Osteoporosis Treatment & Management

Medical care includes the administration of adequate calcium, vitamin D, and antiosteoporotic medication such as bisphosphonates^[69] and parathyroid hormone (PTH). In addition, potentially treatable underlying causes of osteoporosis such as hyperparathyroidism and hyperthyroidism should be ruled out or treated if detected.

Surgical care includes vertebroplasty and kyphoplasty. Vertebroplasty and kyphoplasty are minimally invasive spine procedures used for the management of painful osteoporotic vertebral compression fractures.

A 2008 literature review suggested that the use of "reminders plus education targeted to physicians and patients" can lead to increased bone mineral density (BMD) testing and greater use of osteoporosis medications.^[70] In addition, a physician reminder in conjunction with a patient risk assessment strategy apparently can result in a reduction in patient fractures and an increase in osteoporosis therapy. The authors concluded that multicomponent tools aimed at doctors and patients may support clinical decision making in the management of osteoporosis.

A 2009 study indicated that the use of a case manager for the treatment of patients with hip fractures can, in comparison with a more commonly employed care strategy, can lead to more frequent use of appropriate osteoporosis treatment and may result in fewer fractures, increased life expectancy, and significant health-care cost savings.^[2]

Currently, no treatment can completely reverse established osteoporosis. Early intervention can prevent osteoporosis in most people. For patients with established osteoporosis, medical intervention can halt its progression. If secondary osteoporosis is present, treatment for the primary disorder should be provided.

Patients identified as at risk for osteoporosis (including children and adolescents) should undergo preventive measures, including adequate calcium intake, vitamin D intake, and exercise. Counsel patients to avoid tobacco use. Identify and treat alcoholism.

Protective measures should be taken in patients who must take glucocorticoids for other medical conditions. These include using the minimum effective dose, discontinuing the drug as soon as possible, and supplementing with calcium and vitamin D.

The National Osteoporosis Foundation (NOF) recommends that pharmacologic therapy should be reserved for postmenopausal women and men aged 50 years or older who present with the following:

• A hip or vertebral fracture (Vertebral fracture may clinical or morphometric [ie, identified on a radiograph alone].)
• Other prior fractures and low bone mass (T-score between -1.0 and -2.5 at the femoral neck, total hip, or spine)
• T-score less than -2.5 at the femoral neck, total hip, or spine after appropriate evaluation to exclude secondary causes
• Low bone mass (T-score between -1.0 and -2.5 at the femoral neck, total hip, or spine) and secondary causes associated with high risk of fracture (eg, glucocorticoid use or total immobilization)
• Low bone mass (T-score between -1.0 and -2.5 at the femoral neck, total hip, or spine) and (1) 10-year probability of hip fracture of 3% or more or (2) a 10-year probability of any major osteoporosis-related fracture of 20% or more based on the US-adapted World Health Organization (WHO) algorithm^[52]

The American College of Physicians has reviewed the evidence and has proposed guidelines for pharmacologic treatments of osteoporosis.^[71]

The agents currently available for osteoporosis treatment include bisphosphonates, the selective estrogen-receptor modulator (SERM) raloxifene, calcitonin, denosumab, and one anabolic agent, teriparatide (human recombinant PTH 1-34).^{[19, 72, 73]} All therapies should be given with calcium and vitamin D supplementation.

These medications may be classified into 2 primary categories. The first includes medications that help to stimulate bone formation, such as vitamin D and bisphosphonates. The second includes medications that reduce bone resorption, such as estrogen, bisphosphonates, calcitonin, calcium, and vitamin D.^[74]

Guidelines from the American Association of Clinical Endocrinologists (AACE), published in 2010, include the following recommendations for choosing drugs to treat osteoporosis^[75] :

• First-line agents - Alendronate, risedronate, zoledronic acid, denosumab
• Second-line agent - Ibandronate
• Second- or third-line agent - Raloxifene
• Last-line agent - Calcitonin
• Treatment for patients with very high fracture risk or in whom bisphosphonate therapy has failed - Teriparatide

The AACE guidelines advise against the use of combination therapy.

