Orthoses for Osteoporosis

Key Points

Osteoporosis is a disease characterized by low bone mass and deterioration of the quality of bone tissue, which can lead to an increased risk for fractures.
Prevention of vertebral compression fractures (VCFs) is an important consideration in patients with osteoporosis.
The consequences of VCFs include acute or chronic back pain, functional limitations, respiratory symptoms, and mood impairment.
Comprehensive clinical care for patients with one or more VCFs includes treatment of acute or chronic pain, functional rehabilitation, and secondary prevention of VCFs, including treatment of osteoporosis.
Although orthoses are commonly used in clinical practice, there is very limited scientific support for their use in the treatment of VCFs.
Goals of treatment for VCFs include reducing pain, facilitating correct posture, immobilization for healing, and providing support for patients with significant muscle weakness.
A multidisciplinary team approach is necessary to treat patients with VCFs related to osteoporosis.

Osteoporotic vertebral compression fractures (VCFs) are a rising public health concern because of the associated morbidity and mortality and cost. As the population of older individuals continues to increase, so does the incidence of osteoporosis and, consequently, the incidence of VCFs. A variety of treatment options are available to address osteoporotic VCFs; orthoses are a common component.

Based on prevalence estimates by the National Health and Nutrition Examination Survey from 2005 to 2010 and 2010 population counts, an estimated 10.2 million older adults were affected by osteoporosis and 43.4 million had low bone mass in 2010. These numbers are only expected to continue rising. An estimated 1.5 million fragility fractures occur annually in the United States, including 700,000 spine, 300,000 hip, 250,000 wrist, and 250,000 other fractures related to osteoporosis. More than 260,000 patients with a first-time symptomatic VCF are diagnosed each year. Even more compelling is the economic cost associated with osteoporotic fractures. A 2011 study estimated that osteoporosis and its associated fractures cost $16 billion annually. This cost is expected to continue rising. There are more than 150,000 hospitalizations per year, with an 8-day average stay and $12,300 average charge. Upon discharge from acute care hospitalizations, 50% of patients with a VCF will require skilled nursing facility care.

As early as 1993, the American Academy of Orthopedic Surgeons (AAOS) has proposed that osteoporosis and bone health a national public health priority given the immense impact of osteoporosis on national health and, subsequently economic costs in a country where the older population is increasing. The AAOS urges emphasis on both primary and secondary prevention of osteoporosis, the leading cause of VCFs. Eighty percent of patients diagnosed with osteoporosis are women, though the incidence in men is likely underdiagnosed and underreported. Osteoporosis is also believed to be underdiagnosed in the African American population. Until screening and prevention techniques become more effective, treatment of osteoporosis-related VCFs will remain an important aspect of osteoporosis health care, including the use of orthoses, as further discussed in this chapter.

Pathophysiology of Osteoporosis

An understanding of the potential role of orthotic management of VCFs begins with an understanding of the underlying predisposing condition of osteoporosis. Osteoporosis is a disorder in which mineralized bone density is below normal, resulting in a bone structure that is vulnerable to fragility fractures, which often occur with minimal to no trauma. VCFs can occur during seemingly benign activities such as activities of daily living or even coughing or sneezing.

Osteoporosis is the most common of the metabolic bone diseases. This condition results from an imbalance in bone turnover such that the amount of new bone production cannot keep up with the amount of concurrent bone resorption; thus, bone resorption is greater than bone deposition. A decrease in bone mass typically begins in an individual's early thirties and continues throughout life. Osteoporosis is defined by the World Health Organization (WHO) as a bone mineral density (BMD) greater than 2.5 standard deviations below the young adult mean for normal BMD, using dual-energy x-ray absorptiometry (DXA). Osteopenia is defined as BMD between 1 and 2.5 standard deviations below the adult mean for normal BMD.

Risk factors for osteoporosis include poor nutrition (including vitamin D and calcium intake), sedentary lifestyle, smoking, excessive alcohol consumption, family history of fractures, loss of endogenous sex hormones, chronic glucocorticoid use, and low body mass index.

