Thesis Nurs. 1997 H396g
c.2
Hawley, Tina.
Guidelines for the
treatment of
1997.

GUIDELINES FOR THE TREATMENT
OF

POSTMENOPAUSAL OSTEOPOROSIS

by
TINA HAWLEY

Submitted in Partial Fulfillment of the Requirements
for the Master of Science in Nursing Degree

Approved by:

Judith Schilling, CR
T>, PHD
Committee Chairperson of
of Pennsylvania
Edinboro University c_

V
---- Mary Lou Keller, CRNP, PHD
Committee Member
Edinboro University of Pennsylvania

7 D?te

C •>"

TABLE OF CONTENTS

Acknowledgements

Chapter

ii
Page

Introduction

2

Background

2

Theoretical Framework

5

Definition of Terms

7

Summary

8

Review of Literature

10

Pathophysiology of Osteoporosis..

10

Diagnostic Testing

12

Estrogen Therapy

13

Alendronate

16

Intranasal Calcitonin

19

Sodium Fluoride

21

Calcium

21

Summary

23

Methodology

24

26

References

Appendix
A. Guidelines for the Treatment of

Postmenopausal Osteoporosis

32

ii

Acknowledgement

I would like to express my appreciation to my

thesis committee and to Usha Mohandas MD for their
support with this project.

A very special thank you

to my family, and good friend Peter Raimondo, for
their encouragement throughout this time.
I hope that these guidelines serve to improve
the medical care of women.

2

CHAPTER 1

Introduction
As

under

of

treated

(Miller,

of

1994,

1994) .

osteoporosis

patient.

osteoporosis was one of the most
illnesses

in

the

United

States

This chapter discusses the impact

on

society

and

the

individual

Advances in early detection and treatment

of osteoporosis are discussed.
Background

Osteoporosis, heart disease, and cancer are the
three most serious chronic conditions affecting
United States women (Chung & Maroulis, 1996).

Osteoporosis currently affects more than 20 million
individuals in this country, accounting for about

1.5 million fractures annually (Chung & Maroulis,

1 996) .

It is estimated that as many as 40% of women

over 50 years of age will experience an osteoporotic
fracture during their lifetime (Rupee, 1996).
Osteoporosis causes 250,000 hip fractures and
500,000 vertebral fractures each year (Murray &
O’Brien, 1995) .

Fractures caused by osteoporosis often result
in chronic pain related to poor healing and

deformity.

Disability and death are additional

complications of hip fractures.

The statistics for

20% die within 1
women with hip fractures show th^t

3

year of the injury, and 50% of the
survivors never
walk independently again
(Chung & Maroulis, 1996).

In the United. States, 60,000 nursing home admissions

yearly are attributed to hip fractures, and more

than 8% of all nursing home residents have had a hip
fracture (Butler, Ghrischilles, Davis, & Wallace,

1991).
As of 1994, osteoporosis was one of the most

under treated illnesses in the United States

(Miller, 1994).

Estrogen and subcutaneous

calcitonin were the only treatment for osteoporosis
until 1995.

Not all women are candidates for

estrogen therapy and some women choose not to take

estrogen therapy.

Subcutaneous calcitonin requires

a weekly injection that many patients object to

(Gray,1994).

In the fall of 1995, two new

medications were released for the treatment of
osteoporosis, alendronate and intranasal calcitonin.

Alendronate is a bisphosphonate that inhibits bone
resorption by indirectly interfering with osteoclast

activity, stopping the accelerated bone loss of
osteoporosis (Fleisch, 1992).

The exact mechanism

for alendronate’s effect on increasing bone density
has not been determined.

Calcitonin has a direct

inhibiting the bone
effect on the osteoclasts
osteoporosis (Re^inster, 1993).
resorption of

4

These new medications
replace estrogen therapy.

are not intended to
Alendronate and

calcitonin are indicated for
the treatment of
osteoporosis when estrogen therapy is

contraindicated, or when the patient refuses

estrogen therapy (Chung & Maroulis, 1996).

Estrogen

is the drug of choice for the treatment and

prevention of osteoporosis (Murray & O’Brien, 1995).

Many physicians have not been utilizing estrogen
therapy to the fullest extent and little emphasis
has been placed on osteoporosis prevention.

Fewer

than 15% of U.S. women over 65 are using hormone

replacement therapy (Chung &

Maroulis, 1996).

A

study conducted in Philadelphia found that only 37%
of gynecologists would recommend hormone replacement

therapy for the prevention of postmenopausal

osteoporosis and that only 7% of general internist

would do so (Kroll, Rozenberg, & Vandromme, 1996).
Early diagnosis is another important aspect in

the treatment of osteoporosis.

Until recently,

early diagnosis was not feasible because the only
a plain x-ray.
tool to diagnose bone loss was
Osteoporosis was usually not identified until a
x-rays do not show
fracture occured because plain
is lost
osteoporosis until 30% of bone mass
diagnostic technique is now
(Miller, 1990) . A new

5

available that identifies bone loss earlier, before

fractures occur.

Dual energy x-ray absorptiometry

exposes the patient to only low doses of radiation

and diagnoses early bone loss with a high degree of
accuracy (Chung & Maroulis, 1996). Early diagnosis

allows the health care provider to identify patient's
at risk for osteoporosis, and to begin treatment to

stop the accelerated bone loss.
The incidence of osteoporosis is increasing

with the aging of the population.

