Osteoporosis Update

A Geriatrician’s Perspective
by Michele F. Bellantoni, M.D

• Is it a Disease?
• Screening for Low Bone Mass and Bone Turnover
• Strategies for Management in a Primary Care Setting
• Management of Osteoporosis Fractures and Physical Frailty
• Resources of Patient Education
• References

Hear the lecture! Corticosteroid-Induced Osteoporosis

Is it a Disease?

Current Definition
How common is osteoporosis?
Factors Influencing Bone Mass
Does Bone Mass Predict Fracture Rate?
Do Previous Fractures Predict Future Fractures?
Do Falls Increase Risk for Fracture?

Current Definition
While the loss of bone mass is an expected part of aging, it has consequences for successful aging. The medical literature defines osteoporosis as a disease characterized by abnormalities in the amount and architectural arrangement of bone tissue that leads to impaired skeletal strength and an undue susceptibility to fractures^{(ref 1)}. The World Health Organization has proposed a clinical definition of osteoporosis based on epidemiological data that link low bone mass with increased fracture risk. In study populations of Caucasian postmenopausal women, a bone mineral density that was lower than 2.5 standard deviations (SD) of normal peak bone mass was associated with a fracture prevalence of 50&037;, meaning that 50% of women with bone mass at this level had at least one bone fracture^{(ref 2)}. Based on these data, the WHO defined osteoporosis as bone mineral density 2.5 or more SD below peak bone mass, osteopenia as bone mass between 1.0 and 2.5 SD below peak, and normal as 1.0 SD below normal peak bone mass or higher. However, the WHO criteria apply only to Caucasian, postmenopausal women, and not men, premenopausal women, or women of ethnicity other than Caucasian. We have yet to classify clinically significant low bone mass in this populations.

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How common is osteoporosis?

Using the WHO criteria, 30% of Caucasian postmenopausal women in the US have osteoporosis, and 54% have osteopenia. The prevalence of low bone mass increases with age. Using the WHO definition of osteoporosis, the prevalence in the US of osteoporosis in Caucasian postmenopausal women based on the lowest bone mass at any site is estimated to be 14% of women aged 50-59 years, 22% of women aged 60-69 years, 39% women aged 70-79 years, and 70% women aged 80 years or greater^{(ref 3)}.

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Factors Influencing Bone Mass
Peak bone mass occurs for both men and women by the early thirties. Genetic factors play the greatest role in determining peak bone mass, but there are clinically significant contributions from nutrition, drug exposures, endocrine health following puberty, and weight-bearing status ^{(ref 4)}. For example, most teenagers and young adults do not receive the Recommended Daily Allowance (RDA) for calcium of 1200 mg. Smoking and excessive alcohol use contribute to low bone mass. Systemic glucocorticoid use of 7.5 mg daily or greater impairs bone formation. Phenytoin and other anti-seizure medications impair vitamin D metabolism. Oligomenorrhea and amenorrhea cause accelerated bone loss, as do hyperthyroidism or over-replacement of thyroxine supplementation such that the serum TSH is suppressed. Immobility is associated with thinning of the bone from lack of weight-bearing forces.

The menopausal transition is associated with bone loss that can exceed 4% per year and extend for 10 years or more ^{(ref 4)}. There is individual variation as to the rate and duration of bone loss. It appears that body fat, a non-ovarian source of circulating estrogens, influences the rate of bone loss; with higher amounts of body fat protecting against menopausal bone loss. Studies of African American women have shown that although on average they have higher peak bone mass than Caucasian women, they experience comparable rates of menopausal bone loss that are clinically significant for lean African American women.

Bone loss in women continues into older age, as the Study of Osteoporotic Fractures showed clinically significant bone loss occurring in women 65 years of age and older ^{(ref 5)}. Factors contributing to this bone loss include inadequate intake of calcium and vitamin D, lack of weight-bearing exercise, and possibly age-related changes in endocrine functions beyond those of estrogen deficiency.

