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Osteoporosis: Current Management Guidelines

Harmanjit Singh*, Manoj Goyal**, Jasbir Singh

Osteoporosis is a multifactorial progressive skeletal disorder characterized by reduced bone mass
and deterioration of bone microarchitecture. Fragility fractures, the consequence of
osteoporosis, are responsible for excess mortality, morbidity, chronic pain, admission to hospitals
and economic costs. Approximately 1.6 million hip fractures occur each year worldwide and the
incidence is set to increase to 6.3 million by 2050. Preventive measures should be started at an
early age and should include smoking cessation and weight-bearing exercises. Pharmacologic
prevention methods include calcium supplementation and administration of raloxifene or
bisphosphonates. No treatment can completely reverse established osteoporosis. Early
intervention can prevent osteoporosis in most people. For patients with established
osteoporosis, medical intervention can halt its progression. Currently available therapies include
bisphosphonates, selective estrogen receptor modulators (SERMs), hormone replacement
therapy (HRT), denosumab, teriparatide, calcitonin and strontium ranelate. Cathepsin K
inhibitors (balicatib and odanacatib) are among recent drugs under development. Saracatinib, a
novel orally available competitive inhibitor of Src kinase has been shown to inhibit bone
resorption in vitro. Lasofoxifene, bazedoxifene and arzoxifene are new SERMs in late-stage
treatment trials. Nonpharmacological measures are required when patients experience adverse
effects because of drug therapy, when symptoms are not controlled by drug therapy alone or
when patient is not willing to take drugs for a prolonged duration.

Osteoporosis is a multifactorial progressive skeletal disorder characterized by reduced bone mass

