Bone Bruising and Bone Marrow Edema
Syndromes: Incidental Radiological Findings or Harbingers of Future Joint
M. Niall, FRCS (Orth)
Consultant Orthopaedic Surgeon
Vladimir Bobic, MD, FRCSEd
Consultant Orthopaedic Knee Surgeon
c/o D. Niall
Co. Meath, Ireland.
Increasing use of magnetic resonance imaging for musculoskeletal injuries over
the last decade has alerted clinicians to "bone bruising", a phenomenon
previously undetected on conventional radiographic techniques (1-12). This
entity is recognised as focal signal abnormalities in subchondral bone marrow
and the appearances are thought to represent microtrabecular fractures,
haemorrhage and oedema without disruption of adjacent cortices or articular
cartilage. Since the late 1980's, bone bruising has been increasingly
identified in association with soft tissue knee injury, in particular anterior
cruciate ligament rupture and, to a lesser extent, injuries of the hip joint
and foot. Although some authors suspect these lesions may account for symptoms
of pain and have prognostic implications, there are few substantial reports to
date clarifying the short-term implications, exact time to resolution and
long-term sequelae and their clinical significance is still uncertain.
Bone marrow edema syndromes with no
history of trauma, are also increasingly recognised, particularly in the hip
joint, but increasingly in the knee joint. Whilst initially assumed to be a
precursor of osteonecrosis, the scientific evidence is conflicting and at
present they are best considered closely related diseases with overlapping
clinical and radiological presentations. Most recently, the presence and
persistence of marrow edema patterns in early osteoarthritis are showing
promise as a potential marker of actively progressive disease.
DIAGNOSIS OF BONE BRUISES AND MARROW
The subcortical marrow cavity consists of cancellous bone that usually
demonstrates fatty marrow at all ages. The normal marrow signal on MRI
parallels that of subcutaneous fat-high on conventional T1-weighted and
intermediate on T2-weighted spin echo sequences. A typical bone bruise appears
as an area of signal loss on T1 images and high signal intensity on T2 images,
as a result of increased water content in the injured marrow. Further
information can be gained with Short T1 Inversion Recovery ("STIR") imaging
when signal from normal medullary fat is markedly suppressed and bone bruises
show increased intensity ( Figs 1-2). Distinction between bone bruising and
marrow oedema syndromes is primarily based on a clinical history of trauma, as
the radiological features are largely indistinguishable.
CLASSIFICATION OF BONE BRUISES
Mink (6) was the first to identify bone bruising as a distinct entity in 1987
and several authors have since attempted to classify the lesions (3,5,12). Some
confusion exists however, in distinguishing bone bruises involving only the
marrow, and "occult" fractures, undetected on conventional x-ray, which breach
the adjacent cortex or osteochondral surface on MRI. Vellet (12) divided true
subcortical lesions into three types dependent on their characteristic bruising
pattern - reticular, geographic and linear. He described reticular lesions as
regions of "reticular serpiginous stranding" with variable degrees of
coalescence within the marrow compartment but distant from the adjacent
cortices and articular cartilage. "Geographic" lesions are characteristically
large, amorphous, coalescent and continuous with the adjacent cortical bone and
are the commonest type seen. Scant attention has been paid to these
classifications, as they contribute little to understanding the underlying
INCIDENCE OF BONE BRUISING
Much of the literature to date has focused on bone contusions around the knee
joint. Lynch reviewed 434 consecutive patients with acute knee injury and found
an incidence of 20%, the majority (77%) associated with anterior cruciate
rupture (3). Subsequent authors have almost exclusively focused their attention
on the ACL injured population with strikingly consistent findings
(1,2,7-11,13). Scans in the acute phase following injury consistently found
more than 80% of acute ACL tears had contusions on MRI (8-10,13). Studies done
which included patients scanned over a longer period had a smaller incidence
ranging from 40-56% (1,2,11).
The pattern of bone contusions
associated with ACL tears is very distinctive. In Spindler's series, 86% and
67% of contusions involved the lateral femoral condyle (LFC) and lateral tibial
plateau (LTP) respectively and bruising of both occurred in 56%. Lesions in the
medial femoral condyle (7%) and tibial plateau (21%) were less common (10). The
notion that "matching" lesions in the lateral compartment reflected the valgus
force on the knee at the time of injury was supported by Kaplan in her review
of 100 MRIs of acute ACL tears (2). All 56 knees with contusions had
posterolateral tibial lesions and this was the only finding in 43% of patients,
whilst 48% had lesions in both the posterior LTP and LFC. In 200 MRIs without
radiological ACL injury, posterolateral tibial bruising was found in only 3
patients, all of whom were later found to have an ACL tear at arthroscopy,
suggesting that posterolateral tibial bruising is a pathognomonic sign of ACL
injury. McCauley also found a high specificity of 97% for posterolateral
plateau contusions alone and 100% when combined with lateral femoral condyle
contusions as markers of ACL injury (4).
