Transient Osteoporosis

Anastasios V. Korompilias, MD
Apostolos H. Karantanas, MD
Marios G. Lykissas, MD
Alexandros E. Beris, MD

Dr. Korompilias is Assistant Professor,

Department of Orthopaedic Surgery,
University of Ioannina, Ioannina, Greece.
Dr. Karantanas is Associate Professor,
Department of Radiology, University of
Crete, Heraklion, Greece. Dr. Lykissas is
Resident, Department of Orthopaedic
Surgery, University of Ioannina. Dr. Beris
is Professor, Department of Orthopaedic
Surgery, University of Ioannina.
None of the following authors or a
member of their immediate families has
received anything of value from or owns
stock in a commercial company or
institution related directly or indirectly to
the subject of this article:
Dr. Korompilias, Dr. Karantanas,
Dr. Lykissas, and Dr. Beris.
Reprint requests: Dr. Korompilias,
Department of Orthopaedic Surgery,
University of Ioannina, Ioannina, PC
45110, Greece.
J Am Acad Orthop Surg 2008;16:480489
Copyright 2008 by the American
Academy of Orthopaedic Surgeons.

480

Abstract
Transient osteoporosis is characterized primarily by bone marrow
edema. The disease most commonly affects the hip, knee, and
ankle in middle-aged men. Its cause remains unknown. The
hallmark that separates transient osteoporosis from other
conditions presenting with a bone marrow edema pattern is its selflimited nature. Laboratory tests usually do not contribute to the
diagnosis. Plain radiographs may reveal regional osseous
demineralization. Magnetic resonance imaging is used primarily for
early diagnosis and monitoring disease progression. Early
differentiation from more aggressive conditions with long-term
sequelae is essential to avoid unnecessary treatment. Clinical
entities such as transient osteoporosis of the hip and regional
migratory osteoporosis are spontaneously resolving conditions.
However, early differential diagnosis and surgical treatment are
crucial for the patient with osteonecrosis of the hip or knee.

n 1959, Curtiss and Kincaid1 first

described a syndrome of transient
demineralization of the hip in patients in the third trimester of pregnancy. Since then, various terms
have been used to describe benign
clinical entities characterized by the
common imaging finding of bone
marrow edema (BME), such as transient osteoporosis of the hip (TOH),
regional migratory osteoporosis
(RMO), transient bone marrow edema syndrome, and reflex sympathetic dystrophy (RSD).
Lequesne et al2 in 1977 were the
first to characterize the syndrome of
transient demineralization of the hip
as TOH. Since then, a large number
of cases of TOH have been reported
in the literature.3-10 It is apparent
that these transient clinical entities
share a similar pathogenic mechanism. For this reason, Hofmann et
al11 proposed that such conditions be
included under the general term
bone marrow edema syndrome
(BMES). However, transient osteoporosis (TO) is a clinical term

that more accurately describes bone

marrow disorders characterized primarily by osteoporosis. TO is believed to represent a distinct entity,
with specific clinical and imaging
features.12 Some authors, however,
believe that this syndrome is just an
abortive form of osteonecrosis.13,14
TO affects mostly young and
middle-aged men and, rarely, women
during the last 3 months of pregnancy or the immediate postpartum period.1,7 It is considered idiopathic,
with no correlation to a history of
trauma. TO involves only the lower
extremities, especially the hip joint
and, less frequently, the knee, ankle,
and foot. It is manifested primarily
by spontaneous occurrence, with
sudden-onset pain of the affected
joint. Pain is worse on weight bearing and is associated with limping
and disability; these gradually subside within 4 to 9 months. Recurrence may involve the same or adjacent joints. Physical examination
reveals minimal restriction of range
of movement and pain only at the

Journal of the American Academy of Orthopaedic Surgeons

Anastasios V. Korompilias, MD, et al

extremes of range. This discrepancy

between physical examination findings and disability may help early on
to distinguish this benign and selflimiting clinical entity from other irreversible conditions, and it may aid
in avoiding unnecessary diagnostic
and therapeutic measures.
Bone biopsy of the affected joints
shows irregularly woven bone, osteoid seams, and lining cells.15 These
histopathologic findings reflect radiographic evidence of periarticular
osseous demineralization. Open biopsy often reveals increased synovial
fluid and abnormal synovium; however, microscopic evaluation of the
tissue demonstrates minimal synovial inflammation.3 These findings
are not specific.
Many hypotheses have been proposed to explain the pathogenesis
and characteristic manifestations
of TO, but the cause remains unknown.7,16 Furthermore, the relationship between clinical entities
characterized by pathologic magnetic resonance signals remains controversial. Pathogenesis is variable;
clinical, radiographic, and magnetic
resonance imaging (MRI) findings
are used to diagnose the patient
with TO.