and deterioration of bone microarchitecture, predisposing it to increased fracture risk.
Osteoporosis is called a silent disease because it progresses without symptoms and remains
unnoticed for a long time as bone resorption process in early stages is almost asymptomatic and
at later stages usually presents with a fracture due to trivial trauma.1 Fragility fractures, the
consequence of osteoporosis, are responsible for excess mortality, morbidity, chronic pain,
admission to institutions and economic costs. They represent 80% of all fractures in menopausal
women over age 50. Patients with hip or vertebral fractures have substantially increased risk of
death after the fracture.
With major improvements in diagnostic technology and assessment facilities; it is now possible
to detect the disease before fractures occur. Once the condition is diagnosed, steps can be taken
to prevent further damage, including special exercises, changes in the diet, lifestyle changes and
supplements or medication.
Burden of Osteoporosis
According to various surveys, worldwide one in 3 women over 50 will suffer a fracture due to
osteoporosis; this increases to one in 2 in women over 60. One in 5 men over 50 will suffer a
fracture due to osteoporosis; this increases to one in 3 over 60. Approximately 1.6 million hip
fractures occur each yearvworldwide and the incidence is set to increase to 6.3 million by 2050.
Currently and there is an increasing incidence of hip fractures in the developed cities in Asia. One
out of 4 hip fractures occur in Asia and Latin America. Osteoporosis is also becoming a serious
public health problem in India. Conservative estimates in a study suggest that 20% of women and
about 10-15% of men are osteoporotic in India. Another highly conservative estimate by a group
of experts suggested that 26 million Indians suffer from osteoporosis, and this number is
expected to reach 36 million by 2013.
WHO definition of Osteoporosis
The World Health Organization (WHO) operationally defines osteoporosis as a bone density that
falls 2.5 standard deviations (SD) below the mean for young healthy adults of the same sex - also
referred to as a T-score of 2.5. Postmenopausal women who fall at the lower end of the young
normal range (a T-score 1.0) are defined as having low bone density and are also at increased
risk of osteoporosis. More than 50% of fractures among postmenopausal women, including hip
fractures, occur in this group with low bone density. The WHO definition applies to
postmenopausal women and men aged 50 years or older. This diagnostic classification should
not be applied to premenopausal women, men younger than 50 years or children.
Bone mineral density (BMD) in a patient is related to peak bone mass and subsequently, bone
loss. The T-score is the patients bone density compared with the BMD of control subjects who
are at their peak BMD, while the Z-score reflects a bone density compared with that of patients
matched for age and sex. Several noninvasive techniques are available for estimating skeletal
mass or density. They include dual-energy X-ray absorptiometry (DXA), single-energy X-ray
absorptiometry (SXA), quantitative computed tomography (CT) and ultrasound (US). DXA is a
highly accurate X-ray technique that has become the standard for measuring bone density in
most centers.
Osteoporosis is classified as primary and secondary. Primary osteoporosis by convention is of
relatively unknown origin that occurs with aging and accelerates with menopause or andropause.
There is no direct or singular cause for primary osteoporosis but there are several clinical risk
factors (Table 1). Secondary osteoporosis is the consequence of conditions such as hormonal
imbalances, diseases or medications. It is increasingly being recognized that multiple
pathogenetic mechanisms operate in the development of the osteoporotic state. The hallmark
of osteoporosis is a reduction in skeletal mass caused by an imbalance between bone resorption
and bone formation. Under physiologic conditions, bone formation and resorption are in a fair
balance. A change in either that is, increased bone resorption or decreased bone formation may
result in osteoporosis.
Osteoclasts derived from mesenchymal cells are responsible for bone resorption, whereas
osteoblasts from hematopoietic precursors are responsible for bone formation. These two types
of cells are dependent on each other for production and linked in the process of bone remodeling.
Osteoblasts not only secrete and mineralize osteoid but also appear to control the bone
resorption carried out by osteoclasts. Osteocytes, which are terminally differentiated osteoblasts
embedded in mineralized bone, direct the timing and location of bone remodeling. In
osteoporosis, the coupling mechanism between osteoclasts and osteoblasts is thought to be
unable to keep up with the constant microtrauma to trabecular bone.
Osteoclasts require weeks to resorb the bone, whereas osteoblasts need months to produce new
bone. Osteoclasts resorbs the bone matrix by secreting hydrochloric acid, which dissolves calcium
phosphate, and enzymes such as collagenase and other proteases. Therefore, any process that
increases the rate of bone remodeling results in net bone loss over time. Furthermore, in periods
of rapid remodeling (e.g., after menopause), bone is at an increased risk for fracture because the
newly produced bone is less densely mineralized, the resorption sites are temporarily unfilled
and the isomerization and maturation of collagen are impaired. The receptor activator of nuclear
