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Screening for Postmenopausal Osteoporosis
Information For Clinicians
RECOMMENDATION
There is insufficient evidence to recommend for
or against routine screening for osteoporosis with bone densitometry in postmenopausal
women. Recommendations against routine screening may be made on other grounds
(see Clinical Intervention
). All postmenopausal women should be counseled about
hormone prophylaxis
and be advised of the importance of smoking cessation, regular exercise, and
adequate calcium intake.
For those high-risk women who would consider estrogen prophylaxis only to
prevent osteoporosis, screening may be appropriate to assist treatment decisions
(see Clinical Intervention
).
Burden
of Suffering
An estimated 1.3 million osteoporosis-related fractures
occur each year in the U.S.[1]
About 70% of fractures
in persons aged 45 or older are types that are related to osteoporosis.[2]
Most of these injuries occur in postmenopausal women.
Over half of all postmenopausal women will develop a spontaneous fracture
as a result of osteoporosis.[3]
It has been estimated
that about one quarter of all women over age 60 develop vertebral deformities
and about 15% of women sustain hip fractures during their lifetime.[4]
,[5]
The annual cost of osteoporosis-related
fractures in the U.S. has been estimated to be over $8 billion in direct and
indirect costs.[6]
Most fractures in elderly women
are due in part to low bone mass; osteoporosis-related fractures commonly
involve the proximal femur, vertebral body, and distal forearm.[7]
Of these sites, the proximal femur (hip) has the greatest effect on morbidity
and mortality; there is a 15-20% reduction in expected survival in the
first year following a hip fracture.[8]
Hip fractures
are also associated with significant pain, disability, and decreased functional
independence.[9]
Among persons living at home at the
time of a hip fracture, about half experience a deterioration in social function
within 2.5 years.[10]
Low bone density is
strongly associated with an increased risk of fracture.[11]
By one estimate, a 50-year-old woman in the 10th percentile of bone density
has a 25% lifetime risk of hip fracture (vs. 8% for those in the 90th percentile).[12]
A World Health Organization study group has recommended
that osteoporosis be defined as a bone density more than 2.5 standard deviations
(SD) below the normal bone mass in young women, and that osteopenia (low bone
mass) be defined as bone density 1-2.5 SD below the normal mean.[13]
Risk of postmenopausal osteoporosis is a function of rate
of bone loss as well as peak bone mass. The principal risk factors for osteoporosis
are female sex, advanced age, Caucasian race, low body weight, and bilateral
oophorectomy before menopause.[1]
,[4]
Other historical risk factors such as parity, lactation history, and caffeine
intake have been shown to be poor predictors of bone mass.[14]
[15]
[16]
Smoking is a probable risk factor
for hip fracture, but it is a less reliable predictor of bone mass.[17]
The lower weight and poorer health of smokers compared
to nonsmokers may be responsible for the associations between smoking and
bone mass and fracture risk.[18]
Accuracy of Screening Tests
A number of
radiologic screening tests have been proposed for both clinical and research
purposes to detect low bone mass in asymptomatic persons. These include conventional
skeletal radiographs, quantitated computed tomography, single photon absorptiometry,
dual photon absorptiometry, and dual energy x-ray absorptiometry. Although
skeletal x-rays can detect focal bone disorders and fractures, they do not
reliably detect bone loss of less than 20-30%, and they are of limited
value in estimating bone mass.[19]
The other techniques
vary in their availability, cost, and convenience, and provide measures expressed
as bone mineral content (BMC) in grams/cm, or as bone mineral density (BMD)
in grams/ cm[2]
.