Pathogenesis
Although TO is a well-described clinical entity, its cause and pathogenesis remain obscure. Because of the rarity of the condition, the lack of
specific symptoms at the onset of TO,
and the unpredictability of the episodes, many patients are misdiagnosed. Few extensive investigations
of the pathomechanics of the disease
have been done. In 1959, Curtiss and
Kincaid1 presented a neurogenic compression theory. Rosen7 suggested
that a venous obstruction and secondary localized hyperemia may be the
cause of the transitory demineralization of the femoral head. Other investigators have tried to unify lesions
characterized by TO. For example, the
presence of hyperemia in the initial
Volume 16, Number 8, August 2008

stage of the disease supported the idea

that RSD was the cause of RMO.
However, other investigators indicated that these two clinical entities,
although related, are distinct.12
Pathology of the proximal nerve
roots has been proposed as a possible
pathogenic mechanism of TO. Ischemic events in the small vessels
proximal to nerve roots may be the
cause of the disease. This hypothesis
is based on electromyographic findings indicative of denervation that
were related in location and time to
TO attacks. Restoration of blood
flow in the nerve roots and nerve regeneration may be responsible for
the limited clinical course of TO,
which usually lasts 9 months. Recurrence of such ischemic events in
other vessels may explain the migratory character in patients with
RMO. These theories remain unproved, and further studies are necessary to draw direct conclusions.
BME, as shown on MRI, and focal
osteopenia, as shown on plain radiographs, are typical findings in the patient with TO. A BME pattern on
MRI is characterized by high signal
intensity, compared with normal
bone marrow on fat-suppressed T2weighted and short tau inversion recovery images and by low signal intensity on T1-weighted images.
Although BME is a common finding
on MRI, it has a nonspecific signal
pattern that may be present in various diseases.17,18 Enhancement of the
BME area after intravenous administration of contrast agents is indicative of hypervascularity and increased permeability of the capillary
bed. However, vasodilation and increased permeability may constitute
a result rather than a cause of the
BME disclosed on MRI.
Recent research emphasizes the
role of the regional accelerated phenomenon (RAP) activation. RAP is an
acceleration process by which the rate
of bone modeling and remodeling in
local areas may be increased up to 10
times the normal rate in response to
noxious stimuli. According to this

theory, bone tissue microdamage and

consequent microfracture may be the
noxious stimuli that trigger RAP.19,20
Prolonged or exaggerated activation
of bone foci where normal bone repair
mechanisms are most active may result in TO. In a recent study of bone
mass assessment in three cases of
RMO, Trevisan and Ortolani16 suggested wide systemic bone loss with
prevailing trabecular involvement as
the cause of TO. These findings,
which also have been reported by others, may support Frosts theories of
prolonged or exaggerated active bone
foci as a cause of TO to explain the
influence of local and systemic factors
in both causing and reversing osteoporosis.21 However, this theory
does not explain why certain anatomic areas are involved in TO.
Although many studies have tried
to determine the etiology of BMESs,
no common mechanism has yet
been found that explains the pathogenesis of the multiple clinical entities characterized by regional osteoporosis and BME.

Diagnostic Evaluation
Laboratory Tests
Laboratory findings usually do
not contribute to the diagnosis of
TO. However, blood tests should be
done to distinguish TO from aggressive clinical entities such as metastatic or metabolic bone disease.
Histologic examination of the lesion
is necessary only when these other
pathologies are suspected.
Compared with serum levels, specific biochemical markers of bone
formation, including bone-specific alkaline phosphatase, osteocalcin, procollagen type I N-terminal propeptide, and C-terminal cross-linking
telopeptide were found to be elevated
in aspirates from the femoral head in
patients with TO.22 However, in all
of these bone markers, serum concentration was not different from
that of healthy individuals.
481

Transient Osteoporosis

Figure 1

A, Anteroposterior radiograph demonstrating regional osteopenia (arrows) in a 40-year-old man with a 2-month history of left
hip pain and a final diagnosis of transient osteoporosis of the hip. B, Axial computed tomography scan demonstrating osteopenia
in the trabecular bone and a thinned but present cortex (arrow).

