Spine, Chapter 23, pp.

227-234
Section 5, Systemic Problems

Chapter 23: Osteoporosis of the Spine

By Joseph M. Lane; Harvinder S. Sandhu

There are no metabolic bone diseases that affect the spine exclusively: as
systemic processes, these diseases can appear in all bones. However,
because the spine represents a major portion of the body's bone mass,
contains the largest quantity of metabolically active (cancellous) bone,
and specifically loads this trabecular bone in compression during upright
posture, metabolic bone diseases are often encountered as diseases
primarily of the spine.

The spinal skeleton is more than mere inert, mechanical tissue.

Rather, as in all bones, its component cells are physiologically active and
responsive to an assortment of metabolic and mechanical stimuli. These
activities serve the biochemical role of mineral balance as well as provide
the structural role of remodeling and repair according to skeletal demands.
Bone is a homeostatic organ and, perforce, a metabolically active one.

Metabolic bone disease results either when the bone constituents

(cells and matrices) behave abnormally, when the stimuli to which bone
responds are inappropriately interpreted, or when systemic processes
derange the bones' environment, leading to impairment of either the
biomechanical or structural tasks. The most common widespread metabolic
disease that affects the skeleton is osteoporosis.

Osteoporosis is characterized by decreased bone mass and increased

susceptibility to fracture. Osteomalacia is a disorder of delayed and/or
impaired mineralization. Osteopenia is the general radiographic observation
of decreased mineral content--it includes both the diagnosis of
osteoporosis and that of osteomalacia. Primary osteoporosis occurs in an
individual who has no endocrinopathy or other disease state that would
account for the changes in bone mass. Osteoporosis affects 20 million
individuals in the United States. These individuals sustain more than 1.2
million fractures. The absolute number and percentage of persons who have
osteoporosis are expected to increase because of the prolonged longevity of
the American population. Emotional morbidity in the form of depression,
reclusiveness, and fear of additional fractures may accompany osteoporosis.
Advances in the understanding of the etiology and pathophysiology of
osteoporosis, as well as progress in the prevention and treatment of this
disease, have given the physician the ability to intervene successfully.

Primary osteoporosis can be classified on the basis of the patterns of

bone loss and fracture. Postmenopausal (type-I), or osteoclast-mediated,
osteoporosis is characterized by rapid bone loss and is seen most often in
recently postmenopausal women. It affects women six times more frequently
than men. This pattern is consistent with high-turnover osteoporosis. There
is a rapid phase of bone loss, which predominantly involves trabecular
bone, and an association with vertebral and distal radial fractures.

Senile (type-II), or osteoblast-mediated, osteoporosis affects women

twice as frequently as men. It is related to aging, chronic calcium
deficiency, increased parathyroid hormone activity, and decreased bone
formation. An individual can display traits of both types of osteoporosis
over time.

Osteoporosis is a subject of major interdisciplinary research

efforts. There is a relatively large diversity of opinion regarding the
best approach to the management of osteoporotic patients.

Bone Metabolism

Bone is a living matrix that is in constant flux and under direct cellular
control. Bone is formed by osteoblasts, which are cells of marrow stromal
origin. Newly formed bone contains an organic matrix, which consists
primarily of type-I collagen that undergoes mineralization. Bone resorption
is under the control of osteoclasts. These large, multinucleated cells
arise from macrophage precursors. They cause bone resorption by first
isolating a segment of bone surface, thereby creating a Howship lacuna.
Next, the mineral phase is solubilized by acidification via a carbonic
anhydrase that allows for the enzymatic degradation of the organic
components, including the collagen.

During the course of continued bone formation, the osteoblasts encase

themselves within the bone matrix and become osteocytes. The osteocytes
have direct connections to the outer bone surface through microcanaliculi,
and play a critical role in calcium flux. Bone turnover involves a bone
metabolic unit and is a coupled process in which resorption precedes
formation.

Calcium
Calcium is an essential mineral that participates in many important
physiologic functions. The attainment of peak bone mass and the maintenance
of the skeleton are critical elements directly related to calcium intake.
Calcium requirements change throughout life depending on the activity and
the function of body as well as the efficiency of intestinal absorption
(Table 1).