The preponderance of contusions in
the lateral compartment with ACL rupture correlates with the mechanism of
injury. The tibia subluxes anteriorly relative to the femur, the lateral
plateau subluxing more than the medial side. If this traumatic "pivot shift"
occurs with enough axial and valgus force, it is conceivable that a unique
pattern of "kissing-contusions" may occur in the middle ( weight-bearing)
portion of the LFC and the posterior aspect of the LTP as the bones are
compressed against one another. The posterior aspect of the LTP may be
structurally weaker than the LFC and therefore injured most often. Kaplan's
finding of the invariable presence of posterolateral tibial bruising would
support this theory. It has also been shown that some injury of the
popliteus-arcuate capsuloligamentous complex is commonly associated with bone
contusions of the posterior LTP (13), lending support to contemporary opinion
by clinicians that subtle injury to the posterolateral corner is frequently
overlooked and may account for less optimal outcome after ACL reconstruction.
Murphy made some interesting
observations by distinguishing between complete and partial tears of the ACL
(7). Whilst bruising of the posterolateral tibia (94%) and lateral femoral
condyle (91%) was common with complete tears, only 17% of patients with partial
tears had contusions. He suggested that the presence of these MRI lesions
indicates ACL "insufficiency" and may influence decisions about reconstruction.
These findings were supported by Zeiss, who found that 80% of "partial
tears" with contusions were high grade injuries that eventually led to complete
rupture within 6 months (14).
Whilst the pattern of lateral joint
contusions is explained by axial and valgus load, the mechanism of medial
tibial plateau injury is not clearly understood. In 25 patients with medial
tibial plateau contusions, all associated with ACL rupture and lateral lesions,
Kaplan found consistent injury to the posterior horn of the medial meniscus or
meniscocapsular junction (15). She suggested contusions of the posteromedial
lip of the tibial result from a "contrecoup" impaction injury as the knee
reduces and they imply associated medial meniscal injury. Speer observed a
relatively high incidence (29%) of MTP lesions in alpine skiers (9). It has
been proposed that, at the moment of ACL rupture, the skier's knee is
non-weight bearing and the ultimate tearing force is rotational. The expected
number of contusions from axial loading should be less, but this is not
supported in Speer's group. However, the higher incidence of posteromedial
tibial plateau contusions and meniscal injury may reflect a different mechanism
of injury in skiers and requires further investigation. The mechanism behind
infrequent anteromedial femoral condyle contusion with ACL rupture is also open
to question. Recent work has implicated associated clinical disruption of the
posterolateral corner but this theory needs substantiation in large studies
Recent literature has also
highlighted contusions with other "non-bony" knee injury. Miller reported an
incidence of 45% associated with medial collateral ligament injury, almost all
lesions involving the lateral femoral condyle (17). Contusions of the lateral
femoral condyle (81-100%) and the medial patella (30%) after patellar
dislocation (18-21) and "isolated" bone bruising with uneventful resolution
(22) are both recognised. Traumatic hip dislocation has also been implicated in
lesions of the femoral head (23) and the ipsilateral knee from dashboard
impaction (24). Lesions of the talus and medial malleolus occur in up to 40% of
lateral ligament ankle sprains (25-29) and bilateral calcaneal contusions after
axial loading has also been reported (30).
CLINICAL, OPERATIVE AND HISTOLOGICAL
Difficulty arises in identifying clinical signs and symptoms directly
attributable to the bone bruising, because of the spectra of associated
injuries. However, patients with contusions appear to have a more protracted
clinical recovery, with greater effusions and pain scores at matched time
intervals and a slower return of motion (31).
Arthroscopic evidence of damage to
the joint surface overlying contusions is not universally supported in the
literature. Several authors found no arthroscopic evidence of osteochondral
lesions corresponding anatomically with contusions in the acute phase (1,12).
Coen described normal joint appearance but "dimpling" of the cartilage over
geographic femoral bruises when probed (32). Several authors describe articular
lesions later at the time of ACL reconstruction (9,10). Speer found a small
incidence of fissuring (6%) overlying lateral femoral condyle and
posterolateral tibial plateau contusions (9). Although Spindler found 46% of
patients had articular lesions, many did not correlate with contusion. The only
significant relationship was in the lateral femoral condyle where 40% of
contusions had an overlying lesion (10). In contrast, Johnson consistently
found evidence of articular cartilage injury over femoral condyle contusions,
varying from subtle indentation when probed, to severe fibrillation, fissuring
or overt chondral fracture (33).