factor-k B ligand (RANKL)/receptor activator of nuclear factor-k B (RANK)/osteoprotegerin (OPG)
system is the final common pathway for bone resorption. Osteoblasts and activated T cells in the
bone marrow produce the RANKL cytokine. RANKL binds to RANK expressed by osteoclasts and
osteoclast precursors to promote osteoclast differentiation. Osteoprotegerin is a soluble decoy
receptor that inhibits RANK-RANKL by binding and sequestering RANKL.
Risk factors
Risk factors for osteoporosis, such as advanced age and reduced BMD, have been established by
virtue of their direct and strong relationship to the incidence of fractures; however, many other
factors have been considered risk factors based on their relationship to BMD as a surrogate
indicator of osteoporosis (Table 1).
The most important measure in the management of osteoporosis is treatment of the underlying
cause. Various preventive treatment measures have been described below.
Measures to Prevent Osteoporosis
Primary prevention of osteoporosis starts in childhood. Patients require adequate calcium intake,
vitamin D intake and weight-bearing exercise. Beyond this, prevention of osteoporosis has two
Behavior modification and pharmacologic interventions. The following behaviors should be
modified to reduce the risk of developing osteoporosis: Cigarette smoking, physical inactivity and
intake of alcohol, sodium, animal protein. Patients should be counseled on smoking cessation
and moderated alcohol intake. Patients who have medical disorders and are on medications*
(Table 1) that can cause or accelerate bone loss should receive calcium and vitamin D
supplementation and in some cases, pharmacologic treatment.
Exercises are another way to maintain BMD, prevent the progression of osteoporosis and reduce
the risk of developing bone fractures. A combination of weight- bearing and strength training
exercises are most effective. Even just walking or jogging regularly can help prevent osteoporosis.
A walking program is the best way to start; activities like dancing, aerobics, racquet sports,
running and the use of gym equipment are also recommended, depending upon the patients
preference and general condition. Exercise has beneficial effect on neuromuscular function, and
improves coordination balance and strength, thereby reducing the risk of falling. Weight-bearing
exercises should be started at early age. Exercise habits should be consistent, at least three times
a week as more substantial effect on bone mass is likely if exercise is continued over a long period
of time. The beneficial effect wanes if exercise is discontinued.
Pharmacologic prevention
Pharmacologic prevention methods include calcium supplementation and administration of
raloxifene or bisphosphonates (alendronate or risedronate). Bisphosphonates and raloxifene
should be considered as first-line agents for the prevention of osteoporosis.
Calcium supplementation: The goal of the current recommendations for daily calcium intake is
to ensure that individuals maintain an adequate calcium balance. Current recommendations
from the American Association of Clinical Endocrinologists (AACE) for daily calcium intake are as
Age 0-6 months: 200 mg/day
Age 6-12 months: 260 mg/day
Age 1-3 years: 700 mg/day
Age 4-8 years: 1,000 mg/day
Age 9-18 years: 1,300 mg/day
Age 19-50 years: 1,000 mg/day
Age 50 years: 1,200 mg/day
Pregnant and breastfeeding women 18 years: 1,300 mg/day
Pregnant and breastfeeding women 19 years: 1,000 mg/day
Vitamin D supplementation: Vitamin D is increasingly being recognized as a key element in overall
bone health and muscle function. It plays a significant role in bone health, calcium absorption,
balance (e.g., reduction in risk of falls) and muscle performance. The minimum daily requirement
in patients with osteoporosis is 800 IU of vitamin D3, or cholecalciferol. Many patients require
higher levels (continuously or for a short period) to be considered vitamin D replete, which is
defined as a serum 25-hydroxyvitamin D level of 32 ng/ml. Vitamin D is available as ergocalciferol
(vitamin D2) and cholecalciferol (vitamin D3). Vitamin D is metabolized to active metabolites.
These metabolites promote the active absorption of calcium and phosphorus by the small
intestine, elevating serum calcium and phosphate levels sufficiently to permit bone
Other nutrients
Adequate dietary intake of salt, animal protein.
Adequate vitamin K status (required for optimal carboxylation of osteocalcin).
Dietary phytoestrogens derived from soya products and legumes (exert estrogenic
Pharmacotherapy of Osteoporosis
Currently, no treatment can completely reverse established osteoporosis. Early intervention can
prevent osteoporosis in most people. For patients with established osteoporosis, medical
intervention can halt its progression. If secondary osteoporosis is present, treatment for the
primary disorder should be provided. Therapy should be individualized based on each patients
clinical scenario, with the risks and benefits of treatment discussed between the clinician and
The National Osteoporosis Foundation (NOF, 2010) recommends that pharmacologic therapy
should be reserved for postmenopausal women and men aged 50 years or older who present
with the following:
A hip or vertebral fracture (vertebral fractures may be clinical or morphometric i.e.,
identified on a radiograph alone)
T-score of 2.5 or less at the femoral neck or spine after appropriate evaluation to exclude
secondary causes