______________________________________________________________
Table 1
Recommended calcium intakes
______________________________________________________________
Amount of
Age Elemental Calcium
______________________________________________________________
Infants
birth to 6 months
6 months to 1 year
Children
1 to 10 years
 11 to 24 years
Adult Women
pregnant and lactating, under age 24 1,200 to 1,500 mg
pregnant and lactating, over age 24 1,200
25--49 years (premenopausal) 1,000
50--64 years (postmenopausal taking 1,000
estrogen)
50--64 years (postmenopausal not taking 1,500
estrogen)
65 + years 1,500
Adult Men
25 to 64 years 1,000
65 years and older 1,500
______________________________________________________________
The data in this table were taken from National Institutes
of Health Consensus Panel, Optimal Calcium Intake, 1994.
______________________________________________________________

Bone mass increases during childhood; peak bone mass is obtained by

the middle of the third decade. Ultimate peak bone mass can be affected
adversely by inadequate dietary calcium intake during skeletal growth
years. A large proportion of girls and women older than 13 years of age do
not have adequate calcium intake and, therefore, have a lower potential
peak bone mass. The larger the peak bone mass achieved, the better the
chance of avoiding osteoporosis later in life. After peak bone mass is
reached, bone loss normally occurs at the rate of 0.3% per year in men and
0.5% per year in women. Bone loss of 2% to 3% per year begins at the onset
of menopause. This rate continues for a period of 6 to 10 years and then
declines to a rate of 0.5% per year. Although all adults lose bone with
age, profound osteoporosis develops in only 20% to 30% of women and 10% to
20% of men who are older than 65 years of age.

Calcitropic Hormones
The major hormones that affect calcium turnover include vitamin D,
parathyroid hormone, and calcitonin (Fig. 1). Vitamin D is a sterol hormone
that is converted by sun exposure from 7-dehydrocholesterol in the skin.
It is further hydroxylated in the liver to 25-hydroxy vitamin D and then to
the active form of 1,25-dihydroxyvitamin D in the kidneys under the control
of parathyroid hormone. The active vitamin D metabolite facilitates calcium
absorption across the intestines and acts as an adjunct to parathyroid
stimulation of bone resorption.

Parathyroid hormone responds to low ionic calcium by stimulating the

retention of calcium and excretion of phosphate by the kidneys. In
addition, it stimulates the production of 1,25-dihydroxyvitamin D by the
kidneys and indirectly leads to the resorption of bone by osteoclasts.

Calcitonin is a calcitropic peptide produced in the perifollicular

cells of the thyroid gland. It responds to elevated serum ionic calcium
levels by decreasing the number and activity of osteoclasts.

Estrogen and progesterone, although not directly calcitropic hormones,

are critical for the maintenance of bone mass. There is clear evidence of
estrogen receptors on osteoblast-like cells. Estrogen is effective in the
early phases of growth by inhibiting parathyroid function and preventing
bone resorption, and it is effective in the later phases in the
extraskeletal arena by enhancing calcium resorption from the kidney and
calcium absorption from the intestine.

Bone Mechanics

Cortical bone has a low ratio of surface area to volume, while trabecular
bone proportionately has a much greater surface area. Bone turnover is a
surface event, and therefore, it affects trabecular bone more profoundly
than cortical bone. Bones and bone regions rich in trabecular bone, such as
the vertebral body, are particularly subject to a loss of structural
integrity during the aging process (Fig. 2).

The structural strength of bone is related not only to bone mass and
its anatomic distribution but also to a concept known as connectivity.
Connectivity refers to the degree of trabecular interconnectedness within
the bone. Osteoporosis involves a thinning of the cortex and a change in
the structure of the trabecular bone. Within the trabecular bone there are
areas in which osteoclasts create a discontinuity of the trabeculae by
shifting the structure of the bone from plates to narrow bars, which
further weakens the bone in those areas of discontinuity.

Physical activity is an important factor in bone formation and a

common therapeutic intervention. Impact-loading exercises appear to be
effective and site-specific in the maintenance of bone mass. The effect of
physical activity on peak bone mass is most evident during the years of
skeletal growth and is relatively minor in older adults. The rate of bone
loss among young women who are amenorrheic as the result of chronically
high levels of exercise, however, is substantially greater than that among
young women who maintain normal menstrual cycles but do not exercise.

As a group, women who exercise and maintain normal menstrual cycles

have the greatest bone mass. The constellation of disordered eating,
amenorrhea, and osteoporosis has been recognized as a serious threat to the
health of the female athlete and has been termed the "female triad."