In 1990, 11% of

the population of the U.S. was 65 years or older. By

the year 2050, it is estimated that 22% of that
population will be over 65 (Miller, 1990).

By the

year 2050 over 6 million people are expected to

fracture a hip (Gray, 1994).

Health care costs for

osteoporosis are currently at least $6-10 billion
annually (Edwards, Finch, & Kirkpatrick, 1991).
This cost will increase as the incidence of

osteoporosis increases.

The prevention and

treatment of osteoporosis is a growing health care
concern in the United States.

Theoretical Framework
The theoretical framework for this project is

(Orem,1995). The
Orem's theory of self-care
self-care agent is key to the
patient's role as a
As a
prevention and treatment of osteoporosis.

6

self-care agent the patient
performs activities of
health promotion. This involves
activities that are
beyond those that are life sustaining.
As a selfcare agent, the patient with
osteoporosis has
health-deviation self-care requisites related to
medication compliance, risk reduction, and pain
control.

The patient may also have self-care

deficits related to universal self-care requisites

such as prevention of hazards to human functioning

and adequate rest.

The role of the primary care

provider is to work with patients to determine their
health care needs and to assist patients in meeting

those needs.

The treatment plan must be

individualized according to the self-care deficits
of each patient.
The menopausal woman has primary prevention

self-care

demands related to education about risk

factor reduction for osteoporosis.

Prevention and

early detection of osteoporosis will decrease the

patient’s self-care deficits and increase her
ability as a self-care agent. The patient with
tertiary self-care
osteoporosis has secondary or

demands related to

education about diagnosis and

treatment.

The results of

this project is the development

of clinical guidelines for the treatment of

7

osteoporosis.

Clinical guidelines are a tool for

primary care providers to
use in planning quality
patient care. The guidelines
are based on a review
of the literature and input from experts in the

treatment of osteoporosis.
Definitions of Terms

1 .

Primary Care Provider -

A physician, nurse

practitioner, or physician assistant providing
primary care to patients.

2.

Postmenopausal

The time period in a women’s

life that begins 12 months after menstruation
ceases.
3.

Clinical Practice Guidelines

A set of

diagnosis-specific guidelines developed by an

interdisciplinary team to assist clinicians in
providing quality patient care (Freed & Pare, 1995).

4.

Risk Factors

Factors that identify persons

who are at risk of developing a disease.

Risk

factors for osteoporosis are postmenopausal,
premature menopause, Caucasian or Asian race,

positive family history, small frame, leanness, low

calcium intake, inactivity, history of atraumatic

fractures ,

nulliparity, long-term glucocorticoid

therapy, long-term
hyperthyroidism or

anticonvulsant therapy,
excessive thyroxine, cigarette

smoking, alcohol abuse, and gastrlo/small bowel

8

bowel resection (Chung & Maroulis,
1996).
5. Osteoporosis Skeletal state of decreased bone
mass that may result in
pathologic bone fracture(s).
Osteopenia is a precursor for osteoporosis (Edwards,

Finch, & Kirkpatrick, 1991).
6.

Osteoclasts

Cells located on the bone surface

that break down bone in the remodeling process

(Miller, 1994).

7.

Osteoblasts

Cells located on the bone surface

that build back the bone broke down by the
osteoclasts (Miller, 1994).

Summary

Osteoporosis is one of the most serious chronic
conditions affecting women and is one of the most

under treated illnesses (Chung & Maroulis, 1996).
Osteoporosis results in fractures that cause

disability, chronic pain, and loss of self-esteem.

Osteoporosis uses $6-10 billion annually in health
care costs, and this figure will increase with the

growing population over age 65 years (Edwards,

Finch, & Kirkpatrick, 1991).
There are three medications for the treatment
intranasal
of osteoporosis: alendronate,

calcitonin, and estrogen.

the rapid bone loss

These medications inhibit

of osteoporosis and increase

bone density in varying degrees.

Diagnostic tools

9

are also now available for identifying early bone

loss before fractures occur.
Orem’s theory of self-care is the theoretical
framework for developing these clinical practice

guidelines.

The patient with osteoporosis is a

self-care agent with health-deviation requisites
related to medication compliance, risk reduction,

and pain control.

10

CHAPTER 2
Review of Literature

The pathophysiology, the diagnosis, and the

treatment of osteoporosis are the topics included in

this literature review.

The review of literature

also includes results of studies using medications
for osteoporotic treatment.

This information was

the basis for the osteoporotic treatment guidelines.

Pathophysiology of Osteoporosis
The skeleton of the human body undergoes a

continuous process of remodeling.

This remodeling

process is the body’s mechanism for obtaining free

calcium and phosphate, in addition to responding to
bone stress (Ramamureti, 1979).

The remodeling

process consists of osteoclasts that break down

bone, and osteoblasts that rebuild bone (Riis,
1996).

In osteoporosis, osteoclast activity exceeds

osteoblast activity, resulting in a net loss of bone
mass (Ramamureti, 1979).

Osteoporosis can be described as primary or
secondary, depending upon its etiology.

Primary

and is divided into two
osteoporosis is idiopathic
Secondary
categories, senile and postmenopausal.
an identified underlying
osteoporosis is caused by

11

disease (Gray, 1994)
Postmenopausal osteoporosis is related to

estrogen deficiency (Barzel, 1990).

There are

estrogen receptors located on the bone’s osteoblasts

that trigger osteoblastic activity (Lane, McDonnell,
& Zimmerman, 1987).