Conventional Radiography
Conventional radiographs may be
normal in the early stages of TO.
Plain radiographs may reveal periarticular osseous demineralization,
usually at 3 to 6 weeks from the onset of symptoms (Figure 1, A). Radiographic findings may be present
weeks after the symptoms have resolved. In fact, radiographic evidence
of remineralization may not be apparent until 2 years following symptom resolution.
Despite the described arthralgia
and joint effusion that develops in
most cases, the joint space remains
intact, and no subchondral erosions
are evident.23 Moreover, bony margins are always preserved. Possible
complications from microdamage or
stress damage are not evident on
conventional radiographs.
Radiographs of the femoral head
of patients in the later stages of TO
may reveal complete disappearance of
the osseous architecture, known as
phantom appearance of the femoral head. The trochanters, acetabula,
and iliac wings are rarely affected.
Bone Scintigraphy
Even though findings of radionuclide bone scanning are not specific,
scintigraphy with technetium Tc482

99m methylene diphosphonate is useful in the early diagnosis of TO because increased uptake in the affected
joint usually precedes radiologic features and can be seen within a few
days after the onset of symptoms (Figure 2). During the diagnostic period
in which clinical symptoms are
present but no objective radiographic
findings are evident, bone scanning is
considered to be sensitive but not specific for the detection of TO. Increased radionuclide uptake is detected in all phases of a three-phase
bone scintigram; this represents focal
increase in capillary permeability and
hyperemia as well as increased osteoblast activity. When symptoms subside, reduced activity on the perfusion
and blood pool phases are noted. Increased activity in the delayed bone
phase may be present for many
months after the onset of symptoms,
indicating repair activity.
Scintigraphy is very useful both for
monitoring the progression of the disease and for differentiating TO from
other conditions that are characterized by regional osteopenia. Clinical
entities that should be distinguished
from TO on bone scintigraphy include osteonecrosis of the femoral
head, stress fracture of the femoral
neck, and osteomyelitis. In transient

lesions, bone scintigraphy may reveal

a homogenous, diffuse increased uptake. In the case of TOH, this involves the entire femoral head and
neck. Conversely, in osteonecrosis of
the femoral head, the radionuclide uptake is less intense and is limited to
the femoral head. In the early stages
of osteonecrosis, an important element of the radionuclide bone scan
evaluation is the presence of a cold
spot resulting from decreased isotope
uptake over the anterosuperior region
of the femoral head.
Computed Tomography
CT scanning has insufficient sensitivity for detecting abnormalities
related to TO. However, CT scanning may reveal demineralization in
the early stages of the disease when
plain radiographs are reported to be
normal.24 According to Horiuchi et
al,25 CT findings such as several
spotty defects without any cortex
participation may be useful for distinguishing TO from other clinical
entities (Figure 1, B).
Magnetic Resonance
Imaging
MRI has been the imaging study
of choice for evaluating patients
with bone marrow abnormalities.

Journal of the American Academy of Orthopaedic Surgeons

Anastasios V. Korompilias, MD, et al

TO is primarily characterized by
BME, which is not visible on plain
radiographs or CT scans. MRI is the
only imaging modality that provides
adequate detection of BME.11 In the
presence of BME, MRI scans reveal
low signal intensity on T1-weighted
images and high signal intensity on
T2-weighted images in bone marrow26 (Figure 3). These changes reflect the increased content in intraand extracellular fluid of the bone
marrow, resulting in new bone formation and repair processes. Joint effusion also may be present.
Similar abnormal signal intensity
may indicate BME secondary to an
ischemic process, such as osteonecrosis. That MRI findings in the early stages of osteonecrosis may simulate those of TO has been supported
but is not widely accepted.23 In these
cases, differentiation between irreversible and transient lesions should
be made based on specific imaging
features. To determine the MRI features that most reliably distinguish
these lesions, Vande Berg et al27 reviewed MRI scans of 72 femoral
head lesions with the BME pattern.
According to their study, the lack of
additional subchondral changes other than BME on both T2-weighted
and contrast-enhanced T1-weighted
images had a positive predictive value of up to 100% for transient lesions. However, the presence of a
subchondral area of low signal intensity at least 4 mm thick on either
T2-weighted or contrast-enhanced
T1-weighted images had a strong
positive predictive value for irreversible lesions. Moreover, contour deformity and areas of subchondral
low signal intensity were more frequently found in irreversible lesions.
In these cases, no visible reactive interface between necrotic and viable
tissue is observed. Reversibility of
the findings without persistent abnormalities is suggestive of BME because of the presence of transient lesions.
Volume 16, Number 8, August 2008