Evaluation of Osteoporosis

The evaluation of a patient in whom osteoporosis is suspected should

include a thorough medical history, imaging and laboratory studies, and
possibly bone histomorphometry. Common fractures due to osteoporosis (Fig.
2) include wedge fractures of the thoracic spine, central end-plate cupping
of the lordotic lumbar vertebral body, and fractures of the metaphyseal
area of the long bones. Workup of a patient who has sustained an
insufficiency fracture should proceed in an organized fashion. The
possibility of a bone tumor should be evaluated with the use of plain
radiography, magnetic resonance imaging (MRI), computed tomography (CT),
and/or bone scanning. Endocrinopathy or osteomalacia should be ruled out
with appropriate laboratory tests.
History
The risk factors for osteoporosis that a clinician should seek to identify
include early natural or operatively induced menopause, prolonged periods
of amenorrhea, poor nutrition, a history of inactivity, genetic factors,
and/or a history of excess alcohol intake or smoking. Fifty-seven percent
of women with osteoporosis have scoliosis of at least 10 degrees. Women who
have scoliosis, regardless of whether they are premenopausal or
postmenopausal, have lower bone mass than their peers.

In addition to assessing the risk factors for osteoporosis, the

clinician must evaluate the patient's risk of falling. More than 90% of
fractures of the hip are associated with falls. Although osteoporosis per
se is responsible only for a decrease in bone strength, femoral fractures
due to falls account for the preponderance of the morbidity associated with
osteoporosis. Both experimental and clinical data support the critical role
of the fall as one of the prime causes of hip fracture. The role of
excessive exercise, strenuous lifting, and other mechanical contributions
to the pathogenesis of spinal fractures has yet to be fully clarified.

Imaging Studies and the Measurement

of Bone Mineral Density
The primary goal of the treatment of osteoporosis is to prevent bone loss
beyond the fracture threshold. Measurements of bone mineral density can be
used to assess the risk of a fracture with a high degree of specificity.
There is a 1.5 to threefold increase in the fracture rate for each standard
deviation of decrease in bone mineral density. Although the risk of
fracture increases continuously as bone mineral density declines, it is
useful from a practical standpoint to define cutoff values for the purpose
of intervention. The World Health Organization has divided osteoporosis
into four separate levels, based on bone density. Individuals who are
within one standard deviation of the peak bone mass of young same-gender
individuals are considered to be normal. Individuals who are less than one
to 2.5 standard deviations below peak bone mass are considered to have
osteopenia. Individuals with a bone mass loss of more than two standard
deviations below that of a young individual's peak bone mass are considered
to have osteoporosis. Individuals with significant bone loss and a fracture
are considered to have severe osteoporosis.

Bone mass can be determined by a number of noninvasive techniques. The

current elements of any system include precision, accuracy, and sensitivity
for change of bone mass.

Dual-energy x-ray absorptiometry, commonly called DXA, has a high rate

of precision, subjects the patient to an extremely low dose of radiation,
and is a frequently used method of evaluating bone mass in clinical
practice. Quantitative computed tomography (QCT) scanning can be used to
examine a window within the vertebral body as well as to measure the
trabecular bone mass therein. Among radiographic methods, QCT is the most
sensitive to changes in the bone mass; however, it is less precise, is more
costly, and results in a higher exposure to radiation than DXA. Single-beam
densitometry measures the distal third of the forearm or the ultradistal
radius. Radiographic densitometry methods that evaluate the hand are site-
specific and may not correlate well with the spine.

Determination of precisely when a vertebral deformation resulting from

osteoporosis constitutes a fracture can be difficult with standard
radiographic techniques. The lack of a universally accepted definition of a
fracture has serious implications; for example, as the definition has
expanded to include more minor changes, the specific effect of any drug
intervention on the disease process becomes more difficult to assess. Some
authors have suggested that a 25% change in one dimension or a 40% change
in the total cross-sectional area as the minimum criteria for a vertebral
fracture is essential.

