Feature Article
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Innovative Treatment of Osteoporosis Pathophysiologic Basis for the Treatment of Osteoporosis
"The efficacy of current agents has greatly ameliorated the severity of osteoporosis and, to a certain extent, can prevent it," began Stanley Wallach, MD, Clinical Professor of Medicine at New York University School of Medicine and Codirector of the Osteoporosis Center at the Hospital for Joint Diseases in New York. Dr. Wallach reiterated the accepted definition of osteoporosis as "a systemic skeletal disease characterized by low bone mass and, most importantly, microarchitectural distortion, such that the sum of the two leads to bone fragility and fractures." Although fractures are a complication of osteoporosis, he pointed out that they are also an important end point for assessing the efficacy of treatment.
Bones affected by osteoporosis lose mass and architecture, and as a result they fracture. "The significant change is from normal trabecular bone, with its lacy latticework and interconnections, to bone that is less dense and lacks the connectivity between the trabeculae that provide much of the bone's strength," he said. The bones that fracture in osteoporosis depend predominantly on trabecular bone for structural support.
"With increasing age and increasing entry of patients into long-term care, the incidences of fracture of the vertebral column and of the hips (upper femurs) are the ones to watch in terms of fracture and/or the complications of osteoporosis," he stated. Fracture leads to considerable morbidity and a significant degree of mortality, depending on the patient, and depending on the site of fracture.
Dr. Wallach emphasized that severe osteoporosis results in several types of disability, including a reduction in volume of the chest and abdominal cavities, as well as kyphosis, height loss, and acute and chronic back pain. These less appreciated disabilities "lead to difficulties with gastrointestinal and respiratory activity. There is also loss of self-esteem, depression, a negative impact on activities of daily living, and an increase in overall mortality."
Although the actual amount of mortality is controversial, cumulative five-year excess mortality is 5% to 15% for vertebral fractures. In contrast, within six months after a hip fracture there is a 20% excess mortality resulting from complications. Dr. Wallach also stated that 20% to 30% of individuals with hip fractures end up in long-term care facilities. "They never get to go home again, and those who do, go home with a long-term disability," he stated.
Osteoporosis is an immense problem. "We estimate that one in three women older than age 50 actually have osteoporosis as defined by low bone mass and microarchitectural disruption and will ultimately go on to fracture. One in six will have a hip fracture." It is estimated that the annual cost of health care for osteoporotic fractures currently exceeds $14 billion and may increase fourfold over the next 50 years if no preemptive action is taken.
Because patients' viability and longevity are maintained in the long-term care setting, these patients will live longer and, therefore, fracture more. Dr. Wallach predicted: "Over the next 50 years, this problem could quadruple. We need to exercise damage control now by breaking the chain of low bone mass leading to fragility and then to fracture."
Remodeling
"To understand osoteoporosis, we need to examine the physiology of the skeleton and what happens with age to skeletal homeostasis," he stated. The skeleton comprises 8% of body weight and is a complex tissue consisting of organic material, a matrix predominantly of type I collagen combined with several noncollagenous proteins, and a much larger inorganic fraction. "Bone turns over at an average rate of 8% per year in young adults. But on average, about 25% of trabecular bone is removed each year by bone resorption and is replaced by new bone formation. We call this remodeling," explained Dr. Wallach.
Bone is a biomechanical material that undergoes stress, strain, and microfracture with continued use and, therefore, needs constant replacement. The replacement phase is initiated by the osteoclast system, which arises from hemopoietic stem cells of the macrophage-monocyte series and resorbs the area at hand via acid secretion of the defunct area of bone, producing a pit. Once this pit is created, the osteoclasts recede and are replaced with osteoblasts which form a collagen matrix that is then mineralized, enabling the area to be replaced by normal new bone. "It is a process of continuous remodeling and replacement," he stated.
Dr. Wallach noted that if the processes of remodeling and replacement occurred in a balanced manner throughout life, there would be no disease such as osteoporosis. However, "the problem is that as people enter the second half-century of life, the process loses its quantitative coupling, and total bone mass slowly declines because each time an area of defunct bone is resorbed, a little less bone is made to replace it. Bone loss under normal aging conditions usually does not exceed 20% and does not predispose to fragility fractures. In women there is an additional rapid loss of bone after menopause, so that they can end up with 70% of baseline bone mass, which constitutes only a small risk of fracture. "Unfortunately, in many individuals bone mass drops more rapidly, to levels of 60% or less, and these individuals are very susceptible to overt fractures, predominantly of the spine, wrist, and upper femur," he reported.
