Osteoporosis consists of a heterogeneous group of syndromes in which bone mass per unit volume is reduced in otherwise healthy bone, resulting in fragile bone. The increment in bone porosity results in architectural instability of bone and increases the likelihood of fracture. The mineral/matrix ratio is normal in osteoporosis, but in osteomalacia the mineral content is markedly reduced.
Clinicians can add quality to the years of life of patients with osteoporosis through the use of an interdisciplinary approach. This condition is the most prevalent metabolic bone disease in the United States and is a major public health problem. The direct and indirect cost of osteoporosis in the United States alone is estimated to be more than $14 billion annually. Much of this expense relates to hip fractures. In 15% to 20% of hip fracture cases, the outcome is fatal.
The World Health Organization has defined osteoporosis as bone mineral density (BMD) of 2.5 standard deviations below the peak mean bone mass of young healthy adults. The T score shows the amount of one’s bone density compared with a young adult (at the age of 35 years) of the same gender with peak bone mass. The Z score is calculated in the same way, but the comparison is made with someone of the same age, gender, race, height, and weight. The Z score is adjusted for an individual’s age, and the T score is not. For example, a 75-year-old woman with a Z score of −1.0 is one standard deviation below the BMD of an average 75-year-old woman, but her T score may be −3.0 because she is three standard deviations below the BMD of an average 35-year-old woman. Normal BMD is a T score −1 or greater; osteopenia, a T score between −1 and −2.5; osteoporosis, a T score −2.5 or less; and severe osteoporosis, a T score −2.5 or less with fracture. In the asymptomatic stage, osteoporosis is characterized simply by decreased bone mass without fracture. Osteoporosis becomes clinically problematic only when the bone fractures.
Bone Function and Structure
Bone serves as a mechanical support for musculoskeletal structures, as protection for vital organs, and as a metabolic source of ions, especially calcium and phosphate. Despite its appearance, bone is an active tissue. To maintain its biomechanical competence, bone tissue undergoes continuous change and renewal so that older bone tissue is replaced by newly formed bone tissue. Approximately 20% of bone tissue is replaced annually by this cyclic process. There are two types of bone cells: osteoclasts, which resorb the calcified matrix, and osteoblasts, which synthesize new bone matrix.
Osteoclasts are localized on the endosteal bone surfaces. Their origin is hematopoietic, and they share a common precursor with the monocyte macrophage. Osteoclasts are large multinucleated cells with an average of 10 to 20 nuclei. They have a special cell membrane with folds that invaginate at the interface with bone surface, called the ruffled border . To induce resorption of bone and the mineralized bone matrix, osteoclasts produce proteolytic enzymes in this ruffled border.
Osteoblasts are derived from mesenchymal cells. The role of osteoblasts is mineralization of the matrix through budding of vesicles from their cytoplasmic membrane. These vesicles are rich in alkaline phosphatase. Osteoblasts secrete all the growth factors that are trapped in the matrix.
Bone Remodeling
Bone remodeling is a process that allows removal of old bone and replacement with new bone tissue. This process allows maintenance of the biomechanical integrity of the skeleton, and it supports the role of bone in the provision of an ionic bank for body and mechanical support. Bone remodeling has five phases.
- 1.
Activation: Osteoclastic activity is recruited.
- 2.
Resorption: Osteoclasts erode bone and form a cavity.
- 3.
Reversal: Osteoblasts are recruited.
- 4.
Formation: Osteoblasts replace the cavity with new bone.
- 5.
Quiescence: Bone tissue remains dormant until the next cycle starts.
This process is cyclical, starting with bone resorption and finishing with bone formation. In adult human bone, each cycle of remodeling lasts 3 to 12 months. The signal that stops osteoclastic activity is not yet completely defined. After bone resorption, the reversal phase starts, which involves osteoblastic activity. Osteoblasts start to fill the resorption cavity. During the process of osteoclastic activity, the growth factors that are stored in the bone matrix are released and subsequently stimulate osteoblastic proliferation.
This process of bone resorption and formation is called coupling . The ideal situation in the coupling process is equilibrated bone formation and resorption. In osteoporosis, however, there is disequilibrium between resorption and formation, as coupling favors resorption that results in bone loss.