Calcium and vitamin D supplementation

The goal of the current recommendations for daily calcium intake is to ensure that individuals maintain an adequate calcium balance. In 1994, the National Institutes of Health recommended the following daily calcium intake:

• Birth to age 6 months - 400 mg/d
• Age 6 months to 1 year - 600 mg/d
• Age 1 to 10 years - 800-1200 mg/d
• Age 11 to 24 years - 1200-1500 mg/d
• Age 25 to 50 years - 1000 mg/d
• Age 51 to 64 years - 1000 mg/d
• Age 51 years and older (only women not on hormone replacement therapy [HRT]) - 1500 mg/d
• Age 65 years and older - 1500 mg/d
• Pregnant or lactating women - 1200-1500 mg/d

Current recommendations from the National Osteoporosis Foundation for daily calcium intake are as follows:

• Age 1 to 3 years - 500 mg/d
• Age 4 to 8 years - 800 mg/d
• Age 9 to 18 years - 1300 mg /d
• Age 19 to 49 years - 1000 mg/d
• Age 50 years and older - 1200 mg/d
• Pregnant and breastfeeding women age 18 years and younger - 1300 mg/d
• Pregnant and breastfeeding women age 19 years and older - 1000 mg/d

Vitamin D is increasingly being recognized as a key element in overall bone health and muscle function. The minimum daily requirement in patients with osteoporosis is 800 IU of vitamin D3, or cholecalciferol. Many patients require more, continuously or for a short period, to be considered vitamin D replete, defined as a serum 25-hydroxyvitamin D level of 32 ng/mL.

Several large studies have demonstrated that supplementation with a combination of calcium and vitamin D can reduce fracture risk.^[76]

A meta-analysis of 12 double-blind, randomized, controlled trials of nonvertebral fractures and 8 randomized controlled trials of hip fractures comparing oral vitamin D (with or without calcium) with either calcium alone or placebo showed that nonvertebral fracture prevention with vitamin D is dose-dependent, and a higher dose reduced fractures by at least 20% in individuals aged 65 years or older.^[77]

An additional meta-analysis concluded that vitamin D alone is not effective in preventing fractures, although, when administered with calcium, hip fractures and total fractures (and possibly vertebral fractures) were reduced.^[78] The conclusions were based on 7 large studies that were randomized with at least one intervention arm in which vitamin D was given and included analysis of fractures as an outcome and at least 1000 participants.

More information is needed regarding risks associated with long-term calcium supplementation. Bolland et al conducted a meta-analysis of patients taking calcium supplements (without coadministered vitamin D) and association with cardiovascular risks. An increased risk for myocardial infarction was associated with patients taking calcium supplements.^[79] This increased risk has not been associated with dietary calcium intake.

Bisphosphonates

Bisphosphonates are the most commonly used agents for osteoporosis. They have been employed for both treatment and prevention. (See Prevention of Osteoporosis.) Oral and intravenous (IV) options are available.

Alendronate has been shown to increase spinal and hip mineral density in postmenopausal women. Well-conducted controlled clinical trials using alendronate sodium indicate that treatment reduces the rate of fracture at the spine, hip, and wrist by 50% in patients with osteoporosis. The treatment dose of alendronate is 70 mg/wk, to be taken sitting upright with a large glass of water at least 30 minutes before eating in the morning. The results of a population-based, national register–based, open cohort study of 38,088 patients suggest that elderly patients who use proton pump inhibitors in conjunction with alendronate have a dose-dependent loss of protection against hip fracture.^[80]

Other oral bisphosphonates include risedronate, given weekly or monthly, and ibandronate, given orally once a month. Risedronate reduced vertebral fractures by 41% and nonvertebral fractures by 39% over 3 years. Ibandronate has not shown efficacy in nonvertebral fractures in the clinical trials.

Intravenous bisphosphonates are excellent choices for patients intolerant of oral bisphosphonates or in those in whom adherence is an issue. Ibandronate is available as an intravenous formulation that is given every 3 months. Zoledronic acid is the most potent bisphosphonate available. It increases BMD at the spine by 4.3-5.1% and the hip by 3.1-3.5% compared with placebo. It reduces the incidence of spine fractures by 70%, hip fractures by 41%, and nonvertebral fractures by 25% over 3 years. Zoledronic acid is once-yearly intravenous infusion approved for the treatment of postmenopausal osteoporosis.^[81] A randomized, placebo-controlled, double-blind trial suggests that a once-yearly 5-mg dose of IV zoledronic acid increases bone mass in men within 90 days of hip fracture repair; similar increases were also noted in women.^[82]

