Osteoporosis is a disease of the skeleton characterized by low bone mass and microarchitectural deterioration, with a consequent increase in bone fragility and susceptibility to fracture.¹ It is defined and diagnosed by measurably low bone mineral density (BMD).² Primary osteoporosis in women occurs most often after menopause and is related largely to estrogen deficiency. The terms primary osteoporosis and postmenopausal osteoporosis are often used interchangeably.² Secondary osteoporosis can result from changes in bone health related to certain medications, such as glucocorticoids, antiepileptic drugs, cyclosporine, and heparin, and certain diseases and conditions, such as cystic fibrosis, rheumatoid arthritis, end-stage renal disease, hyperthyroidism and other thyroid abnormalities, amenorrhea, alcoholism, osteogenesis imperfecta, anorexia nervosa, and organ transplant.²

Bone substance is constantly turning over through balanced processes of bone formation and bone resorption. Normally, these processes occur in a tightly coupled fashion, resulting in little net change in bone mass.² Osteoporosis occurs when the rate of bone resorption is greater than the rate of bone formation. As bone mass diminishes, bones become fragile, raising the risk of fractures from even minimal trauma.^3,4 Clinical diagnosis of osteoporosis is based on BMD scores via dual energy X-ray absorptiometry (DXA) which can lead to fragility fractures.⁵ A fragility fracture is caused by an injury that would be insufficient to fracture normal bone – the result of reduced compressive and/or torsional strength of bone.⁶ In the clinical setting, a fragility fracture is often recognized as a fracture related to a fall from standing height or lower, or as the result of minimal or no identifiable trauma.⁷

More than 10 million women and men in the U.S. have osteoporosis, and 34 million more have low bone mass (osteopenia), placing them at increased risk for this disease.⁸ The World Health Organization estimates that up to 70% of women older than 80 have osteoporosis.⁹ Although osteoporosis strikes more women than men, both men and women lose bone mass at approximately the same rate by age 65 or 70. According to the National Osteoporosis Foundation, one in two women and one in eight men over the age of 50 in the U.S. will suffer an osteoporosis-related fracture in their lifetime. One study placed the annual estimated cost of 1.5 million fractures as high as $17 billion¹⁰ and rising. In fact, the National Center for Injury Prevention and Control has projected that cost could escalate to $240 billion by the year 2040.¹¹ As the median age of the population in the U.S. increases, osteoporosis will become a major health concern in almost every setting in which physical therapists work.¹²

Losing Bone

The human skeleton contains 206 bones, which contain various percentages of cortical (compact) and trabecular (cancellous) bone. Cortical bone is densely packed and comprises the exterior of bones. Trabecular bone is spongy, similar to cortical bone in chemical composition and ultrastructure, and found in the distal radius, hip, and vertebra. Metabolism and remodeling occur at higher rates in trabecular bone. Bones with a greater percentage of trabecular bone are most likely to suffer osteoporotic fractures. Although trabecular bone accounts for only 15% of the skeleton, it is the site where the most demineralization occurs.³

Bone is a metabolically active organ that undergoes constant structural change from osteoclasts and osteoblasts found in the marrow. Endocrine glands regulate bone reconstruction by signaling osteoclasts to break down bone and osteoblasts to rebuild it. Genetic and environmental factors as well as the amount of calcium and vitamin D available in the body also influence bone formation. When there is insufficient calcium to supply major organs, such as the heart, nerves, and muscles, osteoclasts release calcium from the bones, leaving minute gaps that lower bone density.¹²

Bone Mass Across the Life Span

During childhood, increased bone production strengthens and augments the skeleton. In adolescence, the lengthwise growth of bones stops, while bone density and strength continue to increase. Peak bone mass is achieved for the interior bone tissue, or trabecular bone, by the early 20s. Cortical bone reaches its peak mass several years later. Throughout young adulthood, a remodeling process of bone resorption and formation ensures that bones fundamentally remain the same. In fact, before a person’s mid-30s, more new bone is gained than lost. However, after the mid-30s, the balance between breaking down old bone and building new bone is disrupted.