Risk Factors
"Why are some people selected out of the population for this negative event? Much depends on the bone mass you start with," Dr. Wallach explained. "Peak bone mass at maturity is a factor that we have overlooked until now because the baseline at which you start the bone loss process determines where you end up.
We've got to do a better job preventing this disease by working with the younger segment of the population," he advised.
Risk factors can affect peak bone mass, postmenopausal bone loss, and age-related bone loss and include several multifactorial components. "Some of these risk factors are controllable and some are not. You can't control your gender, ethnic group, or the genes in your family that may predispose to developing a light skeleton. These are fixed genetically based risk factors," Dr. Wallach explained.
Risk factors that can be controlled, however, include inadequate calcium and vitamin D intakes. "Both nutrients are critical to preventing the disease and also to ameliorating it once it happens," he stated. Other controllable risk factors include excessive smoking, caffeine, and alcohol intake. Strenuous athletic activity or a lack of physical activity are also predisposing factors.
"There are medical conditions that we should be aware of as physicians that also affect bone density," he advised. Early menopause should be controlled by either hormone replacement treatment or some other modality; gonadal hormone deficiency states should be treated; and patients with eating disorders and chronic liver and kidney disease need astute management. In addition, malabsorption is a commonly misdiagnosed or underdiagnosed problem that leads to calcium and vitamin D deficiencies and osteoporosis.
"There are also things we do as physicians that predispose to bone loss: excessive corticosteroid treatment, thyroid hormone replacement beyond the hypothyroid patient's need, chronic heparin therapy, radiotherapy to the skeleton, and long-term use of anticonvulsants," he recited. With all of these predisposing factors, there eventually emerges a clinical picture of osteoporosis in which there are chronic and recurrent backaches, episodes of severe back pain, and disability as new vertebral compression fractures occur, as well as progressive kyphosis (sometimes scoliosis), shortened stature, and peripheral fractures, predominantly of the hip, but also of the ribs, the pelvis, the upper humerus, and especially the wrist."
Diagnosis
A full medical history and physical examination are critical to proper diagnosis and therapy. There are usually few biomechanical indices, and if they are present, physicians should think of other causes of bone loss or of secondary types of osteoporosis. Regarding x-rays, physicians should be aware of the following x-ray changes prior to fracture:
* Increased width of the intervertebral spaces on lateral spine films
* Schmorl's nodes (localized indentations along the cortical plates)
* Relative accentuation of the upper and lower cortical plates of the vertebrae
* Visible vertical striations of the vertebral bodies
"Also, it isn't hard to detect osteoporosis with kyphosis by a good examination of the back," attested Dr. Wallach. However, the best quantification of bone loss in use today is the Dual Energy X-ray Absorptiometry Method (DXA), which measures spinal mass using a dual, filtered x-ray source. The output is displayed on a dedicated computer screen and then quantified to provide exact measurements. These are compared to normative data and a "T" score calculated. A T score is the difference in standard deviations between the patient's spine or hip bone density and the mean normal value for young adults. "If you're no more than one standard deviation below that young, normal value that's built into the computer, you're also normal. If you're down by two and a half standard deviations, you're osteoporotic by definition, and if you're below two and a half and have a fracture, we add the word severe," he summarized.
"Don't wait for fractures to occur," warned Dr. Wallach. "Between a T score of minus one and minus two and a half (standard deviations) there is a range we call osteopenia, which is an ideal time to prevent further loss of bone. Prevent complications with early treatment. Don't wait for a T score of two and a half to develop."
According to Dr. Wallach, an additional assessment of severity of osteoporosis is with the use of urinary markers for bone resorption. "These markers are known as the C- or N-telopeptide cross-links of bone collagen or the deoxypyridinoline component of the cross-link. The cross-link is a side chain that connects the terminal ends of two collagen molecules to the middle of a third to make a collagen fibril. When bone is resorbed, this material is released into the circulation and excreted so that its level in blood or urine is a marker of the degree of bone resorption. We can also use high normal and distinctly high resorption rates as a baseline to follow the course of treatment," he explained.