Decreased estrogen levels

result in less triggering of the osteoblasts and, as

a result, less bone is rebuilt.

Since estrogen also

stimulates the release of calcitonin, which inhibits
bone resorption, an estrogen deficiency results in

less circulating calcitonin (Lane et al., 1987).
The end result of estrogen deficiency is excessive
bone resorption and a loss of bone mass.

Decreased

bone mass causes bone fragility and can result in

pathological fractures (Riis, 1996) .
Senile osteoporosis is related to the
physiological changes of aging (Ettinger, 1987).

With aging there is often a decrease in active
and a
vitamin D, a decline in physical activity,
1987).
decline in osteoblast activity (Lane et al.,

The loss of bone mass

in osteoporosis effects

two types of bone, trabecular and cortical, at
Trabecular bone,
different rates (Riis, 1996).
the skeleton, is concentrated
accounting for 20%
and other flat bones, and
in the vertebrae, pelvis,
Trabecular bone is
at the end of long bones -

12

effected first in postmenopausal osteoporosis

because its surface area is greater (Madson, 1989).
Cortical bone is found in the shafts of the long
bones and comprises 80% of the skeleton.

Trabecular

and cortical bone are effected equally in senile
osteoporosis.
In osteoporosis, fractures can occur with

normal activity or following minimal trauma.

The

most prevalent areas for fractures are the

vertebrae, ribs, proximal femur, proximal humerus,

and the distal radius (Kupec, 1996).

The vertebrae

are composed primarily of trabecular bone, therefore
they fracture earlier than the highly cortical area

of the femoral neck (Lane et al., 1987).

The risk

of fracture in osteoporosis relates to bone density
or mass

(Chung & Maroulis, 1996).

Bone density

correlates with bone strength and accounts for 75%
to 85% of its variance (Riis, 1996).

Diacmostic Testing
Bone density measurement can be used to predict
the risk of fractures (Murray & 0’Brien, 1995). In

in bone density of
postmenopausal women, a decrease
below the mean indicates a
one standard deviation
2.3 times higher than
risk of vertebral fracture
Osteoporosis is
average (Bell et al-, 1•
Health Organizatign as a value
defined by the World

13

for bone mineral density that is
2.5 standard

deviations or more below the young adult mean (Gold

et al. , 1 996) .
Dual energy x-ray absorptiometry (DEXA) is a
new bone density test.

It is an improvement over

the older single energy x-ray absorptiometry (SXA).

The SXA test measured bone density at the wrist and
heel, and the heel site is less predictive of
osteoporosis .

The DEXA test images the spine and

hip, which is more predictive of osteoporosis.

The

effective radiation dose of the DEXA is 1 (uSV) , and
the SXA radiation dose is less than 1 (uSV) .

A bone

density result between 1 and 2.5 standard deviations
below the mean indicates osteopenia; the DEXA should

be repeated in 2 years (Gold et al. , 1996) .
measures
Quantitative computerized tomography (QCT)

bone density using the spine site, but the effective
(Gold et al., 1996).
radiation dose is 60-100(uSV)
of less than 1%
The DEXA has a precision rate
precision rate of 3% to
variation, and the QCT has a
For comparative value,
5% variation (Miller, 1994).

used each time.
the same test must be
Estrogen Therapy

In postmenopausal

osteoporosis, the decrease in

menses ceases and occurs at
bone mass begins before
5 to 10 years after
a higher rate the first

14

menopause (Bush, Ettinger, Lobo, Mishell, & Speroff,

1 995) .

The rate of bone loss during the first 3 to

4 years postmenopausal is typically 2.5% annually.
After that time, the rate of bone loss slows to an

annual rate of 0.75% (Chung & Maroulis, 1996).

Accelerated bone loss occurring in the early
postmenopausal period can be prevented by the use of

estrogen (Bush et al., 1995).

Estrogen is the only

medication currently FDA approved for the prevention
of osteoporosis.

In a study done at the University

of California, San Francisco, 73 women who were

started on estrogen therapy at the beginning of

menopause showed no significant bone loss during a 2
year follow-up period.

Other studies have also

shown a beneficial effect on bone when estrogen was
started within 3-5 years of menopause or
oophorectomy (Barzel, 1990).
Women who use estrogen therapy for 10 years
after menopause, and then discontinue its use,
reduce their relative fracture risk at the age of 80

by 15%.

Women remaining on estrogen therapy longer

than 10 years reduce their relative fracture risk by

50% by the age of 80 (Bush et al., 1995).

Controversy exists concerning the long term use of

estrogen therapy because of the increased risk of
breast cancer with aging and its possible

15

association with estrogen therapy.

Studies have come to conflicting conclusions

concerning the risk of breast cancer with estrogen

therapy.

It is important to consider the risk in

relationship to the benefit of hormone therapy.

A

60 year old woman on hormone therapy has a 1-in-14

chance of breast cancer if she lives to be 80 years
old; but she has an 8-in-14 chance of heart disease
if she lives to age 80 without hormone therapy (Bush
et al., 1995).

There is even benefit for women who start
estrogen therapy 5 or more years after menopause.

A

study done at Mayo Clinic showed a 5% to 7% increase

in bone density, and a reduction in vertebral
fractures , in postmenopausal women on estrogen

therapy beginning more than 5 years after menopause
(Bush et al., 1995).

The greatest benefit of

estrogen therapy in preventing osteoporosis,
however, is gained when it is started early in

menopause (Gambrell, 1991).