Bone Densitometry
The relationship between generalized osteoporosis and osteopenia
associated with TO has been reported by many authors.16,24 However,
only a few cases using quantitative
methods for bone mass assessment
have been described in the literature.16 It is unlikely that the middleaged men who present with TO suffer from systemic osteopenia.

Figure 2

Differential Diagnosis
The most common entities presented
with a BME pattern are briefly addressed herein. Differential diagnosis
includes TOH, RMO, osteonecrosis,
neoplasia, and inflammatory arthritis.
Transient Osteoporosis of
the Hip
TOH usually affects healthy
middle-aged men and affects women
almost exclusively during the third
trimester of pregnancy or in the immediate postpartum period.1,7 TOH
is characterized by acute disabling
pain in the hip and functional disability without a history of previous
trauma. Many authors have considered it to be an abortive form of osteonecrosis of the femoral head or a
type of RSD syndrome. Focal areas of
thin and disconnected bone trabeculae covered by osteoid and active osteoblasts are evident on histologic
examination.
With few exceptions, the clinical
course of TOH is relatively short and
may last up to 6 to 8 months, with
rapid aggravation of pain and functional restriction of the hip during the
first month after onset. Radiologic
findings of bone loss of the femoral
head and/or the femoral neck may be
present within 3 to 6 weeks after the
onset of symptoms. The precise definition of histomorphologic osteopenia is uncertain, but many authors
use it to define a lesser degree of bone
loss. However, this definition is not
appropriate for the patient with TOH
because the degree of bone loss can be

Bone scintigraphy image

demonstrating an abnormal area of
uptake (arrow) in a 65-year-old woman
who presented with sudden-onset
pain that began 4 days before imaging.
The final diagnosis was transient bone
marrow edema syndrome of the medial
femoral condyle.

extensive. In addition, some patients

have other lower extremity joint involvement. Spontaneous clinical and
radiologic recovery is the rule. Recurrence in the same joint or migration
of the disease to the contralateral
femoral head may be seen.
Features of the affected femoral
head noted on imaging include diffuse bone loss (ie, osteopenia) of the
femoral head and neck on plain radiographs and homogenous, diffuse
increased uptake on bone scintigraphy. A delay between the onset of
symptoms and conventional radiographic findings is common. Characteristic BME signal on T1- and T2483

Transient Osteoporosis

Figure 3

A 45-year-old man presented with left hip pain persisting for 10 weeks; the final diagnosis was transient osteoporosis of the
hip. A, Coronal T1-weighted magnetic resonance imaging (MRI) scan demonstrating an area of low signal intensity (long arrow)
extending down to the intertrochanteric area. Spared normal marrow is seen medially (short arrow). B, Axial fat-suppressed T2weighted fast spin-echo MRI scan demonstrating high signal intensity in the involved area (arrow), moderate joint effusion (thin
arrow), and normal marrow (short arrow). C, Coronal short tau inversion recovery MRI scan demonstrating high-signal-intensity
edematous marrow lesion (arrow) and joint effusion (thin arrow). D, Oblique axial fat-suppressed contrast-enhanced MRI scan
demonstrating enhancement of the marrow edema (white arrow), synovitis (thin white arrow), and a thin subchondral low-signalintensity structure in keeping with an insufficiency fracture (black arrow).