In September 2011, the FDA updated the prescribing information for zoledronate (Reclast) to provide improved information regarding the risk of kidney failure. Cases of acute renal failure requiring dialysis or having a fatal outcome following Reclast use have been reported to the FDA. Reclast is indicated to treat or prevent osteoporosis and is administered as a single infusion once every 1-2 years. Zoledronate is contraindicated with moderate-to-severe renal impairment (ie, CrCl < 35 mL/min) or in patients with evidence of acute renal impairment. Other risks for renal impairment include coadministration of zoledronate with nephrotoxic or diuretic medications, severe dehydration before or after zoledronate administration, or advanced age.^[83]

Over time, bisphosphonate therapy decreases bone turnover and, at very high levels in animals, decreases bone strength and resilience. Some limited reports, including that by Odvina et al, describe patients on long-term bisphosphonate therapy developing transverse stress fractures; biopsy specimens of these individuals have suggested extremely low turnover states.^[84]

Therefore, while the bisphosphonates are outstanding in their efficacy, bone turnover markers should be monitored; if these become profoundly suppressed, the patient should be taken off the bisphosphonates and given a rest period until he or she can return to therapeutic levels (N-telopeptide of collagen cross-links [NTx], 20-40).

The limited trial data available on long-term treatment with bisphosphonates has raised questions about the optimal length of treatment with these medications.^[85] This issue has become more important given newly recognized complications of bisphosphonate use, including osteonecrosis of the jaw and atypical (subtrochanteric or femoral shaft) femur fractures.

Some studies have sought to clarify the true risks of complications in patients receiving bisphosphonates. A Canadian study by Park-Willie et al found the estimated absolute risk of a subtrochanteric or femoral shaft fracture among 52,595 women with at least 5 years of bisphosphonate therapy to be low (0.13% during the subsequent year and 0.22% within 2 years).^[86] Overall, a patient’s risk of fracture can be used to help guide length of treatment. Patients at high risk may be continued on bisphosphonates after 5 years; however, in some patients, especially those with a lower risk of fracture, bisphosphonate treatment may be stopped.^[87]

The AACE recommends that clinicians consider a “drug holiday” after 4-5 years of bisphosphonate treatment, if osteoporosis is mild; if fracture risk is high, a drug holiday of 1-2 years may be considered after 10 years of treatment.^[75] BMD and bone turnover markers should be monitored during the drug holiday, and treatment should be restarted if density declines substantially, bone turnover markers increase, or a fracture occurs.^[75]

Raloxifene

SERMs are considered to provide the beneficial effects of estrogen without the potentially adverse outcomes. Raloxifene, a SERM first studied for breast cancer prevention, decreases bone resorption through actions on estrogen receptors. It has been shown to prevent bone loss, and data in females with osteoporosis have demonstrated that raloxifene causes a 35% reduction in the risk of vertebral fractures. It has also been shown to reduce the prevalence of invasive breast cancer.

Raloxifene may be most useful in younger postmenopausal women without severe osteoporosis. It has been shown to increase the incidence of deep vein thrombosis and hot flashes. In 601 postmenopausal women who had daily therapy with raloxifene, BMD was increased, serum concentrations of total low-density lipoprotein cholesterol were lowered, and the endometrium was not stimulated.

Pooled mortality data from large clinical trials of raloxifene (60 mg/d) were analyzed by Grady et al in 2010. When compared with placebo, all-cause mortality was 10% lower among older postmenopausal women receiving raloxifene. The primary reduction was in noncardiovascular, noncancer deaths.^[88]

Teriparatide

Teriparatide (human recombinant PTH 1-34) is the only available anabolic agent for the treatment of osteoporosis. When PTH is given continuously, it is associated with increased osteoclastic and osteoblastic turnover, leading to a net loss of bone. However, in an intermittent subcutaneous administration of 20 mcg/d, PTH has been demonstrated to lead to a very active anabolic phase, with bone mass increasing up to 13% over 2 years in the spine and to a lesser degree within the hip.^{[89, 90, 91]}

Indications for PTH in men and women are a bone density decline while on bisphosphonate therapy, bone density stabilization while on extremely low-level bisphosphonate therapy, a fracture occurring while on bisphosphonate therapy, or a very low initial bone turnover rate for which an anabolic effect is clearly warranted. Teriparatide should be considered in younger and older postmenopausal women with severe osteoporosis.