The use of progesterone with estrogen does not
alter the beneficial effect of estrogen therapy on

bone mass (Barzel, 1990).

The dose of estrogen that

is effective in preventing and treating osteoporosis
is 0.625 mg (Bush et al., 1995) .

A transdermal form

of estrogen is also approved (Miller, 1992)

16

Alendronate

Alendronate is a new medication for the
treatment of osteoporosis, released in the fall of

1 995.

Alendronate is a bisphosphonate which is an

alteration of a naturally occurring substance,
pyrophosphonate (Compston, 1994).

The phosphonate

is altered by adding two carbons that make it
resistant to hydrolysis.

There have been other

medications in this classification used to treat
osteoporosis (Fleisch, 1992).

Etridonate has been

used in European countries in a cyclic pattern, but

studies have shown alendronate to be 100 to 500 fold
more potent (Bell, et al., 1995).

Etridonate is

given parenterally.

Alendronate inhibits osteoclast-mediated bone

resorption and has an indirect effect on osteoblast
activity (Gertz, Kanis, Ortolani, & Singer, 1995).

The decreased osteoclast activity results in fewer
bone areas to refill, so the osteoblasts are able to
keep pace with the osteoclasts and can even exceed

osteoclastic activity.

This results in an increase

in bone density as well as a slowing of bone loss
(Fleisch, 1992).

There is no proven adverse effect on bone
mineralization with alendronate (Papapoulos, 1993).

Normal bone mineralization is important in

17

maintaining bone strength.

Researchers believe that

bone mineralization will not be effected because the

osteoblast activity remains at a normal rate.

Five clinical trials, involving 1,827

postmenopausal women aged 41 to 85 with
osteoporosis, showed an increase in bone density of

the hip and lumbar vertebrae with the use of
alendronate.

These trials were conducted in six

countries and the women were followed for 2 years
(Chung & Maroulis, 1996).

The trials showed an

average increase in bone mineral density of 8.2% at
the spine and 7.2% at the hip, and also reported 48%

fewer new spinal fractures (Lindsay, 1996).
The dosing regime for alendronate that best

balances efficacy and side effects is 10mg daily
(Bell et al., 1995). In clinical trials the

occurrence of side effects with alendronate, 10mg
orally daily, was low (Chung & Maroulius, 1996).
The most common side effect was gastrointestinal

upset which occurred in less than 5% of patients.

There was a rare occurrence of erosive esophagitis
during the first few weeks of treatment.

Alendronate is contraindicated in patients with
dysphagia, gastritis, peptic ulcer disease, or
esophageal irritation (Gold et al., 1996).

Patients

must be instructed to report to their health care

18

provider immediately should symptoms of dysphagia or
esophageal irritation occur.

Information from clinicians prescribing
alendronate has shown a greater occurrence of
gastrointestinal upset then expected from clinical

trials (Nightingaler 1996).

This may be related to

patients’ nonadherance to instructions on how to

take the drug.

To prevent esophageal irritation,

alendronate must be taken with a glass of water and
the patient must not lie down for the next 30
minutes (Lindsay, 1996).

Alendronate is absorbed

poorly from the gastrointestinal tract,
approximately 1% of the administered dose being
absorbed.

Absorption is markedly reduced further in

the presence of food (Gertz et al., 1995).

The

medication therefore must be taken on an empty

stomach and the patient must not eat for 30 minutes.

Alendronate cannot be taken along with any other
medications or liquid other than water (Lindsay,

1996) .
Alendronate is excreted by the kidneys and is
contraindicated in patients with a renal creatinine
clearance less than 35ml/minute (Lindsay, 1996).

The plasma half-life of alendronate is short, but
its bone half-life is about 10 year.

Alendronate is

absorbed specifically by bone, and especially so in

19

areas of resorptive activity (Gertz et al., 1995).

The long bone half-life has not been shown to have
an adverse effect on bone mineralization (Compton,
1994) .

Alendronate therapy, in clinical trials,

resulted in an increased bone mineral density at the
lumbar spine after 6 weeks of treatment

(Gertz et

al., 1995).

Intranasal Calcitonin
Nasal spray calcitonin was FDA approved for use
in treating osteoporosis in the fall of 1995.
Calcitonin is a natural occurring hormone produced

by the thyroid gland (Reginister, 1993).

Calcitonin

directly inhibits osteoclast activity by interfering

with the osteoclast precusor (Christiansen, Hansen,
Jensen, & Overgaard, 1992).

The medication also

binds to receptors on the osteoclasts, causing the

osteoclasts to move away from the bone resorptive
surface (Reginister, 1993).

The end result is to

stop the rapid bone loss.
Salmon calcitonin is used in the intranasal
preparation because its potency is greater than
human calcitonin (Attinger et al., 1987) .

Calcitonin is not absorbed when taken orally.

The

biological effects obtained after intranasal

administration are equivalent to those observed with
parenteral administration (Reginister, 1995).

20

Tolerance to intranasal calcitonin is excellent with
side effects occurring infrequently and transiently
(Chung & Maroulis, 1996).

Side effects with

intranasal calcitonin include nausea, vomiting, and
flushing, but rhinitis is the most common side­

effect (Gold et al., 1996).

Two randomized, placebo controlled trials with
intranasal calcitonin conducted with 325

postmenopausal females with osteoporosis showed a
slowing of bone loss and a 1 % increase in bone
mineral density of the lumber spine.

The increase

in bone density began as early as 6 months after

treatment was started.

