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Painful bone marrow edema of the knee: differential
diagnosis and therapeutic concepts
Siegfried Hofmann, MD
a,
*
, Josef Kramer, MD
b
, Anosheh Vakil-Adli, MD
c
,
Nicolas Aigner, MD
d
, Martin Breitenseher, MD
e
a
General and Orthopaedic Hospital Stolzalpe, 8852 Stolzalpe, Austria
b
Institute MR and CT Diagnostic at the Schillerpark, 4020 Linz, Austria
c
St. Vincents Hospital, 4020 Linz, Austria
d
Orthopaedic Hospital, Speising, Vienna, Austria
e
Department of Osteology, University Radiology Clinic, Vienna, Austria
During the last decade, MRI has been the imaging
modality of choice for evaluating patients with pain-
ful bones or joints with normal or unspecific radio-
graphs [1]. Characteristic MRI signal alterations have
been described for most bone and joint diseases, and
MRI examination has become the diagnostic standard
for many patients with painful knee joints. The most
important functional units of the joint, in particular
cartilage, subchondral bone, the capsular–ligament
complex, and the surrounding soft tissues, can be
visualized simultaneously with MRI [2] . For thera-
peutic decision making, the correct interpretation of
the MRI findings is of utmost importance [3]. Bone
marrow edema (BME), with its typical signal appear-
ance on MRI, is a common but nonspecific signal
pattern that can be found in the bony parts of the
joints in several diseases [4,5]. Bone marrow edema
can be categorized into three distinct groups accord-
ing to cause:
1. Ischemic BME
Osteonecrosis
Bone marrow edema syndrome (BMES)
Osteochondritis dissecans (OCD)
Complex regional pain syndrome (CRPS)
2. Mechanical BME
Bone contusion (bone bruise)
Microfracture
Stress-related BME
Stress fracture
3. Reactive BME
Gonarthritis
Osteoarthritis
Postoperative BME
Tumor-related BME
Because only marrow structures are involved in
BME, plain-film radiographs and CT are unable to
detect changes with sufficient sensitivity. Bone scin-
tigraphy can detect early changes in vascularization
in areas with BME by increased tracer accumulation
[6], but its spatial anatomic resolution is poor, and
differentiation from other disorders characterized by
increased tracer uptake is generally impossible [7].
BME is not visible with arthroscopy. Only MR
imaging provides adequate detection of BME. BME
is characterized by low signal intensity compared
with unaffected bone marrow on T1-weighted
images. O n T2-weighted images, especially when
fat-suppression techniques are used, high signal in-
tensities in the low-signal areas of the T1-weighted
images are typical for BME (Fig. 1). After intrave-
nous administration of contrast agents, enhancement
of the BME lesion is more evident, indicating hyper-
vascularity and repair activity [8]. On histologic
examination, BME is caused by increased intra- and
0030-5898/04/$ – see front matter D 2004 Elsevier Inc. All rights reserved.
doi:10.1016/j.ocl.2004.04.005
* Corresponding author.
E-mail address: hofmann.siegfried@aon.at
(S. Hofmann).
Orthop Clin N Am 35 (2004) 321–333
extracellular fluid within bone marrow inducing new
bone formation and repair processes [9].
Pain is caused by the increased intraosseous
pressure (normal pressusre, 20–30 mm Hg) because
of the abnormally high fluid content in the marrow
spaces [10–12]. The characteristic symptom of BME
in the knee is pain during mechanical loading com-
bined with more or less severe complaints during
night. Also typical is pain in the affected area when it
is tapped [4]. Until now there has been no explana-
tion why the intensity or extent of BME in MRI does
not always correlate with pain. Sometimes BME of
the knee is observed in asymptomatic patients [13];
on the other hand, BM E is som etimes th e only
definite morphologic alteration in long- lasting com-
plaints [5]. This article discusses the various causes of
painful BME of the knee joint. The aim is to allow
proper diagnosis using clinical, radiographic and
MRI findings. The therapeutic concepts for the dif-
ferent BME entities are also addressed.
Ischemic bone marrow edema
A common cause of BME is an ischemic process,
which frequently is combined with other causative
factors. Ischemic BME includes osteonecrosis, OCD,
and CRPS.