Most studies with PTH have been performed on women. The medication decreases the risk of vertebral and nonvertebral fractures to the same extent as bisphosphonates. Teriparatide is given for a maximum of 2 years, after which time the gains in BMD achieved with PTH are secure and can even be augmented with bisphosphonate therapy, otherwise the BMD slowly deteriorates to pretreatment levels.^[92]

According to Finkelstein et al in 2003, initial studies using a combination of concurrent PTH and bisphosphonate therapy showed decreased benefit compared with therapy with either agent alone; therefore, the general recommendation is that these drugs be given separately and in sequence.^[93]

A 2005 study by Cosman and colleagues challenged this conclusion by giving 3-month-on, 3-month-off pulses of teriparatide while the subjects were on weekly alendronate; BMD in the spine increased above that of the alendronate-only arm.^[94] This pulsed regimen appears to take advantage of the 3- to 4-month so-called anabolic window, in which the markers of bone formation rise more quickly than the markers of bone resorption.

Studies by Deal et al and Ste-Marie et al on women have shown that the concurrent use of estrogen or raloxifene can enhance the bone-forming effects of teriparatide.^{[95, 96]} Data on the use of PTH in men are much more limited, but they appear to have relatively comparable efficacy.

Bouxsein et al retrospectively analyzed data from the Fracture Prevention Trial and the Multiple Outcomes of Raloxifene Evaluation trial for the risk of new vertebral fractures adjacent to existing vertebral fractures in postmenopausal osteoporotic women in patients on teriparatide or raloxifene and found that teriparatide reduced fracture risk to a greater extent than raloxifene.^[97]

In this study, 1226 untreated postmenopausal women had 1 or more vertebral fractures at baseline. During the 2-year follow-up, 196 (16%) had a total of 292 new vertebral fractures; 47% of fractures were adjacent to a previously existing fracture. Teriparatide reduced the risk of any new, new adjacent, and new nonadjacent vertebral fractures by 72%, 75%, and 70%, respectively, compared with placebo, whereas raloxifene reduced the risk by 54%, 54%, and 53%, respectively, compared with placebo.

A study performed by the Austrian group using PTH 1-84 to treat pelvic fractures demonstrates clearly that the anabolic agent used in osteoporosis also has the ability to both increase the rate of union and enhance the speed of the process. Using CT evaluation of the fracture site, the authors not only proved their primary goal of improved fracture healing, but also noted a significant decrease of pain and improved function over the placebo arm. This clinical study supports the extensive animal data that predicted a clear role for PTH in fracture repair.^[98]

Calcitonin

Calcitonin is a hormone that decreases osteoclast activity, thereby impeding postmenopausal bone loss. It is delivered as a single daily intranasal spray that provides 200 U of the drug. The drug can be delivered subcutaneously, but this route is rarely used.

Results from a single controlled clinical trial indicate that calcitonin may decrease osteoporotic vertebral fractures by approximately 30%. In the first 2 years, calcitonin has been found to increase spinal BMD by approximately 2%. Calcitonin also has an analgesic property that makes it ideally suited for the treatment of acute vertebral fractures.

Calcitonin is an option for patients who are not candidates for other available osteoporosis treatments.

Denosumab

Denosumab is a humanized monoclonal antibody directed against receptor activator of nuclear factor-kappa B ligand (RANKL), which is a key mediator of the resorptive phase of bone remodeling.^[96] It decreases bone resorption by inhibiting osteoclast activity. Denosumab was approved by the US Food and Drug Administration (FDA) in June 2010. It has been studied in cancer patients and in patients with postmenopausal osteoporosis.^{[99, 100]} It is indicated for patients with postmenopausal osteoporosis at high risk for fracture.

In patients with multiple myeloma or bone metastases from breast cancer, a single subcutaneous dose of denosumab decreases bone turnover markers within 1 day, and this effect is sustained through 84 days at the higher doses used in one study. Denosumab was shown to increase BMD and decrease bone resorption in postmenopausal women with osteoporosis over a 12-month period.