The number of active remodeling units in trabecular bone is approximately three times greater than in cortical bone. The physical endurance of any bone is affected by the percentage of cortical bone involved in its structure. Trabecular bone is more active metabolically than cortical bone because of the considerable surface exposure areas. Consequently, more bone loss occurs at the trabecular areas when resorption is greater than formation. The vertebrae consist of 50% trabecular bone and 50% cortical bone, whereas the femoral neck consists of 30% trabecular bone and 70% cortical bone. When bone turnover increases, bone loss and osteoporosis occur in the vertebrae before they occur in the femoral neck.
Pathogenesis
Peak adult bone mass is achieved between ages 30 and 35 years. Bone mass at any point in life thereafter is the difference between the peak adult bone mass and the amount that has been lost since the peak was reached. Age-related bone loss is a universal phenomenon in humans. Any circumstances that limit bone formation or increase bone loss increase the likelihood that osteoporosis will develop later in life. Measures that can maximize peak adult bone mass are clearly desirable.
Trabecular (or cancellous) bone represents approximately 20% of skeletal bone mass and makes up 80% of the turnover media. The cortex makes up only 20% of the turnover media and is made of compact bone, which represents 80% of skeletal bone mass. In both cortical and trabecular bone, bone remodeling is initiated with the activation of osteoclasts. The resulting resorption sites are then refilled by osteoblastic activities, a process called bone formation . If the amount of bone resorbed equals the amount formed, the bone loss is zero. The remodeling process does not result in zero balance after age 30 to 35 years, however, and after this age the normal process of remodeling results in bone loss.
Certain conditions, such as hyperparathyroidism or thyrotoxicosis, can increase the rate of bone remodeling. These conditions increase the rate of bone loss, which results in high-turnover osteoporosis. The secondary causes of osteoporosis are associated with an increased rate of activation of the remodeling cycle. Although factors such as calcium intake, smoking, alcohol consumption, physical exercise, and menopause are important factors in determining BMD, genetic factors are the major determinant and contribute to 80% of the variance in peak BMD. Fracture incidence related to osteoporosis is lower in men than in women because the diameter of vertebral bodies and long bones is greater in men at maturity and bone loss is less (about half that of women) throughout life.
Classification of Osteoporosis
Osteoporosis can be primary or secondary to other disorders that result in bone loss. The most common causes of osteoporosis are listed in Box 34-1 . The most common type of osteoporosis is either postmenopausal or age-related.
Hereditary, Congenital
- •
Osteogenesis imperfecta, neurologic disturbances (myotonia congenita, Werdnig-Hoffmann disease), gonadal dysgenesis
Acquired (Primary and Secondary)
Generalized
- •
Idiopathic (in premenopausal women and middle-aged or young men; juvenile osteoporosis)
- •
Postmenopausal
- •
Age-related
- •
Endocrine disorders: Acromegaly, hyperthyroidism, Cushing’s syndrome (iatrogenic or endogenous), hyperparathyroidism, diabetes mellitus (?), hypogonadism
- •
Nutritional problems: Malnutrition, anorexia or bulimia, vitamin deficiency (C or D), vitamin overuse (A or D), calcium deficiency, high sodium intake, high caffeine intake, high protein intake, high phosphate intake, alcohol abuse
- •
Sedentary lifestyle, immobility, smoking
- •
Gastrointestinal diseases (liver disease, malabsorption syndromes, alactasia, subtotal gastrectomy) or small bowel resection
- •
Nephropathies
- •
Chronic obstructive pulmonary disease
- •
Malignancy (multiple myeloma, disseminated carcinoma)
- •
Drug use: Phenytoin, barbiturates, cholestyramine, heparin, excess thyroid hormone replacement, glucocorticoids
Localized
- •
Inflammatory arthritis, fractures and immobilization in cast, limb dystrophies, muscular paralysis
Primary osteoporosis is the rare disorder of idiopathic juvenile osteoporosis. This type of osteoporosis typically occurs before puberty (between ages 8 and 14 years), and patients present with osteoporosis that is progressive over 2 to 4 years in association with multiple axial or axioappendicular fractures. Remission usually occurs by the end of the 2- to 4-year course. In this type of osteoporosis, the process of bone formation is normal but osteoclastic activity increases, resulting in increased bone resorption. Idiopathic juvenile osteoporosis is most evident in the thoracic and lumbar spine and needs to be distinguished from juvenile epiphysitis or Scheuermann disease. It is usually self-limiting, but the radiographic appearance might not return to normal. The laboratory values are typically normal, and the diagnosis is made by exclusion.