Low bone mass (T-score between 1.0 and 2.5 at the femoral neck or spine) and a 10-
year probability of a hip fracture of 3% or greater or a 10-year probability of a major
osteoporosis-related fracture of 20% or greater based on the US-adapted WHO algorithm.
Guidelines from the AACE, published in 2010, include the following recommendations for
choosing drugs to treat osteoporosis:
First-line agents: Alendronate, risedronate, zoledronic acid, denosumab
Second-line agent: Ibandronate
Second- or third-line agent: Raloxifene (SERMs)
Last-line agent: Calcitonin
Treatment for patients with very high fracture risk
or in whom bisphosphonate therapy has failed: Teriparatide.
The most commonly prescribed drugs to treat osteoporosis are bisphosphonates. Alendronate
was the first bisphosphonate to be approved for treatment of osteoporosis in the US in 1995.
Since that time, newer bisphosphonates with less frequent dosing intervals have been
introduced, partially in an attempt to improve compliance. Risedronate is an oral medication that
can be administered daily, weekly or monthly at varying doses. Zoledronic acid is the newer
medication, which is administered once yearly by intravenous (IV) transfusion.
Bisphosphonates bind to hydroxyapatite crystals and thus have a very high affinity for bone.
Bisphosphonates are released from the bone matrix upon exposure to acid and enzymes secreted
by an active osteoclast. Out of all bisphosphonates, zoledronic acid has the highest affinity for
binding to the bone mineral matrix followed by pamidronate > alendronate > ibandronate >
risedronate > etidronate > clodronate. Bisphosphonates with higher affinity like zoledronic acid
bind avidly to the bone surface, but spread through bone slowly, whereas lower affinity agents
like clodronate distribute more widely through the bone, but they have shorter time of residence
when the treatment is stopped. Suppression of bone resorption occurs within approximately
three months of initiation of oral bisphosphonate therapy regardless of dosing frequency, but it
is more rapid after IV administration. After three years of treatment, bisphosphonates have been
shown to increase BMD of the hip by 3-6% and at the spine by 5-8%. In women with osteoporosis,
zoledronic acid, alendronate and risedronate also reduced nonvertebral fractures by 25-40%,
including hip fractures by 40-60%.
Dose: Zoledronic acid: 5 mg single IV infusion annually, alendronate: 10 mg/day orally,
ibandronate: 2.5 mg oral daily or 150 mg once monthly, risedronate: 5 mg/day oral.
Some important adverse events associated with bisphosphonates therapy: Orally administered
bisphosphonates may cause irritation in the esophagus. It is recommended to swallow oral
bisphosphonates with full glass of plain water on arising in the morning, remaining upright for at
least 30 minutes after swallowing the tablet and discontinuing the drug promptly if esophageal
symptoms develop. Rapid IV administration of parenteral bisphosphonates may cause renal
toxicity. For patients with creatinine clearance <30-35 ml/min, use of parenteral
bisphosphonates is not recommended. Other concerns are risk of kidney damage, osteonecrosis
of jaw (Zoledronic acid), atypical fractures and atrial fibrillation.
Selective estrogen receptor modulators
Selective estrogen receptor modulators (SERMs) are
nonsteroidal molecules that bind with high affinity to the
estrogen receptor (ER) and act as agonists or antagonists
depending on the target tissue. The ER agonist effects
of SERMs in bone have proven to be important for the
treatment of osteoporosis in postmenopausal women.
Currently, raloxifene is the only SERM approved by the
US Food and Drug Administration (FDA) for prevention
and treatment of postmenopausal osteoporosis. Clinical
studies have clearly demonstrated the efficacy of
raloxifene in significantly reducing the risk of vertebral
fracture. Raloxifene is indicated for the treatment and
prevention of osteoporosis in postmenopausal women.
The usual dose is 60 mg given orally daily. It can also
be given in combination with calcium and vitamin D.
Raloxifene is the first SERM studied for breast cancer
prevention, and it decreases bone resorption through
actions on ER. It has been shown to prevent bone
loss, and data in females with osteoporosis have
demonstrated that raloxifene causes a 35% reduction in
the risk of vertebral fractures. It has also been shown
to reduce the prevalence of invasive breast cancer.
Prospective clinical trial data have not shown efficacy
at nonvertebral and hip sites. An additional benefit and
indication is prevention of ER-positive breast cancer.28-30
The limited antifracture efficacy of raloxifene has led
to interest in developing other SERMs that might have a
broader antifracture profile. Lasofoxifene, bazedoxifene
and arzoxifene are new SERMs in late-stage treatment
RANK-Ligand inhibition: Denosumab
Denosumab is a fully human monoclonal antibody that
binds with high affinity and specificity to the RANKL,
a key mediator of osteoclast formation, activity and
survival. The inhibition of RANKL by denosumab
reduces osteoclast-mediated bone resorption. It is
indicated for the treatment of postmenopausal women
with osteoporosis who are at high-risk of fracture
(defined as a history of osteoporotic fracture), have
multiple risk factors for fracture, are intolerant to
other available osteoporosis therapies or in whom
osteoporosis therapies have failed. In postmenopausal
women with osteoporosis, denosumab reduces the
incidence of vertebral, nonvertebral and hip fractures.