In a randomized placebo-controlled trial of 7868 women aged 60-90 years with osteoporosis who received either denosumab 60 mg SC or placebo every 6 months for 36 months, Cummings et al found that denosumab decreased the risk of vertebral, nonvertebral, and hip fractures in women with osteoporosis.^[101]

Smith et al reported a reduction in incident vertebral fractures when denosumab was used in 734 men receiving androgen-deprivation therapy for prostate cancer compared with placebo.^[102] In this study, denosumab significantly increased lumbar spine, hip, femoral neck, and radial BMD.

Because the overactivity of RANKL is a major factor in bone loss in patients with autoimmune and inflammatory disorders, such as ulcerative colitis, denosumab may become first-line therapy for these patients.^[103]

Hormone replacement therapy

Hormone replacement therapy (HRT) was once considered a first-line therapy for the prevention and treatment of osteoporosis in women. Although HRT is not currently recommended for the treatment of osteoporosis, it is important to mention because many osteoporosis patients in a typical practice still use it for controlling postmenopausal symptoms.

Data from the Women's Health Initiative confirmed that HRT can reduce fractures.^[104] However, the results of the Women's Health Initiative were distressing with respect to the adverse outcomes associated with combined estrogen and progesterone therapy (eg, risks for breast cancer, myocardial infarction, stroke, and venous thromboembolic events) and estrogen alone (eg, risks for stroke and venous thromboembolic events).

Strontium ranelate

Evidence indicates that strontium ranelate (available in Europe) reduces the risk of fracture.^{[105, 106]} Strontium is not approved for the treatment of osteoporosis in the United States.

Other medical treatments

Based on preliminary data that suggest women on nitrates have higher BMDs and lower fracture risk, Jamal et al conducted a randomized placebo-controlled trial of women who applied daily nitroglycerin ointment for 24 months.^[107] The nitroglycerin ointment increased BMD and decreased bone resorption, although headaches were a limiting factor for many patients. Other nitrate preparations may be better tolerated and could show efficacy for fracture risk reduction.

The goals of surgical treatment of osteoporotic fractures include rapid mobilization and return to normal function and activities. Traditional operative management of vertebral compression fractures is uncommon and is usually reserved for gross spinal deformity or for threatened or existing neurologic impairment.

Operative interventions include anterior and posterior decompression and stabilization with placement of such internal fixation devices as screws, plates, cages, or rods. Bone grafting is routinely performed to achieve bony union. The failure rate of spinal arthrodesis is significant because achieving adequate fixation of hardware in osteoporotic bone is difficult. Moreover, patients who are elderly have a reduced osteogenic potential.

Vertebroplasty and balloon kyphoplasty are indicated in patients with incapacitating and persistent severe focal back pain related to vertebral collapse. At the primary author's institution, vertebroplasty is used for lesions above T8 and kyphoplasty is used for the remainder.

Vertebroplasty

Percutaneous vertebroplasty (PVP) with polymethylmethacrylate (PMMA) was developed in 1984. PMMA is the principal component of bone cements used for rapid stable fixation of implants, such as metal and plastic prosthetics placed in living bone during orthopedic procedures. PMMA is used in PVP to fortify a collapsed vertebral body and stabilize the vertebral column.

The first indication for this treatment was aggressive vertebral angiomas. PVP with PMMA was then used for other lesions that weakened the vertebral body, such as malignant tumors. PVP is one therapeutic alternative for the treatment of pain associated with compression fractures.

The procedure involves percutaneous injection of PMMA into a fractured vertebral body, either through a transpedicular or an extrapedicular route (see the image below). This procedure can be performed on an outpatient basis under local or general anesthesia with fluoroscopic assistance.

Because this is a continuous insertion into an unprepared bed, a venographic injection is often used to ensure that the needle is not directly aligned with an exiting vein. After verification of appropriate placement, 1-4 mL of a specially prepared PMMA-containing enhanced radiographic visualization material is then inserted directly with a syringe. One or more levels of the spine can be treated in a single setting.

One drawback of PVP with PMMA is that, although the bone cement is injected under pressure, the procedure does not have the potential to correct compression deformities. In addition, extravasation of the cement into the epidural space is a potential complication of this method.

Jensen et al studied age-related or steroid-induced osteoporotic vertebrae with partial compression fractures in patients who underwent PVP with PMMA.^[108] A total of 48 vertebrae in 30 patients were injected, and 90% of the patients described marked improvement of pain within 1 week of treatment. All the patients who experienced pain relief noted increased mobility and decreased need for narcotics. The patients were tracked for an average of 9 months, and the rate of long-term pain relief was reported to be approximately 80%. Whether this pain relief was related to mechanical stabilization of the spine or was secondary to neurotoxic effects of PMMA remains to be determined.