Hormones and Physiology of Bone
The rate of bone remodeling can be increased by parathyroid hormone (PTH), thyroxine, growth hormone, and vitamin D (1,25-dihydroxyvitamin D 3 [1,25(OH) 2 D 3 ]) and decreased by calcitonin, estrogen, and glucocorticoids.
The major hormone for calcium homeostasis is PTH. It is secreted by the parathyroid glands, which are located behind the thyroid glands. The level of plasma calcium is the major moderator of the secretion of PTH, which regulates the plasma calcium ion (Ca 2+ ) concentration in three ways:
- 1.
In the presence of active vitamin D, PTH stimulates bone resorption and the release of calcium and phosphate.
- 2.
Through production of calcitriol in the kidneys, it indirectly increases intestinal absorption of calcium and phosphate.
- 3.
It increases active reabsorption of calcium ions in the renal distal tubal area.
PTH also reduces proximal tubular reabsorption of phosphate. In general, PTH increases serum calcium concentration and primarily tends to decrease serum phosphate concentration.
Calcitonin is a hormone secreted by the parafollicular cells of the thyroid gland. The major stimulus of calcitonin production is the serum level of calcium. Calcitonin directly prohibits calcium and phosphate resorption through inhibition of osteoclastic activity, lowering the serum calcium level.
The main regulators of vitamin D synthesis are the serum concentrations of 1,25(OH) 2 D 3 , calcium, phosphate, and PTH. Vitamin D can also be synthesized through exposure to the sun and conversion in the liver. PTH is the major inducer of the production of the active form of vitamin D in the kidney. This function is accomplished through the effect of the enzyme 1-α-hydroxylase, which transforms the inactive form of vitamin D to the potent form. The active form of vitamin D increases intestinal absorption of calcium and phosphate. Vitamin D is also required for appropriate bone mineralization. The influence of the active form of vitamin D is both a direct effect through stimulating osteoblastic activity and an indirect effect through increasing the intestinal absorption of calcium and phosphorus.
Role of Sex Steroids
The main endocrine function that occurs at menopause is loss of secretion of estrogen and progesterone from the ovaries. The premenopausal ovary produces primarily estradiol. Progesterone secretion, which occurs cyclically after ovulation in the premenopausal stage, also decreases to very low levels in the postmenopausal stage. These changes in circulating sex steroids are gradual in a woman’s sexual reproductive life. The premenopausal ovary also produces androgens, especially testosterone. The circulating testosterone levels decrease after menopause. The major source of estrogen in postmenopausal women is conversion from dehydroepiandrosterone. The latter is then converted into androstenedione, which changes into estrone in fat cells. Estrone is the major source of estrogen in postmenopausal women.
Men do not have the equivalent of menopause, but in some elderly men bone mass decreases along with a decline in gonadal function. The testosterone level in men decreases with age as a result of a decreased number of Leydig cells in the testes. Male hypogonadism is typically associated with bone loss.
Other Factors Affecting Bone Mass
Several other factors can contribute to the reduction of sex-related steroid levels. In hyperprolactinemia, which is attributable to a prolactin-secreting pituitary tumor, failure of the gonadal axis results in a substantial loss of bone. Amenorrheic athletes who exercise excessively, such as high-mileage runners or ballet dancers, who have lower-than-normal body weight, have lower circulating estradiol, progesterone, and prolactin levels. Their amenorrhea is associated with hypothalamic hypogonadism, which leads to excessive bone loss. This bone loss can be mostly reversed when training distances are decreased. With weight gain and improvement in nutrition, these young women can facilitate resumption of menses and reversal of bone loss. Reduction of sex steroid concentrations is not the only cause of bone loss. Other factors such as race, genetics, nutrition, physical exercise, and lifestyle can also contribute to the rate of bone loss after an ovariectomy or natural menopause. It is well known that bone must be physically stressed to be maintained. A considerable body of data shows that the rate of change in strain also influences bone growth and remodeling.
Effect of Aging on Bone Mass
In the normal aging process, there is an imbalance between resorption and formation because osteoblastic activity is not equal to osteoclastic activity. The result of the remodeling process is bone loss during each cycle of remodeling. Bone loss occurs even when the remodeling process is not increased. In fact, activation of skeletal remodeling is decreased as a result of the aging process. This decreased activation gives rise to the concept of low-turnover osteoporosis, which occurs concomitantly with the aging process.