Single photon absorptiometry
(SPA), in which radioisotopes are the photon source, can measure BMC or BMD
in cortical bone in the radius or calcaneus.[20]
Dual
photon absorptiometry (DPA), dual energy x-ray absorptiometry (DXA), and quantitative
computed tomography (QCT) provide direct measures of BMD and are most useful
in evaluating the trabecular bone density in locations beneath large amounts
of soft tissue (e.g., lumbar vertebrae, proximal femur). DPA and DXA use
radioisotopes (DPA) or x-rays (DXA) to emit photons at two different energy
levels, thereby correcting for the effect produced by layers of soft tissues.[20]
[21]
[22]
DXA
is now widely used in the clinical setting, and provides more reproducible
measures of bone density, with shorter examination times (5-10 vs. 20-40
minutes) than DPA.[20]
[21]
[22]
The precision of DXA (variation in results on repeated
measurement) is about 0.5-2%, compared to 1.5-4.0% for DPA.[23]
Current data on the performance of these devices have been
obtained primarily at specialized research centers, however. Most experts
agree that DXA is a safe, accurate, and precise modality for measuring bone
density that may be useful in the clinical setting.[24]
Reproducibility of SPA is similar to DPA and DXA, but the cost per scan is
significantly lower than DXA. Evidence suggests that SPA of the radius or
calcaneus is also predictive for future risk of nonspine fracture.[25]
QCT is highly accurate in examining the anatomy
and density of transverse sections and trabecular regions within the spine,
but it is less practical as a routine screening test due to cost and higher
radiation exposure. Ultrasound technology for assessing bone density and
architecture is under development and may be of value in the future. Other
screening tests under investigation include biochemical markers of bone turnover,
which may be able to identify those women who will develop more significant
bone loss.[26]
Effectiveness of Early Detection
There is little evidence
from controlled trials that women who receive bone density screening have
better outcomes (improved bone density or fewer fractures) than women who
are not screened. The primary argument for screening is based on evidence
that postmenopausal women with low bone density are at increased risk for
subsequent fractures of the hip, vertebrae, and wrist,[27]
[28]
[29]
[30]
[31]
[32]
[33]
[34]
[35]
and that interventions can slow
the decline in bone density after menopause.
Prospective cohort
studies have demonstrated the dose-response relationship between BMD and fracture
risk.[11]
,[36]
,[37]
In 2-year follow-up of 8,134 women over 65, annual risk of hip fracture for
women in the lowest quartile of femoral neck BMD was approximately 1%, almost
twice that of women in the second lowest quartile and more than 8 times that
of women in the highest quartile.[11]
Various studies
have estimated that each standard deviation decrease in BMC or BMD is associated
with a 1.5-2.8-fold increase in risk of fracture.[38]
There are no studies, however, determining how well perimenopausal bone density
predicts long-term risk of fracture. Because the rate of postmenopausal bone
loss varies among women, bone mass at menopause correlates only moderately
with bone mass 10-20 years later, when most fractures occur.[39]
Randomized trials have demonstrated that calcium
supplementation and estrogen are effective in preserving bone density in postmenopausal
women.[40]
[41]
[42]
[43]
Due to the long delay between menopause and fracture, few
prospective studies have been able to demonstrate directly that these interventions
reduce fractures. Calcium plus vitamin D reduced hip fractures among very
elderly women in France (mean age 84).[43]
In a randomized
trial in healthy postmenopausal women, calcium supplementation slowed bone
loss and significantly reduced symptomatic fractures over 4 years.[43A]
Numerous observational and nonrandomized experimental
studies suggest that risk of fracture can be reduced 25-50% by estrogen
replacement therapy (see Chapter 68).
The benefits of hormone prophylaxis on bone mass and fracture risk appear
greatest with treatment begun close to menopause (before the period of rapid
bone loss), and continued for longer periods (>5 years). Benefits appear
to wane after stopping estrogen.[44]
As a result, preventing
fractures in older postmenopausal women may require continuing hormone therapy
indefinitely. Other agents that inhibit bone resorption (e.g., calcitonin,
bisphosphonates) or stimulate bone formation (e.g., sodium fluoride) can preserve
or increase bone mass, but their use in asymptomatic persons remains investigational.[40]
There is limited evidence that screening influences
treatment decisions, and that women appreciate the more precise estimates
of risk provided by BMD measurement. Women who had below average bone density
were more likely to take calcium, vitamins, or estrogen than those with above
average values (84% vs. 38%) in one study.[45]
Compared
to the low rates of compliance with hormone therapy in average women (see Chapter 68), 60% of women with low bone density
detected by screening were still taking hormone therapy 8 months after screening.[46]
The effect of BMD screening on long-term compliance is
not known.