weighted MRI scans has been

repeatedly demonstrated in patients
with TOH (Figure 3). The typical
BME changes are seen on MRI within the first 48 hours after the onset of
symptoms. MRI findings in the patient with TOH are commonly characterized by self-limited BME in the
affected area, indicating hypervascularity and repair activity.11
Regional Migratory
Osteoporosis
RMO is defined as sequential
polyarticular arthralgia of the
weight-bearing joints associated
with severe focal osteoporosis. Although RMO primarily affects the
lower appendicular skeleton, several
484

recent reports describe combined axial skeleton involvement.12 Regional osteoporosis is a distinctive feature of the disease.
RMO primarily affects middleaged men. Its presentation and clinical course are identical to those of
TOH, with the patient typically reporting no history of trauma or injury.
Although RMO was first described by
Duncan et al28 in 1969, BME migration and its etiology and relationship
to TOH have not been addressed adequately in the literature.29 According to the original description, this
clinical entity involves only the lower
extremities, especially the knee, ankle, and foot, with lesser involvement
of the hip joint, which further differ-

entiates RMO from TO.20,28,30,31 Migration occurs in 5% to 41% of patients with hip BME.30,32,33 Migration
may occur in the same or a different
joint, and in an unpredictable time interval after the onset of the first
symptoms (Figures 4 and 5). Usually,
the joint nearest the diseased one is
the next to be affected.
Clinical examination often reveals generalized tenderness and a
warm edematous affected joint with
decreased range of motion secondary
to severe pain. The overlying skin
is characterized by inflammatory
changes, and muscle atrophy is frequently noted.20,28 This is clearly different from descriptions of TO,
which does not include inflammato-

Journal of the American Academy of Orthopaedic Surgeons

Anastasios V. Korompilias, MD, et al

Figure 4

Contrast-enhanced magnetic resonance imaging (MRI) study of a 55-year-old man with regional migratory osteoporosis.
A, Coronal MRI scan taken 4 weeks after the onset of symptoms, demonstrating diffuse bone marrow edema in the proximal
femur on the left side and joint effusion. B, Three months later, the pain migrated to the left foot. Axial MRI scan demonstrating
diffuse bone marrow edema in the navicular bone (long arrow), cuneiform bones (arrows), and proximal metatarsals (small
arrows). C, Six months later, the pain migrated to the left knee joint. Coronal MRI scan demonstrating bone marrow edema in
the medial femoral condyle (arrows) and, to a lesser degree, in the lateral femoral condyle (short arrow).

ry skin changes or subcutaneous

swelling of the involved area.
The diagnosis of RMO is mainly
dependent on the benign and selflimiting clinical and radiologic behavior of the condition. The finding
that separates RMO from other similar conditions, such as TOH and
RSD, is its migratory nature.25 The
retrospective MRI findings of BME
migration to a neighboring joint or
to another site within the same joint
confirms the diagnosis of RMO.
Some authors have classified TOH
and RMO under the term transient
regional osteoporosis.12
Osteonecrosis
Approximately 15,000 new cases
of osteonecrosis are reported annually in the United States.34 Osteonecrosis is a multifactorial disease,
caused by either genetic predilection
or exposure to certain risk factors.
TO has been considered as a point
on a spectrum of pathology, with
Volume 16, Number 8, August 2008

Figure 5

A, Coronal T1-weighted magnetic resonance imaging (MRI) scan demonstrating

bone marrow edema in the medial femoral condyle (arrows) and a low-signal-intensity subchondral dark line, presumably representing trabecular microfractures, in a
51-year-old man who experienced nontraumatic sudden-onset pain 6 weeks before
imaging. B, Coronal T1-weighted MRI scan made 3 months after the image in
panel A; the patients symptoms were less intense, but a new sudden pain developed. The scan demonstrates a new bone marrow edema lesion in the medial femoral condyle (arrow). The patient experienced complete resolution of the previous
lesion (thick arrow).
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Transient Osteoporosis

Figure 6

The double-line sign seen in femoral head osteonecrosis. A, Coronal T2-weighted fast spin-echo magnetic resonance imaging
scan demonstrating the low-signal-intensity outer rim (arrow) and the high-signal-intensity inner rim. B, Image demonstrating
the same sequence as in panel A, with the only difference being the shift of the frequency encoding axis. The bright rim is now
located peripherally (arrow).

transient BME at one end and osteonecrosis at the other.