Age plays a considerable role in the rate of bone turnover. It has been clearly determined that bone turnover increases in women at menopause, but bone turnover does not increase substantially in men with aging. Most studies have shown that plasma levels of the active form of vitamin D, 1,25(OH) 2 D 3, decrease with age by approximately 50% in both men and women.
Growth hormone stimulates renal production of 1,25(OH) 2 D 3 . Growth hormone production decreases with age. Secretion of growth hormone is reduced in patients with osteoporosis. Growth hormone and insulin-like growth factor 1 have several positive effects on calcium homeostasis, including synthesis of 1,25(OH) 2 D 3 , osteoblast proliferation, osteoclast formation, and bone resorption.
It appears that special forms of vitamin K therapy in elderly persons can be associated with a reduction in the rate of bone resorption, demonstrated by decreased excretion of urinary hydroxyproline. Further studies are needed in this area. Studies have shown that calcium absorption is less efficient in elderly people. Bone loss has also been related to deficiencies in trace metal elements, such as copper, zinc, and magnesium, but this issue is not fully resolved.
Plasma calcitonin levels are higher in men than in women. Calcitonin levels do not change with age. Studies have shown that estrogens stimulate calcitonin secretion. Thyroid hormone levels typically show no change or are slightly decreased with age. The PTH level increases with age, perhaps because of mild hypocalcemia and decreased 1,25(OH) 2 D 3 concentration. This reduction in the active form of vitamin D can be as a result of decreased consumption of dietary vitamin D, decreased exposure to sunlight, decreased skin capacity for vitamin D conversion, reduced intestinal absorption, and reduced 1-α-hydroxylase activity.
Several studies have shown that the level of physical activity decreases with aging. This is important because physical strain and mechanical load also positively affect bone mass. Female gymnasts, both children and college-aged athletes, reportedly have higher BMD than swimmers. Exercise is known to stimulate the release of growth hormone or other trophic factors that can stimulate osteoblastic activity. Optimal nutrition and physical activity are necessary to achieve the genetic potential for bone mass. The peak bone mass attained by early adulthood is a major determinant of bone mass in later life. Nutrition can also affect both bone matrix formation and bone mineralization. In general, in estrogen-deficient women, calcium intake of 1500 mg/day and 800 international units/day of vitamin D are recommended.
Clinical Manifestations of Osteoporosis
Osteoporosis is typically a “silent disease” until fractures occur. Osteoporotic vertebral fractures can go unnoticed until they are incidentally seen on a chest radiograph. Appendicular fractures, however, typically require immediate attention. The fact that a fracture resulted from osteoporosis should not affect the orthopedic method of management. The most common areas for osteoporotic fractures are the midthoracic and upper-lumbar spine ( Figure 34-1 ), hip (proximal femur), and distal forearm (Colles fracture). The highest incidence of fractures is in white women. The female/male ratio is approximately 7 : 1 for vertebral fractures, 2 : 1 for hip fractures, and 5 : 1 for Colles fractures. It has been estimated that after menopause, a woman’s lifetime risk of sustaining an osteoporotic fracture is 1 in 2 or 3.
Hip fracture is the greatest concern clinically because the risk of death with osteoporotic hip fracture is 15% to 20%. This is despite all the modern developments in surgical and nonsurgical intervention. The management of an osteoporotic spine fracture requires immobilization of the involved vertebral bodies and analgesia. Fortunately, these fractures heal through becoming more condensed and, unlike appendicular fractures, typically do not require any specific treatment. If there is nonunion of the appendicular fracture, one needs to look for conditions other than osteoporosis, such as osteomalacia or hyperparathyroidism. The duration of immobilization should be for only a limited time, sufficient to ensure the primary fracture-healing process. Prolonged immobilization is discouraged because it can contribute to additional osteoporosis.
The orthopedic management for most osteoporotic fractures is generally noncontroversial, except for the management of hip fracture. The management of femoral neck fracture creates a great deal of controversy because of the high complication rate. Efforts are ongoing to solve these controversies through prospective studies. Despite these efforts, the treatment of hip fracture remains a challenge, and each case creates an emergency situation. Shoulder fracture, especially fracture in the surgical neck of the proximal humerus, is not uncommon in elderly women. This type of fracture usually occurs from an impact force directly to the shoulder during a fall. A conservative treatment regimen typically suffices for this fracture.