There are several important limitations to screening
as a means of preventing fractures. In a single measure of bone density,
there is a small risk of inaccurate values, and there is no value of BMD that
discriminates well between patients who develop a fracture and those who do
not.[44]
Other risk factors that independently influence
falls or bone strength may be more important than low BMD for identifying
older women at high risk of fracture. In a prospective study of over 9,500
women over 65, the presence of multiple risk factors (e.g., age >=80, fair/poor
health, limited physical activity, poor vision, prior postmenopausal fracture,
psychotropic drug use, among others) was a much stronger predictor of hip
fracture than low bone density: incidence of first hip fracture in women
with 5 or more risk factors was 19/1,000 woman-years versus 1.1/1,000 in women
with two or fewer risk factors.[18]
Screening perimenopausal
women is less predictive of risk later in life, and even women with "normal"
bone density are likely to benefit from measures to prevent postmenopausal
bone loss. Equally important, there is no consensus on what interventions
are indicated for any particular level of bone density. Hygienic measures
such as adequate calcium and vitamin D intake, exercise, and smoking cessation
can be recommended irrespective of bone density. The decision to begin estrogen,
in contrast, often depends on factors other than risk of osteoporosis (see Chapter 68).
Screening could have adverse
effects, if it leads to "labeling" in patients diagnosed with osteopenia or
osteoporosis, or false reassurance in those with normal bone density. In
one study of women referred for screening, women with low bone density were
more likely to restrict their activities, and those with normal bone density
were less likely to follow routine hygienic measures to prevent osteoporosis
(e.g., calcium or vitamin D).[45]
Interpreting and explaining
the values obtained is complex and may require considerable time for patient
counseling about the significance of an abnormal bone density. Although the
absolute benefit of preserving bone mass may be greatest in women with low
bone density, the overall balance of risks and benefits of hormone therapy
in an individual patient is likely to depend on other factors.[39]
If estrogen therapy is likely to be recommended on other grounds, the clinical
usefulness of routine screening is limited.[47]
If other
more specific and expensive therapeutic modalities (e.g., bisphosphonates,
calcitonin) are shown to be effective in reducing fractures in asymptomatic
high-risk women, however, this may increase the role of screening to identify
appropriate candidates for treatment.
Recommendations of Other Groups
Recommendations against
routine radiologic screening for osteoporosis have been issued by the Canadian
Task Force on the Periodic Health Examination[18]
and
the American College of Physicians (ACP)[48]
; updated
ACP guidelines are due out in 1996. Both of these organizations and a World
Health Organization study group[49]
concluded, however,
that bone density measurements may be useful to guide treatment decisions
in selected postmenopausal women considering hormone replacement therapy.