On average, men achieve higher peak bone mass than women, and they do not experience as dramatic a change in reproductive function with aging as do menopausal women. However, levels of circulating testosterone as well as those of growth hormone and adrenal androgens decrease with normal healthy aging. These age-related endocrine changes combined with nutritional and lifestyle changes result in a gradual loss of bone mass with normal aging in men. Accelerated bone loss occurs with abrupt loss of testosterone production such as that experienced during the treatment of prostate cancer.

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Does Bone Mass Predict Fracture Rate?
For every one standard deviation below peak bone mass the risk of vertebral fracture is two times that of normal bone mass, and for the hip, the risk is 2.5 times.^{(ref 6)} Low bone mass is a modifiable risk factor for fracture analogous to hypercholesterolemia or hypertension for myocardial infarction and stroke.

The clinical consequence of low bone mass is fracture. Pain and immobility result from fractures of the limbs and spine. Multiple vertebral fractures result in irreversible spinal deformity and chronic pain syndromes. However, hip fractures result in institutionalization and excess mortality. One year mortality according to age at hip fracture are estimated to be roughly 20% in individuals less than age 70 years; 30% for ages 70-79.9 years, and almost 40% ages 80-89.9.^{(ref 7)} In summary, bone loss is a natural consequence of aging that if untreated, results in loss of independence and quality of life. Yet, preventive and treatment strategies have been developed (see below), thus making bone health an appropriate part of preventive health care in the primary care setting.

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Do Previous Fractures Predict Future Fractures?
One vertebral fracture is associated with a 5-fold increase in risk for subsequent vertebral fractures and a 2-fold increase in hip fracture. Two or more vertebral fractures increase the risk of subsequent vertebral fracture by 12-fold.^{(ref 8)} In our experience, almost half of frail elders admitted to an inpatient rehabilitation unit following a fracture had experienced a previous fracture.^{(ref 9)} The majority of the earlier fractures were of minimal or short-term impact on functional state; whereas the more recent fracture greatly impacted physical function. Yet, none of the earlier fractures resulted in an effective treatment program that may have prevented the more recent fracture.

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Do FAlls Increase Risk for Fracture?
The great majority of all fractures in older women result from falls.^{(ref 10)} Fall risk factors include leg weakness, impaired gait, and balance dysfunction. These can occur from global physical deconditioning as well as specific syndromes such as stroke, osteoarthritis of selective joints, and medical conditions such as polypharmacy, use of psychoactive medications, and orthostasis.^{(ref 11)}

The occurrence of fracture during a fall is determined by the intensity of the trauma and by bone strength. Risk factors identified for injurious falls include fear of falling, reduced knee extension strength, and poor distance visual acuity.^{(ref 12)} A simple test that predicts risk of injurious falls is the one-leg balance test – the ability to stand unassisted for 5 seconds on one leg.^{(ref 13)} Inability to perform this task increased relative risk of injurious falls by 2.1 (confidence intervals 1.04-4.3).

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Screening for Low Bone Mass and Bone Turnover

Available Testing
Medicare Guidelines for Bone Densitometry
SCORE Screening Quiz

Available Testing
The current standard for assessing bone mass is dual energy x-ray absorptiometry, or DEXA. Measurement of the bone mass of the lumbar spine and hip are currently used for diagnostic purposes and monitoring of treatment. Peripheral sites such as wrist and heel can be useful screening tools in older individuals; however there is discordance between bone sites in rates of loss with aging. Thus, many newly postmenopausal women will have a normal bone mass of the heel, and yet have clinical significant low bone mass of the spine. The FDA recently approved ultrasound techniques for use as a screening test for low bone mass.^{(ref 14)} Currently, the different manufacturers of bone densitometers all use different reference populations from which the standard deviations from normal are calculated, also called T scores. There are differences in calibration between companies as well, so that an individual patients bone density reading can differ by as much as 12% from one machine to the next. Thus, to monitor a patients response to treatment, the same bone densitometer must be used. This is a challenge when patients are often referred to centers based on insurance coverage.

While the T score is used to assess bone mass, diagnose osteoporosis, and predict fracture risk, the Z score, or comparison with age-matched individuals is used to determine whether the patients bone mass is unexpectedly low. A Z score of -2.0 or more negative is often used to determine whether a more extensive laboratory assessment is done to assess for secondary causes of bone loss such as myeloma, vitamin D deficiency, and hyperparathyroidism.