Fractures and Management
The relationship between bone mass and spinal fractures has been extensively studied, and it is known that fracture risk increases as bone mass decreases. For every standard deviation of decrease in BMD, the risk of osteoporotic fracture of the spine increases 1.5- to 2-fold, and the risk of hip fracture increases 2.6-fold. Another predictor of fracture risk is age itself. The risk of fracture as a result of osteoporosis doubles every 5 to 7 years. It is not clear whether age-related changes in bone density or bone quality are factors that increase the risk of fractures caused by falls.
Vertebral Fracture
The incidence of vertebral fractures is poorly understood because 50% of these fractures can be subclinical and the patient might not seek medical attention. Vertebral fractures can create both acute and chronic pain.
Acute pain that occurs in the absence of a previous fracture is usually as a result of compression fractures of the vertebrae. Sometimes, a minor fall or even an affectionate hug can cause a compression fracture. The compressed vertebrae might not be apparent on radiographs for up to 4 weeks after the injury. Compression fractures usually result in acute pain that later resolves ( Box 34-2 ). The spinal deformity that can result from these fractures can produce chronic pain.
- •
Bed rest (2 days): Substantial bone loss is not likely to occur with 2 days of bed rest
- •
Analgesics: Avoid constipating medicines, such as codeine derivatives
- •
Avoidance of constipation
- •
Physical therapy: Initially cold packs, then mild heat and stroking massage
- •
Avoidance of exertional exercises
- •
Knowledge of lifting and standing principles to avoid excessive spinal strain
- •
Back supports if needed to decrease pain and expedite ambulation
- •
Gait aids if needed
Kyphotic postural change is the most physically disfiguring and psychologically damaging effect of osteoporosis. The incidence of osteoporosis and kyphosis can be substantially decreased only by early detection and subsequent intervention in high-risk patients.
Disproportionate weakness in back extensor musculature relative to body weight or spinal flexor strength considerably increases the possibility of compressing the vertebrae in the fragile osteoporotic spine. Recognition and improvement of decreased back extensor strength can enhance the ability to maintain proper vertical alignment. The geriatric population has an increased risk of debilitating postural changes because of several factors, the two most apparent being a greater prevalence of osteoporosis and an involutional loss of functional muscle motor units. Development of kyphotic posture not only can predispose to postural back pain but can also increase the risk of falls. Several other factors can also contribute to the risk for falls ( Box 34-3 ).
Extrinsic
- •
Environmental: Obstacles, slippery floors, uneven surfaces, poor illumination, stairs not well defined, pets, icy sidewalks
- •
Extraskeletal: Inappropriate footwear, obstructive clothing
Intrinsic
- •
Intraskeletal: Lower-extremity weakness (neurogenic or myopathic), balance disorder (vestibular dysequilibrium, peripheral neuropathy, hyperkyphosis), visual impairment, bifocal use, vestibular changes, cognitive decline, decreased coordination (cerebellar degeneration), postural changes, imbalance, gait unsteadiness, gait apraxia, reduced muscle strength, reduced flexibility, orthopnea, postural hypotension, cardiovascular deconditioning, iatrogenically reduced alertness
Chronic spinal pain can be attributable to the deformity caused by vertebral wedging and compression, as well as by secondary ligamentous strain. These deformities are often difficult to distinguish from the usually associated disk deterioration. The intervertebral disks undergo the most dramatic age-related changes of all connective tissues. With aging, there is an increase in the number and diameter of the collagen fibrils in the disk. This change is accompanied by a progressive decrease in disk resilience, and loss of distinction between the nucleus pulposus and the annulus fibrosus eventually occurs.
Chronic back pain secondary to osteoporosis is related to postural changes resulting from vertebral fractures. Strong back muscles contribute to good posture and skeletal support ( Figure 34-2 ). One controlled study showed the long-term effects of back extensor resistance training 8 years after cessation of the exercise. None of the women in either group in the study received hormone replacement therapy. Compared with the exercise group, the control group had a 2.7-times greater number of vertebral fractures at 10-year follow-up evaluation. The pain and skeletal deformity associated with osteoporosis might secondarily reduce muscle strength. The reduction in muscle strength can further exacerbate the postural abnormalities associated with this condition ( Figure 34-3 ).
Chronic pain can also be attributable to microfractures that are visible only on bone scanning and can occur continuously. Management of chronic osteoporosis-related pain is outlined in Box 34-4 . Prescription of opiate analgesics, such as codeine sulfate or its derivatives, should be undertaken judiciously, as their use can cause constipation.