Osteonecrosis most frequently involves the hip, followed by the knee
joint. Osteonecrosis of the knee may
be secondary to ischemic risk factors
or may be spontaneous. Osteonecrosis should be distinguished from TO
of the knee, which affects middleaged men, while spontaneous osteoporosis of the knee is typically observed in women older than age 55
years.
In the patient with osteonecrosis
of the femoral head, plain radiographs indicate a mottled radiolucent area surrounded by an area of
sclerosis. In later stages of the disease, following subchondral bone
collapse, a crescent sign may develop. In the initial phase of the disease,
bone scintigraphy may reveal a cold
in hot imagean area of increased
uptake in the shape of a half-moon
(crescent) that circumscribes a
cold zone of decreased tracer uptake equivalent to the necrotic zone.
In the advanced stages of osteonecrosis, a nonspecific area of increased
uptake is usually observed.
In osteonecrosis of the femoral
head, MRI findings are similar to
those of BME. Because BME is a nonspecific finding that also has been
486

described in association with many

transient self-limited conditions (eg,
RMO, THO, epiphyseal stress fractures),35 early differentiation is crucial to prevent overtreatment of the
benign conditions and to reserve
more aggressive therapy for patients
with osteonecrosis. Studies have
shown that patients with osteonecrosis of the femoral head do not
have clinical or imaging findings of
BME typical for TOH in the early
stages of the disease.36
In their study presenting early
findings in patients with osteonecrosis, Fujioka et al37 found no evidence
of BME prior to the appearance of
band patterns on MRI scans. A similar study showed that a band pattern is the initial finding of early osteonecrosis on MRI, with no prior
evidence of diffuse BME.38 The
double-line sign, which is seen on
T2-weighted spin-echo or fast spinecho sequences, consists of a lowsignal-intensity outer rim and a
high-signal-intensity inner rim (Figure 6). Mitchell et al39 first described
this sign, which was considered
pathognomonic for osteonecrosis of
the femoral head; the outer rim represents the reactive bone and the inner rim, the vascular and repair tissue at the necroticviable osseous

interface. Recently, it was suggested

that the double-line sign has the
characteristics of a chemical shift artifact; however, this does not reduce
its value for diagnosing hip osteonecrosis for surgeons who use nonfatsuppressed T2-weighted spin-echo
or fast spin-echo magnetic resonance
sequences.40
A circumscribed subchondral
band-like lesion with low signal intensity on T1-weighted images is
pathognomonic for hip osteonecrosis39 (Figure 7). BME has been shown
to appear after the onset of hip pain
and to correlate significantly with the
subsequent collapse of the femoral
head, suggesting progression to osteonecrosis; BME therefore is considered to be a poor prognostic
indicator of osteonecrosis.41,42 Newer
techniques, such as diffusionweighted imaging, do not seem to
provide useful data for differentiating
osteonecrosis-associated BME from
transient BME.43 Absence of areas of
subchondral low-signal-intensity lesions on T2-weighted images and on
contrast-enhanced T1-weighted images seems to have a positive predictive value for a transient pattern of
the disease.27 Therefore, concomitant
subchondral changes with the typical
BME pattern may help to differenti-

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Anastasios V. Korompilias, MD, et al

Figure 7

T1-weighted magnetic resonance imaging scans demonstrating osteonecrosis of the femoral head. A, Coronal image
demonstrating bilateral osteonecrotic lesions with the typical band-like lesion (arrows) in a 45-year-old man. B, Axial image
demonstrating an osteonecrotic lesion on the left hip with the typical band-like lesion (arrow) in a 51-year-old man.

ate transient from irreversible lesions.

According to a recent study, delayed
enhancement in contrast-enhanced
images is another MRI finding that is
highly suggestive of a transient lesion.15
Neoplasia
Metastatic carcinoma, multiple
myeloma, leukemia, and lymphoma
can resemble TO. Usually, physical
examination and laboratory tests help
to distinguish these aggressive conditions from TO. Plain radiographs reveal characteristic distraction of the
metaphyses and diaphyses of long
bones in cases of neoplastic processes.
On the contrary, TO usually involves
epiphyses in which diffuse osteoporosis with preservation of the articular
cartilage is the rule.24 However, in the
patient with multiple myeloma, diffuse rather than regional demineralization may be present.
CT is of great value in further analyzing the lesion matrix and integrity of the cortex. Bone scintigraphy
may reveal the presence of multifocal tracer uptake, whereas MRI determines involvement of bone and the
surrounding soft tissues in neoplastic cases. BME may be present in various tumors or tumor-like conditions.44 In such cases, MRI with
intravenous contrast administration
Volume 16, Number 8, August 2008

distinguishes tumor tissue from concomitant BME.

