Osteoporosis is a major epidemic
in industrialized nations. In the United States, 1.2 million fractures
occur each year (mostly in women) as a direct result of osteoporosis.
In recent years, there has been increasing interest in various methods
of measuring an individual’s risk of developing osteoporotic fractures.
Detection of bone loss at an early stage would presumably lead to earlier
and therefore more effective interventions aimed at slowing and possibly
reversing the process.
Currently, several technologies are
available to measure bone mineral density. The most commonly used method
is called dual-energy X-ray absorptiometry (DEXA). This technique can
measure the bone density of the hip and spine within a few percent.
DEXA has largely taken the place of dual-photon absorptiometry, because
the latter may fail to distinguish true bone mineral from osteophytes
in the lumbar spine. Bone density measurements at the distal radius
(in the wrist) or calcaneous (in the foot) are more convenient and less
expensive than DEXA. However, while these tests may help predict fracture
risk, bone density at distal sites do not necessarily correlate with
bone density of the hip and spine (where most of the medically significant
fractures occur). Even hip and spine measurements provide only a rough
estimate of fracture risk. For example, some individuals with very “dense”
bones develop osteoporotic fractures, whereas many people with frank
bone loss never suffer a fracture. Evidently, bone mineral content is
only one factor; the quality of the bone crystal (which cannot be readily
measured) also appears to be important.
During the past several years, urine
and blood tests have become available which measure various markers
of bone resorption (such as urinary N-telopeptide crosslinks and pyridinoline)
and bone formation (such as serum osteocalcin and bone-specific alkaline
phosphatase). Studies have shown that these markers can predict, at
least to some extent, changes in bone density as determined by DEXA.
However, there is little or no research on how the use of bone-building
agents (such as progesterone, DHEA, testosterone, or magnesium) would
affect the predictive value of these tests. For example, if a woman
is taking estrogen (which functions as an anti-resorptive agent), a
decline in markers of bone resorption would predict a reduction in bone
loss. On the other hand, a patient who is taking bone-building compounds
might show an increase in markers of bone formation, as well as a compensatory
rise in markers of bone resorption. If only the latter were being measured,
the results could suggest a net loss of bone is occurring, even though
the opposite might be the case. Thus, biochemical tests should be interpreted
with caution, and only after considering what treatments the patient
is using.
Doctors often recommend that DEXA
studies be repeated annually, in order to monitor the progress of treatment.
However, the precision of DEXA is only about 3%, whereas bone density
may change by less than 3% per year. Repeating the test too soon may
therefore provide nothing more than expensive and unreliable data points.
I usually advise my patients to wait 18-24 months before repeating their
DEXA test.
Although testing for osteoporosis
can provide a rough estimate of fracture risk, no single test or combination
of tests is 100% reliable. Considering the epidemic nature of osteoporosis,
everyone should consider a prevention program, including a diet of whole
foods, supplementation with calcium and other micronutrients,1
regular weight-bearing exercise, and abstaining from cigarettes and
excessive amounts of caffeine and alcohol. The tests mentioned above
may help identify individuals who are at increased risk. In those cases,
treatment with hormones and possibly other medications may be advisable.
Alan R. Gaby, MD
1. Gaby AR. Preventing and Reversing
Osteoporosis. Prima Publ., Rocklin, CA, 1994.
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