Once menopause occurs, a lack of estrogen increases bone resorption and decreases calcium absorption, resulting in bone loss and a corresponding reduction in bone mass.⁴ In the first five to 10 years after menopause, bone loss is about 2% to 3% per year, tapering off to 0.3% to 1% yearly. By the age of 80, a woman could lose up to 30% of her bone mass.³ The physical consequences of osteoporosis can be devastating, including hip fractures, vertebral compression fractures, reduced height, poor posture, fear of falling, back pain, and limited mobility.² Osteoporotic fractures most commonly occur in the vertebrae, the femur, and the radius. Hormonal changes associated with menopause affect the trabecular portions of the vertebrae and distal wrist the most, putting them at a greater risk for fractures. These fractures can significantly affect the elderly, causing chronic pain disability that, in some cases, require extensive physical therapy and assistance with daily activities. Hip fractures – the most serious of the osteoporotic fractures – generally require surgical intervention, physical therapy, and often, admission to a chronic care facility. After 50 years of age, approximately 40% of white women will suffer one or more fractures, with at least 15% of these being fractures of the hip.^13,14 According to the 2004 Surgeon General’s Report, 180,000 patients were placed in chronic care facilities due to osteoporotic fractures. Fewer than half of the hospitalized hip fracture patients recover to their prefracture ability to manage their everyday lives.¹⁵ The first year after these injuries is characterized by 12% to 24% mortality, which may be caused by complications or prolonged immobilization.³

Risk Factors

Physical therapists are in a key position to educate young women about the modifiable risk factors for osteoporosis. Advising patients to cease smoking, avoid excessive alcohol intake, get appropriate levels of sunlight exposure, improve calcium and vitamin D intake, maintain a healthy body weight, exercise regularly, and treat stress or depression can all reduce the likelihood of developing osteoporosis.² Nonmodifiable risk factors, such as advanced age, female gender, genetic background, having a family history of osteoporosis or hip fracture, and vitamin D resistance² should also be discussed with patients.

Characteristic Findings in Osteoporosis

Due to an absence of early symptoms, osteoporosis has been labeled a “silent disease.” At the same time, people may overlook symptoms of back pain, height loss, weak extremities, and kyphosis that reflect an advanced stage of the disease. Many women have osteoporosis for years without realizing it until a bone fracture occurs. For example, height loss of up to an inch is normal in an older person, indicating intervertebral disc space narrowing with aging, but greater height loss often indicates prevalent vertebral fracture(s).¹⁶ A fractured bone after the age of 50 could indicate the first sign of osteoporosis.³ In advanced cases, simply coughing, lifting groceries, or standing too long may produce a compression fracture.¹⁷

Once vertebrae are fractured, normal anatomical positioning is changed. A dowager’s hump or hyper-kyphotic posture may develop, which causes a loss of stature. As demineralization continues, the waistline disappears and the abdomen protrudes.¹² Significant kyphotic changes can produce chronic neck and back pain. Dyspnea can occur from the crowding of internal organs and interference with chest expansion. In severe cases, the ribs will rest on the pelvic bones.

Diagnostic Tests and Evaluation

Although an accurate and early diagnosis is essential for halting further bone destruction, osteoporosis is rarely diagnosed before advanced bone loss occurs. Osteoporosis is so difficult to detect that it may not show up by X-ray until bone loss of 30% or greater has occurred. Many times healthcare providers only accidentally discover the disease while examining X-rays taken for some other medical condition, such as chronic back pain, height loss, a curving spine, or a fractured bone.¹⁸

Assessment of medical history, risk factors, the patient’s lifestyle, and family history can help determine the risk of osteoporosis. However, conditions that mimic osteoporosis also need to be ruled out. For example, degenerative arthritis, disc disease, and osteomalacia — conditions that involve loss of calcium and other minerals from the bones — are associated with symptoms of low back pain and loss of bone mass similar to osteoporosis. Patients should have urine and blood tests, including a complete blood cell count and thyrotropin level, because excessive serum thyroid-stimulating hormone can accelerate bone loss. Due to its important role in calcium absorption and bone integrity, vitamin D deficiency should be ruled out. Vitamin D production slows in the elderly, the housebound, and those subjected to long periods of cloudy weather, because it is synthesized through sun exposure.⁴