Osteonecrosis
Osteonecrosis is characterized by ischemic necro-
sis of bony structures (bone marrow, trabecula e,
cortex) in the epiphysis of convex joint compart-
ments. By far the most frequently involved location
is the hip joint, followed by the knee. In osteonecrosis
Fig. 1. Bone marrow edema syndrome (BMES): typical signal pattern of diffuse BME in different MRI sequences of coronal
images. (A) T1-weighted image. (B) Fat-suppressed T2-weighted image. (C) Fat suppressed T2-weighted image after contrast
media. Note the diffuse extension of one complete quadrant of the knee.
S. Hofmann et al / Orthop Clin N Am 35 (2004) 321–333322
of the knee joint, two distinct types, secondary and
spontaneous osteonecrosis [SONK]) can be differenti-
ated [14,15]. Secondary osteonecrosis can be observed
in younger patients ( 20 – 55 years) who frequently
have typical risk factors for osteonecrosis. Multiple
necrosis and infarcts involving both knee joints and
other sites can be detected in most of these cases. The
etiology of secondary osteonecrosis is similar to that
of osteonecrosi s of th e hip for s ever al ische mic
factors [16]. In addition, the course of the disease
can be staged like osteonecrosis of the hip joint [4].
Initially, in the reversible initial stage (ARCO I), there
are only focal subchondral areas of BME. Frequently,
however, the location is not confined to the loading
zone. At this time the BME pattern is nonspecific.
In irreversible early stage (ARCO II), a subchondral
osteonecrotic area is surrounded by a reactive inter-
face (Fig. 2). In this stage, plain radiographs are still
negative and therefore are not useful for diagnostic
evaluation. Concomitant BME is commonly seen ad-
jacent to the necrotic area. This appearance may en-
large the necrotic area on T2-weighted images or even
hide a small subchondral necrotic lesion in the early
phase. Diagnosis of secondary osteo necrosis with
concomitant edema can be made without difficulty
in most cases, however, by the pathognomonic signal
changes on MR [15,17].
SONK is observed in older patients ( > 55 years)
without the classic osteonecrosis risk factors. There is
a predominance of females with isolated involvement
of the medial femoral condyle [15,16]. In a prospec-
tive MR study of 176 patients suffering from knee
pain, 3.4% had SONK. For patients over 65 years of
age, the prevalence was even higher (9.4%) [18]. MRI
and histology demonstrate subchondral microfrac-
tures combined with ischemic necrosis [19,20]. The
course of SONK can be also divided into different
stages, but the appearance and course differ signifi-
cantly from second ary osteonecrosis [20]. Initially
(stage I), subchondral BME is observed in the load-
bearing zone of the femoral condyle (Fig. 3). Involve-
ment of the weight-bearing zone of the tibia is
uncommon [15]. Normally, because of this typical
location and the age of the patient, a definite diagno-
sis can be made in this early phase. The initial stage is
reversible. Further progression leads to early sub-
chondral fracture with flattening of the condyle (stage
II), to osteochondral fracture (stage III) and, subse-
quently, to secondary osteoarthritis (stage IV) [20].
Bone marrow edema syndrome
Whether BMES represents a distinct disease (tran-
sient osteoporosis, algodystrophy, transient bone mar-
row edema syndrome) [21,22] or is a subtype of
osteonecrosis [23–25] remains controversial. Most
likely, BMES is caused by diffuse subacute ischemia,
which completely heals in most cases because of a
sufficient repair mechanism [12]. No pathologic plain
radiographic findings can be observed during the
initial period of 4 to 6 weeks. Afterwards, a slight
demineralization of the affected area can be seen. As
a result, BMES is often also referred to as transient
osteoporosis. Histologic examination shows no signs
characteristic of osteoporosis, although loss of hy-
droxyapatite content within the bone is observed in
BMES of the hip [9]. A reasonable diagnosis of
Fig. 2. Secondary osteonecrosis. (A) T1-weighted and (B) fat suppressed T2-weighted images with two typical osteonecrosis
lesions, reactive interface, and concomitant BME in the patella and femoral condyle.
