NURS6521: Bisphosphonates And Osteoporosis
NURS6521: Bisphosphonates And Osteoporosis
NURS6521: Bisphosphonates And Osteoporosis
A postmenopausal patient is prescribed bisphosphonates to treat osteoporosis. The nurse will instruct the patient to take the drug
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Oral therapy with bisphosphonates suppresses biochemical indices of bone resorption to about 50% of
baseline at one month and to a stable nadir of 50–70%
below baseline by three months (7-9). Bone formation
falls more slowly, reaching a steady state after six to
twelve months of treatment. Overall, bone turnover is
reduced to the levels seen in healthy young adults.
Bone mineral density increases modestly (2–6%)
during the first year of treatment. Values in the lumbar spine continue to increase at a slower rate for several years, while BMD in the proximal femur plateaus
after about two years of treatment (10-12). The initial
increase in BMD is a consequence of the reduced
number and depth of bone remodeling units (13).
Subsequent increase is due to a progressive increase in
the mineral density of bone, a consequence of reduced
remodeling and increasing age of the bone tissue (14).
Therapy preserves but does not increase bone volume
or restore bone structure (15,16).
In patients with osteoporosis, bisphosphonate
therapy results in clinically relevant reduction in the
incidence of vertebral and non-vertebral fractures
(including hip fractures) (10,12,17-21). Fracture protection occurs within a few months of beginning therapy (10,12,22-24) and is sustained for at least several
years (19,25). Importantly, the cycle of progressive,
multiple vertebral fractures is reduced by 77–96%
(10,18,20).
The specific mechanisms by which bisphosphonates prevent fracture are not known. The observed
effects on fractures exceed the estimates effects based
on BMD changes, and the correlation between
changes in fracture rates and changes in BMD is, at
best, modest (26). Estimates of the contribution of the
change in BMD to vertebral fracture reduction with
bisphosphonates have ranged from 17–28% (27,28),
and no differences in fracture risk reduction are
observed with different doses of individual bisphos-
Bisphosphonates
McClung
Arq Bras Endocrinol Metab vol 50 nº 4 Agosto 2006 737
phonates that cause varied BMD responses
(12,17,19,21). The time course of fracture reduction
more closely follows the effects of treatment on indices
of bone turnover than on BMD, and a significant correlation exists between the change in these markers
with therapy and fracture protection (29,30). It is likely that the direct effect of bisphosphonates — the suppression of osteoclastic bone resorption — reduces
fracture risk by decreasing the number of bone remodeling sites and stress risers, preserving or slightly
increasing bone density and maintaining bone structure (5)
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