- •
Improve faulty posture; may need weighted kypho-orthosis
- •
Manage pain (ultrasound, massage, or transcutaneous electrical nerve stimulation)
- •
If cause of pain is beyond correction, apply back support to decrease painful stretch of ligaments
- •
Advise the patient to avoid physical activities that exert extreme vertical compression forces on vertebrae
- •
Prescribe a patient-specific therapeutic exercise program
- •
Start appropriate pharmacologic intervention
New Hypothesis on the Most Effective Exercise to Reduce the Risk for Vertebral Fracture
After a 10-year follow-up study, the author developed the following hypothesis: “Back resistive exercises performed in a prone position (nonloading) rather than in vertical loading position can decrease risk of vertebral fractures through improvement of horizontal trabeculae.” The exercise needs to be progressive, resistive, and nonloading to avoid vertebral compression fracture.
Vertebroplasty and Kyphoplasty
Vertebroplasty and kyphoplasty procedures are used for the management of vertebral fractures. These procedures involve the injection of acrylic cement (such as polymethylmethacrylate) into a partially collapsed vertebral body. Jensen et al. found that 63% of patients with osteoporosis who underwent vertebroplasty decreased their use of opiates and analgesics for pain control, 7% increased their use, and 30% continued on the same use. More recently, two multicenter randomized controlled trials evaluating vertebroplasty demonstrated no significant difference in pain relief when compared with a sham procedure. Vertebroplasty does not substitute for rehabilitative measures that are needed after fracture. One study showed considerably fewer vertebral refractures after vertebroplasty in patients who received instruction for back extension exercises. The author recommends a rehabilitation program, especially back extension exercises, for osteoporosis management.
Hip Fracture
Falls and hip fractures can be life-threatening. In addition to weakness of the lower limbs, one of the contributing factors to falls is disequilibrium of individuals with spinal kyphotic posture. The kyphotic posture places the center of gravity closer to the limit of stability. Measures that reduce instability, such as exercise programs for equilibrium, including tai chi, some yoga poses, and use of a weighted kypho-orthosis (WKO), as in the Spinal Proprioceptive Extension Exercise Dynamic (SPEED) program, can reduce both the fear of falls and the risk of falls ( Figure 34-4 ).
Hip fracture is an emergency situation. In typical cases, the limb is rotated outward (externally rotated) and shortened. It is difficult to tell from the clinical evaluation whether the fracture is intracapsular (femoral neck fracture) or extracapsular (trochanteric fracture). Radiographs are necessary to make this distinction because the operative treatment and the outcome of intracapsular versus extracapsular hip fractures differ considerably. The consensus is that surgery is the treatment of choice for both femoral neck fracture and trochanteric hip fracture. In some unusual cases of impacted fracture, however, conservative treatment might be advisable. This is particularly true when the patient is severely debilitated and has impaired general health.
Femoral neck fracture requires fixation, and the type of fixation differs among surgeons. Because of the high incidence of operative failures after internal fixation of these fractures, most orthopedists prefer arthroplasties. Some orthopedists prefer total joint replacement, whereas others prefer hemiarthroplasty only for the femoral neck and head. The rationale is that total hip arthroplasties are considered to stay intact longer than hemiarthroplasties. The hemiarthroplasty, however, is a considerably smaller surgical trauma for the patient and is advocated for the very old or frail patient with a prognosis of limited mobility.
The trochanteric hip fracture creates fewer problems, despite the fact that the fracture engages more bone than the femoral neck fracture. The operative treatment of choice is internal fixation ( Figure 34-5 ). The postoperative course for all hip fractures, regardless of whether internal fixation or joint arthroplasty is done, is less eventful if physical therapeutic measures are used postoperatively, including the use of gait aids with partial weight-bearing on the operative side. Only for patients with severely comminuted fractures, or fractures in which the operative result has been unsatisfactory, is the restriction of weight-bearing to no weight-bearing needed.
Hip Pads for Fracture Prophylaxis
There is conflicting evidence as to whether hip protectors can reduce the incidence of hip fractures in the elderly, high-risk population. Compliance with use of the hip protectors has been a concern in the nursing home population. One study showed no substantial difference in the incidence of hip fractures, even in the participants who were compliant with the use of the hip protectors. It appears that at-risk elderly individuals, especially those with a history of falls, impaired balance, and decreased cognition, would benefit from use of hip pads in addition to use of gait aids. Also, rehabilitation for patients to learn how to fall and land safely can decrease the risk of hip fracture resulting from high-impact contact during a fall. Landing on the buttocks is less traumatic to hips than landing on the greater trochanters.