A bone density study provides information on the patients current bone mass, but does not assess whether bone loss is accelerated. Blood and urine studies have been developed to assess bone turnover. Most of these markers are breakdown products of proteins specific to bone, including n-telopeptide (NTX or Osteomark®), C-telopeptide (CTX) and deoxypyridinoline crosslinks (Pyrilinks-D®). The appropriate use of these markers in clinical practice is controversial.^{(ref 15)} There are data to show that they predict bone loss as assessed by bone densitometry over one to two years. Small studies show potential use to monitor response to treatments such as bisphosphonates and estrogen. Studies are repeated three months after treatment with a clinical response assessed at three months. The variablity in measurements is estimated at 20%; a decrease in value of 30% is considered a treatment response. Effective October 1, 1999, Medicare will provide reimbursement for biomarkers to monitor bone loss, at costs of roughly $30 per study.

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Medicare Guidelines for Bone Densitometry

Medicare Guidelines for bone densitometry became effective 7/1/98.^{(ref 16)}

Patients must meet one of the following criteria:

• Estrogen deficient woman at clinical risk for osteoporosis (the clinician can refer a postmenopausal woman who is receiving hormone replacement if there is concern that the therapy may not be preventing bone loss)
• Vertebral abnormalities as demonstrated by x-ray to be indicative of osteoporosis, osteopenia, or vertebral fracture.
• Chronic glucocorticoid use; defined as 7.5 mg/day or greater of prednisone or equivalent steroid for 3 months or greater, or anticipated use of such therapy.
• Primary hyper-parathyroidism
• Individual being monitored to assess the response to, or efficacy of, an FDA-approved osteoporosis drug therapy.

**Medicare will cover a bone mass measurement for a beneficiary once every two years.

**More frequent central bone densitometry will be covered if medically necessary such as with steroid use, or to confirm the findings of a screening study such as ultrasound or peripheral bone densitometry.

**The National Osteoporosis Foundation also suggests that bone densitometry is appropriate in the setting of positive family history of osteoporosis, chronic thyroxine use, height loss, vertebral deformity without x-ray confirmation, and any fracture for which the degree of trauma is disproportionate to the degree of injury.^{(ref 1)}

Medicare reimbursement for central bone densitometry is roughly $140; peripheral and ultrasound studies are reimbursed at approximately $50. It is now possible for patients to receive peripheral densitometry at locations such as pharmacies and health fairs. Again, because bone mass at peripheral sites changes more slowly with time, and there is discordance in bone mass between different anatomical sites, a normal peripheral bone mass measurement in a patient with significant risk factors for osteoporosis should be screened with a bone mass measurement of the spine and hip. The peripheral ultrasound technologies are accurate, but there is insufficient data to access precision over time. Thus they are not currently used to monitor response to treatment, although this recommendation may change with more data.^{(ref 17)}

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SCORE Screening Quiz
Located below is a six question screening questionnaire for osteoporosis, SCORE (Simple Calculated Osteoporosis Risk Estimation). SCORE has been shown to have 89% sensitivity and 50% specificity in an ambulatory population of postmenopausal women.^{(ref 18)} The questionnaire below can be used by office support staff to identify individuals for whom bone densitometry is warranted to confirm the clinical suspicion of osteoporosis.

1. What is your current age in years? ____

Enter the number in redhere. ______

2. What is your race or ethnic group?

If African-American/Black American, enter 0. For all other groups, enter 5 here. ______

3. Have your ever been treated for or told you have rheumatoid arthritis?

If yes, enter 4 If no, enter 0 ______

4. Since the age of 45, have you experienced a fracture (broken bone) at any of the following sites?

Hip: If yes, enter 4; If no, enter 0 ______ Rib: If yes, enter 4; If no, enter 0 ______ Wrist: If yes, enter 4; If no, enter 0 ______

5. Do you currently take or have you ever taken estrogen? (ie, Premarin®, Estrace®, Estraderm®, Estratab®, Evista®)

If yes, enter 0 If no, enter 1______

6. Subtotal

Add 1 thru 5, enter here ______

7.What is current weight in pounds? __ ____

Enter the number(s) in redhere. ______

8. Calculate Final Score

Subtract subtotal on line 6 from the value on line 7. Enter here. ________

If your final score is greater than or equal to 6, you could be at risk for osteoporosis. Speak with your doctor about further evaluation.