S. Hofmann et al / Orthop Clin N Am 35 (2004) 321–333 323
BMES can be made by MRI only. Extensive, diffuse
BME involving an entire quadrant of the knee joint is
typical (see Fig. 1). An important differentiation from
other diseases with BME is the diffuse extension, the
lack of any other morphologic alterations, no history
of trauma, and the reversible course in most cases
[12]. Spontaneous healing lasts from 3 to 12 months
(average, 6 months). In contrast to BMES of the hip,
a concomitant extensive joint effusion is uncommon
in BMES of the knee. A special migratory form can
be observed in rare cases [22,26]. After BME dis-
appears from an initially affected quadrant, new BME
may be observed in a different site in the knee (Fig. 4)
[27,28].
Osteochondritis dissecans
OCD usually affects the knee. OCD is the mani-
festation of osteonecrosi s in j uveniles, when the
growth plate is partly still open. The cause is probably
multifactorial and the consequence of abnormal ossi-
fication or focal stress combined with ischemia [29].
The prognosis and the course of the disease are much
better than for osteonecrosis in adults [30]. OCD can
even be observed in the convex epiphysis of joints
and can be separated into five different stages. Unlike
secondary osteonecrosis in adults, the affected area in
OCD appears relatively small in most cases [31].
Initially on MRI a nonspecific subchondral BME
Fig. 4. Fat-suppressed T2-weighted coronal images showing migratory BMES. (A) Primary lesion (lateral). (B) Three months
later the lateral lesion has healed; there is new BME in the medial condyle.
Fig. 3. T2-weighted fat-suppressed images of stage II spontaneous osteonecrosis of the knee (SONK). (A) Coronal view.
(B) Sagittal view. Note the diffuse extension of the BME and the low signal line indicating subchondral fracture.
S. Hofmann et al / Orthop Clin N Am 35 (2004) 321–333324
(stage I) can be seen. Location, extension, and age of
the patient allow diagnosis in most cases. In stage II,
plain radiographs are still negative, but in MRI the
demarcation of a necrotic area from surrounding bone
is already visible (Fig. 5). In contrast to osteonecrosis
in older patients, stage II is still reversible. Stages III
through V can be diagnosed on plain radiographs.
Concomitant BME can occur in all stages, but it is not
as common as in osteonecrosis [29].
Chronic regional pain syndrome
CRPS is also known as algodystrophy, reflex
sympathetic dystrophy, or Morbus-Sudeck syndrome
[32]. Following a trauma or i njury of unknown
origi n, a continuous burning pain, trophic distur-
bances, sensorimotor alterations, and, frequently,
psychic imbalance are observed. Initially one joint
is affected, but in chronic cases the entire extremity
may be involved. In CRPS three different stages
(acute, dystrophy, and atrop hy) can be sep arated
[33]. In most cases, the diagnosis can be suspected
by history and clinical findings. In the initial stage,
bone scintigraphy shows intense tracer uptake by the
involved joint and periarticular tissues [7]. On plain
radiographs, the earliest signs are typically patchy
structural changes after 6 to 12 weeks. MRI is not
the modality of choice in the diagnostic process of
CRPS [32], but it can contribute to diagnosis in ques-
tionable cases in the acute stage [7]. Characteristic
findings on MRI in acute CRPS are diffuse BME on
both sides of the affected j oint and edematous
changes in periarticular soft tissue. In most cases,
joint effusion is visible [7,34]. In the initial stage, an
acute infection must be excluded. Differentiation
from edema caused by other disease is possible in
most cases. In migratory BMES, however, soft tissue
involvement is possible too. A continuous transition
from migratory BMES to CRPS may be possible [7].
Mechanical bone marrow edema
In almost all cases plain radiographs and CT allow
sufficient diagnosis in the acute phase following
injury to the extremity. Patients with nonspecific pain
that does not respond to therapy following a trauma
or overloading and who have negative plain radio-
graphs present a difficult diagnostic situation. Al-
though its specificity is very low, the advantage of
bone scintigraphy in occult trauma or mechanical
overload lies in its high sensitivity. In a consecutive
series of 176 patients, BME was detected on MRI in
72% after trauma [31]. MRI significantly facilitates
diagnosis of posttraumatic or overloading pain.