Some interesting histological
information has arisen from biopsy at varying time periods (33-35). In acute
lesions, Rangger found microfractures of the trabecular bone, oedema and
bleeding in the fatty marrow (34). In Johnson's series, all patients had
articular cartilage and subchondral bone changes at ACL reconstruction.
Chondrocytes in the superficial zone of the articular cartilage showed
different stages of degeneration, and loss of matrix proteogylcan and variable
osteocyte necrosis in the underlying subchondral bone was noted (33). Fang
supported the evidence for proteoglycan loss and also found a 10-fold increase
in matrix protein degradation products in the synovial fluid from injured
compared with uninjured knees (35). This clinical data supports previous animal
studies suggesting blunt trauma to articular cartilage produces profound
changes in its histologic, biochemical and ultrastructural characteristics in
the absence of surface disruption (36,37) and lends scientific evidence to the
notion that bone bruising may be a precursor of posttraumatic arthritis.
RESOLUTION OF BONE BRUISING
Few studies to date address resolution of bone contusions or long-term
sequelae. Vellet demonstrated complete resolution of MRI contusions at 6-12
months but osteochondral sequelae in 67% of lateral femoral condyle lesions
(12). The commonest finding was an overt cartilage defect (48%), but features
of osteosclerosis, cartilage thinning and osteochondral defects were also seen.
No articular defects occurred over associated reticular bruises in the
posterolateral tibial plateau. Bretlau recently reported persistent bruising in
69% and 12% of patients rescanned at 4 and 12 months respectively (38). Miller,
in contrast, suggested the majority of lesions resolved in 2-4 months but his
study involved patients with isolated medial collateral ligament injury, the
benign nature of which may have influenced the rate of recovery (17).
Much anecdotal evidence that
contusions resolve within the first few months is inferred from earlier studies
on incidence. In Graf's series with a 48% incidence of contusions, no lesions
were seen in scans later than 6 weeks (1). Tung reported a significantly
shorter interval from injury to MR imaging when bone bruising was present (mean
4.3 weeks) than in those with normal medullary signal (mean 24 weeks) (11).
Dimond found scans were consistently negative for contusions by 6 months, but
showed a greater incidence of meniscal tears and chondromalacia (39). Whether
these are secondary injuries from instability, or indeed sequelae of a resolved
bone bruise is open to question. Two year follow-up studies suggest that 10-15%
of patients have persistent marrow oedema at 2 years and up to one third have
some evidence of subchrondral osteonecrosis or articular cartilage degeneration
BONE MARROW EDEMA SYNDROMES
The first use of the term ''bone marrow edema'' was by Wilson and collaborators
in 1988 (75). They found ill-defined bone marrow hyperintensities on
T2-weighted MR images in patients with debilitating knee and hip pain.
Corresponding standard radiographs were normal or demonstrated non-specific
osteopenia. The authors termed this condition bone marrow edema because of "the
lack of a better term and to emphasize the generic character of the
condition''. According to findings of a Medline search starting at 1966, this
term was not mentioned before 1988 in the radiology or pathology literature,
which probably relates to the fact that MR imaging was not used widely for
musculoskeletal disease before the mid-1980s. However, Roemer et al. (41)
conclude that widely used term BME should be replaced by "ill-defined signal
intensity" as there are many similar but unrelated and non-specific MRI
abnormalities. They claim that post-traumatic osteonecrosis, as reported in the
literature, must be a rare event after acute knee trauma.
Whilst marrow edema is a recognised
non-specific finding in pathologies such as infection, neoplasms and avascular
necrosis, the phenomenon of transient bone marrow edema syndrome (BMES) has
received much attention in recent years. Most commonly seen in the hip joint,
it was initially thought to be synonymous with transient osteoporosis and a
possible precursor of avascular necrosis. However, the onset of radiological
osteopenia within weeks of clinical symptoms distinguishes transient
osteoporosis from BMES, although both are characterised by complete recovery,
It has been suggested that
transient osteoporosis or the bone marrow edema syndrome may be the initial
phase of femoral head osteonecrosis but there is little radiological or
histological evidence to date to support this hypothesis. In a series of 200
hips, Kim could not identify a bone marrow oedema pattern on MRI in the early
stages of femoral head necrosis (42). Structural damage of the head seemed to
result in the later appearance of marrow edema and the development of pain,
suggesting that the edema pattern is a secondary reaction associated with the
inflammatory response to subchondral fracture.