Denosumab was approved by the US FDA in June 2010.

Approved dosage is 60 mg given subcutaneously every
six months. Several recent studies have demonstrated
the efficacy of this new antiresorptive therapeutic class
in terms of increasing BMD, decreasing bone turnover
markers (BTMs) and most important, reducing
fractures at vertebral, hip and other nonvertebral
sites. Because RANKL is expressed in lymphocytes,
safety concerns relate to inhibition of this important
immunomodulator and to potential consequences
such as infections. The clinical trials did not report
an increased rate of serious infections related to
denosumab, but there was a significantly increased
incidence of eczema and hospitalization for cellulitis
compared with placebo.31,32
Calcitonin is a hormone that decreases osteoclast
activity, thereby impeding postmenopausal bone
loss. It acts like the endogenous form of the hormone
on the calcitonin receptor on osteoclasts to decrease
their activity. Out of all recombinant or synthetic
calcitonins that have been used for medical purposes,
the salmon calcitonin preparation (SCT) is the
most widely used. SCT as a nasal spray is the most
commonly used calcitonin formulation due to its
convenience of administration. It is recommended
in conjunction with adequate calcium and vitamin D
intake to prevent the progressive loss of bone mass.
The intranasal spray is delivered as a single daily
spray that provides 200 IU of the drug. The drug can
be delivered subcutaneously, but this route is rarely
used. It has reduced the incidence of vertebral fractures
in women with pre-existing vertebral fractures. As a
desirable additional effect, calcitonin has been noted to
reduce the pain of clinical vertebral fractures. Calcitonin
is an option for patients who are not candidates for
other available osteoporosis treatments. Common
side effects of nasally administered calcitonin include
nasal discomfort, rhinitis, irritation of nasal mucosa
and occasional epistaxis. Nausea, local inflammatory
reactions at the injection site, sweating and flushing are
side effects noted with parenteral use.33-35
Strontium ranelate
Strontium ranelate, a novel orally active agent, has
been developed for the treatment of osteoporosis.
It consists of two atoms of strontium and an organic
moiety ranelic acid. Strontium ranelate acts by both
stimulating bone formation and decreasing bone
resorption. In vitro, strontium ranelate has been shown
to increase osteoblastic activity, including increasing collagen synthesis and modulating the
system in favor of OPG, as well as decrease bone
resorption by decreasing osteoclast differentiation and
resorbing activity and increasing osteoclast apoptosis.
Strontium ranelate is approved for the treatment of
osteoporosis in some countries in Europe. It reduces the
risk of both spine and nonvertebral fractures. Strontium
is not approved for the treatment of osteoporosis in
the United States. Dose is 2 g sachet nightly taken
at bedtime, mixed with >30 ml of water at least two
hours after food. Strontium ranelate has rarely been
associated with venous thromboembolism and severe
hypersensitivity reactions, including Stevens-Johnson
syndrome and drug rash with eosinophilia and
systemic symptoms. Patients should be advised to seek
immediate medical advice if they develop a rash.36-38
Teriparatide is a synthetic form of human parathyroid
hormone, which acts by inhibiting bone resorption and
increasing bone formation. Normally in response to low
serum calcium, parathyroid hormone (PTH) is secreted
from parathyroid glands, which acts to increase the
concentration of calcium in serum by mobilizing
calcium from bone. Pharmacologically, when PTH is
administered intermittently at low doses, it has been
shown to have predominantly anabolic effects on
osteoblasts. PTH initiates bone formation first and only
later promotes bone formation, which is indicated by
bone turnover markers. Teriparatide is also indicated
for use in men with a high-risk of fractures and where
other treatments are unsuitable. Following a course
of teriparatide it is recommended that patients use
an antiresorptive medicine (e.g. a bisphosphonate) to
further increase BMD and maintain the antifracture
effect. Dose is 20 g subcutaneous injection daily in the
thigh or abdomen. Use is restricted to 18 month lifetime
exposure (caused osteosarcoma in animal studies);
informed consent is required. Transdermal teriparatide
is also under development.39-41
Hormone replacement therapy
Hormone replacement therapy (HRT) was once
considered a first-line therapy for the prevention and
treatment of osteoporosis in women. Although HRT
is not currently recommended for the treatment of
osteoporosis, it is important to mention because many
osteoporosis patients in a typical practice still use it
for controlling postmenopausal symptoms. Data from
the Womens Health Initiative confirmed that HRT can
reduce fractures. However, the results were distressing
with respect to the adverse outcomes associated
with combined estrogen and progesterone therapy