Bone contusion (bone bruise)
Bone bruise is caused by direct injury to the bone.
On histologic evaluation, diffuse BME, microfrac-
tures of trabeculae, and hemorrhage can be found
[35]. Bone contusions of the knee joint are a common
finding and are frequently observed after direct con-
tact, compression, or distraction injuries [36].By
definition, a bone bruise is not visible as a fracture
on plain-film radiographs or CT. In bone scintigra-
phy, increased tracer uptake in the affected area may
help diagnosis. Today, MRI is the modality of choice
for detecting bone contusions. A diffuse subcortical
BME is visible in the painful area with enhancement
Fig. 5. Stage II osteochondritis dissecans (OCD) with concomitant BME sagittal images. (A) T1-weighted image. (B) Fat-
suppressed T2-weighted image.
S. Hofmann et al / Orthop Clin N Am 35 (2004) 321–333 325
after administration of contrast agents. Besides the
diffuse BME pattern, no signs of osteonecrosis or
fractures are visible on MRI (Fig. 6). A focal demin-
eralization zone may be observed on plain radio-
graphs 6 to 12 weeks after injury [37].
Microfracture
Microfractures are traumatic injuries of the bone
marrow in which cortical involvement is common.
There is no clear delimitation between bone bruise
and microfracture. Even in bone contusion of joint
structures, osteochondral microfractures may be pos-
sible. Plain-film radiographs are not helpful for
detecting microfractures. The fra cture line can be
detected on high-resolution CT, however. On T1-
weighted MRI, the microfracture is characterized by
a broad band of low signal in the bone marrow
coursing until the cortic al surface . Even on T2-
weighted MRI a thin band of low signal indicates
the fracture line surrounded by BME (Fig. 7) [38].
Sometimes the concomitant edema partially hides the
fracture line, and diagnosis is more difficult. In
compression fractures, extensive BME can usually
be observed. In contrast, distraction injuries may
show only minimal BME, and therefore misdiagnosis
with MRI is possible [39,40].
Stress-related bone marrow edema
Frequently, with mechanical stress or frontal mal-
alignment, subchondral BME of the overloaded com-
Fig. 6. Fat-suppressed T2-weighted images of bone bruise after anterior cruciate ligament rupture.(A) Sagittal view shows BME
of the lateral posterior tibia and central femoral condyle. (B) Coronal view of the same lesion.
Fig. 7. Microfracture: osteochondral microfracture not visible on radiographs. (A) Sagittal T1-weighted image. (B) Coronal fat-
suppressed T2-weighted image shows fracture in the lateral tibia plateau.
S. Hofmann et al / Orthop Clin N Am 35 (2004) 321–333326
partment can be observed [41]. In most patients this
chronic mechanic overloading leads to progressive
early arthritic changes (subchondral sclerosis and
thinning of the hyaline cartilage) on radiographs.
Stress-related BME can be observed without any
arthritis in the knee, however. In MR examinations
in a healthy population without arthritis, subchondral
BME could be demonstrated after mechanical stress
combined with artificial malalignment of the mechan-
ical axis [42]. On MRI, stress-related BME is char-
acterized by wedge-shaped subchondral BME in the
femur and tibia of the involved compartment with the
base of the wedge located at the site of the greatest
load (Fig. 8). Frequently, there are additional arthritic
signs with typical chondral and subchondral signal
changes, as discussed later. Therefore a continuous
transition from stress-related BME to activated oste-
oarthritis may be considered.
Stress fractures
Stress fractures can be divided into fatigue and
insufficiency fractures. A fatigue fracture is caused
by repeated overloading of normal bony structures.
In contrast, insufficiency fractures occur sponta-
neously, without any trauma or overloading in patho-
logic, altered bony tissues (eg, osteoporotic bones)
[43]. Differentiation between microfractures and
stress-related fractures is not possible with conven-
tional imaging modalities. The patient’s history can
help differentiate between microfracture (with a his-
tory of trauma) and stress fracture (with a history
of overloading).