Prevention and Treatment
Dr. Wallach emphasized the need to (1) improve nutrition, increase physical activity, adjust life style, minimize medical and iatrogenic factors, and address other modifiable risk factors in all patients to identify women at greatest risk as soon after menopause as possible, (2) consider hormone replacement treatment in postmenopausal women, (3) identify other patients at risk, and (4) initiate full treatment programs when indicated.
Because the ideal osteoporotic diet involves large intakes of calcium and vitamin D, and dietary intake in most individuals may not be adequate, supplements are often used. "If you look at the long-term care population, postmenopausal women and men above age 65, the required calcium intake is 1500 mg per day. Very few people are getting this. A glass of milk contains 300 mg of calcium, and at least four glasses of milk or the equivalent in other dairy and calcium-rich foods would be needed. Since there are few significant dietary sources of calcium except dairy products, we must be more imaginative in our nutritional counseling," emphasized Dr. Wallach.
Vitamin D deficiency is another concern in this population. Fortified milk is the only significant source of vitamin D in the diet. "Because many long-term care patients do not get much sunlight or milk, especially if they are lactose-intolerant, vitamin D reserves tend to be low. Also, old people, as a group, don't convert precursors to vitamin D in their skin efficiently, regardless of their sun exposure. Finally, there are several other age-related defects in the vitamin D cascade, and supplements are usually needed to get the recommended 600-900 units into the long-term care population."
Preventive approaches to osteoporosis should be initiated at an early age. There is an increasing segment of the population who reach the long-term care age range with inadequate skeletal mass and therefore are potential or established osteoporotics. As long as reasonable longevity is expected in such candidates, prevention and treatment modalities must be intensified, including decreasing the risk of falls. "Fortunately, the aged skeleton responds to preventive and therapeutic agents as well as that of younger people. Therefore, we must seek improved economic, social, and survival outcomes in the long-term care population," concluded Dr. Wallach.
Pharmacotherapeutic Strategies for Treating Osteoporosis Under PPS
"The management of osteoporosis addresses the prevention of falls and fractures with prudent medication management and an understanding of underlying risk fac tors," began Manju T. Beier, PharmD, FASCP, President, Geriatric Consultant Resources LLC, and Clinical Assistant Professor of Pharmacy, University of Michigan, Ann Arbor. Understanding medication-related secondary causes of osteoporosis during drug regimen reviews is essential to minimize the effect of drugs that cause bone loss, decrease blood pressure, impair cognition, and increase the risk of falls. "Although no medications are currently available that stimulate bone formation, there are several antiresorptive agents that retard the resorption of the bone and the bone remodeling cycle," stated Dr. Beier.
Prospective Payment System
The Prospective Payment System (PPS) is compelling nursing home administrators, medical directors, pharmacists, and other health care professionals to carefully scrutinize management approaches to chronic conditions affecting the frail elderly. "How will the management of osteoporosis be impacted by the PPS? When does the role of the skilled nursing facility end in terms of Medicare beneficiaries within the Prospective Payment System?" she asked. Dr. Beier stated that the skilled nursing facility's role possibly ends when a beneficiary is away from the facility for more than 24 consecutive hours on an outpatient basis.
"I think this is a very important point in terms of trying to manage osteoporosis appropriately. We can minimize the need for an ambulance, decrease paramedic expenses, and reduce hospitalization of a nursing home resident for a suspected hip fracture by effective osteoporosis management," she explained. Section U of the Minimum Data Set will be implemented in October 1999 and will track medication use. "By tracking these data, we're hoping that we can get some quality indicators: Are there any negative outcomes related to selection of medications? What kinds of drugs have been used? Has there been a compromise in the quality of care and the choice of drugs?"
The medication assessment on admission to the facility is designed to decrease drug-related morbidity and mortality from fractures and to increase the quality of life. "When the patient is admitted to the facility, it is important to have a fact sheet to assess what this patient is already on. In conjunction with a diagnosis, perhaps we can prevent drug interactions. We also need to encourage documentation of osteoporosis based on clinical cues, such as height loss, kyphosis, and changes on spinal x-rays, and to ensure optimal calcium and vitamin D intake. Other measurable outcomes are assessment of appropriateness of antiresorptive therapy and collaboration with the rest of the team to assess the risk of falls and to implement fall-reduction programs," she counseled.