In general, initial studies report good results.^[109] However, success with vertebroplasty may be limited by the lack of significant height restoration and the high rate of cement extravasation.

Kyphoplasty

The second therapeutic alternative for vertebral compression fractures is balloon kyphoplasty, which has been used since the mid 1990s. Kyphoplasty is similar to vertebroplasty, but a few key differences exist.^[110]

Kyphoplasty involves the insertion of an inflatable balloon tamp into the vertebral body under fluoroscopic guidance. An extrapedicular approach is used in the midthoracic region, while a pedicular route may be used in the thoracolumbar or lumbar spine. The balloon is instilled with radiographic contrast material at pressures up to 360 pounds per square inch, which compacts the cancellous bone and re-expands the vertebral body, thus reducing the fracture.

The balloon is then removed, thereby creating a cavity. PMMA is infiltrated into the cavity, stabilizing the vertebral body and restoring vertebral body height. Because the cement is injected into the cavity under lower pressure than is used in PVP, the risk of cement extravasation is reduced (see the images below).

This procedure has been successful both in reducing the amount of kyphosis and in restoring vertebral body height. It also has successfully reduced pain. Studies have shown kyphoplasty to be a safe and minimally invasive spine procedure that results in improved function in elderly patients, allowing them to participate in increased activities, with resulting improvements in independence and quality of life.

Adequate calcium and vitamin D intake are important in persons of any age, particularly in childhood as the bones are maturing. Patients who ingest inadequate amounts of vitamin D and calcium should receive oral supplementation.

A diet that includes adequate vitamin D and calcium is essential. Recommendations for patients with osteoporosis include daily dosages of 400-800 IU of vitamin D and 1200-1500 mg of calcium.

Premenopausal women and men younger than 50 years without risk factors for osteoporosis should receive a total of 1000 mg of calcium daily. Postmenopausal women, men older than 50 years, and other persons at risk for osteoporosis should receive a total of 1200-1500 mg of calcium daily. Good sources of calcium include dairy products, sardines, nuts, sunflower seeds, tofu, vegetables such as turnip greens, and fortified food such as orange juice. See the National Osteoporosis Foundation Web site for further calcium recommendations.

Adults younger than 50 years should receive 400-800 IU of vitamin D₃ daily. All adults older than 50 years should receive 800-1000 IU of vitamin D₃ daily. Good sources of vitamin D include eggs, liver, butter, fatty fish, and fortified food such as milk and orange juice. See the National Osteoporosis Foundation Web site for further vitamin D recommendations.

A meta-analysis of 12 double-blind, randomized, controlled trials (RCTs) for nonvertebral fractures and 8 RCTs for hip fractures that compared oral vitamin D (with or without calcium) with either calcium alone or placebo found that nonvertebral fracture prevention with vitamin D was dose dependent and that a higher dose reduced fractures by at least 20% for individuals aged 65 years or older.^[77]

The following conditions can interfere with nutrition:

• Alcohol intake - Excessive alcohol intake can interfere with calcium balance by increasing PTH production and by inhibiting the enzymes that convert inactive vitamin D to its active form; in addition, alcohol can result in hormonal deficiencies and can increase the tendency for falls
• Anorexia nervosa - Poor nutritional states, such as in anorexia nervosa, an eating disorder,^[111] have been strongly associated with bone loss; nutritional and endocrine factors contribute to bone loss (in particular, low estrogen states, which result from low body weight, result in significant bone loss)

The first goal of rehabilitation in osteoporosis patients is to control pain if a fracture has occurred. Spinal compression fractures can be extremely painful and can cause short- and long-term morbidity. Oral analgesics on a regular schedule can be implemented. Pain-relieving modalities such as moist hot packs and transcutaneous electrical nerve stimulation should also be considered. During this period, monitoring the patient carefully for signs of constipation, urinary retention, and respiratory depression, which can occur with the use of narcotic analgesics, is essential.