Osteoporosis can be categorized based on etiology (see Table 10.1 ). In 1948 Albright and Reifenstein suggested that primary osteoporosis stems from one of two causes: menopausal estrogen loss or aging. This initial description has since evolved into primary osteoporosis, categorized as type I or type II. Type I osteoporosis affects women and is associated with estrogen deficiency, occurring 5 to 10 years after menopause ( Table 10.1 ). Trabecular osteogenesis is primarily affected in type I, resulting in a diminished capacity to support compressive loads. Thus vertebral bodies, the distal radius, and the hip are common sites at increased risk for fracture. Type II osteoporosis affects both men and women and occurs secondary to aging-associated calcium deficiency. In type II osteoporosis, both trabecular and cortical bone are affected. Because cortical bone provides support, especially for bending and torsional loads, the femoral neck, proximal tibia, humerus, pelvis, and vertebral bodies are at higher risk for fracture. Children and young adults may also be affected with idiopathic juvenile osteoporosis or young adult osteoporosis, respectively, which tends to resolve spontaneously.

TABLE 10.1

Classification of Osteoporosis

From O'Young BJ, Young MA, Stiens SA, eds. Physical medicine and rehabilitation secrets . 2nd ed. Philadelphia: Hanley & Belfus; 2002.

Classification	Clinical Course	Remarks
Primary
*Involutional*
Type I (postmenopausal)	Affects women only, postmenopause, lasts 15–20 years	Predominantly trabecular bone loss in axial skeleton
Type II (age-associated)	Men or women >70 years	Proportional loss of trabecular and cortical bone
Idiopathic juvenile	Age 8–14 years, self-limited (2–4 years)	Normal growth; consider secondary forms
Idiopathic young adult	Mild to severe, self-limited (5–10 years)
Secondary (Type III)
Endocrine Gastrointestinal Bone marrow disorders Connective tissue disorders Malnutrition Lymphoproliferative diseases Medications Calcium poisoning Others	Dependent on underlying cause	Usually reversible to some extent after treatment of primary disease
Regional
Reflex sympathetic dystrophy	Three overlapping clinical stages: typical course lasts 6–9 months, followed by spontaneous or assisted resolution	Radiographic changes may be seen in the first 3–4 weeks as patchy demineralization of the affected area; triple-phase bone scan shows increased uptake in involved extremity before radiographic changes; brief tapering dose of corticosteroids often warranted
Transient regional osteoporosis	Localized, migratory, predominantly involves hip, usually self-limited (6–9 months)	Rare; diagnosis by clinical suspicion, radiograph, and bone scan; treatment similar to that for reflex sympathetic dystrophy

Secondary osteoporosis tends to be less common but can occur from numerous causes, as further described in Table 10.1 . Corticosteroids are a common cause of secondary osteoporosis. Other common medications associated with osteoporosis include thyroid hormone excess, loop diuretics, proton pump inhibitors, and selective serotonin reuptake inhibitors.

Osteoporosis can also be regional. Transient regional osteoporosis is a disease in which the affected individuals have migratory arthralgias in the weight-bearing joints of the lower extremities. Another disease involving regional osteoporosis is reflex sympathetic dystrophy, or type I complex regional pain syndrome, which consists of pain, swelling, and vasomotor dysfunction of an extremity without a clear etiology. This syndrome can be associated with severe osteoporosis.

Overview of Vertebral Compression Fractures

A VCF occurs when a vertebral body collapses, most commonly because of low bone density and often as a result of minimal or no trauma. VCFs can present with acute back pain; however, more than two thirds of VCFs are asymptomatic and found incidentally on imaging. Symptomatic acute VCFs most commonly occur from level T8–L4. In addition to acute-onset back pain, clinical signs of VCF include loss of height, spinal deformity (hyperkyphosis), protuberant abdomen, and diminished vital capacity. Many patients with acute pain go on to experience persistent chronic pain.

Radiographically, VCFs are diagnosed via lateral spine imaging that reveals a loss of vertebral body height of at least 20% or a 4-mm reduction from baseline height. A large percentage of cases go undiagnosed, and nearly half of those who are diagnosed will require more than one physician visit before successful diagnosis.