Available Agents
Medications for the prevention and treatment of osteoporosis can be grouped into two categories: agents that decrease bone resorption and those that promote bone formation. Antiresorptive drugs balance bone resorption with bone formation, thereby reducing the overall rate of bone turnover. "These agents have the greatest effect on trabecular bone during the early postmenopausal period when bone turnover is increased," stated Dr. Beier. Treatment with antiresorptive medications results in either no change in bone mass or a minimal increase. Therefore, patients with low bone density may continue to have fractures, although less frequently, while on antiresorptive agents.
The following agents are currently FDA-approved for the prevention of osteoporosis: estrogen replacement therapy (ERT), alendronate, and raloxifene (a selective estrogen receptor modulator). Available treatment agents include ERT, alendronate, and calcitonin-salmon.
Dr. Beier also supported the use of calcium and vitamin D: "We need to keep in mind appropriate calcium and vitamin D dosages. There are studies that have shown that plain old calcium and vitamin D can reduce the risk of fractures in elderly patients," she advised.
In 1996, guidelines for osteoporosis were published by the American Association of Clinical Endocrinologists (AACE).1 In 1996, the National Osteoporosis Foundation (NOF) issued a consensus development statement, and in November 1998 the NOF issued guidelines for defining osteoporosis in terms of awareness and treatment. "One thing to remember about guidelines," she mentioned: "They're very time-sensitive documents. Indications are changing, and new trials are coming through. We have to keep up with the data to be as current as possible." Ultimately, she recommended that practitioners use their informed judgment to select the appropriate therapy.
Estrogen
Consensus panels and strong epidemiologic data have defined estrogen as the best measure for preventing and treating osteoporosis. "Estrogen has been categorically defined as the gold standard for prevention and treatment of osteoporosis in postmenopausal women," stated Dr. Beier. By conserving bone mass, estrogen therapy reduces the risk of osteoporosis-related fractures and results in an approximately 40% to 75% reduction of vertebral fractures and a 25% decrease in nonvertebral fractures with five years of use. "If a woman selects estrogen replacement therapy and has an intact uterus, she needs to be on a progestational agent to decrease the risk of endometrial hyperplasia."
Women who do not receive ERT rapidly lose bone mass in the immediate postmenopausal period, approximately five to seven years after menopause. After this intermediate period, bone loss becomes age-dependent. "Bone loss will be reduced in women who receive ERT at age 50. Women who start ERT around age 65 and continue will increase and maintain their bone mineral density within 10 years," stated Dr. Beier. She then mentioned that the percentage difference in bone mineral density between those who start ERT early (right after menopause) and those who start late (around age 65) is not dramatic. "This tells us that it's never too late to start ERT," she asserted. This assertion, however, may not be strong in terms of preferences, contraindications, and a series of benefits and drawbacks for ERT in the long-term care population.
Risk Factors. The development of breast cancer is the most predominant risk factor associated with ERT. Risk increases with duration of ERT use. "If you want to maintain bone mineral density, you need to be on ERT. As soon as you stop ERT, however, your bone mineral density starts to decline. With this argument in mind, if you want to maintain bone mass, and if you start at the age of 50, you may be on ERT for 35 years. You can start later on in life (around age 65) and perhaps minimize the number of years you're on ERT and perhaps minimize the breast cancer risk as well," Dr. Beier advised.
Unopposed ERT substantially increases the risk of endometrial cancer in women with an intact uterus. Risk increases with elevated dose and longer duration.
Benefits. ERT reduces fracture risk. In the controversial Heart and Estrogen/progestin Replacement Study (HERS), women with cardiovascular disease were prospectively examined. In over four years of follow-up in this particular HERS study, there was no conferred secondary cardiovascular benefit. However, there are epidemiologic data for primary cardiovascular protection from ERT.
ERT has also been studied for improvements of vasomotor and genitourinary tract symptoms, as well as possible cognitive effects. "Studies are currently underway of ERT's neuroprotective benefits in delaying dementia caused by Alzheimer's disease," reported Dr. Beier.
Calcitonin-Salmon
Calcitonin-salmon is a polypeptide hormone secreted by the parafollicular cells of the thyroid gland that inhibits osteoclast-mediated bone resorption. Calcitonin-salmon has been approved by the FDA for the treatment of osteoporosis. "Calcitonin is an antiresorptive drug that inhibits osteoclast-mediated bone resorption, acts to decrease high serum concentrations of calcium, and opposes the action of the parathyroid hormone in the body," explained Dr. Beier.