Bone mineral density (BMD) and skeletal imaging studies are the primary diagnostic tools for osteoporosis. Bone density refers to the amount of mineral contained in a specific bone and therefore the relative strength of the bone. A World Health Organization working group defined osteoporosis as a bone mineral density value (T score) that is 2.5 standard deviations (SD) below the mean peak value in young adult women 20 to 29 years of age. Osteopenia, a less severe decline in BMD, is similarly defined as a T score that is 1 to 2.5 SD below the mean peak value in young adult women.² The precise measurements of bone densitometry can identify fracture risks, candidates for intervention, and initial therapy for osteoporosis. However, subsequent changes in BMD are an imperfect indicator of the efficacy of treatment.¹⁹ Nevertheless, physical therapists can be instrumental in preventing or halting osteoporosis and its sequelae by educating patients about the BMD test, as well as osteoporosis, its risk factors, and fall prevention.

Specific tests and indicators can evaluate the risk or detect progress of osteoporosis.^20,21

• Dual Energy X-ray Absorptiometry (DXA), which uses X-rays without radioactive isotopes to estimate the bone mass of the entire skeleton, is the single most important test to confirm the diagnosis of osteoporosis. DXA measurements are typically taken of the lumbar spine and femoral neck. Peripheral DXA (pDXA) measures BMD at the wrist or heel.
• Quantitative Computed Tomography (QCT) measures the amount of trabecular bone inside the vertebrae. Although precise, the QCT uses more radiation, time, and money; the peripheral version (pQCT) is also accurate, though less costly, and measures BMD of the forearm.
• Quantitative Ultrasound (QUS) is a new, noninvasive method that measures bone density of the heel and provides information about the structure and mechanical properties of bone. QUS has advantages of low cost, portability, speed (five minutes), and nonionizing radiation. However, it is a screening, not a diagnostic tool.
• Biochemical markers, revealed in blood and urine tests, can assess bone disease. Used primarily in research centers, in conjunction with densitometry measurements, they can determine the rate of bone turnover and evaluate the efficacy of therapy.

Prevention And Therapy

Osteoporosis irreversibly damages bone tissue. Therefore, therapy strives to prevent further degeneration and to correct underlying medical conditions that cause bone demineralization.

Bisphosphonates were approved by the Food and Drug Administration (FDA) in 1995 for treatment and in 1997 for prevention of osteoporosis.⁴ Bisphosphonates, such as alendronate (Fosamax) and risedronate (Actonal) prevent bone loss and can stabilize the microarchitecture of the bone, thereby decreasing risk of fracture. However, these drugs, which are taken orally once a week or once a month, are difficult for the body to absorb.²² Recently the FDA approved an IV bisphosphonate, ibandronate (Boniva), for quarterly administration by a healthcare professional; this agent can also be taken orally once a month.²³

Hormone therapy (also known as HT, or ET for estrogen therapy) can increase BMD at the spine and hip and reduce the risk of spine and hip fracture in older women. Unfortunately, significant bone loss can occur shortly after therapy is discontinued, sometimes negating any gain. However, the big issue is that findings from the Women’s Health Initiative (WHI)²⁴ suggest that HT increases events related to heart disease as well as the risk of stroke and breast cancer, although new types and doses of HT may address some of these risks.²²

Selected estrogen receptor modulators (SERMs) are a category of therapeutic agents that mimic estrogen in some tissues and act as estrogen antagonists in others. They have been shown to increase BMD at the hip and spine and to reduce spine fractures by 50% in postmenopausal women (although they appear to have no impact on hip or nonspine fractures). Efficacy begins three years after a treatment begins, but bone loss occurs after discontinuation of treatment.²²

Approved in 1997 by the FDA for the prevention of osteoporosis, raloxifene (Evista) is a second-generation SERM. The drug not only reduces the risk of vertebral fractures, but apparently prevents breast cancer in postmenopausal women at increased risk of breast cancer.²⁵ Adverse effects include venous thrombosis, hot flashes, and leg cramps.²⁶