Various authors have treated BMES
of the hip with core decompression, showing marked acceleration in recovery
compared with conservative measures (43-45). Interestingly, no osteonecrosis
followed with either treatment. Histological examination of the core specimens
from the earliest series suggested evidence of early necrosis (46). However,
recent studies report edema without osteoporosis or osteonecrosis (43-45).
Increased osteoblast activity and transient decrease in mineral density are
described but osteoclast resorption is rarely seen. Live trabeculae and active
bone formation, however, infer increased repair capacity and may explain the
spontaneous reversibility of this syndrome.
The pathophysiological event that
triggers BMES is still a complete enigma. Ischaemia has been suggested as the
initiating factor. Koo reported angiographic findings of increased femoral head
perfusion suggesting a vasomotor response in the pathogenesis (47). The present
consensus of opinion is that bone marrow edema syndrome, transient osteoporosis
and avascular necrosis may have a common pathophysiology but are distinguished
by the early potential for reversibility.
The recent increasingly frequent
findings of non-traumatic bone marrow edema in the knees and feet of
asymptomatic athletes (48,49) and others with pain (50,51), suggests that BMES
is more common than previously recognised.
MR imaging is sensitive to changes
in subchondral bone marrow (especially if fat suppression is used), which are
difficult, if not impossible, to assess arthroscopically. Those changes reflect
changes in overlaying cartilage, but the nature of bone lesions remains
unclear. In recent years advances in MRI imaging of articulating surfaces have
shown previously unknown subchondral bone changes following cartilage repair:
edema-like signal, cysts, irregularity of subchondral bone plate, mismatch with
adjacent plate, intralesional osteophytes, etc. Persistent BME and pain
following autologous chondrocyte implantation (ACI) repair seem to suggest
complications or failed repair. Abnormal subchondral bone marrow signal after
cartilage repair is associated with failure of repair tissue integration at
different levels. Failed integration of the repair tissue to bone appears as
diffuse edema-like signal, while failed integration of the repair tissue to
adjacent cartilage appears as focal edema-like signal, fissures, cysts, etc. In
summary, early edema-like MRI changes may reflect normal healing, while
persistently abnormal marrow signal usually indicates a problem with cartilage
BONE MARROW EDEMA AND OSTEOARTHRITIS
Recent studies provide some evidence that marrow edema in osteoarthritis joint
is strongly associated with both pain and disease progression. In a large
series of arthritic knees, Felson found bone marrow lesions in 77.5% of
patients with pain, compared with 30% in those without pain (52). In a further
study, he suggested that BME lesions increase the risk more than six-fold for
disease progression at a year (53). Pessis also examined the predictive value
of subchrondral edema and found no patient without oedema on initial MR
assessment but 40% of those with lesions developed worsening chondropathy at
one year (54).
Cartilage degeneration, although
fundamental to the pathogenesis of osteoarthritis, is not the site of origin of
pain, which is the predominant symptom of osteoarthritis. Patients with
osteoarthritis of the knee often report no or minimal pain while walking but
considerable pain after activity, especially at night. These delayed responses
can be explained by findings such as those reported by Felson and colleagues -
they reflect the time it takes for the marrow spaces to react. Edema of the
bone marrow has also been observed in patients with painful, transient regional
osteoporosis, which is usually symptomatic for 6 to 12 months. Periosteal edema
along with marrow edema has been seen on MRI in patients with otherwise
unexplained medial tibial pain after trauma. MR imaging has demonstrated other
bone marrow lesions in patients with bone pain, such as those in osteoid
osteoma and with sickle-cell crises. Magnetic resonance imaging can also detect
early subarticular erosions in rheumatoid arthritis.
Impaired venous drainage from the
bone marrow has been suggested as a cause of pain in patients with
osteoarthritis, since the resulting venous hypertension would increase
intraosseous pressure in the closed spaces of the bone marrow compartments.
Such venous hypertension would contribute to the development of marrow edema
and may be an aspect of the phenomenon that Felson and colleagues observed. The
development of venous hypertension and bone marrow edema may also be related to
the development of cysts in the subchondral bone in osteoarthritis. These
observations may explain pain that occurs before OA changes are visible on
standard radiographs. Ordinary radiographs show the effect of degeneration of
joint cartilage as narrowing of the space between articulating surfaces.
However, patients can have considerable pain despite a normal-looking cartilage
space, or pain can be mild despite marked narrowing. (77).
It is possible in the future that
MR may be a useful screening tool for identifying patients with marrow oedema
and high risk of arthritic progression.