The 5-year PROOF (Prevent Recurrence of Osteoporotic Fractures) study with calcitonin-salmon examined the effects of calcitonin on osteoporotic fractures. "More than 1000 postmenopausal women with established osteoporosis were recruited at many sites in the United States and the United Kingdom," Dr. Beier explained. "These women had existing osteoporosis with a particular definition in mind: one to five vertebral compression fractures and an average age of 68. They were randomized to one of these four groups: placebo, 100 international units (IU), 200 IU, or 400 IU of a nasal calcitonin spray daily. All patients also received supplements of 1000 mg of elemental calcium and 400 IU of vitamin D," she reported.
Dr. Beier noted that across the board supplementation with calcium and vitamin D is significant because then one can determine calcitonin's effect on bone mass density and fracture risk over and above the effect of calcium and vitamin D. "At four years the results show a 36% reduction in new vertebral fractures with 200 IU of salmon calcitonin a day, which is the recommended dose for the treatment of osteoporosis." In addition, treatment with nasal calcitonin in the PROOF study resulted in a 50% nonsignificant reduction in the risk of hip fractures. Dosage of nasal calcitonin is 200 IU daily, or one spray once daily in alternate nostrils to prevent nasal-mucosal irritation. Calcitonin may be given regardless of meals or other medications and does not seem to have any drug–drug interactions.
Calcitonin has also been examined in terms of its analgesic properties. "In the 1970s, animal studies explored calcitonin's analgesic effect, and since then some studies have been published on the parenteral and intranasal formulations of calcitonin that have demonstrated efficacy in osteoporotic patients with chronic pain after vertebral fractures." The AACE guidelines state that calcitonin may be useful in the immediate postfracture period because of its analgesic effects. Although calcitonin decreases the risk of vertebral fractures, includes an analgesic component, and has a good safety record, the spray may cause nasal irritation. In addition, there are currently no prospective data on its reduction of hip fractures.
Bisphosphonates
Bisphosphonates are synthetic compounds that are adsorbed to the bone's surface and then directly inhibit the action of osteoclasts, thereby inhibiting bone resorption. The bisphosphonates are then covered with new bone during the formation phase of the remodeling cycle. Alendronate is the only particular bisphosphonate that has been approved for the prevention and treatment of osteoporosis.
A large prospective study called the Fracture Intervention Trial (FIT)2 included more than 2000 women initially receiving 5 mg of alendronate and then switched to 10 mg over four years. Vertebral fractures at the end of four years decreased by 47%, wrist fractures decreased by 48%, and hip fractures decreased by 51%. "It's certainly a very efficacious drug in terms of treatment," she attested.
Dr. Beier mentioned another source that assessed the FIT data from an age standpoint, stating that alendronate is effective in women with advanced age and also with severe osteoporosis. There was a 50% reduction in fracture rate at the vertebral site, the hip site, and the wrist site. In addition, the EPIC study compared the effects of 2.5 mg or 5 mg per day of alendronate versus estrogen for the prevention of bone loss in postmenopausal women under 60 years of age. "This is a prevention study. These are not women with established osteoporosis. This is one of the studies that led to an indication of 5 mg of alendronate per day for prevention of osteoporosis," Dr. Beier explained.
The adverse effects of alendronate include abdominal and musculoskeletal pain, nausea, dyspepsia, constipation, and other gastrointestinal effects. There have been case reports of severe esophagitis, although the rate is less than 1%. Guidelines have been issued to minimize the risk of chemical esophagitis or severe esophagitis. "There are important guidelines to be followed with any particular drug, and these guidelines should be followed to decrease the risk of side effects," recommended Dr. Beier.
Among some of the administrative guidelines for alendronate are the following: alendronate should be taken on waking in the morning. The patient should not lie down for at least 30 minutes after ingestion. It should be taken with 6 to 8 ounces of water. Alendronate is contraindicated in patients with delayed esophageal emptying, an inability to stand or sit upright for at least 30 minutes, or hypocalcemia, and in women who have estimated creatinine clearances less than 35 ml per minute.
Raloxifene
Raloxifene is currently approved in the United States for the prevention of osteoporosis only. "It's a selective estrogen receptor modulator with agonist and antagonist effects. The agonist effects are in the bone and the antagonist effects are in the breast and the endometrial tissue," explained Dr. Beier. Studies with raloxifene have not shown any increase in breast cancer or any endometrial hyperplasia. At the recommended dose of 60 mg per day, raloxifene has demonstrated an approximately 38% reduction in the risk of new vertebral fractures. Common adverse events associated with raloxifene include hot flashes and leg cramps. "There's a great deal of interest in this compound, but we are still awaiting its approval for the treatment of osteoporosis," she stated.