These studies did not show a

decrease in the fracture rate for the spine or hip,
but the length of the study was only 2 years.

A 2

year prospective study with elderly women having low

forearm bone density showed a reduced fracture rate
of 66% with nasal salmon calcitonin, as compared

with oral calcium supplements alone (Reginister,

1995).
The usual dose of nasal calcitonin is 200
I.U./day or one spray, alternating the nostril side

used (Lindsay, 1996).

Calcitonin has also been

shown to relieve bone pain, but the exact mechanism

is unknown (Chan & Pun, 1989).

The use of

calcitonin decreases the need for daily consumption

21

of analgesic drugs for bone pain.

Sodium Fluoride
Sodium fluoride has been studied for some years

for its usefulness in treating osteoporosis.

There

is a significant increase in bone mass with sodium
fluoride, but with abnormal bone mineralization.

Recent clinical trials have shown that the abnormal

mineralization with sodium fluoride is dose
dependent and does not occur at doses less than 20
mg daily (Kanis, 1993).

Extended release sodium

fluoride has been shown not to effect bone

mineralization (Meunier & Ringe, 1995) .

Sodium fluoride has a bone-anabolic effect, and

in patients with extensive bone loss would reduce

the risk of bone fractures (Meunier & Ringe, 1995).
The antiresorptive agents, alendronate and

calcitonin, are not as effective in these cases.
The effects of sodium fluoride on bone mass has not

been consistent with up to 40% of patients showing

little or no improvement.
not clear (Kanis, 1993).

The reason for this is
Enteric coated forms

decrease the gastointestinal upset that occurs with

other forms of sodium fluoride.

Calcium
Calcium supplementation is not effective

22

treatment for established osteoporosis although

calcium helps to build bone and low calcium intake
contributes to low bone mass (Todd, 1985).

A recent

study of 118 healthy white women 3 to 6 years after
menopause demonstrated that calcium augmentation
alone retarded bone loss from the femoral neck, but
that the effect was less pronounced compared to the

group taking calcium combined with hormone

replacement therapy (Chung & Maroulis, 1996).

It is

unclear whether calcium supplements actually
decrease fractures (Todd, 1985).

Calcium supplements are to be taken along with

alendronate or calcitonin. The recommended dose of
calcium is 1,000 mg per day for premenopausal women

or women on hormone replacement therapy, and 1,500
mg after menopause without hormone replacement.
Vitamin D increases the absorption of calcium but

does not increase bone density independently (Todd,
1 985) .

It is recommended that patients take 400 to

800 I.U. of Vitamin D along with calcium supplements
(Chung & Maroulis, 1996).

Vitamin D insufficiency

is common among the frail elderly, especially those
living in northern climates, or in institutions
where they are exposed to little sunlight (Murray &

O’Brien, 1995).

23

Summary
Estrogen therapy is approved for use in

preventing postmenopausal osteoporosis, and is
effective in stopping the accelerated bone loss that
occurs in the first 5 years of menopause.

Alendronate slows the rate of bone loss and
increases bone density.

Alendronate increases bone

density at the spine by 8.2% and at the hip by 7.2%,

with 48% fewer new spinal fractures (Lindsay, 1996) .
Intranasal calcitonin stops the accelerated bone

loss of osteoporosis, and increases the bone density

of the spine by 1%.
The studies done with alendronate and
intranasal calcitonin have extended over only a 2

year period.

This is not long enough to determine

the effect on hip fractures.

Sodium fluoride is not

FDA approved for use in the United States.
supplementation should be taken by all

postmenopausal women, along with vitamin D.

Calcium

24

CHAPTER 3
Methodology-

Written guidelines for treating medical
conditions provide for standardized patient care

that promotes quality.

Guidelines serve as tools to

use in determining the treatment plan for an
individual patient.

Research data, a review of the

literature r and expert opinion are the basis for the

development of treatment guidelines (Freed & Pare,

1995) .
In order to develop guidelines for the
treatment of postmenopausal osteoporosis, a review

of the research data on alendronate, calcitonin, and
estrogen was done.

Information collected concerned

the safety and efficacy, side effects, and
contraindications for each medication.

Effective

dosage and indications for use were also studied.

Risk factors for postmenopausal osteoporosis
were also identified from the literature.

Risk

factor identification is an integral part of
determining the need for diagnostic testing for

osteoporosis.

These guidelines, therefore, include

screening patients for osteoporosis risk factors;

indications for diagnostic testing are also
included.

25

Patient education is an important aspect of the
treatment of postmenopausal osteoporosis.

Education

involves information about taking the medication,
side-effects, and other means of risk factor

reduction.

Intervention in osteopenia is included

in the guidelines, because this can prevent the
development of osteoporosis and the occurrence of

fractures.

Guidelines for the follow-up of

osteoporotic treatment are included.
The development of the guidelines involved the

input from experts in the field who are experienced
in using the medications.

These experts were a

board certified internal medicine physician and a

pharmacist.

The experts reviewed the guidelines,

and appropriate corrections were then made in the

wording of the guidelines.
are in Appendix A.

The revised guidelines

26

References
Attinger, M., Azria, M., Buclin, T.,
Burckhardt, P•, Gomez, F., Jacquet, A., & Randin, J.

(1987). The effect of rectal and nasal

administration of salmon calcitonin in normal
subjects . Calcified Tissue, 41, 252-25
Barzel, U.