Reactive bone marrow edema
Reactive BME occurs in a group of disorders in
which the underlying disease or a prior s urgical
procedure dominates the history, clinical findings,
prognosis, and course of the disease. BME in
these patients represents only a severe concomitant
component without any main influence on the ther-
apeutic management. In most cases there are no
essential differential diagnostic difficulties in separat-
ing reactive BME from the other types of BME de-
scribed previously.
Gonarthritis
The most important diseases in which reactive
BME is noted are chronic polyarthritis, reactive
arthritis, bacterial arthritis, and osteomyelitis. Differ-
ential diagnosis is of utmost importance for ther-
apeutic management. In contrast to other imaging
modalities, MRI allows early detection, exact assess-
ment of bony involvement (location and extent),
evaluation of the severity of disease, and its differ-
entiation from other diseases [1]. MRI should not be
used as the primary modality but should be used
when the diagnosis is questionable. In the initial stage
of chronic polyarthritis, MR imaging allows evalua-
tion of a joint effusion, synovial involvement, bony
erosions, periarticular soft tissue involvement, and
relatively early alterations of hyaline cartilage [44].
Intravenous administration of contrast agent may be
helpful for assessment of inflammatory activity [45].
In the acute phase of chronic polyarthritis a more or
less severe concomitant BME may be observed [46].
Fig. 8. Sagittal views of stress-related BME: lateral compartment osteoarthritis with valgus deformity and beginning
osteoarthritis. (A) T1-weighted image. (B) Fat-suppressed T2-weighted image.
S. Hofmann et al / Orthop Clin N Am 35 (2004) 321–333 327
In most cases, however, a correct assignment of this
reactive BME is not difficult [44]. Reactive arthritis
can be observed as a concomitant finding in several
diseases. It is important to differentiate reactive
arthritis from bacterial arthritis. Normally in reactive
arthritis there are no pathologic changes within the
bone marrow, but in rare cases BME can be observed
on MRI [47]. Frequently, in these cases, differentia-
tion from an initial stage of chronic polyarthritis is
not possible by MRI [1].
In bacterial gonarthritis, MRI is helpful for evalu-
ating the involvement of cartilage, joint capsule, soft
tissue structures, and the bone marrow. MRI, however,
is indicated in unclear cases only [48]. A concomitant
BME in bacterial arthritis must be conside red as
possible direct involvement of the bony structures
[1]. In the initial stage of osteomyelitis, only diffuse
BME is visible, and differentiation between acute
infectious alterations within the bone and concomi-
tant BME may be difficult. In this situation intrave-
nous administration of contrast agent may facilitate
diagnosis [1]. Changes in signal intensity are non-
specific, however, and it can be difficult to differen-
tiate concomitant BME from other forms of diffuse
BME. In most cases an exact diagnosis can be made
by history, clinical and laboratory findings, plain-film
radiographs, and appearance in MR imaging [49].
Assessment of osteomyelitis following to trauma or
surgery remains still a problem, however.
Osteoarthritis
Normally MRI is not used f or diagnosis and
therapy planning in chronic degenerative joint dis-
eases. In unclear cases, however, MRI may be helpful
in detecting additional changes such as joint effusion,
subchondral edema, geodes, and reactive synovitis
(Fig. 9). Histologic evaluation of subchondral BME
in arthritic knee joints shows several pathologic
changes in the bone marrow [50]. In a recent study
it has been shown that subchondral BME is correlated
to pain in patients with painful osteoarthritis of the
knee [10]. A longitudinal follow-up study of these
patients over 30 months documented for the first
time that, besides mechanical malalignment, BME
represented the main risk factor for osteoarthritic
progression [41]. There is no strong delimitation
between stress-related BME, described previously,
and subchondral BME in osteoarthritis.
Postoperative bone marrow edema
MRI is indicated for follow-up examinations after
surgery and when there is continued or recurrent pain
after surgery. In the knee joint postoperative BME is
frequently observed after reconstructions of liga-
ments, dri lling, and surgical procedures involving
the osteochondral compartment (Fig. 10). This reac-
tive BME can be seen up to 6 to 12 months after
surgery [51], and an appropriate diagnosis and as-
signment are not difficult in most cases. In patients
with persisting or recurrent pain after arthroscopies
with partial meniscectomies [52 –54] or ligament
reconstructions [55], subchondral signal alterations
have been described on MRI. In 94 patients with
meniscal tears who did not show any subchondral
signal alterations on MRI before surgery, a partial
meniscectomy was performed arthroscopically. MRI
Fig. 9. Coronal views of medial osteoarthritis. (A) T1-weighted image. (B) Fat-suppressed T2-weighted image shows BME in the
tibial plateau and focal in the femoral condyle.