Vertebral Fractures
"Although 5% of women over age 50 and 25% of white women between age 80 and 85 have vertebral compression fractures, only 30% of these fractures come to clinical attention," began Kenneth W. Lyles, MD, Associate Professor of Medicine, Director of the Sarah W. Stedman Nutrition Center, and Director of the Geriatric Physician Fellowship Program, Duke University Medical Center, Durham, NC. "When you've identified a vertebral fracture, this person is much more at risk for further fractures. Men have half the prevalence of vertebral fractures of women. The presence of a vertebral fracture increases a woman's risk for subsequent fracture fivefold. The most common fracture sites are T-8--that's right at the base of the scapula--and then T-12 and L-1 vertebrae. There's probably something we don't fully understand there. It's probably in part a transmission of force," explained Dr. Lyles.
Vertebral fractures in the lower spine are associated with much more pain, functional difficulties, and impaired quality of life. "Vertebral fractures higher up are not associated with as much pain and disability, but remember, they put people at risk for further fractures," he stated. Dr. Lyles then cited a Swedish study from the American Society for Bone and Mineral Research, which demonstrated that a person who is admitted to a hospital for a vertebral fracture has a 35-fold increase in the fracture rate over the next 12 months compared to the general population.3 "When you identify these people with fractures, you need to be very concerned about trying to intervene and prevent further fractures," he emphasized.
In 1993, survival rates for patients with vertebral fractures were 61% compared to a population survival rate of 76%.4 "When our colleagues in Europe looked at this, they did not find similar rates. There's a modest excess mortality, in fact, that may be explained by comorbid diseases. Because two-thirds of these fractures are clinically silent, we must identify these people, although we still probably don't understand the full scope of this problem," he explained.
Vertebral fractures result in several problems, including back pain, scoliosis, degenerative disk disease, idiopathic kyphosis, spinal stenosis, Paget's disease, and metastatic neoplasm, among others. There are two types of vertebral fractures: those that can be radiographically determined and involve a 15% to 20% reduction in height, and those that are clinically evident. Two-thirds of patients with vertebral fractures have no symptoms. "There may be some pain, there may be some height loss, but rarely will you see someone develop an ileus as a result of these fractures," he reported. Dr. Lyles reviewed six studies that assessed outcomes associated with radiographically determined vertebral fractures. Four of these six studies showed that severe deformities (ie, four standard deviations; 20% reduction in height) are associated with pain and disability. "If you have a four-standard-deviation reduction in your vertebrae, you have a twofold increased likelihood of reporting disability with vertebral fractures."
Outcomes associated with clinically diagnosed fractures include pain, reduced physical function, and reduced self-esteem. Dr. Lyles explained that these outcomes are often overlooked: "For many years, physicians overlooked people with vertebral compression fractures because they were healthy enough to come to clinics. These patients were not associated with patients in long-term care facilities who had really severe problems associated with osteoporosis."
Patients with clinically apparent fractures must be identified because they are more likely to have an additional fracture. This population is identifiable by height loss. "When patients have lost an inch in height, and if they don't have severe scoliosis, there's a very good chance of finding a vertebral fracture." These fractures cause chronic impairments, such as pain and deformity, as well as movement, activities of daily living, and psychosocial impairments.
Vertebral fractures often worsen other comorbidities. Two studies have shown that reduced pulmonary function is correlated with clinical and radiologic severity of spine deformity from vertebral fractures. "Vertebral fractures that exacerbate kyphosis may worsen dyspnea, for example, if a patient has an existing chronic obstructive pulmonary disease," he illustrated.
Both clinically diagnosed and asymptomatic vertebral fractures are associated with impairments. A study published in the Annals of Internal Medicine that followed 7223 women, 65 years and older, pointed out that a person who had a vertebral fracture during the study was four to five times more likely to experience subsequent fractures.
An exercise program in women with vertebral fractures decreased pain and the use of analgesics and showed that quality of life was improved even beyond the period of active intervention. "This is one of the ways you improve function and improve mobility in people with vertebral compression fractures," he explained. Annals of Long-Term Care - ISSN: 1524-7929 - Volume 7 - Issue 07 - July 1999 |