(1990). Estrogen therapy for

osteoporosis: Is it effective? Hospital Practice, 2
(7), 95-198.

Bell, N., Chesnut, C., Delmas, P., Ensrud, K.,
Genant, & Harris, H.

(1995). Alendronate treatment

of the postmenopausal woman: Effect of multiple
dosages on bone mass and bone remodeling. American
Journal of Medicine, 99(2), 144-151 .

Bush, T., Ettinger, B., Lobo, R., Mishell, D.,
& Speroff, L. (1995) . New concepts in managing

menopause. Symposium, Patient Care, 18-24.
Butler, D., Chrischilles, E., Davis, C., &

Wallace, R. (1991). A model of lifetime osteoporosis
impact.

Archives of Internal Medicine,151, 2026-

2032.
Chan, L., & Pun, K.

(1989). Analgesic effect of

intranasal salmon calcitonin in the treatment of

osteoporosis vertebral fractures. Clinical
Therapeutics^ 11(2), 205-208.

Christiansen, C., Hansen, M., Jensen, S., &

27

Overgaard, K.

(1992). Effect of calcitonin given

intranasally on bone

mass and fracture rates in

established osteoporosis:
A dose-response study.
British Medical Journal, 305, 477-479.
Chung, P., & Maroulis, G.

(1996). Osteoporosis:

An update on prevention and treatment. Physician
Assistant , 12(4), 83-96.
Compston, J.

(1994). The therapeutic use of

bisphosphonate. British Medical Journal, 309 (1 7) ,
711-715.
Edwards, M., Finch, N., & Kirkpatrick, M.
(1991). Assessment and prevention of osteoporosis

through use of a client self-reporting tool. Nurse
Practitioner, 16(7) , 16-25.
Ettinger, B.

(1987). Estrogen and

postmenopausal osteoporosis. American Association of

Occupational Health Nursing, 35112), 543-546.
Fleisch H.

(1992). Editorial: Prospective use

of bisphosphonates in osteoporosis. Journal of
Clinical Endocrinology and Metabolism, 76(6),

1397-

1398.

Freed, M., & Pare, S.

(June, 1995). Clinical

practice guidelines for quality patient outcomes. In
P. A. Hickey (Ed.), Nursing Clinics of North America
(pp-

183-196)- Philadelphia: W. B. Saunders Co.
Gambrell, R-

(1991)- Estrogen replacement

therapy and osteoporosis. Hospital Practice, 26

28
(suppl. 1)

0-5.

Gertz, B-, Kanis,
J-, Ortolani, S., & Singer,

F.

(1995). Rationale for the use of alendronate in

osteoporosis. Osteoporosis International, 5, 1-11.

Gold, D., Lee, L., & Tresolini, C.

(1996) .

Working with patients to prevent, treat, and manage

osteoporosis (Curriculum Guide For Health
Professions). San Francisco, CA: National Fund for
Medical Education.

Gray, M. A.

(1994). Osteopororsis medications:

What’s your source of information? Orthopaedic

Nursing, 13(5), 55-58.
Kanis, J.

(1993). Treatment of symptomatic

osteoporosis with fluoride. The American Journal of

Medicine, 95 (suppl. 5A) , 5 3 s-6 0 s.
Kroll, M. , Rozenberg, S., & Vandromme, J.
(1996) .

Decision factors influencing hormone

therapy. Journal of Obstetrics and Gynecology
1 0 3 (suppl. __1 3) t 92-98.

Kupec, D.

(1996). Alendronate for the treatment

of osteoporosis. Nurse Practitioner, 21(1), 86.

Lane, J.z McDonnellr J., & Zimmerman, P.
(1987). Osteoporosis: Definition, risk factors,

etiology, and diagnosis. American Association of
Occupational Health Nursing^ 35112), 527-530.

Lindsay, L.

(1996) . The new treatment options

for osteoporosis. Modern Medicine^ 64_l 6-7.

29

Madson, s.

(1989). How to reduce the risk of

postmenopausal osteoporosis. Journal of

Gerontological Nursing, 1_5 (9) , 20-23.

Meunier, p_, & Ringe, J.

(1995). What is the

future for fluoride treatment of osteoporosis?
Osteoporosis International, 5, 71-73.

Miller, C.

(1992). Estraderm for osteoporosis.

Geriatric Nursing, 13 L6) , 337-338.

Miller, J.

(1994). Clinical evaluation of

osteoporosis. Physician Assistant, 18(3), 23-24.

Miller, P.

(1990). Osteoporosis: New

developments in prevention and treatment. Physician

Assistant, 14(6), 17-18.

Murray, C., & O’Brien, K. (1995). Osteoporosis

workup: Evaluating bone loss and risk of fractures.
Geriatrics,

50(9)t

Nightingale,

41-53.

S.

(1996). Important Information

regarding alendronate adverse reactions. Journal of

American Medical Association^ 275(20), 1534.

Orem,D.

(1995) . Nursing concepts of practice

(5th ed.) St. Louis, MO: Mosby.

Papapoulos, S.

(1993). The role of

and treatment of
bisphosphonates in the prevention
,
osteoporosis.

American Journal of Medicine,
—-------------------

95(suppl. 5A), 48s-51s.

Senile osteoporosis. In
Ramamurti, C. (1979).
R. V. Tinker (Ed-), Orthopaedics in Primary Care

30

(PP- 366-368). Baltimore: Williams & Wilkins.

Riis, B.