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Strategies for Osteoporosis Management in a Primary Care Setting

Pharmacologic Therapies for Prevention and Treatment
Fall Prevention
Estrogen Replacement and Selective Receptor Modulators

Pharmacologic Therapies for Prevention and Treatment
Primary health care should routinely address bone health. Young adults should be encouraged to achieve normal peak bone mass through:

• adequate dietary calcium (1000 mg daily)
• weight-bearing exercise
• maintenance of normal body weight and reproductive function
• hormone replacement (often in the form of estrogen containing oral contraceptives) in young women who experience prolonged amenorrhea

For newly menopausal women, estrogen replacement is the standard of practice to prevent bone loss. There is evidence to suggest that initiating estrogen therapy in older women may be of benefit to bone mass, although the maximum benefits are achieved through early menopausal hormone replacement and maintenance of estrogen replete state long-term. For example, The Study of Osteoporotic Fractures provided epidemiological data that bone loss continues in older women and that estrogen may decrease this loss.^{(ref 20)} The average rate of bone loss from the total hip in this study was sufficient to increase the risk of hip fracture by 21% per 5 years in women aged 80 years or older. However, compared with nonusers, current estrogen users had a 33% lower age-adjusted mean rate of loss at the total hip. There are no completed long-term clinical trials of estrogen in older women; however the Womens Health Initiative is an ongoing study to determine the risk-benefit ratio of estrogen use in older postmenopausal women.

Testosterone replacement for hypogonadal men preserves bone mass. Testosterone replacement for age-related declines in testosterone levels in healthy older men is currently being studied to determine the risk/benefit profile. Studies are underway to determine if there is a role for bisphosphonate therapy in prevention of bone loss due to hypogonadal state from the anti-hormonal therapies for the treatment of prostate cancer.

Osteoporosis Management^{(ref 4, 19)} is evolving. There is consensus that calcium and vitamin D intake is needed to increase bone mass. There are three FDA approved, non-sex steroid treatments for for postmenopausal osteoporosis; alendronate, risedronate and etidronate. Likely, other oral bisphosphonates will receive FDA approval. Data were recently published that support the combination of estrogen and bisphosphonate as additive to increase bone mass.^{(ref 27)} Calcitonin and sodium monofluorophasophate plus calcium have also been shown to reduce vertebral fractures. The table below lists the dosing and side effects of these nonhormonal treatment options.

Calcium Intake	1500 mg daily (through diet and supplements)
Vitamin D	800 units daily is needed to increase bone mass
Alendronate* (a biphosphonate, FDA approved	Dosage: 10 mg daily to treat osteoporsis and 5 mg daily to prevent bone loss in women who are unable to take estrogen replacement. There are data to show that alternative alendronate dosing of 35 mg twice weekly, or 70 mg once weekly results in similar increases in bone density at one year to daily alendronate therapy, but with less gastrointestinal adverse reactions.(ref 21)(:also see EULAR meeting highlights) Efficacy: Alendronate is shown in three year clinical trials to reduce the risk of new vertebral and hip fractures by 50%. Side Effects: Gastrointestinal are most common, especially nausea, acid reflux symptoms, and constipation. To maximize absorption, should be taken on an empty stomach with water only, waiting 30 minutes before eating or drinking. To minimize acid reflux, patients should not recline for one hour after a dose. To optimize treatment response, adequate calcium and vitamin D as described above are essential.
Risedronate (a biphosphonate, FDA approved in April, 2000)	Dosage: The recommended regimen is 5 mg orally daily for the treatment and prevention of postmenopausal osteoporosis”glucocorticoid-induced osteoporosis. Efficacy: In clinical trials, administration of risedronate to postmenopausal women resulted in decreases in biochemical markers of bone turnover. Data on bone mineral density increases and reductions in vertebral compression fractures are comparable to alendronate.(ref 24)Side Effects: Gastrointestinal are most common, especially nausea, acid reflux symptoms, and constipation. To maximize absorption, should be taken on an empty stomach with only water, waiting 30 minutes before eating or drinking. To minimize acid reflux, patients should not recline for one hour after a dose. To optimize treatment response, adequate calcium and vitamin D as described above are essential. Risedronate is not recommended for use in patients with severe renal impairment (creatinine clearance < 30 mL”min).
Etidronate (FDA approved for treatment in Pagets Disease)	Efficacy: Ealier studies showed efficacy in preventing vertebral fractures with cycled etidronate; however later data suggested that long-term etidronate may lead to impairment in new bone formation.
Calcitonin (for those who do not tolerate bisphosphonate therapy)(ref 22)	Dosage:200 units, or one metered puff daily alternating nostrils Efficacy: Calcitonin is shown to reduce the risk of vertebral fractures, but the effects on the hip appear to be less than that of bisphosphonate therapy.
Sodium Monofluorophosphate Plus calcium (does not have FDA approval)	Dosage: Not available for patient use except under research protocols. Efficacy:: Although shown to reduce vertebral fractures, the effects on bone mineral density of the total hip were not significant.(ref 23)