As a recently recognised entity, the natural history of bone bruising is
unknown. If it represents trabecular microfracture, as the histological
evidence to date suggests, one can reasonably expect bony healing of the
subchrondral lesion. Certainly, there is a consensus that most bone contusions
heal in the short term. It has been proposed however, that increased stiffness
of the healed bone may decrease the potential for the joint to dissipate load
by deformation and this may also increase shear-stress at the bone cartilage
interface, precipitating cartilage degeneration (55). However, it is also
likely that the initial trauma insults the cartilage microstructure in its own
right and the relative influence of the underlying bone bruise on chondral
degeneration is still open to question. Further understanding of articular
cartilage microstructure in the acute phase is needed, as evidence for chondral
injury to date is based on macroscopic appearances and histology at the time of
The high prevalence of bone bruises
with ACL rupture has raised questions about its prognostic implications for
this injured population. Posttraumatic arthritis is an established complication
of nonoperative treatment of ACL rupture (56-66). Some radiological
degeneration is seen in up to 80% of patients as early as 3 years post injury
(60,62). McDaniel and Dameron found 37% of patients had profound degeneration
at 14 years (63). Whilst associated meniscal injury was often considered the
determining factor, several authors have shown similar rates of long-term
degeneration, regardless of initial meniscal damage (64,66). Two possible
explanations exist. Chronic instability may provoke secondary injury to menisci
seen to be intact at the time of ACL rupture (67,68). Alternatively, initial
damage to the articular cartilage may be the predominant prognostic factor and,
if so, bone bruising may be the missing link. Sherman's observation that knees
with concomitant medial collateral ligament injury degenerated significantly
earlier than those with ACL/ meniscal tear patterns could be explained by a
more traumatic impact to the lateral compartment with extensive bone
The commonly held belief that a
knee with a chronic ACL injury develops cartilage wear and degeneration because
of instability requires further review. The literature to date shows lack of
documentation that ACL reconstruction prevents degenerative arthritis
(57,59,69-71). Friederich and O'Brien have shown a similar incidence of
radiographic arthritis at 5-10 years in surgically and conservatively treated
knees, whilst Daniel found an increased incidence of degenerative change after
reconstruction (57,59). Both these studies suggest that initial injury to the
articular cartilage is the predominant precursor to joint degeneration and bone
bruising may be the etiological factor. Long-term prospective trials comparing
matched reconstructed groups, with and without bone bruising, will clarify this
issue in the future.
Most of the literature to date has
focused on ACL associated bone bruises. However, the long-term manifestations
of bone bruising will be difficult to clarify in these patients because of the
injury complexity and we need to identify better natural history models for
follow-up studies. "Isolated" contusions and those associated with medial
collateral ligament injury would seem ideal. The speculation that lesions may
also occur with meniscal tears must also be explored. The incidence of
posttraumatic arthritis after meniscectomy has historically been attributed to
increased load-bearing in the affected compartment (72-74). However, contusions
in the adjacent bone may be contributory in part.
Many answers on the enigmas of bone
contusions will not be answered in the short-term. Future research needs to
focus on longitudinal studies to establish natural history and further
investigation into the pathophysiology of the lesions and the adjacent
cartilage. Until such time as long-term studies are available, as clinicians we
must assume that bone bruising as a specific entity is a harbinger of
posttraumatic arthritis and practice a cautious approach to management of
associated knee injuries.
(1) Graf BK, Cook DA, De Smet AA et al. "Bone bruises" on magnetic
resonance imaging evaluation of anterior cruciate ligament injuries. Am J
Sports Med 1993; 21(2):220-3.
(2) Kaplan PA, Walker CW, Kilcoyne
RF et al. Occult fracture patterns of the knee associated with anterior
cruciate ligament tears: Assessment with MR imaging. Radiology 1992; 183:835-8.
(3) Lynch TCP, Crues JV, Morgan FW
et al. Bone Abnormalities of the knee: prevalence and significance at MR
imaging. Radiology 1989; 171:761-6.
(4) McCauley TR, Moses M, Kier R et
al.. MR diagnosis of tears of anterior cruciate ligament of the knee:
importance of ancillary findings. AJR 1994; 162:115-9.
(5) Mink JH, Deutsch AL. Occult
cartilage and bone injuries of the knee: Detection, classification and
assessment with MR imaging. Radiology 1989; 170:823-9.
(6) Mink JH, Reicher MA, Crues IH.
(eds). Magnetic resonance imaging of the knee. New York: Raven 1987.
(7) Murphy BJ, Smith RL, Uribe JW
et al. Bone signal abnormalities in the posterolateral tibia and lateral
femoral condyle in complete tears of the anterior cruciate ligament: A specific
sign? Radiology 1992; 182:221-4.