VCFs can lead to progressive sagittal deformity, or hyperkyphosis, and the subsequent changes in spinal biomechanics increase the risk of further fractures in the vertebrae above or below the fracture site. Severe hyperkyphotic deformity involving wedging of one or more adjacent vertebrae is referred to as a dowager's hump or gibbous deformity. Hyperkyphosis can lead to ligamentous stretching, diminished functional vital capacity, inferior costal margin and pelvic rim contact and discomfort, chronic low back pain, abdominal crowding, muscle imbalance, pain, pseudarthrosis, and depression. In these patients, lung function is significantly reduced. The presence of one thoracic VCF causes 9% loss of vital capacity. The degree of kyphosis in individuals has been found to correlate with physical function and mobility (independent of pain), pulmonary function, mental well-being, and risk of new fractures. In the case of muscle imbalance, the kyphotic deformity progressively elongates the paraspinal muscle extensors and leads to overall muscle weakness. Involutional muscle loss, also known as sarcopenia, is common in the elderly and can be an important factor contributing to muscle weakness. The severity of a VCF and its associated pain can lead to diminished function, decreased mobility, physical deconditioning, and, consequently, accelerated bone loss. Patients with a VCF have a 23% to 34% increased mortality rate compared to patients without a VCF. The most common cause of death is pulmonary disease, including chronic obstructive pulmonary disease (COPD) and pneumonia (hazard ratio 2.1).

Prevention of Vertebral Compression Fractures

Osteoporosis often goes undiagnosed until after the first symptomatic fragility fracture occurs, at which point an osteoporotic condition is considered to be severe. Women who have been diagnosed with one VCF are at fivefold higher risk of developing an additional VCF. With the acute fracture, attention is often focused on relieving pain and returning the patient to the usual activities of daily living.

Given that preventing a fracture is preferable to treating one, screening for osteoporosis in the at-risk population is an important consideration. As a result, prevention programs, which include regular screening for osteoporosis, are emphasized. Although opinions vary on the value of screening for osteoporosis based on BMD measurements alone, there is general agreement that groups that should be screened using DXA include women older than 65 years and younger women with major risk factors. Other groups that may benefit from osteoporosis screening include those with a history of fragility fractures and/or chronic corticosteroid treatment, those with diseases associated with bone loss and/or fractures, men with hypogonadism, and men older than 70 years. Other methods for evaluating BMD exist; however, DXA is considered the most accurate method for BMD measurement, and current screening guidelines are based on DXA as the method of choice. DXA is also notable in that it can detect changes in BMD in a period of time as short as 6 to 12 months, which is useful when assessing response to osteoporosis treatment. Prevention also includes counseling the patient regarding modifiable risk factors for osteoporosis and appropriate adjustments such as participation in regular exercise, increased calcium intake, smoking cessation, and decreased alcohol consumption.

The WHO has come up with a fracture risk algorithm (FRAX), which uses clinical risk factors and BMD to determine an individual's 10-year estimated hip fracture probability and major osteoporotic fracture probability. An important limitation of FRAX is that it may only be used in an individual who has not been treated for osteoporosis previously.

Primary prevention of osteoporosis is the obvious goal; however, the AAOS emphasized in its position statement, most recently updated in December 2014, on “Osteoporosis/Bone Health in Adults as a National Public Health Priority” that secondary prevention of fractures is also crucial, particularly given the rising population of older individuals.

Treatment of Vertebral Compression Fractures

Treatment of osteoporosis is divided into pharmacologic, nonpharmacologic, and surgical options. Comprehensive clinical care for patients with one or more VCFs includes (1) treatment of acute or chronic pain; (2) functional rehabilitation; and (3) secondary prevention of VCFs, including treatment of osteoporosis. Identifying the goals of therapy is key when initiating treatment in patients with osteoporotic VCFs, because the treatment methods and timelines are different. The following sections discuss the current treatment methods available for VCFs. Later in the chapter, the goals of treatment with orthoses, specifically, are addressed.

