  
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  Resorption—osteoclast precursors convert to active osteoclasts and create an acidic environment, thus dissolving the mineral content of bone.

  
  
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  Reversal—osteoclasts undergo apoptosis and are replaced by osteoblast precursors.

  
  
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  Bone formation—osteoblast precursors undergo activation to osteoblasts and deposit collagen.

  
  
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  Mineralization—osteocytes embedded within the collagen matrix contribute to its mineralization and hardening into new bone.

Bone remodeling occurs under the control of various hormones and cytokines, including estrogens and androgens, vitamin D, parathyroid hormone (PTH), osteoprotegerin, and receptor activator of nuclear factor-κB (RANK) and its ligand (RANK-L). Many of these factors have provided targets for the pharmacological treatment of osteoporosis. A schematic of the bone remodeling process is shown in Fig 1.10-1 .

The remodeling process favors new bone formation until the 20s, when an individual′s bone mass peaks. African Americans achieve the highest peak bone mass with Caucasians reaching lower peaks and Asians the lowest. A trend toward bone loss begins immediately after peak bone mass is reached. In women, bone loss accelerates after menopause, when lower estrogen levels allow increased bone resorption by osteoclasts without a corresponding increase in bone deposition by osteoclasts. In the seventh decade of life, age-related decreases in calcium absorption lead to a secondary hyperparathyroidism, which also increases bone resorption. Finally, in the very old, renal vitamin D production decreases while resistance to endogenous vitamin D increases, resulting in a further net increase in bone resorption. As she ages, a woman′s bone mass may decrease by 30–40% from peak level.

Osteoporosis represents a pathological imbalance between bone resorption and bone formation, with the former predominating. In addition to decreased bone mass, osteoporosis is characterized by disruptions in the microarchitecture of bone, with fewer, more fragile bone trabeculae, as well as decreased viability of the osteocytes that maintain bone mineralization. Figure 1.10-2 depicts the microscopic structure of normal and osteoporotic bone.

6 Osteoporosis risk assessment, diagnosis, and evaluation

Any fracture at a major skeletal site, particularly at the hip or spine, in an adult 50 years or older should be considered osteoporosis-related unless clinical circumstances point to another clear etiology for the fracture, and the patient should be evaluated accordingly.

In addition, the National Osteoporosis Foundation (NOF) suggests assessment of osteoporosis and fall risk in all postmenopausal women and all men older than 50 years. Common risk factors for low BMD are listed in the following:

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  Increasing age

  
  
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  Early menopause

  
  
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  Caucasian or Asian race

  
  
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  Personal or family history of fragility fracture

  
  
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  Inadequate calcium and vitamin D intake

  
  
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  Excessive alcohol or tobacco use

  
  
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  Low level of physical activity

  
  
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  Medications:

  
  
  
  
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    Glucocorticoids

    
    
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    Anticonvulsants

    
    
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    Heparin

    
    
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    Excessive thyroid hormone

    
    
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    Proton pump inhibitors

Patients deemed to be at high risk for osteoporosis or falls should undergo BMD determination. The contribution of falls to fracture risk is discussed separately in chapter 1.11 Sarcopenia, malnutrition, frailty, and falls. Regardless of risk factors and fall and fracture history, the US Preventive Services Task Force recommends screening DEXA in all women 65 years and older; the NOF suggests screening in men 70 years and older as well.

Central DEXA as measured at the total hip, femoral neck, or spine is the most common method of BMD determination. A given patient′s BMD, expressed in units of grams of mineral per square centimeter scanned (g/cm²), is compared to two databases, one comprising an age-, gender-, and ethnicity-matched population and another comprising a young adult, gender-matched population. The SDs of the patient′s BMD from these two database norms yield Z- and T-scores, respectively. As shown in Table 1.10-1 , DEXA-based diagnoses of osteoporosis and osteopenia are defined by T-scores. Methods other than central DEXA also exist for the determination of BMD, but these have limitations. Quantitative computed tomography, for example, involves increased radiation exposure and cost compared to central DEXA. Heel ultrasonography and peripheral DEXA, which measures BMD at the forearm, heel, and fingers, are portable but do not correlate as well with fracture risk as do central DEXA measurements.

Vertebral fractures define osteoporosis even in the absence of a DEXA diagnosis. These fractures often produce no symptoms and may go undiagnosed for months or years, but their presence is an indication for pharmacological treatment of osteoporosis. Therefore, some groups recommend yearly measurement of height in older patients. In addition, vertebral imaging should be considered in:

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  Women older than 70 and men older than 80 years with DEXA-defined osteopenia

  
  
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  Women from 65–69 years and men from 70–79 years with T-scores of less than -1.5

  
  
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  Postmenopausal women and men older than 50 years with low-trauma fracture during adulthood, height loss of 4 cm or more or long-term treatment with glucocorticoids [18]

The majority of postmenopausal women with osteoporosis have no identifiable secondary cause. However, 50% of men and premenopausal women may have an underlying treatable condition, as the list of selected causes of secondary osteoporosis shows:

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  Medications, eg, glucocorticoids, anticonvulsants, lithium, proton pump inhibitors, and others

  
  
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  Rheumatic disease, eg, rheumatoid arthritis, systemic lupus erythematosus, and ankylosing spondylitis

  
  
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  Endocrinopathies, eg, cushing syndrome, hyperthyroidism, hyperparathyroidism, hypogonadism, type 2 diabetes, and others

  
  
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  Other medical conditions, ie, cystic fibrosis, chronic obstructive pulmonary disease, human immunodeficiency virus infection, renal insufficiency, and liver disease

  
  
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  Nutritional factors, eg, excessive alcohol intake, anorexia, celiac disease, and vitamin D deficiency

While no formal guidelines exist for further evaluation, a careful clinical evaluation followed by laboratory testing may be warranted in patients suspected of having a secondary etiology of osteoporosis.