(8) Rosen MA, Jackson DW, Berger
PE. Occult osseous lesions documented by magnetic resonance imaging associated
with anterior cruciate ligament ruptures. Arthroscopy 1991; 7:45-51.
(9) Speer KP, Warren RF, Wickiewicz
TL et al. Observations on the injury mechanism of anterior cruciate ligament
tears in skiers. Am J Sports Med 1995; 23(1):77-81.
(10) Spindler KP, Schils JP,
Bergfeld JA et al. Prospective study of osseous, articular and meniscal lesions
in recent anterior cruciate ligament tears by magnetic resonance imaging and
arthroscopy. Am J Sports Med 1993; 21(4):551-6.
(11) Tung GA, Davis LM, Wiggins ME
et al. Tears of the anterior cruciate ligament: Primary and secondary signs at
MR imaging. Radiology 1993; 188:661-7.
(12) Vellet AD, Marks PH, Fowler PJ
et al. Occult post-traumatic osteochondral lesions: Prevalence, classification
and short-term sequelae evaluated with MR imaging. Radiology 1991; 178:271-6.
(13) Speer KP, Spritzer CE, Bassett
FH et al. Osseous injury associated with acute tears of the anterior cruciate
ligament. Am J Sports Med. 1992 Jul;20(4):382-9.
(14) Zeiss J, Paley K, Murray K et
al. Comparison of bone contusion seen by MRI in partial and complete tears of
the anterior cruciate ligament. J Comput Assist Tomogr. 1995
(15) Kaplan PA, Gehl RH, Dussault
RG et al. Bone contusions of the posterior lip of the medial tibial plateau
(contrecoup injury) and associated internal derangements of the knee at MR
imaging. Radiology 1999 Jun;211(3):747-53.
(16) Ross G, Chapman AW, Newberg AR
et al. Magnetic resonance imaging for the evaluation of acute posterolateral
complex injuries of the knee. Am J Sports Med. 1997 Jul;25(4):444-8.
(17) Miller MD, Osborne JR, Gordon
WT et al. The Natural History of bone bruises. A prospective study of magnetic
resonance imaging-detected trabecular microfractures in patients with isolated
medial collateral ligament injuries. Am J Sports Med 1998; 26(1):15-19.
(18) Lance E, Deutsch AL, Mink JH.
Prior lateral patellar dislocation: MR imaging findings. Radiology 1993
(19) Kirsch MD, Fitzgerald SW,
Friedman H et al. Transient lateral patellar dislocation: diagnosis with MR
imaging. Am J Roentgenol 1993 Jul;161(1):109-13.
(20) Virolainen H, Visuri T,
Kuusela T. Acute dislocation of the patella: MR findings. Radiology 1993
(21) Sallay PI, Poggi J, Speer et
al. Acute dislocation of the patella. A correlative pathoanatomic study. Am J
Sports Med. 1996 Jan-Feb;24(1):52-60.
(22) Wright RW, Phaneuf MA, Limbird
TJ, Spindler KP. Clinical outcome of isolated subcortical trabecular fractures
(bone bruise) detected on magnetic resonance imaging in knees. Am J Sports Med.
(23) Laorr A, Greenspan A, Anderson
MW, et al. Traumatic hip dislocation: early MRI findings. Skeletal Radiol. 1995
(24) Bealle D, Johnson DL.
Subchondral contusion of the knee caused by axial loading from dashboard
impact: detection by magnetic resonance imaging. J South Orthop Assoc. 2000
(25) Nishimura G, Yamato M, Togawa
M. Trabecular trauma of the talus and medial malleolus concurrent with lateral
collateral ligamentous injuries of the ankle: evaluation with MR imaging.
(26) Pinar H, Akseki D, Kovanlikaya
I et al. Bone bruises detected by magnetic resonance imaging following lateral
ankle sprains. Knee Surg Sports Traumatol Arthrosc. 1997;5(2):113-7.
(27) Alanen V, Taimela S, Kinnunen
J et al. Incidence and clinical significance of bone bruises after supination
injury of the ankle. A double-blind, prospective study. J Bone Joint Surg Br.
(28) Labovitz JM, Schweitzer ME.
Occult osseous injuries after ankle sprains: incidence, location, pattern, and
age. Foot Ankle Int. 1998 Oct;19(10):661-7.
(29) Sijbrandij ES, van Gils AP,
Louwerens JW et al. Posttraumatic sudchrondral bone contusions and fractures of
the talotibial joint: occurrence of "kissing" lesions. Am J Roentgenol. 2000
(30) Dienst M, Blauth M. Bone
bruise of the calcaneus. A case report. Clin Orthop. 2000 Sep;(378):202-5.