Laboratory Studies
Laboratory studies are used to exclude other diseases that can cause
osteoporosis or osteopenia and to determine the type of osteoporosis. As
indicated in the algorithm for the workup of a patient who has an
insufficiency fracture, a complete blood-cell count with differential,
determination of the erythrocyte sedimentation rate, and serum protein
immunoelectrophoresis identify most bone marrow abnormalities. These
abnormalities are seen in approximately 2% of the patients who have
osteopenia. One half of these abnormalities are related to multiple
myeloma. If such an abnormality is suspected, a bone marrow aspiration is
performed. If no bone abnormality is noted, common endocrinopathies are
sought. Initially, the physician should screen for hyperparathyroidism and
hyperthyroidism by determining serum levels of parathyroid hormone and
thyroid-stimulating hormone using radioimmunoassay. Corticosteroid-induced
osteoporosis (Cushing disease) and type-I diabetes are sought if they are
suspected as a result of the clinical history.

After endocrinopathies have been excluded, as many as 10% of older

individuals who live in the northern communities in the United States and
who have osteopenia will be found to have varying levels of osteomalacia.
Osteomalacia can be diagnosed in more than 50% of these individuals on the
basis of simple blood tests that show low to low-normal serum calcium
levels, low phosphate, low 25-hydroxyvitamin D, and high alkaline
phosphatase and parathyroid levels.

Recently, new laboratory markers of bone metabolism have been

developed. Bone specific alkaline phosphatase, osteocalcin, and
procollagen-I extension propeptides specifically reflect bone formation.
Markers of bone degradation are more nonspecific, but collagen breakdown
products isolated in the urine (pyridinoline, deoxypyridinoline, and
N-telopeptides) correspond well with histologic indices of bone
resorption.

Results of the more advanced laboratory tests, which screen using

precise markers of bone formation and degradation in blood and urine,
accurately reflect the metabolic activity of bone in most patients. The
determination of bone mass does not characterize the qualitative status of
the bone. A biopsy of tetracycline-labeled, undecalcified, iliac crest bone
is the best method for differentiating among high turnover and low turnover
osteoporosis, osteomalacia, secondary hyperparathyroidism, and complicated
combinations of these conditions.

Treatment of Osteoporosis

Calcium
Calcium is one of the most widely used agents in the treatment of
osteoporosis. Because most children have an inadequate calcium intake, the
peak bone mass achieved is often lacking its true potential. This lack
creates a major risk for osteoporosis later in life. Girls at puberty are
probably the optimum population for the early use of calcium to prevent
osteoporosis. It has been suggested that the administration of calcium
supplements during growth may accelerate the attainment of peak bone mass;
there is no evidence that increases in actual peak bone mass are ultimately
achieved. However, calcium deficiency can lead to a diminished peak bone
mass. Calcium supplementation varies with age (Table 1). Calcium
supplementation is helpful for patients who have senile type-II
osteoporosis, especially when therapy is combined with vitamin-D
supplementation. A marked decrease in the rate of fractures of the hip has
been demonstrated in a study of elderly patients from France who received
dietary supplements of calcium (1,200 mg) and vitamin D (800 units).

Vitamin D
Vitamin D deficiency is common in elderly individuals who have
osteoporosis, in strict vegetarians, in the population residing in northern
locations during the winter, and in individuals who are institutionalized.
Individuals who have vitamin D deficiency typically have poor calcium
absorption as well. Vitamin D receptors on the osteoblast display
heterogeneity. It has been postulated that weaker receptor binding sites
may account for some etiologic factors leading to osteoporosis.

Estrogen
Estrogen deficiency plays a prominent role in the pathogenesis of type-I
osteoporosis. Estrogen inhibits bone resorption and positively affects
calcium balance, either directly, by stimulating the estrogen receptors in
bone, or indirectly, by suppressing the production of bone-resorbing
cytokines. Administration of estrogen to postmenopausal women not only
prevents bone loss but also protects against vertebral and femoral
fractures, with a greater effect on the spine. Discontinuation of the
therapy is followed by an immediate resumption of bone loss at a rate
similar to that in women who have not received such therapy.