A comfortable mechanical support for the spine and, in some cases, a thoracic orthosis, may need to be prescribed. The primary reason for the application of a thoracic orthosis is to limit motion in the spine. The length of time a patient should wear a rigid spinal orthosis is undetermined. What is well known is that immobilization contributes to bone demineralization. During the early mobilization period, deep breathing exercises, pectoral and intercostal strengthening, and back conservation techniques need to be implemented.

Physical therapy then focuses on improving a patient's strength, flexibility, posture, and balance in order to prevent falls and maximize his/her physical function.^{[112, 113]} Postural retraining is key in this population. Spinal BMD is directly correlated with the strength of the back extensors; therefore, maintaining and strengthening the back extensors should be emphasized.^[114] Sinaki and others found that strengthening the back extensor muscles reduced kyphosis and decreased the risk of sustaining vertebral compression fractures.^{[115, 116]}

As soon as the course of therapy allows, weightbearing exercises should be initiated. Regular weight-bearing exercises are essential for the maintenance of bone mass^[24] and should be encouraged in all patients, including children and adolescents (in order to strengthen the skeleton during the maturation process). Exercise also improves agility and balance, thereby reducing the risk of falls.

Aerobic low-impact exercises, such as walking and bicycling, generally are recommended. During these activities, ensure the patient maintains an upright spinal alignment. In 1984, Sinaki and Mikkelsen showed that exercises that place flexion forces on the vertebrae tend to cause an increase in the number of vertebral fractures in patients.^[114]

In postmenopausal women, impact exercises can increase BMD in the hip and spine. Chien et al examined the efficacy of a 24-week aerobic exercise program consisting of treadmill walking followed by stepping exercises in osteopenic postmenopausal women aged 48-65 years. Women who exercised had increased bone mineral density in L2-L4 and the femoral neck, as well as improved quadriceps strength, muscular endurance, and peak exercise oxygen consumption (VO₂ max), while values in the control group declined.^[117]

Also, Snow et al found increased BMD of the femoral neck, trochanter, and total hip in 18 postmenopausal women (average age 64 y), who wore weighted vests and participated in jumping exercises 3 times per week for 32 weeks of the year over 5 years.^[118]

The results of a Cochrane Database of Systematic Reviews study found that exercise may help prevent bone loss and fractures in postmenopausal women. The most effective type of exercise on BMD for the neck of the femur was non–weight bearing, high-force exercise such as lower limb resistance strength training; combination exercise programs were most effective for BMD at the spine.^[119]

Although swimming is not a weightbearing exercise that will improve BMD, it does provide chest expansion, spinal extension, and low-impact cardiopulmonary fitness. Isometric exercises should also be used to strengthen abdominal muscles, aiding in the prevention of a kyphosis.

Proper therapy for osteoporosis includes 3-5 sessions per week of weight-bearing exercises, such as walking or jogging, with each session lasting 45-60 minutes. The patient should be instructed in a home exercise program that incorporates the necessary elements for improving his/her posture and overall physical fitness.

The physical therapist must address balance training, because fall prevention is important in eliminating the complication of fracture. Improving one's balance can significantly lower the risk of falling. Balance training incorporates the strengthening of various parts of the body (eg, trunk, legs), proprioception, and vestibular input. Several different exercises have been shown to be beneficial in patients with osteoporosis.^{[120, 121, 122, 123]}

Tai Chi Chuan and specific physical therapy programs have been shown to be particularly effective in improving balance and reducing falls. Wolf et al monitored 200 elderly community dwellers who received Tai Chi and computerized balance training. After a 15-week intervention, the authors documented decreased fear of falling responses. In addition, Tai Chi was shown to reduce the risk of multiple falls by 47.5%.^[124]

Campbell et al monitored 233 elderly community dwellers randomized to an individually tailored physical therapy program in the home compared with usual care and an equal number of social visits. The authors found that after one year, the mean rate of falls was lower in the exercise group than the control group (0.87 versus 1.34, respectively). In addition, after 6 months, subjects in the exercise group had improved balance.

Other types of exercise training programs may also positively impact balance and strength. Carter et al demonstrated that osteoporotic women aged 65-75 years who underwent a 10-week community-based physical activity intervention program improved their static balance, dynamic balance, and knee extension strength, although they did not benefit from a significant reduction in fall risk factors.^[125]

Training in the performance of activities of daily living (ADLs) and in the proper use of adaptive equipment are essential to the prevention of future falls.^[113] Home modification focuses on reducing the risk of falling by installing handrails and grab bars in hallways, stairs, and bathrooms. The use of a shower chair, tub bench, and adaptive bathing devices also can be beneficial. The application of nonskid tape to steps (indoors and outdoors), as well as the removal of throw rugs, greatly improves home safety.