The American Academy of Family Physicians recommends measuring BMC in women
40-64 years old with risk factors for osteoporosis (e.g., Caucasians,
bilateral oophorectomy before menopause, slender build) and in women for whom
estrogen replacement therapy would otherwise not be recommended; these recommendations
are under review.[50]
The American College of Obstetricians
and Gynecologists does not recommend routine screening for osteoporosis.[51]
The National Osteoporosis Foundation is in the process
of revising its guidelines for screening for osteoporosis.[20]
Discussion
Routine bone
densitometry of all postmenopausal women is likely to be time-consuming and
very expensive. Screening times vary from 5-15 minutes for SPA and
DXA to 20-45 minutes for QCT and DPA.[24]
Average
costs of screening have been estimated to be $75 with SPA, $75-100 with
DXA, $100-150 with DPA, and $100-200 with QCT.[23]
,[24]
The costs and inconvenience of screening may be justified
if screening reduces the burden of osteoporosis, but further research is necessary
to demonstrate both the clinical effectiveness and cost-effectiveness of different
screening and treatment strategies.[40]
,[52]
Although routine screening may not be appropriate for asymptomatic women,
measurement of bone density may be useful for identifying persons at high
risk of fracture who might not otherwise consider effective treatments such
as estrogen. Measures of bone density provide more reliable estimates of
risk than clinical assessment, and they may help both the patient and the
clinician make more informed decisions about the potential benefits and risks
of therapies such as estrogen.[45]
Women who have been
identified as having low bone density may be more likely to take estrogen
and comply with other preventive measures, but the effect of screening on
long-term outcomes (compliance with therapy, bone density, or fracture) has
not been adequately studied. The net benefit of screening may be small if
high-risk women do not continue long-term therapy, or if screening causes
those with normal BMD to forego preventive measures. There is little reason
for screening if the information is not likely to influence decisions by the
patient or provider. For most women, osteoporosis prevention is only one
of many factors that go into the decision whether or not to take estrogen.
CLINICAL INTERVENTION
There is insufficient evidence to recommend for
or against screening for osteoporosis or decreased bone density in asymptomatic,
postmenopausal women ("C" recommendation). Recommendations against routine
screening may be made on the grounds of the inconvenience and high cost of
bone densitometry, and lack of universally accepted criteria for initiating
treatment based on bone density measurements. All perimenopausal and postmenopausal
women should be counseled about the potential benefits and risks of hormone
prophylaxis (see Chapter 68). Although
direct evidence of benefit is not available, selective screening may be appropriate
for high-risk women who would consider hormone prophylaxis only if they knew
they were at high risk for osteoporosis or fracture.
All women should also receive counseling regarding
universal preventive
measures related to fracture risk, such as dietary calcium and vitamin D intake
(Chapter 56), weight-bearing exercise
(Chapter 55), and smoking cessation
(Chapter 54). Elderly persons should
also receive counseling regarding preventive measures to reduce the risk of
falls and the severity of fall-related injuries (Chapter
58).
The draft update of this chapter was
prepared for the U.S. Preventive Services Task Force by Robert B. Wallace,
MD, MPH, Denise Tonner, MD, and David Atkins, MD, MPH.
REFERENCES
1.
National
Institutes of Health.
Consensus conference: osteoporosis.JAMA 1984;252:799-802.
2.
Iskrant AP, Smith RW Jr.
Osteoporosis in women 45 and over related to
subsequent fractures.Public Health Rep 1969;84:33-38.
3.
Christiansen C, Riis BJ, Ridbro
P.
Prediction of rapid bone loss in postmenopausal women.Lancet 1987;1:1105-1108.
4.
Cummings SR, Kelsey JL, Nevitt C, et al.
Epidemiology of osteoporosis
and osteoporotic fractures.Epidemiol Rev 1985;7:178-208.
5.
Melton LJ III.
Epidemiology
of fractures.In: Riggs BL, Melton LJ III, eds. Osteoporosis: etiology, diagnosis,
and management.New York:Raven Press, 1988.
6.
Peck WA, Riggs BL, Bell NH, Wallace RB, Johnston CC Jr, Gordon SL, Shulman
LE.
Research directions in osteoporosis.Am J Med 1991;84:275-282.
7.
Seeley DG, Browner WS, Nevitt MC, et al.
Which fractures are associated
with low appendicular bone mass in elderly women?Ann
Intern Med 1991;115:837-842.
8.
Jensen GF, Christiansen C, Boesen J, et al.
Epidemiology
of postmenopausal spinal and long bone fractures: a unifying approach to
postmenopausal osteoporosis.Clin Orthop 1982;166:75-81.
9.
Chrischilles EA, Butler CD, Davis
CS, et al.
A model of lifetime osteoporosis impact.Arch Intern Med 1991;151:2026-2032.
10.