*Recent data support the use of alendronate 10 mg daily in the treatment of steroid-induced osteoporosis in both women and men.^{(ref 25)} The dose of 5 mg daily has been shown to prevent accelerated bone loss in newly postmenopausal women, and may be useful for women who are unable to take estrogen due to history of estrogen-sensitive cancers or clotting disorders.^{(ref 26)}

In addition to oral therapy, bisphosphonate treatment is also possible via intravenous infusion. Although not FDA approved for treatment of osteoporosis, pamidronate 30 or 60 mg infused intravenously over 2 hours every three months for two years has been shown to increase bone mineral density of the spine and hip by roughly 11% and 5.5% respectively.^{(ref 28)} Ibandronate has been given by intravenous push rather than lengthy infusion, but is not yet available in the U.S. for clinical use.^{(ref 29)}

Weight-bearing exercise has been shown to increase bone mass, strengthen muscle, and reduce the risk of falls. There is a role for exercise prescriptions in osteoporosis management. The National Osteoporosis Foundation offers an exercise program via video cassette that includes safe and effective exercises that can be performed in the home setting.

Is it reasonable to implement an osteoporosis treatment program in the setting of a recent fracture? Our experience to date is yes. At the Rehabilitation Center of the Johns Hopkins Geriatrics Center, the post-fracture admission orders include calcium and vitamin D supplementation. Bisphosphonate therapy in this setting has been difficult due to the high prevalence of gastroesophageal reflux and constipation. We currently defer bisphosponate or calcitonin therapy until the acute and subacute rehabilitation is complete, which is usually one to two months post-fracture.

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Fall Prevention
For those at risk for falls, a fall prevention strategy is warranted to reduce the number of fall-related fractures. A multi-disciplinary approach includes both medical and physical assessments.^{(ref 30)} Medications are reviewed to determine if any are impairing judgment, balance, or postural hemodynamic stability. Orthostatic and postprandial hypotension are considered. Vision and hearing assessment may target appropriate intervention. Gait assessment is performed during physical therapy evaluation. Training with assistive devices and the use of rubber soled shoes often improve fall risk. Physical therapy should include an exercise program for muscle strengthening and physical reconditioning. A home safety evaluation is used to identify dangers from throw rugs, inadequate lighting, and cluttered walkways, and to provide in-home safety equipment such as bathroom grab bars and raised toilet seats.