S. Hofmann et al / Orthop Clin N Am 35 (2004) 321–333328
control examinations performed in all patients within
2 years revealed that 34% had femoral or tibial
subchondral BME in the region of the meniscectomy.
There was no correlation between the incidence of
BME and age, gender, or constitution of the hyaline
cartilage. The percentage of the removed meniscus
was identified as a risk factor, however [52]. This
subchondral BME will disappear in many cases if
partial weight bearing is induced by early diagnosis
[54]. The risk of developing manifest osteonecrosis
after partial meniscectomy seems to increase in
patients older than 50 years [53,56]. Clinical symp-
toms, course, and imaging findings of postoperative
BME after arthroscopy are the same as for SONK
[57]. Furthermore, histologic examinations demon-
strated subchondral microfractures comp arable to
SONK in these cases [58]. Predisposing factors may
be ischemia and local traumatizing during arthros-
copy as well as mechanic overloading (missing effect
of shock absorption and further deterioration of the
mechanical axis because of the removal of the me-
niscus) [54,58].
Tumors and tumorlike lesions of the knee joint
Benign and malignant tumors of the knee joint are
fairly common. After initial plain radiographs, MRI
with contrast administration should be performed for
exact assessment of bone involvement and involve-
ment of soft tissue structures [44]. MRI morphology
of tumors in the knee joint is the same as in other
joints. Concomitant reactive BME can be observed in
almost all stages of various tumors [59]. In most
cases better delineation of concomitant edema from
tumor tissue is possible by using intravenous contrast
agent [1]. Characteristic MRI findings of tumors
together with specific plain-film abnormalities allow
a clear differentiation from other entities with BME in
almost all cases [44].
Therapeutic concepts
Therapeutic management of BME depends es-
sentially on the disease that causes the BME. Non-
steroidal anti-inflammatory drug (NSAID) or pain
medications have shown only a limited effect, espe-
cially for the night pain. Mechanical unloading by
partial weight bearing or drilling the edematous bone
may lead to pain relief [23]. An interesting new
treatment is the medication therapy with Iloprost
(Ilomedin, Schering, Berlin, Germany), a prostacyclin
analogue [60]. The effect of iloprost has been evalu-
ated in two prospective MRI studies in patients with
painful BME of the knee (BMES, bone bruise, stress-
related BME, and reactive BME with osteoarthritis).
The preliminary data have shown clinical success for
pain relief and rapi d reg ression of the BME and
subchondral lesions on MRI [61]. Iloprost may be a
successful therapeutic approach for patients with
painful BME in the future.
Ischemic bone marrow edema
In osteonecrosis differentiating secondary osteo-
necrosis from SONK is important for therapeutic
decision making. In secondary osteonecrosis, de-
creasing intraosseous pressure by core decompres-
sion, a minimal surgical procedure, can lead to
immediate pain relief [17]. Repair of manifest necro-
sis (irreversible stage II osteonecrosis) is not possible
by drilling only, however [8]. In early-stage osteo-
necrosis without joint space destruction (stages I–II),
core decompression has shown clinical success in
79% with an average follow-up of 7 years [17].
Fig. 10. Postoperative BME: sagittal views 6 weeks after osteochondral transplantation (mosaicplasty). (A) T1-weighted image.
(B) Fat-suppressed T2-weighted image shows perifocal BME around the cylindrical transplants.