(1996) . The role of bone turnover in

the pathophysiololgy of osteoporosis. British
Journal of Obstetrics and Gynaecology, 103(suppl
13), 9-15.

Reginister, J.

(1993). Calcitonin for

prevention and treatment of osteoporosis. The
American Journal of Medicine, 95, 44s-46s.

Todd, B.

(1985). Can osteoporosis be treated?

Geriatric Nursing, 6_L6) , 359-360.

31

Appendix A

32

Guidelines for the Treatment
of

Postmenopausal Osteoporosis

Osteoporosis is defined as a metabolic disorder

of bone in which decreased bone mass and strength
lead to an increased incidence of fractures with

minimal or no trauma [1] .

In osteoporosis,

osteoclast activity exceeds osteoblast activity,
resulting in a net loss of bone mass.

Osteoporosis

can be described as primary or secondary, depending
upon its etiology.

Primary osteoporosis is

idiopathic and is divided into two categories,

senile and postmenopausal. Secondary osteoporosis is
caused by an identified underlying disease [2].
The following guidelines are designed to assist
the practitioner in planning the treatment of

osteoporosis.

These guidelines are based on a

review of the literature and input from experts in

the field.

The guidelines include prevention,

diagnosis, use of medications, patient education,
and follow-up.

It is hoped that these guidelines

will promote quality patient care that meets the

needs of the individual patient.

33

Prevention of Osteoporosis

Women during the transitional years before
menopause should be evaluated for osteoporosis risk
factors. Hormone replacement therapy
should be

discussed with women during this time, and they
should be evaluated for contraindications to hormone
therapy.

Women that choose not to use hormone

replacement therapy, or those in which it is

contraindicated, may be at risk for osteoporosis.
Bone density testing should be considered for these

women at menopause and thereafter.
Osteopenia is decreased bone density without
the occurrence of fractures [2] .

It is defined as a

bone density between 1 and 2.5 standard deviations
below the young adult mean [3] .

Bone mineral

density correlates highly with the risk of

fractures, and osteopenia is a risk factor for

osteoporosis.

Identification of osteopenia, along

with the presence of additional osteoporotic risk

factors, allows for early intervention before the
occurrence of a fracture.

Determining the need for bone density testing
should be based on the overall patient profile.

Risk factors

osteoporosisz health motivation,

and financial status should be considered in
of bone density
determining the

34

testing.

Refer to Figure 1 for an outline of the

guidelines for prevention of postmenopausal

osteoporosis.

Risk factors for osteoporosis
- Postmenopausal

- Premature menopause
Caucasian or Asian race

- Positive family history

Small frame
Leanness

Inactivity
Low calcium intake

- History of atraumatic fracture

- Nulliparity
- Long-term glucocorticoid therapy
- Long-term anticonvulsant therapy

_ Hyperthyroidism or excessive thyroxine
- Cigarette smoking
- Alcohol abuse
- Gastric/small bowel resection

35
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36

Candidates for bonP ■density

tie sting.

- Postmenopausal women without hormone
replacement
Women concerned about
osteoporosis
- Women undecided
concerning hormone replacement
therapy
Persons on long-term

Presence of

corticosteriods

dowager’s hump”

— Persons that have suffered a nontraumatic fracture
after 40 years of age

Estrogen therapy.
Postmenopausal osteoporosis is related to

estrogen deficiency.

Osteoblasts have estrogen

receptors that trigger osteoblastic activity, and

with a decrease in estrogen there is a decrease in
bone building [4] .

When estrogen therapy is started

in the first 3 to 5 years of menopause, bone loss
can be prevented.

The dose of estrogen that is

effective in preventing osteoporosis is .625 mg
daily.

The use of progesterone with estrogen does

not alter its effectiveness.

estrogen is also approved.

A transdermal form of

The longer that estrogen

is used after menopause the greater the reduction in
fracture risk.

The use of estrogen for 10 years

discontinued, reduces the
postmenopausally , then
risk of fractures by 15% at the age of 80.

Remaining on estrogen

therapy beyond 10 years

37

postmenopausally reduces

the risk of fractures by

50% at the age of 80 [5] .

Alendronate

LFosamax)

Alendronate is another medication that
effectively treats osteopenia.

Alendronate is a

bisphoshonate medication that stops bone loss by

interfering with the osteoclasts.

The recommended

dose is 10 mg orally daily, to be taken on an empty

stomach.

The patient must then remain NPO for 30

minutes.

Alendronate needs to be taken with a full

glass of water and with no other medication, liquid,
or food.

Diagnosing Osteoporosis
Osteoporosis is defined by the World Health
Organization as a value for bone mineral density

that is 2.5 standard deviations or more below the
young adult mean.

Dual energy x-ray absorptiometry

(DEXA) measures bone density at the spine and hip.
DEXA testing uses low dose radiation with a
precision rate of less than 1% variation.
Quantitative computerized tomography (QCT) measures

bone density using the spine site with an effective

DEXA and a precision rate
radiation dose higher than
For comparative value,
of 3 to 5% variation [3] .
the same test must be

used each time.

38

Osteoporosis Treatment
Estrogen therapy, alendronate,
and intranasal
calcitonin are the medications
approved for treating
osteoporosis. Which medication
used depends on the
individual patient. The practitioner needs to

discuss various treatment options with the patient
and decide which one best meets the patient's needs.

Refer to figure 2 for an outline of the guidelines
for treatment of postmenopausal osteoporosis.