Pharmacologic Treatments

Pharmacologic therapy is a cornerstone of osteoporosis treatment. Medications are used to address multiple treatment goals, including the management of pain and treatment of osteoporosis by slowing or reversing progression of osteoporotic disease that underlies fragility fractures. There are a number of classes of medications that are used to slow or reverse progression of osteoporotic disease. Bisphosphonates are considered first- (and second-) line treatment for osteoporosis, per American Association of Clinical Endocrinologists recommendations. Bisphosphonates work to decrease bone resorption. There is also evidence that bisphosphonates may decrease bone pain, but concern exists for bisphosphonates inducing deregulation of bone remodeling that could potentially affect the healing of acute fractures. Thus treatment with bisphosphonates in the acute phase of fracture healing is questionable. Though uncommon, select bisphosphonates have been associated with atypical femoral shaft fractures.

Intermittent parathyroid hormone (PTH) replacement with recombinant PTH may be used to activate osteoblasts more than osteoclasts to stimulate bone remodeling and, thus, increase BMD. Because of the high cost and long-term toxicity, recombinant PTH is only used in individuals with very high fracture risk who have failed bisphosphonate therapy.

Hormone replacement therapy (HRT) with estrogen with or without progestin can be used to counteract the postmenopausal increased rate of bone loss in women; unfortunately, discontinuation of HRT is associated with a decrease in BMD and eventual loss of the fracture prevention benefit. HRT is also associated with increased risk for endometrial and breast cancer and cardiovascular events, risks that tend to outweigh the benefits of HRT.

Calcitonin can be used to reduce osteoclastic bone resorption, reducing bone turnover and increasing lumbar spine BMD while also improving fracture pain. The 2010 AAOS guidelines recommend treatment with 4 weeks of calcitonin after acute compression fracture.

The monoclonal antibody receptor activator of nuclear factor kappa-B ligand (RANKL) inhibitors are used to reduce osteoclastogenesis, subsequently decreasing bone turnover and increasing BMD. RANKL inhibitors have also been associated with atypical femoral shaft fractures.

Selective estrogen receptor modulators (SERMs) affect estrogen receptors to improve BMD; SERMs can be associated with an increased risk of venous thromboembolism and stroke. Notably, many of the mentioned medications can have serious side effects, a few of which were discussed previously. All of these medications should be used cautiously with appropriate medical monitoring.

Notably, pharmacologic therapy for the treatment of osteoporosis should not be indefinite. The individual's osteoporosis risk profile and changes in bone density should be assessed serially, 1 to 2 years after initiating therapy and every 2 years thereafter to determine whether therapy should be continued, given the side effects and risks that these medications carry.

Regarding supplementation with vitamin D and calcium, the Institute of Medicine recommends adequate intake and provides parameters consisting of 1000 to 1200 mg daily of calcium and 600 to 800 international units daily of vitamin D based on gender and age group.

Options for pain management include nonsteroidal antiinflammatory drugs (NSAIDs), acetaminophen, opioids, lidocaine patches, muscle relaxants, calcitonin, tricyclic antidepressants (TCAs), and membrane-stabilizing agents such as gabapentin. Ringe and Body suggested treatment of fracture pain based on the WHO three-step analgesic ladder, which includes acetaminophen and NSAIDs as the first tier of treatment, with weak opiates following in the secondary tier, and stronger opiates in the final tier. Adjuvant agents such as TCAs and membrane-stabilizing agents have also shown benefit when used concurrently with the three-step ladder. Of note, there is evidence that NSAIDs may inhibit healing of fractures, though this evidence is primarily based on rodent studies. Further studies are needed to elucidate the risks and benefits of the use of NSAIDs for fracture pain.

NSAID side effects primarily consist of gastrointestinal bleeding and cardiovascular events. Possible side effects of opioids that may compromise rehabilitation include drowsiness and dizziness. Pain medications should be tapered as soon as possible as pain improves. It is also possible that complete elimination of pain may allow individuals to overload and overuse their fracture site because of the lack of pain inhibition. This could potentially inhibit bone repair. Direct effects of opiates on bone repair have not been thoroughly investigated at this time.

Improving pharmacologic treatments of osteoporosis is a topic of ongoing research. Variability in the response to pharmacotherapy makes the prediction of success or failure difficult in an individual. Moreover, the outcome of pharmacologic treatment may not be known for years. The emerging field of pharmacogenomics of osteoporosis aims to use genetic information to predict the outcomes of pharmacologic treatments and could lead to new drug therapies for osteoporosis.