Jensen JS, Baggar J.
Long term social prognosis after hip
fractures.Acta Orthop Scand 1982:53:97-101.
11.
Cummings SR, Black DM, Nevitt
MC, et al.
Bone density at various sites for prediction of hip fractures.Lancet 1993;341:72-75.
12.
Black DM, Cummings SR, Melton LJ.
Appendicular bone mineral
and a woman's lifetime risk of hip fracture.J Bone Min
Res 1992;7:639-646.
13.
Kanis JA, Melton LJ, Christiansen C, et al.
The diagnosis of osteoporosis.J Bone Min Res 1994;8:1137-1141.
14.
Kelsey JL, Browner WE, Seeley DSG, et al.
Risk
factors for fractures of the distal forearm and proximal humerus.Am J Epidemiol 1992;135:477-489.
15.
van Hemert AM, Vanderbroucke JP, Birkenhager JC,
et al.
Prediction of osteoporotic fractures in the general population
by a fracture risk score.Am J Epidemiol 1990;132:123-135.
16.
Cooper C, Shah S, Hand DJ (The
Multicentre Vertebral Fracture Study Group).
Screening for vertebral osteoporosis
using individual risk factors.Osteoporosis Int
1991;2:48-53.
17.
Slemenda CW,
Hui SL, Longcope C, et al.
Predictors of bone mass in perimenopausal women.Ann Intern Med 1990;112:96-101.
18.
Cummings SR, Nevitt MC, Browner WS, et al.
Risk
factors for hip fracture in white women.N Engl J Med 1995;332:767-773.
19.
Canadian Task Force on the Periodic Health Examination.
Canadian guide
to clinical preventive health care.Ottawa: Canada Communication
Group, 1994:620-631.
20.
Johnston CC, Melton LJ, Lindsay R, et al.
Clinical indications for bone
mass measurement. A report from the Scientific Advisory Board of the National
Osteoporosis Foundation.J Bone Min Res 1989;4
(Suppl 2):1-28.
21.
Johnston
CC, Slemenda CW, Melton LJ.
Clinical use of bone densitometry.N Engl J Med 1991;324:1105-1109.
22.
Wahner HW, Dunn WL, Brown ML, et al.
Comparison
of dual energy absorptiometry and dual photon absorptiometry for bone mineral
measurements of the lumbar spine.Mayo Clin Proc
1988;63:1075-1084.
23.
Johnston
CC, Slemenda CW.
Measuring bone density and what it means.Endocrinologist 1991;1:83-87.
24.
Kellie SE.
Diagnostic and therapeutic technology assessment
(DATTA).JAMA 1992;267:286-294.
25.
Black DM, Cummings SR, Genant HK, et al.
Axial
and appendicular bone density predict fractures in older women.J Bone Min Res 1992;7:633-638.
26.
Hansen MA, Kirsten O, Riis BJ, et al.
Role of peak bone mass
and bone loss in postmenopausal osteoporosis.BMJ
1991;303:961-964.
27.
Krolner
B, Nielsen SP.
Bone mineral content of the lumbar spine in normal and
osteoporotic women: cross-sectional and longitudinal studies.Clin Sci 1982;62:329-336.
28.
Cann CE, Genant HK, Folb FO, et al.
Quantitated computed tomography for
prediction of vertebral fracture risk.Bone
1985;6:1-7.
29.
Firooznia H,
Golimbu C, Rafii M, et al.
Quantitated computed tomography assessment
of spinal trabecular bone. II. In osteoporotic women with and without vertebral
fractures.J Comput Tomogr 1984;8:99-103.
30.
Wasnich RD, Ross PD, Heilburn
LK, et al.
Prediction of postmenopausal fracture risk with use of bone
mineral measurements.Am J Obstet Gynecol 1985;153:745-751.
31.
Nillson BE, Westlin NE.
The
bone mineral content in the forearm of women with Colles' fracture.Acta Orthop Scand 1974;45:836-844.
32.
Cummings S.