Estrogen therapy
Estrogen therapy increases bone density by 5%
to 7% and reduces the risk of vertebral fractures,

even when started 5 or more years after menopause
[5] .

The dose is .625 mg daily and is used with

progesterone if the patient has an intact uterus.
The additional benefits of estrogen therapy, over

and above bone density, need to be considered when

deciding on treatment.

The patient with a high risk

of heart disease, for example, may obtain particular
benefit from estrogen therapy.

Estrogen therapy is

not a treatment option for men.

Alendronate therapy. (Fosamaxl
Alendronate increases bone density by 8.2% at

the spine and 7.2%

at the hip, and there is a 48%

reduction in new spinal

fractures [6]-

Alendronate

after being started,
increases bone density 6 weeks

39

and there is some effect for 2

years after it is
Contraindications to alendronate
are
dysphagia, gastritis,
peptic ulcer disease,

stopped.

esophageal irritation, and creatinine
clearance less
than 35 ml/min.

Side effects of alendronate include
gastrointestinal upset, and a rare occurrence of
esophageal erosion which usually occurs in the first

few weeks of therapy.

Patients should be instructed

to notify their health care provider of symptoms of
esophageal irritation.

The patient must remain

upright for 30 minutes after taking alendronate to
reduce the incidence of esophageal irritation.

Only 1 % of alendronate is absorbed orally, so
the patient must take it on an empty stomach and not
eat or drink for 30 minutes.

No other medications

can be taken with alendronate, and it should be
taken with a full glass of water [7] .

The primary care provider needs to assess the

patient’s ability to comply with these instructions

before ordering alendronate.

The patient with

difficulty obtaining an
severe kyphosis may have
benefit from a different
upright position, so may
with a poor memory may have
treatment. The patient
difficulty remembering

consistently.

Patient

with the success

the instructions
motivation plays a big part

of alendronate therapy-

40

Intranasal ■Calcitonin
.therapy (Miacalcin)
Calcitonin decrease osteoclast
activity
inhibiting the accelerated bone loss of

osteoporosis.

Administrated as an intranasal spray,

calcitonin has been shown to increase bone density

by 1% at the lumbar spine.

An increase in bone

density is seen 6 months after starting therapy, and
there is some effect for 2 years after stopping

intranasal calcitonin.

The only contraindication to

its use is an allergy to salmon calcitonin [8] .

Side-effects include rhinitis, nausea,

vomiting, and flushing.

The effective dose is 200

I.U./day taken as one intranasal spray, alternating

nostrils each day.

Side-effects, when they do

occur, are often transient.
Intranasal calcitonin has an additional benefit

of reducing bone pain.

Patients suffering from pain

associated with osteoporotic fractures may benefit

from this medication.

Intranasal calcitonin can be

given along with hormone replacement therapy -

Patient Education

explained to the patient
Osteoporosis should be
started, and all treatment
before treatment is
discussed. It is important that
options should be
of osteoporosis
the patient understand the role
treatment.

41

Calcium
All women after menopause,
and men after 50
years of age, should be instructed
on calcium
supplementation. The recommended daily calcium

requirement is 1000 mg with hormone replacement or

1500 mg without hormone replacement.

It is

recommended that the calcium be taken in divided

doses.

Vitamin D 400 I.U. to 800 I.U. should also

be taken to aid calcium absorption [9]

Exercise
Weight bearing exercises, such as walking, are

recommended to reduce the risk of osteoporosis.

All

people should begin a regular exercise routine as an

adolescence and continue it throughout their adult

lives.
Fall prevention

Instruct the elderly patient to avoid throw
rugs in the home, to use a cane or walker as needed,
to maintain good posture and body mechanics, and to

avoid medications that may cause dizziness.
Consultation with physical therapy may be beneficial

with some patients for fall precautions.

Follow-up
should be done in 1 to
A follow-up bone density
receiving medication to
2 years for the patient

42

treat osteopenia.

Dual energy X-ray absorptiometry

may not be sensitive enough to detect therapeutic

effects within the first year or so [10].

The

patient receiving medication to treat osteoporosis

should have a follow-up bone density in 3 years.
The primary care provider may want to change

medications after the follow-up bone densities.

For

example, the patient with osteopenia treated with

alendronate may be able change to hormone therapy if

bone density returns to normal.

The patient with

osteopenia or osteoporosis on hormone replacement

who shows no improvement after 2-3 years may benefit

from additional medication.

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References

1 - Stein J: Osteoporosis. In:
Internal Medicine, 4th
ed. St. Louis, MO:
Mosby-Year Book, 1994:1515.
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Tinker, ed. Orthopaedics in
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: Williams & Wilkins, 1979:366-368.

3. Gold D, Lee L, & Tresolini C: Working with
patients to prevent, treat, and manage osteoporosis:
Curriculum Guide For Health Professions. San

Francisco, CA: National Fund for Medical Education,

1996.
4. Lane J, McDonnell J, & Zimmerman P: Osteoporosis:

Definition, risk factors, etiology, and diagnosis.

American Association of Occupational Health Nursing
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7. Gertz B, Kanis J, Ortolani S, & Singer F:
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5:1-11Osteoporosis International 1995;
8. Reginister

j: Calcitonin for prevention and

The American Journal of
treatment of osteoporosis.

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Medicine 1993; 95:44s-46s.

9. Todd B: Can osteoporosis be treated? Geriatric
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primary care setting. Contemporary Internal Medicine

1 997; 9 (1 ) :55-56.