(e.g., risks for breast cancer, myocardial infarction,

stroke and venous thromboembolic events) and
estrogen alone (e.g., risks for stroke and venous
thromboembolic events).42
Drugs Under Clinical Development
Cathepsin K inhibitors
Cathepsin K is critical for normal osteoclastic
bone resorption. The two agents, which are under
development are balicatib (AAE581) and odanacatib
(MK-0822). Clinical trials with these agents have
demonstrated increase in hip and lumbar spine BMD,
with a significant reduction in bone resorption markers.
A newer highly potent cathepsin K inhibitor named
relacatib is presently being studied in experimental
Src kinase inhibitors
Src kinase is a nonreceptor tyrosine kinase and a
member of the Src family of protein kinases, which
plays an important role in activity and survival of
osteoclast cells. Osteopetrosis was caused in mouse
due to Src inactivation, therefore it clearly indicated
that Src is an important requirement for osteoclastic
bone resorption. Saracatinib is a novel orally available
competitive inhibitor of Src kinase shown to inhibit
bone resorption in vitro. In a randomized, double-blind,
placebo-controlled, multiple-ascending- dose Phase I

trial, treatment with saracatinib inhibited osteoclast-

mediated bone resorption in healthy men without any

significant adverse effects. The results of this study

show that saracatinib has the potential to become an
agent for the treatment of osteoporosis.45-47
Lasofoxifene: Lasofoxifene is a nonsteroidal SERM
under development for the prevention and treatment of
osteoporosis and for the treatment of vaginal atrophy.
In a dose of 0.5 mg/day, the dose that is intended for
clinical use, it was associated with a reduction in the
risk of ER-positive breast cancer, major coronary heart
disease events and stroke, although the numbers of
these events were small in all groups. Lasofoxifene
was significantly associated with the risk of venous
thromboembolic events and pulmonary embolism.48
Bazedoxifene: Bazedoxifene is a third-generation SERM
under development for the prevention and treatment
of postmenopausal osteoporosis. It is approved in the
European Union (marketed in Italy and Spain) and is
currently in the late phases of review by the US FDA.
Bazedoxifenes combination with conjugated estrogens, Aprela, is currently undergoing Phase III
studies for the
treatment of postmenopausal symptoms (including the
prevention of postmenopausal osteoporosis/treatment
of osteopenia).49
Emerging therapy: The Wnt/-catenin pathway
regulates gene transcription of proteins important
for osteoblast function. Study of the pathway has led
to further discovery of inhibitors of Wnt signaling
secreted by osteocytes. These include sclerostin and
dickkopf1 protein (DKK1), both of which block binding
of Wnt to LRP5 (lipoprotein receptor-like protein 5),
thereby inhibiting osteoblast stimulation. Monoclonal
antibodies designed to block the inhibiting action of
both sclerostin and DKK1 are being considered for
clinical trials based on promising results in animal
models. Because both of these molecules appear to be
secreted only by bone, it is hoped that they will have
fewer systemic adverse effects. Therapies targeted at
other molecules in the pathway, for example a small
molecule inhibitor of GSK3, the enzyme, which
causes degradation of -catenin in the absence of Wnt
signaling, are considered less desirable targets due to
their action in many tissues in addition to bone.50
Nonpharmacologic Management
Although pharmacologic approaches represent the
cornerstone of treatment, some patients cannot comply
with medication regimens, particularly because of
potential adverse effects, but also because some patients
cannot afford certain medication options or are not
willing to take medications for prolonged time periods.
For such patients nonpharmacologic management may
be helpful.

51 Bracing, or orthoses, such as

thoracolumbar (mid to low back) braces are often
prescribed for osteoporotic patients with vertebral
compression fractures. Some braces are rigid and
attempt to straighten the spine backward and
are traditionally used in patients with an acute
vertebral compression fracture.
Fall prevention:

52 Falls in the elderly represent

a significant cause of morbidity and mortality.
Fall prevention involves environmental
modifications, medication review, exercise, gait
assessment and treatment, provisions for assistive
devices and attention to concomitant conditions
resulting in unsteady gait. Environmental
modifications can consist of minimizing clutter,
altering slippery surfaces and providing grab
bars and other supports in tubs and near toilets.
Multiple medications can have a key role in falls.
Medication review should, therefore, be performed

on a regular basis, with unnecessary and potentially

harmful medications eliminated.

53 Kyphoplasty is a minimally
invasive spine procedure that involves the
infiltration of bone cement into a fractured vertebral
body after fracture reduction using a balloon tamp.
Indications for this procedure include relatively
acute, painful compression fractures refractory to
conservative treatment. Kyphoplasty can result in
diminished pain and reduce kyphosis; multiple
studies have shown it to be an effective treatment
for painful compression fractures with sustained
improvements in back pain, back function and