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Estrogen Replacement and Selective Receptor Modulators
Patient compliance is limited by side effects of breast tenderness, weight gain, and vaginal bleeding associated with progestin co-therapy, as well as the increasing evidence that long-term estrogen use is associated with increased risk of breast cancer. However for the majority of women, the benefits of long-term estrogen outweigh the side effects and risks. All forms of estrogen replacement offer benefit if given in proper dose; patient preference, cost, and compliance are considered in the choice of therapy. For a woman who has undergone hysterectomy, estrogen therapy alone is needed. For a woman with an intact uterus, progestin cotherapy prevents endometrial hyperplasia. This can be achieved with daily progestin such as medroxyprogesterone acetate 2.5 mg daily, or 5 mg daily if vaginal bleeding occurs with the lower dose. Alternatively, progestin can be cycled either monthly or quarterly in doses of medroxyprogesterone acetate 5 to 10 mg daily for two weeks. Cycled progestin therapy results in scheduled vaginal bleeding that typically lasts for several days to one week. Over time, the amount of bleeding and the duration decrease, and many women can switch from cycled progestin to daily low dose in one to two years. Recent FDA approved forms of hormonal therapy include oral plant derived estrogens, oral natural progesterone, and a combination estradiol”progestin skin patch.

The largest impact on health from estrogen may relate to cardiovascular disease protection. The Heart and Estrogen”Progestin Replacement Study (HERS) recently published the results of randomized estrogen”progestin replacement for a mean of 4.1 years in 2763 women with established coronary disease.^{(ref 31)} While there were no significant differences between the hormone and placebo groups in the primary outcomes of myocardial infarction and coronary heart disease death, there was a time trend that was significant, with more coronary heart events in the hormone group at year one, and fewer in years 4 and 5. The hormone group experienced 11% net lower LDL cholesterol and 10% higher HDL cholesterol than the placebo group. As a result of these data the research team has elected to continue collecting data on this cohort of women, expecting that the benefits of estrogen as secondary prevention of coronary heart disease requires long-term treatment. In addition to benefits to lipids and direct effects of estrogens on coronary artery atherosclerosis and vasodilatation, long-term estrogen use has been shown to prevent central obesity that may be associated with glucose intolerance.^{(ref 32)}

A recent area of active research in the benefits of estrogen replacement is cognition, and prevention of dementia. In basic science studies, estrogens have been shown to promote neuronal survival and dendritic sprouting, increase acetylcholine activity, and prevent cerebral ischemia. Epidemiological data support a role for estrogen to improve cognition, prevent dementia,^{(ref 33)} although studies on the efficacy of estrogen to treat dementia have contradictory results with the most recent placebo controlled study showing no significant treatment effect.^{(ref 34)} It is possible that the role of estrogen in cognitive function is similar to that in bone metabolism, preventive effects rather than treatment once clinically significant disease is present.

Educating women that the risk of death from hip fracture is equal to the risk of death from breast cancer enhances compliance with long-term estrogen. Indeed, the risk of breast cancer is a large detriment to long-term compliance with estrogen use. A recent metaanalysis of studies involving over 54,000 women found that the risk for breast cancer increases by 2 extra cases by age 70 in 1000 women who have used hormone replacement for five or greater years.^{(ref 35)} Cases of breast cancer per 1000 women for 10 and 15 years of estrogen exposure were 6 and 12, respectively. Thus, the epidemiological data suggest increased risk of breast cancer with five or greater years. For women with positive family history of breast cancer, the Iowa Women’s Health Study did not find an increase in breast cancer with hormone replacement.^{(ref 36)} However, it is difficult to persuade a woman with a family history of breast cancer to initiate estrogen. The Women’s Health Initiative, a randomized trial of hormone replacement, is expected to provide data on the overall benefits such as primary prevention from coronary heart disease and risks of estrogen such as breast cancer in the Year 2007.

Selective estrogen receptor modulators such as raloxifene 60 mg daily offer choice to women who are unable to take estrogen. The effects of raloxifene on bone and lipids are comparable to estrogen replacement.^{(ref 37)} There appear to be no growth promoting effects on breast or endometrium, thus reducing the risk profile of hormone replacement. The down side to raloxifene is that hot flushes are not improved over Placebo, and the risk of clotting is at least comparable to estrogen. Cost is also an issue, with estrogen/progestin therapy roughly $25 per month, whereas raloxifene is over $60. As there are no long-term data on the benefits and risks of these newer pharmacologic agents, it is reasonable to recommend more traditional estrogen and progestin treatments as initial hormone replacement, and limit selective estrogen receptor modulator therapy to those who do not tolerate estrogen therapy or who are unwilling to use estrogen due to increased risk of breast cancer. For example, many women who have first degree relatives with breast cancer will not consider estrogen, although there are no data to support increased risk of breast cancer due to estrogen beyond that of their family history.