Estrogen is a useful agent for prevention of osteoporosis. Its

acceptance is uncertain. Prolonged use of estrogen appears to increase the
risk of breast cancer up to 30% in certain women and in men in the fifth
and sixth decades. Women taking estrogen should have regular mammograms.
The concomitant administration of progestin decreases any increased risk
for uterine cancer. Continuous combination of progestin and estrogen
therapy can minimize cyclical uterine bleeding in older women. Estrogen
with or without progestin is associated with a significant improvement in
cardiovascular lipid profile and leads to the enhancement of life. It is
useful for women who have had a high risk of cardiovascular disease, no
family history of early breast cancer, a strong family history of
osteoporosis, and substantial postmenopausal symptoms, and for those who
are receiving thyroid hormone replacement therapy. Conversely, patients
who do not have coronary artery disease or substantial risk factors for
these diseases and who have a history of thrombophlebitis or a family
history of early breast cancer are poor candidates for estrogen
supplementation. The usual daily dose of estrogen to prevent bone loss is
0.625 mg. One half of this dose may suffice when it is combined with
calcium supplementation. Estrogen therapy usually is initiated in
individuals who are in the perimenopausal period. Several centers have
initiated estrogen in the elderly, noting its beneficial effects in
cardiovascular disease.

Calcitonin
Calcitonin can be used to treat osteoporosis, although patients who have
osteoporosis do not appear to have a deficiency of this hormone. Calcitonin
is used commonly in some countries for the short-term amelioration of pain
associated with fractures due to osteoporosis because it has an analgesic
property, which results either from elevating the level of endorphins or
from competing for the binding site of calcitonin gene-related peptides.
Calcitonin binds to specific receptors on the osteoclast and exerts an
inhibitory effect on its activity. Calcitonin initially was used as a
subcutaneous injection, but it recently has been released as a nasal spray.
Its analgesic and osteoporotic protective activities are well maintained in
this form. The typical dose is 200 units daily in alternate nostrils. This
agent is helpful as an osteoporotic agent for the individual who cannot
take estrogen, for premenopausal individuals who have osteoporosis, for
osteoporotic men, and specifically, for those individuals who have
osteoporotic fragility fractures.

Bisphosphonates
Bisphosphonates are stable, active analogs of pyrophosphate that both
inhibit osteoclastic resorption and to a lesser degree depress bone
turnover. Etidronate increased bone mass and decreased spinal fractures
when used for 2 years. However, it has not been approved by the U.S. Food
and Drug Administration (FDA) because of reported reduction in benefit
after 2 years and some evidence of focal osteomalacia. The second-
generation bisphosphonates are more potent and cause essentially no
inhibition of mineralization. These agents appear to have positive effects
on both vertebral and femoral neck bone density. Alendronate, recently
approved by the FDA, appears to prevent vertebral fracture loss in patients
with osteoporosis and does not alter the mechanical properties of bone. In
addition, it appears to continue to work after it is no longer being
administered. Alendronate is associated with some epigastric distress
(approaching 30%). However this can largely be circumvented by working up
to the therapeutic dose gradually over 4 to 8 weeks. The drug has a very
poor absorption and must be given half an hour before breakfast on an empty
stomach with a full glass of water. The half life of alendronate is 10
years and, therefore, the agent will have a long residence within the bone.
Due to this property, it has not been approved by the FDA for women of
childbearing ages. Trials currently are being carried out to test its
efficacy, in a synergistic role, when combined with estrogen as well as in
the prevention of steroid-induced osteoporosis. Alendronate has not been
approved for men. However, there appears to be theoretic indication for it
to be effective in this population.

Fluoride
All the previously mentioned agents work predominantly in antiresorptive
functions. Sodium fluoride and parathyroid hormone appear to be the only
agents that may directly stimulate osteoblasts. Neither of them are
approved by the FDA for this use.

Fluoride causes osteoblast proliferation and stimulates new bone

formation. Researchers have found substantial increases in trabecular bone
in patients who had received fluoride. Enthusiasm for fluoride has been
tempered by studies that have shown impaired bone mineralization and
increased rates of fractures of the hip and vertebrae despite increased
bone density in the lumbar spine. Alternate forms of fluoride, such as
slow-release fluoride, coupled with lower dosage and large concurrent
calcium supplementation show promise. Patients in whom postmenopausal
senile osteoporosis is treated with a preparation of slow-release sodium
fluoride demonstrate a lower rate of vertebral fracture and a higher
fracture-free rate, compared with a group of controls receiving only
calcium. The role of fluoride in the future may be to augment bone density
at the initiation of therapy before switching to antiresorptive agents for
long-term maintenance of bone density.