Nonpharmacologic Treatments

The primary types of conservative nonpharmacologic treatments of osteoporosis include appropriate activity limitations combined with therapeutic exercise, physical bracing with orthoses (as discussed in the next section), gait training and fall prevention, and optimization of nutrition and lifestyle. Additional pain management options may also include passive physical therapy modalities, facet joint injections, and nerve root blocks or epidural steroid injections. One study showed that postural taping resulted in immediate improvements in thoracic kyphosis. Improving muscle strength, especially in the lower extremities, can reduce the risk of falls. Wearing spinal orthoses has been found to improve gait stability in women both with and without osteoporotic VCFs. Bed rest may be used when pain is intractable but should be avoided otherwise given the numerous costs of immobility, including decreased bone mass and muscle strength as well as the risk of pressure sores and deep venous thrombosis. Conservative care has been shown to provide sufficient pain reduction in 50% of patients by 3 months post-fracture. Postural taping can provide immediate improvements in thoracic kyphosis.28 Improving muscle strength, especially in the lower extremities can reduce the risk of falls.

Spinal extension inducing “postural reduction” of VCFs has also been demonstrated, revealing the dynamic mobility of VCFs. In a prospective study of 41 consecutive patients with 65 VCFs who underwent vertebroplasty, McKiernan et al. achieved improvement of kyphotic deformity in 23 fractures using spinal extension. In a prospective clinical study, Kim et al. described the ability of postural reduction to achieve significant correction of anterior vertebral body height and vertebral kyphotic deformity in 90% of patients with acute VCFs of onset less than 8 weeks.

A cadaveric study showed that spinal extension was effective in recovering anterior height loss. However, of note, the middle height of the fractured vertebra was better restored by balloon inflation, as in kyphoplasty (as discussed in the Surgical Treatments section). The combination of balloon inflation and spinal extension resulted in improved correction of both the vertebral and segmental kyphotic deformities, better than that achieved with individual modalities alone.

The above studies suggest that orthoses may have a role in postural reduction of VCF deformity given potential improvements seen with spinal extension. Orthotic management of osteoporotic VCFs is often used as part of nonpharmacologic treatment in the first 6 to 8 weeks after VCF and is further discussed in the next section.

Surgical Treatments

If VCFs are severe or conservative therapy fails, surgical options are the next line of treatment. As a consequence of diminished bone strength, many patients with acute VCFs from osteoporosis are not candidates for spinal fusion, though this may be a last resort option for some persistently symptomatic VCFs that fail to heal. Thus, less invasive procedures such as vertebroplasty and kyphoplasty are more appropriate.

Treatment augmentation of VCFs with bone cement has emerged as a minimally invasive surgical treatment for patients who have not responded to conservative therapies. There are two distinct procedures: vertebroplasty, in which bone cement is percutaneously injected into the fractured vertebral body to stabilize it but does not correct the deformity, and kyphoplasty, in which bone cement is injected after percutaneous reduction of the vertebral body deformity using inflatable balloons. Kyphoplasty requires greater surgical expertise and is more expensive. The goals of cement augmentation are to reduce pain and to restore the normal weight-bearing function of the spine so that the risk of future fractures is reduced. One of the primary complications associated with these procedures is cement leakage.

Vertebroplasty can result in pain reduction, but it does not correct spinal alignment. The excessive kyphosis that can result from a VCF leads to increased forward bending moments, which can lead to paraspinal muscle fatigue and increased strain at the facet capsules, contributing to chronic pain. Some patients attempt to improve standing posture by flexing their knees to counterbalance the increased forward bending moments. This can lead to muscle contractures, impaired gait velocity and balance, and increased risk of falls. In contrast, kyphoplasty can reduce the vertebral deformity and restore normal spinal alignment.

Development of adjacent VCFs is a concern for patients who already have at least one VCF. A well-recognized risk factor for adjacent VCF is kyphotic deformity about the fractured vertebrae ; this vertebral deformity is caused by a loss of anterior height and regional kyphotic deformity that contributes to increased forward bending moments. With kyphoplasty, the reported percentage of vertebral kyphosis reduction ranges from 39% to 65%, and the restoration of vertebral body height ranges from 35% to 68%.