Sacral Insufficiency Fracture
Other axial skeletal fractures, such as fractures of the sacral alae and pubic rami, can also occur ( Figure 34-6 ). Pelvic fractures are particularly common in patients with osteoporosis. Fractures of the pubic rami can occur with minimal strain, and most patients can hardly recall having a traumatic event or an incident of severe strain. Healing typically occurs without invasive procedures. Ambulatory activities are reduced temporarily, and a wheeled walker is initially recommended to decrease pain. Later in the treatment, crutches and a cane can be used. Weight bearing is limited, as dictated by the level of pain in the pelvic area. Fracture of the sacrum with minimal trauma can also occur, and the goal of management is to decrease weight-bearing pain with use of proper assistive devices for ambulation. For management of pelvic pain, physical therapeutic measures are recommended.
Diagnostic Studies in Osteoporosis
Who is at risk? The National Osteoporosis Foundation recommends that individuals who are at risk for osteoporosis have a BMD evaluation. This group includes estrogen-deficient women with risk factors, women aged 65 years or older (regardless of risk factors), women in the postmenopausal stage who have at least one risk factor for osteoporosis including having fractured a bone, and people who have a vertebral abnormality indicative of bone loss or take a medication such as prednisone that can cause osteoporosis. This group also includes individuals who have type 1 diabetes mellitus, liver disease, kidney disease, thyroid disease, or family history of osteoporosis, as well as women who had early menopause. In addition to the above recommendations, it is thought that individuals who abuse alcohol or are cigarette smokers are at increased risk. A follow-up BMD study should be done after 2 years or longer, depending on the baseline T score and the patient’s risk factors. Bone markers can also be used for additional information on follow-up evaluations, especially those for shorter intervals (i.e., <3 months).
The diagnosis of osteoporosis requires a thorough history and physical examination, including family history of osteoporosis, type and location of musculoskeletal pain, general dietary calcium intake, height and weight measurements, and level of physical activity ( Table 34-1 ).
| Evaluation | Details |
|---|---|
| History and physical examination | Family history of osteoporosis, type and location of pain, general dietary calcium intake, level of physical activity, height and weight |
| Radiographs of chest and spine | To rule out lymphomas, rib fractures, compression fractures, etc. |
| Bone mineral density (spine and hip) | At menopause and every 2 years for high-risk patients and every 5 years for low-risk patients |
| Complete blood cell count | To rule out anemias associated with malignancy, etc. |
| Chemistry group (serum calcium, phosphorus, vitamin D, parathyroid hormone, bone-specific alkaline phosphatase, osteocalcin) | To assess the level of alkaline phosphatase, which may be increased in osteomalacia, Paget’s disease, bony metastasis and fracture, intestinal malabsorption, vitamin D deficiency, chronic liver disease, alcohol abuse, phenytoin (Dilantin) therapy, hypercalcemia of hyperparathyroidism, hypophosphatemia of hyperparathyroidism and osteomalacia, malabsorption, or malnutrition |
| Erythrocyte sedimentation rate and seroprotein electrophoresis | To determine changes indicative of multiple myeloma or other gammopathies |
| Total thyroxine | Increased total thyroxine concentration may be a cause of osteoporosis because of increased bone turnover |
| Immunoreactive parathyroid hormone | Hyperparathyroidism (accompanied by hypercalcemia) |
| 25-Hydroxyvitamin D and 1,25-dihydroxyvitamin D 3 | Gastrointestinal disease, osteomalacia |
| Urinalysis and 24-h urine | To check for proteinuria caused by nephrotic syndrome and for low pH resulting from renal tubular acidosis; a 24-h urine test can exclude hypercalciuria (normal calcium value in men is 25-300 mg/specimen; in women, 20-275 mg/specimen) * |
| Optional: Bone scan, iliac crest biopsy | After tetracycline double-labeling for bone histomorphometry, bone marrow biopsy may be indicated to exclude multiple myeloma and metastatic malignancy |
| Biochemical markers of bone turnover (Eastell) | Formation: Serum osteocalcin, alkaline phosphatase (bone), procollagen type 1, C and N propeptides Resorption: Serum acid phosphatase, pyridinoline, deoxypyridinoline, hydroxyproline, cross-linked telopeptides of type 1 collagen, urinary calcium, or creatinine |
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