One current protocol for osteoporosis in women involves a separation

of premenopausal and postmenopausal patients into two groups (Outline 1).
Premenopausal women who are eumenorrheic should have physiologic calcium
intake (to 1,200 to 1,500 mg/day), vitamin D supplementation (400
international units/day), and appropriate exercise. Premenopausal women
who are amenorrheic should be managed as just described and should also
consider cyclical estrogen and progestin therapy. They also should be
encouraged to have appropriate caloric intake. All postmenopausal women
should have calcium intake of 1,500 mg/day and vitamin D supplementation
of 400 international units/day. Postmenopausal women are subdivided
according to their bone mineral density. Women who have a bone mineral
density that is within 2.0 standard deviations of peak youthful women
should be placed on physiologic doses of calcium, 400 to 800 units of
vitamin D, and consider the possibility of cyclical estrogen and progestin
supplementation. Women who have a bone density that is more than two
standard deviations below peak bone mass without fractures should be
treated with calcium, vitamin D, and recommended to take either cyclical
estrogen and progestin, alendronate (10 mg/day), or nasal calcitonin.
Patients who additionally have a fragility fracture should be placed on
nasal calcitonin until the fracture pain has resolved, and then the more
appropriate agent can be provided.

__________________________________________________________________
Outline 1
Osteoporosis treatment protocol
__________________________________________________________________
Premenopause
 Eumenorrheic
Physiologic calcium (1,000 mg/day)
Vitamin D (400 international units/day)
Exercise
Amenorrheic
Physiologic calcium (1,000 mg/day)
Cyclical estrogen and progestin*/or birth control pills
Vitamin D (400 international units/day)
Appropriate caloric intake
Exercise
Postmenopause
Bone mineral density within 1 standard deviation of normal peak
bone mass
Calcium (1,500 mg/day)
Vitamin D (400 international units/day)
Consider cyclical estrogen and progestin*
Bone mineral density 1 to 2.5 standard deviations less than that
of peak bone mass and no fracture
Calcium (1,500 mg/day)
Vitamin D (400 international units/day)
Cyclical estrogen and progestin* or alendronate (10mg/day)
if bone density > 2.0 standard deviations below peak bone
mass
Bone mineral density > 2.5 standard deviations less than that of
peers, or fracture
Calcium (1,500 mg/day)
Vitamin D (400 international units/day)
Calcitonin (50 to 100 units subcutaneously 3 to 7 days/wk)
Cyclical estrogen and progestin*, or alendronate (10mg/day)
if bone mineral density > 2.0 standard deviations less than
that of peak mass, as per Food and Drug Administration
recommendations
__________________________________________________________________
* A typical regimen consists of 0.625 milligram of estrogen per
day and 2.5 to 10.0 milligrams of progestin per day
__________________________________________________________________

Specific Management of Fragility Fractures of the Spine

Acute management of the spinal fragility fracture in most centers is based
on empiric, rather than objective, data. The absence of a universally
accepted definition of insufficiency (fragility) fracture, combined with
the scarcity of prospective studies on specific fracture patterns, has
resulted in this circumstance. Management aims that are incontrovertible,
however, include alleviation of pain, early mobilization, preservation of
sagittal and coronal plane stability, and prevention of late neurologic
complications.

Neurologic compromise after low-energy trauma to the osteoporotic

spine is extremely uncommon and, as a result, urgent surgical intervention
is rarely indicated. Nonetheless, sequential osteoporotic insufficiency
fractures, or progressive deformity of a prior insufficiency fracture, can
produce gradual kyphosis and late devastating neurologic compromise
resulting from anterior impingement on neural tissues. The mechanisms
causing such late neurologic sequelae are not completely understood.
Further, the true incidence, or risk, of developing compromise following
specific fractures has not been determined.

A retrospective review of patients who have required decompressive and

reconstructive surgery for late neurologic deficits following insufficiency
fracture suggests associated risk factors. These risk factors include
involvement of the thoracolumbar region (T11--L2) with either compromise of
the anterior and middle columns (burst fracture) or wedge compression
fracture with greater than 30 degrees sagittal angulation; vacuum shadow
within the fractured body, implying ischemic necrosis of bone; and/or the
presence of segmental instability or hypermobility, combined with MRI
evidence of retropulsed vertebral fragments. Neurologic involvement can
occur from 1 month to 1.5 years (average: 5.3 months) after the fracture.
Despite lack of prospective data, careful observation of patients
satisfying these criteria is warranted for at least 6 months.