Cement augmentation can relieve pain more quickly and stabilize VCFs, but the long-term benefits in preventing additional fractures are not well understood. The percentage of compression of the vertebral body can help in the decision regarding vertebroplasty versus kyphoplasty, given that kyphoplasty can assist with vertebral height and segmental kyphosis correction. One study showed greater improvements in quality of life and pain at 1 month after kyphoplasty or vertebroplasty for a VCF compared with conservative treatment; at 12 months, however, quality of life and pain were similar. On the other hand, a meta-analysis conducted in 2013 of multiple randomized controlled trials showed improvements in pain, function, and quality of life at both 3 months and 12 months in those who underwent cement augmentation compared with conservative treatment. Based on current scientific evidence, most patients should not undergo cement augmentation. The 2010 AAOS guidelines strongly recommend against vertebroplasty in patients without neurologic deficits; the AAOS also reports limited evidence for kyphoplasty in such patients.

Orthoses for Treatment of Vertebral Compression Fractures

Orthoses are generally low-risk and cost-effective methods for the treatment of VCFs. Goals of treatment with orthoses include (1) reducing pain, (2) facilitating correct posture and immobilization for healing, and (3) providing support in patients with significant muscular weakness. The AAOS reports that the evidence regarding benefits of bracing for VCFs is inconclusive and recommends neither for nor against their therapeutic use. Few studies have investigated the efficacy of specific orthotic interventions in spinal osteoporosis. One small study investigating thoracolumbar bracing revealed improvements in posture, strength, and quality of life. Wearing spinal orthoses has been found to improve gait stability in women both with and without osteoporotic VCFs.

Given the limited evidence for use of orthoses in management of VCFs, it is essential that a carefully designed physical therapy routine be included when utilizing orthoses for treatment. The primary risks associated with use of orthoses are risk for pressure sores and decreased pulmonary capacity. These orthoses can potentially be restrictive about the chest wall; thus, patients are more susceptible to atelectasis and related pulmonary complications if not actively prevented with tools such as incentive spirometry. Orthoses can also generally be uncomfortable, leading to patient noncompliance. And notably, orthoses are rarely indicated for treatment of chronic pain.

There is limited research evidence examining the relationship between orthotic interventions for osteoporotic VCFs and negative effects on the spine such as development of additional VCFs or worsening of pathologic curvatures of the spinal column. Moreover, even fewer studies support the efficacy of available orthoses. The use of some conventional orthoses, such as the total-contact polymer thoracolumbosacral orthosis (TLSO) seen in Fig. 10.1 , often can be ruled out because of the large spinal deformities that may be present, uncomfortable fit over bony prominences, or restriction of pulmonary capacity. Orthotic management that may be considered for use with VCFs includes posture-training support (PTS), lumbosacral or dorsolumbosacral corset, three-point hyperextension orthoses, Spinomed (TLSO–sagittal plane control), and the posterior-shell TLSO.

Figure 10.1, Total-contact polymer thoracolumbosacral orthosis (TLSO).

Posture-Training Support

The PTS is one of only two spinal orthoses for osteoporosis that have any scientific study supporting or refuting their efficacy. The PTS or “weighted kypho-orthosis” provides a weight suspended just inferior to the scapulae ( Fig. 10.2 ). The weight can be increased to as much as 2.5 lb in several increments. Patients are encouraged to try different levels of weight to determine which is most effective. Too much weight will not benefit the patient, and compliance will suffer.

The PTS is indicated in cases of excess dorsal kyphosis possibly involving iliocostal contact or iliocostal friction syndrome. Two mechanisms of action are hypothesized. First, anterior compression forces on the spine are reduced by the countermoment produced by the posterior weight. Second, the device encourages active back extension through proprioceptive input and helps increase back extensor strength. The PTS is designed to aid physical therapy and increase the strength of the paraspinal muscles.

The PTS appears to be the least invasive orthotic recommendation and is more cosmetically acceptable, resulting in a high level of patient compliance. Because of its unobtrusive nature, the PTS does not appear to have any serious disadvantages. However, the challenge is determining which candidates are suitable for this orthotic recommendation. Also, a patient's desire for a less-invasive orthotic intervention should not result in substituting this orthosis for one that is more appropriate given the patient's clinical presentation.

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