(31) Johnson DL, Bealle DP, Brand
JC et al. The effect of a geographic lateral bone bruise on knee inflammation
after acute anterior cruciate ligament rupture. Am J Sports Med. 2000
(32) Coen MJ, Caborn DN, Johnson
DL. The Dimpling phenomenon: articular cartilage injury overlying an occult
osteochondral lesion at the time of anterior cruciate ligament reconstruction.
Arthroscopy 1996 Aug;12(4):502-5.
(33) Johnson D, Urban WP, Caborn
DNM et al. Articular cartilage changes seen with magnetic resonance imaging
detected bone bruises associated with acute anterior cruciate ligament rupture.
Am J Sports Med 1998; 26(3):409-14.
(34) Rangger C, Kathrein A, Freund
MC et al. Bone bruise of the knee: histology and cryosections in 5 cases. Acta
Orthop Scand. 1998 Jun;69(3):291-4.
(35) Fang C, Johnson D, Leslie MP
et al. Tissue distribution and measurement of cartilage oligomeric matrix
protein in patients with magnetic resonance imaging-detected bone bruises after
acute anterior cruciate ligament tears. J Orthop Res. 2001 Jul;19(4):634-41.
(36) Donohoe JM, Buss D, Oegema TR
Jr,et al. The effects of indirect blunt trauma on adult canine articular
cartilage. J Bone Joint Surg 1983; 65A:951-7.
(37) Thompson RC Jr, Oegema TR Jr,
Lewis JL et al. Osteoarthritic changes after acute transarticular load. J Bone
Joint Surg 1991; 73A:990-1001.
(38) Bretlau T, Tuxoe J, Larsen L
et al. Bone bruise in the acutely injured knee. Knee Surg Sports Traumatol
Arthrosc. 2002 Mar;10(2):96-101.
(39) Dimond PM, Fadale PD, Hulstyn
MJ et al. A comparison of MRI findings in patients with acute and chronic ACL
tears. Am J Knee Surg 1998; 11(3):153-9.
(40) Costa-Paz M, Muscolo DL,
Ayerza M et al. Magnetic resonance imaging follow-up study of bone bruises
associated with anterior cruciate ligament ruptures. Arthroscopy. 2001
(41) Roemer FW, Bohndorf K.
Long-term osseous sequelae after acute trauma of the knee joint evaluated by
MRI. Skeletal Radiol 2002, 31:615-623.
(42) Kim YM, Oh HC, Kim HJ. The
pattern of bone marrow oedema on MRI in osteonecrosis of the femoral head. J
Bone Joint Surg Br. 2000 Aug;82(6):837-41.
(43) Calvo E, Fernandez-Yruegas D,
Alvarez L. Core decompression shortens the duration of pain in bone marrow
oedema syndrome. Int Orthop. 2002;24(2):88-91.
(44) Krause R, Glas K, Schulz A et
al. The transient bone marrow edema syndrome of the hip. Z Orthop Ihre
Grenzgeb. 2002 May;140(3):286-96.
(45) Plenk H, Hofmann S, Eschberger
J et al. Histomorphology and bone morphometry of the bone marrow edema syndrome
of the hip. Clin Orthop. 1997 Jan;334:73-84.
(46) Hofmann S, Engel A, Neuhold A
et al. Bone marrow oedema syndrome and transient osteoporosis of the hip. An
MRI-controlled study of treatment by core decompression. J Bone Joint Surg Br.
(47) Koo KH, Ahn IO, Song HR et al.
Increased perfusion of the femoral head in transient bone marrow oedema
syndrome. Clin Orthop 2002 Sep;(402):171-5.
(48) Major NM, Helms CA. MR imaging
of the knee: findings in asymptomatic collegiate basketball players. Am J
Roentgenol. 2002 Sep;179(3):641-4.
(49) Trappeniers L, De Maeseneer M,
De Ridder F et al. Can bone marrow edema be seen on STIR images of the ankle
and foot after 1 week of running? Eur J Radiol. 2003 Jul;47(1):25-8.
(50) Fernandez-Canton G, Casado O,
Capelastegui A et al. Bone Marrow edema syndrome of the foot: one year
follow-up MR imaging. Skeletal Radiol. 2003 May;32(5):273-8.
(51) Papadopoulos Ech,
Papagelopoulos PJ, Kasete M et al. Bone marrow edema of the knee: a case report
and review of the literature. Knee. 2003 Sep;10(3):295-302.