Initial management of the isolated spinal insufficiency fracture,

which commonly is at the thoracic kyphosis, thoracic-lumbar junction, and
the sacral alar, is focused on pain relief and early mobilization to avoid
further bone loss associated with inactivity. Treatment includes narcotic
analgesics as tolerated, sagittal and coronal plane immobilization with
external orthosis, and initiation of nasal calcitonin therapy. As discussed
previously, calcitonin, in addition to its antiresorptive effect, has an
analgesic property and is useful for acute fragility fractures. The
preferred orthotic, although patient dependent, is the tri-pad Jewitt
extension brace because of ease of fitting and application, lack of
restriction on the chest cage and torso, allowance for axial loading, and
greater compliance within the geriatric population. Dorsolumbar corsets may
also be tolerated and provide some pain relief, but not immobilization.

The pain of acute fracture generally lasts 4 to 6 weeks but may extend
to 3 months. Analgesics should be continued until the patient has resumed
weightbearing activities with relative comfort. Orthotics should be
continued until acute pain has subsided and the absence of progressive
deformity is confirmed. Calcitonin is continued until the acute pain has
resolved and a subsequent agent has been chosen (an option is to continue
calcitonin for a full 18-month course).

Osteoporotic patients who require surgical intervention because of

late neurologic sequelae or chronic pain due to progressive deformity pose
particular challenges. Spinal decompression and/or reconstruction can be
approached anteriorly, posteriorly, or both. This decision depends, in
part, on the nature of the deformity and/or the source of the neural
insult. The presence of significant kyphosis and substantial retropulsed
fragments causing anterior canal compromise generally favor an anterior
approach. Prospective studies on this population are lacking, and opinions
regarding surgical approach vary.

Maintainence of correction following reconstruction requires

intersegmental fusion facilitated by spinal column instrumentation. In the
case of vertebrectomy, structural graft replacement is also mandated.
Specific surgical problems associated with mineral-deficient spines include
subsidence or dislodgement of anterior structural grafts and hardware
failure at the metal-bone interface. Particular attention has been directed
toward the use of transpedicular bone screws in the osteoporotic spine.
Fixation of the transpedicular screw as reflected by pull-out resistance is
correlated with insertional torque. Torque less than 4.0 inch-pounds leads
to early screw pullout from cyclic loading in cadaveric models. On the
other hand, transpedicular screws that are "protected" by offset laminar
hooks at two adjacent levels have significantly greater pull-out resistance
in osteoporotic spines. Many advocate the use of methylmethacrylate
augmentation of both transpedicular and transvertebral bone screws in
mineral-deficient vertebral segments. Although immediate fixation and pull-
out resistance is superior, long-term mechanical consequences have not
been evaluated in prospective trials or in in vivo experimental models.

Conclusion

A review of the treatment of osteoporosis indicates that at the present

time prevention is clearly the best solution. Maximization of peak bone
mass and reduction of post-menopausal and age-associated bone loss are
crucial. Adequate calcium intake during growth and calcium and vitamin D
supplementation postmenopausally constitute the fundamental strategies
applicable to all patients. A lifetime habit of physical exercise and
elimination of falls, as well as attenuation of the severity of falls, are
important for the elderly. Estrogen is the drug of choice for the
prevention of postmenopausal bone loss. Calcitonin is the agent of choice
for those who cannot take estrogen or who have pain due to a fracture. The
newly approved bisphosphonate, alendronate, appears to have substantial
antiresorptive properties with minimum side effects. Fluoride has been
shown to positively affect bone formation and may have a role in treatment,
but at this time has not been approved by the FDA.

Chapter Figure Legends

NOTE: Individual Legends are also viewable in the image window

FIGURE 1: Illustration of vitamin-D production and the hormonal regulation

in the control and coordination of total body calcium. (Reproduced with
permission from Mohler DG, Lane JM, Cole BJ, et al: Skeletal failure in
osteoporosis, in Lane JM, Healey JH (eds): Diagnosis and Management of
Pathologic Fractures. New York, NY, Raven Press, 1993, p 24.)

FIGURE 2: Left, Lateral radiograph demonstrating thoracic insufficiency

fracture. Center, Lateral radiograph three years later demonstrating
progression of thoracic fractures. Right, MRI of same patient demonstrating
central end plate cupping of lumbar vertebrae secondary to insufficient
fracture.