Are patients with hip fractures more
osteoporotic? Review of the evidence.Am J Med
1985;78:487-494.
33.
Melton W,
Wahner HW, Richelson LS, et al.
Osteoporosis and the risk of hip fracture.Am J Epidemiol 1986;124:254-261.
34.
Riggs BL, Wahner HW, Dunn WL, et al.
Differential
changes in bone mineral density of the appendicular and axial skeleton with
aging.J Clin Invest 1981;67:328-335.
35.
Ross PD, Davis JW, Epstein RS,
et al.
Pre-existing fractures and bone mass predict vertebral fracture
incidence in women.Ann Intern Med 1991;114:919-923.
36.
Hui SL, Slemenda CW, Johnston
CC Jr.
Age and bone mass as predictors of fracture in a prospective study.J Clin Invest 1988;81:1804-1809.
37.
Gardsell P, Johnell O, Nilsson BE.
The predictive
value of bone loss for fragility fractures in women: a longitudinal study
over 15 years.Calcif Tissue Int 1991;49:90-94.
38.
Ross P, Davis J, Vagel J, et al.
A
critical review of bone mass and the risk of fractures in osteoporosis.Calcif Tissue Int 1990;46:149-161.
39.
Cummings SR, Browner WS, Ettinger B.
Should prescription
of postmenopausal hormone therapy be based on the results of bone densitometry?Ann Intern Med 1990;113:565-567.
40.
Riggs BL, Melton LJ.
The prevention and treatment
of osteoporosis.N Engl J Med 1992;327:620-627.
41.
Cumming RG.
Calcium intake
and bone mass: a quantitative review of the evidence.Calcif Tissue Int 1990;47:194-201.
42.
Aloia JH, Vaswani A, Yeh J, et al.
Calcium supplementation
with and without hormone replacement therapy to prevent postmenopausal bone
loss.Ann Intern Med 1994;120:97-103.
43.
Chapuy MC, Arlot ME, Delmas PD,
et al.
Effect of calcium and cholecalciferol treatment for three years
on hip fractures in elderly women.BMJ 1994;308:1081-1082.
43A.
Reid IR, Ames RW, Evans MC,
et al.
Long-term effects of calcium supplementation on bone loss and fractures
in postmenopausal women: a randomized controlled trial.Am J Med 1995;98:331-335.
44.
Law MR, Wald NJ, Meade TW.
Strategies for prevention of osteoporosis and
hip fracture.BMJ 1991;303:453-459.
45.
Rubin SM, Cummings SR.
Results of bone
densitometry affect women's decisions about taking measures to prevent fractures.Ann Intern Med 1992;116:990-995.
46.
Ryan PJ, Harrison R, Blake GM, et al.
I. Compliance
with hormone replacement therapy (HRT) after screening for postmenopausal
osteoporosis.Br J Obstet Gynaecol 1992;99:325-328.
47.
Hall FM, Davis MA, Baran DT.
Bone
mineral screening for osteoporosis.N Engl J Med
1987;316:212-214.
48.
Melton
LJ, Eddy DM, Johnston CC.
Screening for osteoporosis.Ann Intern Med 1990;112:516-528.
49.
Alexeera L, Burkhardt P, Christiansen C, et al.
Assessment
of fracture risk and application of screening for postmenopausal osteoporosis.
World Health Organization Technical Report Series 843.Geneva: World Health Organization, 1994.
50.
American Academy of Family Physicians.
Age charts for periodic
health examination.Kansas City, MO: American Academy
of Family Physicians, 1994.(Reprint no. 510.).
51.
American College of Obstetricians and Gynecologists.
Guidelines
for women's health care.Washington, DC: American College
of Obstetricians and Gynecologists, 1996.
52.
Tosteson AN, Rosenthal DI, Melton LJ, et al.
Cost effectiveness
of screening perimenopausal white women for osteoporosis: bone densitometry
and hormone replacement therapy.Ann Intern Med
1990;113:594-603.
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