(52) Felson DT, Chaisson CE, Hill
CL, Totterman SM et al. The association of bone marrow lesions with pain in
knee osteoarthritis. Ann Intern Med. 2001 Apr 3;134(7):541-9.
(53) Felson DT, McLaughlin S,
Goggins J et al. Bone marrow edema and its relation to progression of knee
osteoarthritis. Ann Intern Med. 2003 Sep 2;139(5):330-6.
(54) Pessis E, Drape JL, Ravaud P
et al. Assessment of progression in knee osteoarthritis: results of a 1 year
study comparing arthroscopy and MRI. Osteoarthritis and Cartilage
(55) Radin EL, Rose RM. Role of
subchrondral bone in the initiation and progression of cartilage damage. Clin
(56) Arnold JA, Coker TP, Heaton LM
et al. Natural history of anterior cruciate tears. Am J Sports Med 1979;
(57) Daniel DM, Stone ML, Dobson BE
et al. Fate of the ACL-injured patient-A prospective outcome
study.Am J Sports Med 1994; 22(5):632- 44.
(58) Fetto JF, Marshall JL. The
natural history and diagnosis of anterior cruciate ligament insufficiency. Clin
Orthop 1980; 147:29.
(59) Friederich NF, O'Brien WR.
Gonarthrosis after injury of the anterior cruciate ligament: A multicenter,
long-term study. Z Unfallchir Versicherungsmed 1993; 86:81-9.
(60) Jacobsen K. Osteoarthrosis
following insufficiency of the cruciate ligaments in man. Acta Orthop. Scand
(61) Kannus P, Jarvinen M.
Conservatively treated tears of the anterior cruciate ligament-long-term
results. J Bone Joint Surg 1987; 69A(7):1007-12.
(62) McDaniel WJ, Dameron TB.
Untreated ruptures of the anterior cruciate ligament. J Bone Joint Surg 1980;
(63) McDaniel WJ, Dameron TB. The
untreated anterior cruciate ligament rupture. Clin Orthop 1983;(172):158-63.
(64) Noyes FR, Mooar PA, Matthews
DS et al. The symptomatic anterior cruciate deficient knee-Part 1: The
long-term functional disability in athletically active individuals. J Bone
Joint Surg 1983; 65A(2):154-162.
(65) O'Brien WR, Warren RF,
Friederich NF. Degenerative arthritis of the knee following anterior cruciate
ligament injury: A multi-center, long-term folow-up study. Orthop Trans 1989;
(66) Sherman MF, Warren RF,
Marshall JL. A Clinical and radiographical analysis of 127 anterior cruciate
insufficient knees. Clin Orthop 1988; 227:229-37.
(67) Noyes FR, McGinniss GH.
Controversy about the treatment of the knee with anterior cruciate laxity. Clin
Orthop. 1980; 198:61-76.
(68) Hirshman HP, Daniel DM,
Miyasaka K. The fate of unoperated knee ligament injuries. Knee
ligaments: structure, function,injury and repair (eds). New York. Raven Press
(69) Lohmander LS, Roos H. Knee
ligament injury, surgery and osteoarthrosis-truth or consequences? Acta Orthop
Scand 1994; 65(6):605-9.
(70) Maletius W, Gillquist J.
Long-term results of anterior cruciate ligament reconstruction with a Dacron
prosthesis- the frequency of osteoarthritis after 7-11 years. Am J Sports Med
(71) Sommerlath K, Lysholm J,
Gillquist J. The long-term course after treatment of acute anterior cruciate
ligament ruptures-a9 to 16 year follow-up. Am J Sports Med 1991; 19(2):156-162.
(72) Appel H. Late results after
meniscectomy in the knee joint. A clinical and roentgenologic follow-up
investigation. Acta Orthop Scand (suppl 133) 1970;41:1-111.
(73) Hede A, Larsen E, Sandberg H.
Partial versus total meniscectomy. A prospective randomized study with
long-term follow-up. J Bone Joint Surg 1992; 74B:118-21.
(74) Joergensen U, Sonne-Holm S,
Lauridsen F et al. Long-term follow-up of meniscectomy in athletes. J Bone
Joint Sur 1987; 69B:80-3.
(75) Wilson AJ, Murphy WA, Hardy
DC, Totty WG. Transient osteoporosis: transient bone marrow edema? Radiology
(76) Winalski CS. Personal
communication and presented but unpublished material. 2003.
(77) Bollet JA. Edema of the Bone
Marrow Can Cause Pain in Osteoarthritis and Other Diseases of Bone and Joints.
Editorial. Annals of Internal Medicine, 2001;134:591-3.