S. Hofmann et al / Orthop Clin N Am 35 (2004) 321–333 329
Because osteonecrotic areas are relatively large, and
multiple sites are involved, a bone–cartilage trans-
plantation is not a reasonable alt ernative in most
cases. After an osteochondral fracture and clinical
and radiographic progression (stages III and IV), total
knee arthroplasty is recommended [17]. In SONK
with subchondral BME in the initial stage, a prog-
nostic assessment is important. Lesions that involve
more than 50% of the bone in the joint have a
worse prognosis [15]. In a retrospective MRI study
of 23 patients who received no treatment, the pres-
ence of a subchondral hypointense line more than
4 mm thick or 14 mm long on T2-weighted images
indicated a significant risk for early osteochondral
fracture and progression (see Fig. 3) [62].Inthe
initial stage, conservative therapy with partial weight
bearing can be recommended, because in many cases
the necrosis may stabilize. In pat ients with risk
factors or flattening of the fem oral condyle an d
mechanical malalignment, a realignment osteotomy
should be consi dered, depending on the patient’s
age [63]. Additionally de
´
bridement, curettage, and
drilling can be tried arthroscopically [14]. In most
cases cartilage transplantation seems not to be rea-
sonable because of the patient’s age. A good thera-
peutic solution in advanced stages is a minimally
invasive unicondylar prosthesis [15].
In BMES the aim of treatment is pain relief and
shortening of the spontaneous course. NSAID and
pain medications are not very successful. Mechanic
unloading by partial weight bearing decreases com-
plaints but has only a limited effect on night pain.
In BMES of the hip joint, core decompression has
demonstrated immediate pain relief and significant
shortening of the spontaneous clinical course [23].
For the knee joint similar data are not available. In
OCD the therapeutic considerations are not influ-
enced by concomitant BME. In stage I and II OCD
conservative therapy (mechanical unloading by par-
tial weight bearing) or drilling in selected cases seems
to be reasonable. In lat e stages surgical t herapy
includes simple drilling, stabilization of the fragment,
curettage combined with drilling, and lastly osteo-
chondral or chondrocyte transplantation [64]. In the
therapeutic management of CRPS several considera-
tions must be taken in account. Sympathiolytic
agents, various drugs, and physiotherapy have been
recommended with varying degrees of success [32].
Mechanical bone marrow edema
In bone bruises the primary goal of treatment
is symptomatic pain relief by mechanical unloading
and interruption of sports activities for at least
6 weeks. After pain is relieved and before full weight
bearing resumes, a control examination with MRI
can be recommended [36]. In stress-related BME
the main goal of therapy is relief of pain by NSAID
or analgesics as well as mechanical unloading by
partial weight bearing. Pat ients with stress-related
BME combined with malalignment of the mechani-
cal axis show a great risk for decompensation of
the compartment, and therefore realignment should
be considered in patients younger than 60 years of
age. The treatment of microfractures and stress frac-
tures is similar to the treatment for bone bruises, but
unloading is recommended for 6 to 12 weeks. Fur-
thermore, the cause of a stress fracture should be
evaluated, and prophylactic recommendations should
be included.
Reactive bone marrow edema
Reactive BME represents only a more or less
severe concomitant component without any main
influence to the therapeutic management. Only in
osteoarthritis of the knee does subchondral BME
represent an important risk factor for progression,
indicating the beginning decompensation of the joint
[41]. Therefore arthroscopic de
´
bridement in osteo-
arthritis should be combined with decompression
and/or mechanical realign ment of the mechanical
axis. In patients with osteoarthriti s who are older
than 60 years, the indication for arthroscopy should
be restrictive, because there is a high risk of less
postoperative pain relief, rapid progression of osteo-
arthritis, and eventually development of postopera-
tive SONK [18,52,54].
Summary
BME is a common finding when patients with
knee pain are evaluated by MRI. The typical MRI
signal patterns for BME are nonspecific, however,
and occur in several diseases of the knee. This article
categorizes painful BME of the knee joint into three
distinct etiological groups: ischemic BME (osteone-
crosis, OCD, BMRS, and CRPS), mechanical BME
(bone bruise, microfracture, stress-related BME, and
stress fracture), and reactive BME (inflammatory
gonarthritis, degenerative gonarthrosis, postoperative
BME, and tumor-related BME). The therapeu tic
concepts have been described briefly in a short
overview of the different therapeutic approaches.
S. Hofmann et al / Orthop Clin N Am 35 (2004) 321–333330
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