A study of tamoxifen use in older nursing home residents found that 10 mg daily was associated with a lower rate of hip fracture than in women not receiving such therapy, but that a dose of 20 mg was similar to no therapy.^{(ref 38)}

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Management of Osteoporosis Fractures and Physical Frailty

Outpatient Management
Acute Hospital Management
Subacute Rehabilitation
Post-Rehabilitation Care

Outpatient Management
Fractures can occur even with the most aggressive osteoporosis management. Fractures of distal extremities such as forearm and ankle are often managed in the outpatient setting. The orthopedic surgeon performs either open or closed reduction of the fracture and casting for bone healing. The primary health care provider manages pain and immobility that result from the fracture. Pain management is challenging in the elderly as the adverse effects of narcotics including over sedation, delirium, and constipation must be balanced with effective pain relieve and preservation of physical function. Outpatient physical and occupational therapy, often in the home setting for homebound elderly are helpful in maintaining muscle strength and in providing adaptive responses to the injury.

The management of vertebral compression fracture is evolving. Vertebroplasty is FDA approved for the management of pain and physical deformity that result from chronic vertebral compression fracture. Studies are being conducted to assess the benefits vs. risks of vertebroplasty in the management of acute vertebral compression fractures. Calcitonin has been shown in short-term studies to reduce the pain and physical dysfunction of acute vertebral compression fractures. There are data to suggest that bisphosphonates can impact bone pain, but insufficient to recommend their use for pain management. Often in the setting of new fracture the gastrointestinal side effects of daily bisphosphonates outweigh their potential benefits. Data do not show that any of the anti-resorptive treatments impair bone healing after acute fracture. What are strategies for reducing risk of poor prognosis following fracture?

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Acute Hospital Management
The acute hospital course requires a team approach for effective management of hip fractures and other fractures that require operative procedures and inpatient care. Ideally, the orthopedic surgeon provides management of fracture stabilization, whether that be operative or nonoperative. Early mobilization may prevent postoperative complication resulting from deconditioning and bed rest, and is promoted if surgery takes place within 24 to 48 hours of hospital admission followed by high frequency physical and occupational therapy.^{(ref 39)} The orthopedic surgeon makes recommendations regarding wound care, weight-bearing status, and limitations of fractured bones. The internist provides management of cardiopulmonary function, particularly peri-operative fluid and electrolyte management and patient focused assessment of ischemia; pain control, and prevention of common complications such as delirium, deep venous thrombosis, pulmonary emboli, infections, incontinence, constipation, depression, anemia, and pressure sores. Physical and Occupational Therapists assess the functional state of the patient and make recommendations for the rehabilitation setting; inpatient vs outpatient ambulatory, vs in home program. Social workers coordinate rehabilitation based on team recommendations, and arrange for the rental or purchase of equipment such as assistive devices, portable commodes, and wheelchairs.

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Subacute Rehabilitation
A multi-disciplinary team provides optimal patient care.^{(ref 40)} A randomized controlled trial has shown that accelerated rehabilitation reduces the cost of care by approximately 17%.^{(ref 41)}
 

–Medical care– most medical issues require adjustments in care based on patients increased frailty as a result of fracture. An example is adjustment of diabetes regimen in the setting of decreased oral intake due to limited access to food, depression, and/or nausea secondary to pain medications, constipation, or other causes. Rehabilitation is the time when cardiac ischemia and symptomatic orthostasis first present as the patients oxygen consumption increases during ambulation with an assistive device, often in the setting of post-fracture blood loss and new medications that contribute to orthostasis.

–Physiatrists provide recommendations improve rehabilitation outcomes. They focus on pain management, functional impairments and methods to improve function using physical and pharmacologic modalities. For example, a physiatrist may recommend an individualized exercise program to strengthen isolated muscle groups, or to reduce weight-bearing to areas to improve pain.