Annotated Bibliography
Belchetz PE: Hormonal treatment of postmenopausal women. N Engl J Med
1994;330:1062--1071.
This is a superb review of hormonal treatment.

Chapuy MC, Arlot ME, Duboeuf F, et al: Vitamin D3 and calcium to prevent
hip fractures in elderly women. N Engl J Med 1992;327:1637--1642.
The authors present strong evidence that calcium prevents hip
fracture.

Colditz GA, Hankinson SE, Hunter DJ, et al: The use of estrogens and
progestins and the risk of breast cancer in postmenopausal women. N Engl J
Med 1995;332:1589--1593.
The authors discuss the use of estrogens and breast cancer. Courtney
AC, Wachtel EF, Myers ER, et al: Age-related reductions in the strength of
the femur tested in a fall-loading configuration. J Bone Joint Surg
1995;77A:387--395.
This excellent paper addresses the strength of the femur as related to
age.

Cummings SR, Nevitt MC, Browner WS, et al: Risk factors for hip fracture in
white women: Study of Osteoporotic Fractures Research Group. N Engl J Med
1995;332:767--773.
This is a strong discussion and analysis of factors affecting hip
fracture.

Flawn LB: Amenorrhea, anorexia, and osteoporosis: The female triad. Curr
Opin Orthop 1994;5:16--20.
This is an excellent review of the critical elements of the athletic
triad.

Gennari C, Agnusdei D, Camporeale A: Use of calcitonin in the treatment of

bone pain associated with osteoporosis. Calcif Tissue Int 1991;49(suppl
2):S9--S13.
The authors of this strong paper discuss and prove the role of
calcitonin.

Heaney RP: Bone mass, nutrition, and other lifestyle factors. Am J Med
1993;95:29S--33S.
This is an overview and discussion of factors related to vertebral
crush fractures.

Johnston CC Jr, Slemenda CW: Peak bone mass, bone loss and risk of
fracture. Osteoporos Int 1994;4(suppl 1):43--45.
This strong article reviews the importance of peak bone mass.

Lane JM, Riley EH, Wirganowicz PZ: Osteoporosis: Diagnosis and treatment. J
Bone Joint Surg 1996;78A:618--632.
This article reviews the etiology and treatment of osteoporosis.

Matkovic V, Jelic T, Wardlaw GM, et al: Timing of peak bone mass in

Caucasian females and its implication for the prevention of osteoporosis:
Inference from a cross-sectional model. J Clin Invest 1994;93:799--808.
This article addresses the role of peak bone mass.

National Institutes of Health: Optimal calcium intake. NIH Consens

Statement 1994;12:1--31.
This statement presents the newest recommendations for calcium
treatment.

Pak CY, Sakhaee K, Adams-Huet B, et al: Treatment of postmenopausal

osteoporosis with slow-release sodium fluoride: Final report of a
randomized controlled trial. Ann Intern Med 1995;123:401--408.
The authors demonstrate strong efficacy for fluoride therapy.

Price CP, Thompson PW: The role of biochemical tests in the screening and
monitoring of osteoporosis. Ann Clin Biochem 1995;32:244--260.
This is a comprehensive review of the biochemical markers used in
evaluation of osteoporosis.

Watts NB, Harris ST, Genant HK, et al: Intermittent cyclical etidronate
treatment of postmenopausal osteoporosis. N Engl J Med 1990;323:73--79.
The authors report the first large scale multi-institutional study
demonstrating the efficacy of bisphosphonates in treating osteoporosis.

Classic Bibliography

Christiansen C, Christensen MS, Transbol I: Bone mass in postmenopausal

women after withdrawal of oestrogen/gestagen replacement therapy. Lancet
1981;1:459--461.

Ettinger B, Genant HK, Cann CE: Long-term estrogen replacement therapy

prevents bone loss and fractures. Ann Intern Med 1985;102:319--324.

Healey JH, Lane JM: Structural scoliosis in osteoporotic women. Clin Orthop
1985;195:216--223.

Riggs BL, Melton LJ III: Evidence for two distinct syndromes of

involutional osteoporosis. Am J Med 1983;75:899--901.

Velis KP, Healey JH, Schneider R: Osteoporosis in unstable adult scoliosis.

Clin Orthop 1988;237:132--141.