Inflammatory Arthritis
Infectious arthritis, rheumatoid
arthritis, gout, multifocal osteomyelitis, and tuberculosis should be
distinguished from TO. A thorough
history and physical examination
may reveal predisposing conditions
and associated systemic symptoms
of these conditions. Asymmetric
polyarthritis, which usually involves the upper extremities, periarticular soft-tissue swelling, and
marked joint effusion, are some of
the clinical findings that differentiate inflammatory arthritis from TO.
Laboratory examinations of inflammatory markers are helpful in establishing the diagnosis.
In most cases, an accurate diagnosis can be made based on evaluation
of plain radiographs and MRI scans.
Juxta-articular demineralization resulting from disuse or hyperemia
may be found at both sides of the affected joint.24 In patients with inflammatory or reactive arthritis,
BME pattern may be present. This
MRI feature represents only a concomitant component and has no
influence on the therapeutic algorithm. In patients with inflammatory arthritis, periarticular rather

than regional BME is usually found.

In contrast, the patient with TO exhibits regional BME. Similar findings are obtained with bone scintigraphy at the symptomatic sites.
Other potential MRI findings include hyaline cartilage abnormalities, bony erosions, joint effusion,
and synovial and periarticular softtissue involvement. In septic arthritis, associated osteomyelitis and infectious myositis are better seen
with MRI because of its ability to
demonstrate high tissue contrast.

Treatment
TO is a self-limiting disease. Therefore, surgeons should use a treatment
approach based on the clinical symptoms. Current, therapeutic strategies include partial weight-bearing,
mild analgesics, and administration
of nonsteroidal anti-inflammatory
drugs. Although glucocorticoids were
thought to alter the process of the
disease, many authors indicated that
remineralization was not achieved
with the use of glucocorticoids.33
Sympathetic blockade provided no
improvement of results in the treatment of TO.12
The patient with TO experiences
a significant loss of trabecular microarchitecture, leading to a decline
487

Transient Osteoporosis

in local bone strength. Although the

marrow edema resolves, the mechanical strength remains decreased.
Therefore, the aim of treatment is not
only pain relief and shortening of the
spontaneous clinical course of the disease but also protective weight bearing until there is restoration of bone
mineral density. One study indicated
that intravenous administration of
pamidronate, a potent bisphosphonate, was efficacious for the treatment of both RSD and TOH.45 These
conditions are closely related to TO
and RMO, and Horiuchi et al25 speculated that pamidronate may have
promising results in patients with
RMO. It is of paramount importance
to recognize TO and then start the patient on calcium, correct the vitamin
D level (25[OH]vit D), and start bisphosphonates, especially if the collagen type I metabolite PINP (procollagen type I N-terminal propeptide) is
elevated.
Pamidronate has been used to
minimize the extensive bone loss
that occurs during acute episodes.46
Furthermore, iloprost (Ilomedin;
Schering, Berlin, Germany), a prostacyclin analogue, has shown clinical
success in patients with painful
BME of the knee.47 Pain relief and
rapid regression of the BME were attributed to the ability of prostacyclin
to dilate vessels and reduce the permeability of capillaries.
Although nonweight bearing has
a beneficial effect on the affected
joint, prolonged disuse may lead to
further demineralization. Trevisan
and Ortolani16 recommended densinometric assessment during the
clinical management of TO and
RMO. According to their study,
quantitative evaluation of bone mineral content and density during
acute attacks may be useful for managing weight-bearing restriction on a
case-by-case basis.16

transient demineralization of the hip

joint, a large number of TO cases
have been reported in the literature.
Despite the use of new imaging modalities, the diagnosis of TO remains
a challenge. In the initial stage, clinical and radiographic findings are nonspecific. Local regional osteoporosis
and BME are common features that
may be present in all types of TO,
such as TOH, RMO, and RSD. Moreover, a clinical overlap between these
conditions is usually found. Consequently, determining the pathophysiologic commonalities and distinctions between these diseases remains
difficult.
Spontaneous recovery distinguishes TO from other aggressive
pathologic bone conditions. However, the unpredictable recurrence of
symptoms in a different joint (or to
the same joint) makes treatment decision making difficult. The possibility of such pathologically serious
bone lesions should be considered
in patients with demonstrated regional demineralization on plain radiographs and a BME pattern on
MRI. Early differentiation from aggressive conditions with long-term
sequelae and poor prognosis is essential to provide correct diagnosis and
treatment.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

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