–Nursing care– nursing provides frequent assessments for changes in vital signs or clinical symptoms that suggest the early signs of the above mentioned complications (ischemia, pulmonary emboli, infection). Nursing extends the rehabilitation plan established by physical and occupational therapies. Nursing also prevents pressure sores through positioning, establishes bladder retraining programs for incontinence, and educates patients and families on the rehabilitation plan.

–Physical Therapy– This discipline addresses mobility and lower body function. Physical therapy provides gait retraining, safe and proper use of assistive devices, fall prevention, and pain management through local modalities of heat, cold, massage, ultrasound, and electrical stimulation.

–Occupational Therapy– This discipline addresses activities of daily living and upper body function. Occupational therapy provides retraining in bathing, grooming, dressing, toileting, meal preparation, and housekeeping.

–Nutrition Assessments– Assessments of the patients nutritional status and caloric needs are made. This should include assessment of dietary calcium and vitamin D for osteoporosis management.

–Psychology– Depression is common after loss of independence. Counseling and pharmacotherapy may improve patients motivation and performance during rehabilitation.

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Post-Rehabilitation Care
Most inpatient rehabilitation programs are of one to several weeks duration. Many older people will need longer term management of pain or functional impairments. In home physical therapy and occupational therapy should be considered in those who have not regained their prefracture level of physical function at the time of discharge due to plateau in function. Osteoporosis management should begin post-fracture and should be continued long-term.

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Resources of Patient Education

National Osteoporosis Foundation 1-800-223-9994	22 page pamphlet at no charge
National Institute on Aging 1-800-222-2225	Fact sheets on menopause, osteoporosis, fall prevention
Library/Bookstores Paperback text	Managing Your Menopause by Wulf H. Utian, M.D., Ph.D. and Ruth S. Jacobowitz
Arthritis Foundation 1-800-365-3811	Information on exercise programs including programs appropriate for those with back pain and frailty.

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References

1. Consensus Development Conference: Diagnosis, prophylaxis, and treatment of osteoporosis. Am J Med 94:646-650, 1993

2. The WHO Study Group: Assessement of fracture risk and its application to screening for postmenopausal osteoporosis. Geneva, World Health Organization, 1994.

3. Melton LJ III. How many women have osteoporosis now? J Bone Miner Res 10:175-177, 1995.

4. Bellantoni M. Osteoporosis and Other Metabolic Bone Diseases, ClinicalAspects of Aging, 5^th edition, William Reichel, M.D., ed., Williams and Wilkins, Baltimore, MD, 1999.

5. Cummings SR et al. Appendicular bone density and age predict hip fracture in women. JAMA 263:665-668, 1990.

6. Melton LJ III et al. Long-term fracture prediction by bone mineral assessed at different skeletal sites. J Bone Miner Res 8:1227-1233, 1993.

7. Miller PD. Management of osteoporosis. Advances in Internal Medicine 44:175-207, 1999.

8. Ross PD et al. Pre-existing fractures and bone mass predict vertebral fracture incidence in women. Annals of Int Med114:919-923, 1991.

 

9. Humphrey K, Bellantoni MF, Remsburg R. Evaluation of a multidisciplinary care plan for the treatment of osteoporosis in the frail elderly. Abstract presented at the annual meeting of the American Geriatrics Society, Seattle, WA, May 1998.

10. Cummings SR, Nevitt MC, for the Study of Osteoporotic fractures Research Group. Non-skeletal determinants of fractures: The potential importance of the mechanics of falls. Osteoporosis Int 1(suppl):657-670, 1994.

11. Tinneti ME, Speechley M, Ginter SF. Risk factors for falls among elderly persons living in the community. N Engl J Med 319:1701-1707, 1988.

12. Luukinen H, Koski K, Laippala P, et al. Factors predicting fractures during failing impacts among home-dwelling older adults. J Am Geriatr Soc 45:1302-1309, 1997.

13. Vellas B, Wayne S, Romero L, et al. One-leg balance is an important predictor of injurious falls in older persons. J Am Geriatr Soc 45:735-738, 1997.

14. Cheng S, Tylavsky F, Carbone L. Utility of ultrasound to assess risk of fracture. J Am Geriatr Soc 45(11):1392-1394, 1997.

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