Calcitonin is a hormone secreted by the thyroid in response to increased calcium in the blood. With aging, the calcitonin level decreases and is less effective at inhibiting osteoclastic-mediated bone resorption. Calcitonin taken as a medication has been shown to moderately increase BMD at the spine in postmenopausal women.²² Pharmaceutically produced calcitonin cannot be taken orally and must be administered subcutaneously, intramuscularly, or via a nasal spray preparation. Minor adverse effects associated with calcitonin include nausea, vertigo, tingling of the hands, and facial flushing.²⁷

Parathyroid hormone (PTH) by subcutaneous injection is approved for the treatment of osteoporosis in postmenopausal women and men who are at extremely high risks for having first or subsequent fracture.²² Unlike other available treatments that reduce the activity of osteoclasts, PTH actually increases the bone-building of osteoblasts. PTH studies found the vertebrae increased in size as well as bone density.²² This is a significant advance in the prevention of fractures by ensuring stronger bones that are bigger and more resistant to fractures.

Kyphoplasty Revolutionizes Vertebral Fracture Treatment

Research indicates that kyphoplasty is making significant progress in the treatment of pain associated with osteoporotic vertebral fractures. Kyphoplasty is a minimally invasive procedure that involves inserting an orthopedic balloon into the fractured vertebral body; inflating the balloon causes fractured bone fragments to elevate, thus restoring vertebral anatomy. Next, the balloon is removed and the vertebral cavity is filled with methylmethacrylate bone cement. Kyphoplasty has been shown to provide a 90% pain relief from an acute vertebral compression fracture as well as restore body height.²⁸

Although kyphoplasty may reduce or relieve the pain associated with a vertebral fracture as well as correct the spinal deformity, it is not indicated for all vertebral fractures. It is performed if the fracture causes intractable pain that is unresponsive to analgesics and rest, and if the fracture is acute, rather than healed. The procedure may also be beneficial if there are negative consequences associated with the vertebral fracture deformity. Significant height loss may diminish the vital capacity in patients with pulmonary disease. Serious complications associated with the procedure include spinal cord compression.^12,29,30

A Bone-Saving, Preventative Triad

Calcium, vitamin D, and exercise are traditional weapons in the fight against osteoporosis. Although they will not halt the bone resorption that occurs with osteoporosis, they are essential adjuncts to the medical regimen or preventative measures for those at risk.

Adults over 65 typically take less than 600 mg/day of calcium, which is inadequate to maintain bone integrity.²⁹ The Institute of Medicine advises women and men to have a daily calcium intake of 1,000 mg/day until age 50 and 1,200 mg/day over age 50. Women who are on HRT need at least 1,000 mg/day of calcium, while postmenopausal women not taking HRT require 1,500 mg/day. Adolescent, pregnant, and breastfeeding women need 1,200 mg/day of calcium. If a diet is deficient in calcium, supplements should be added,³¹ although the preferred source of calcium is dietary. Vitamin D is integral to calcium absorption and bone metabolism. Adequate levels of vitamin D can be obtained from sunlight, diet, or vitamin supplementation. Usual daily requirements are 200 IU for premenopausal women, 400 to 800 IU for postmenopausal women, and 400 IU for men over 65.⁴

A regular routine of weight-bearing exercises is another important aspect of prevention. This type of exercise puts stress on long bones to augment their mass and improves agility and balance. A complete osteoporosis exercise prevention program also includes isometric strength training. Additionally, lifestyle adjustments, such as quitting smoking, reducing alcohol consumption, and maintaining appropriate body weight, can help preserve bone mass and prevent osteoporosis.