Primary prevention of osteoporosis starts in childhood. Patients require adequate calcium intake, vitamin D intake, and weight-bearing exercise. Beyond this, prevention of osteoporosis has 2 components, behavior modification and pharmacologic interventions.

The National Osteoporosis Foundation (NOF) specified that the following behaviors should be modified to reduce the risk of developing osteoporosis: cigarette smoking; physical inactivity; and intake of alcohol, caffeine, sodium, animal protein, and calcium.^{[126, 127]} Patients should be counseled on smoking cessation and moderated alcohol intake. Patients who have disorders or who take medications that can cause or accelerate bone loss should receive calcium and vitamin D supplementation and, in some cases, pharmacologic treatment.^[128]

Pharmacologic prevention methods include calcium supplementation and administration of raloxifene or bisphosphonates (alendronate or risedronate). Raloxifene and bisphosphonates should be considered as first-line agents for the prevention of osteoporosis.^[129]

When alendronate or risedronate is used for prevention, the recommended dosage is the equivalent of 5 mg/d. In a study by Hosking et al, doses of 2.5 mg and 5 mg of alendronate were evaluated in postmenopausal women who did not have osteoporosis.^[130] They found that the women who received placebo lost BMD at all measured sites, whereas the women treated with 5 mg/d of alendronate had a mean increase in BMD of 3.5% ± 0.2% at the lumbar spine, 1.9% ± 0.1% at the hip, and 0.7% ± 0.1% for the total body.

In 2010, the American College of Rheumatology published revised recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis. Recommendations included the categorization of patients by fracture risk (using the FRAX score) and initiation of treatment in appropriate patients including alendronate, risedronate, zoledronic acid, and teriparatide (in those patients at highest risk).^[131]

Estrogen-progestin therapy is no longer considered a first-line approach for the treatment of osteoporosis in postmenopausal women, because it is associated with an increased risk for breast cancer, stroke, venous thromboembolism, and perhaps coronary disease. Estrogen is now only recommended if patients are also seeking relief of postmenopausal symptoms.

Regular monitoring may be helpful. Periodic bone densitometry helps in diagnosing osteoporosis in the early phase and aids in preventing fractures. According to the NOF, evaluating BMD on a periodic basis is the best way to monitor bone density and future fracture risk.^[64] Bone density checks are recommended every 2 years in postmenopausal women. Regular weight-bearing exercises and back extensor strengthening help to delay bone loss.

For a patient with osteoporosis in the diagnostic and therapeutic phases, the most important consultation is with a rheumatologist or an endocrinologist. These specialists are helpful in the diagnosis of osteoporosis; they can aid in the obtainment of the proper laboratory tests and imaging studies needed to rule out causes of secondary osteoporosis. In patients with uncontrolled pain that does not respond to conventional therapies, an invasive pain specialist may be consulted for proper interventional procedures.

A rheumatologist may also provide useful assistance with management and determination of underlying etiologies in complex cases.

Consultations can include discussions of nonmedical/nonpharmacologic management of osteoporosis.^{[132, 133]} Consult an orthopedist to assist with fracture management. Consultation with a spine surgeon is appropriate for patients with intractable, severe, function-limiting symptomatology that has not been relieved by noninterventional techniques. Consultation with a nonsurgical spine specialist is appropriate for a patient who is not a surgical candidate or whose symptoms persist despite surgical fixation.

Dual-energy x-ray absorptiometry (DEXA) should be repeated every 2-3 years if the baseline test results are normal. DEXA should be performed every 1-2 years in patients who are undergoing osteoporosis treatment.

The USPSTF 2011 recommendations, however, state that evidence is lacking about optimal intervals for repeated screening.^[65]

Orthotics are used to decrease the flexion forces to prevent the worsening of kyphosis and to reduce the pressure on the fracture site in the acute phase of disease.^{[134, 135]} Common orthotics used include the following:

• Thoracolumbosacral orthosis (TLSO)
• Cruciform anterior spinal hyperextension (CASH) brace
• Jewett brace