What Physical Therapists Can Do

The five main goals of physical therapy intervention for individuals with osteoporosis include: (1) promotion of bone formation, (2) fall prevention, (3) fracture prevention, (4) postfracture rehabilitation, and (5) treatment of other musculoskeletal conditions that limit mobility and increase the risk of fall or fracture.⁵ Individualized exercise prescription, pain management, ergonomic advice on safe bending and lifting strategies, mobility aids, protective equipment, manual therapy, flexibility exercises, balance training, environmental modifications, fall risk assessment, and bone health education are essential modes of physical therapy treatment that should be used to achieve these goals.⁵

Specific Intervention

Research has widely recognized that weight-bearing exercise is beneficial to bone health. Dynamic loading is crucial for bone formation and intermittent loading was found to be more osteogenic than continuous loading.⁵ Key recommendations for optimal bone health include weight-bearing endurance activities and resistance training 30 to 60 minutes, three to five times per week, adhering to healthy nutritional habits, avoidance of smoking, and taking in the recommended daily amounts of calcium and vitamin D. PTs should further encourage patients at significant risk for osteoporosis to follow up with a primary care provider.^32,33 Research suggests that aerobic walking for one hour a day, four days per week for 12 months significantly increases lumbar spine BMD as compared to a nonexercising control group.³⁴ Strength training of moderate intensity (three hours of exercise per week, consisting of walking, stretching, and 30 minutes of resistance training, three sets with eight repetitions, maximum) has been shown to be an effective means to increase BMD.³⁵

Sara Meeks, PT, MS, G.C.S., K.Y.T., has spent 23 years specializing in the unique management implications of persons with osteopenia and osteoporosis. She has developed a 12-part program for the conservative management of these conditions as well as back pain and postural problems.³⁶ Her approach incorporates patient assessment, education, site-specific exercise, body mechanics, postural correction, balance, weight-bearing exercise, modalities, bracing, breathing, relaxation, and advanced exercise to prevent and/or arrest avoidable postural changes that can result from bone loss.³⁶ The Meeks Method further focuses on specifically strengthening the erector spinae, gluteus medius, and gluteus maximus muscles, which provide primary support to the spine and hips. Great emphasis is also placed on stretching the hip flexors. Meeks advocates strengthening the erector spinae muscle groups to reduce the incidence of compression fracture in persons with osteoporosis. In comments to an annual meeting of the American Physical Therapy Association, Meeks notes that bending forward compresses the spine. Spinal vertebrae that have been weakened from bone loss can crush or break easily. She advocates caution with common exercises, such as abdominal crunches and partial sit-ups, due to vertebral body compression that can cause back pain and even spinal fractures.³⁷

PTs can help patients reduce the risk of developing osteoporosis throughout their life cycle. Encouraging families to adopt healthy habits such as regular exercise and a proper diet can maximize bone density, especially during the peak bone growth that takes place during childhood, adolescence, and young adulthood. Advising children to participate in weight-bearing exercise, such as jumping, hopping, dancing, skipping, running, and resistance training can be highly beneficial to bone health. In a study of 16- to 18 year-old girls who were given calcium supplements of 1,000 mg/day in conjunction with exercise 45 minutes a day, three days a week, a significant increase in size-adjusted bone mineral content (5%) at the femoral trochanteric site was noted.³⁴

Home care providers have a special opportunity to prevent falls and potential fractures by evaluating their patients’ use of sedatives, identifying sensory deficits, and assisting patients in making their homes safe environments. The Timed Up and Go test is a simple yet effective functional mobility screen that can help therapists identify patients at risk for falls in the home and clinical settings. The test is used to measure the ability of patients to perform sequential locomotor tasks that incorporate walking and turning.³⁸ The patient is observed and timed while rising from an arm chair; he or she then walks 3 meters, turns, walks back, and sits down again. Data suggests that the Timed Up and Go test is a reliable and valid test for quantifying functional mobility that may also be useful in following clinical change over time. The test is quick, requires no special equipment or training, and is easily included as part of routine examination.³⁹

With new treatment modalities aimed at prevention, more research is needed to develop criteria to identify those at risk who would benefit from bone density screening studies and early intervention to avoid this costly and debilitating disease. Osteoporosis does not have to be an inevitable part of the aging process.

Along with weight-training, Helen begins an intensive walking program and a diet supplemented with calcium and vitamin D. She declines HT because of her fears of cancer. She initially takes a prescribed 10 mg daily dose of alendronate, but discontinues the medication after experiencing gastrointestinal distress. She is now taking 200 mg of raloxifene every day with a follow-up BMD test in one year.