Knee Surg Sports Traumatol Arthrosc (2011) 19:1326–1333
DOI 10.1007/s00167-011-1433-0
KNEE
Anterior cruciate ligament mucoid degeneration: a review
of the literature and management guidelines
Francois Lintz • Nicolas Pujol • Philippe Boisrenoult
Kevin Bargoin • Philippe Beaufils • David Dejour
Received: 21 May 2010 / Accepted: 1 February 2011 / Published online: 18 February 2011
Ó Springer-Verlag 2011
Abstract
Purpose Anterior cruciate ligament (ACL) mucoid
degeneration is a rare encounter in clinical practice, dif-
ferent, but often confused with ACL mucoid cysts. Its
pathophysiology remains unclear. However, recent publi-
cations have suggested that it might be underdiagnosed or
misdiagnosed, and that the adverse effects of treatment by
ACL resection might be underestimated. The object of this
work was to summarize this scattered knowledge to
improve patient management.
Methods The authors carried out an exhaustive and
comprehensive review of up-to-date literature. An exten-
sive search of the MEDLINE database was carried out
using MESH terms (ganglion cyst, anterior cruciate liga-
ment) and generic search terms (mucoid degeneration,
hypertrophy).
Results Anterior cruciate ligament mucoid degeneration
is determined by interstitial glycosaminoglycan deposits
amidst the collagen bundles causing ACL hypertrophy,
knee pain, and limited range of motion. It is thought to
arise from a primary synovial lesion and is associated with
arthritic change or subsequent to acute or repeated trauma.
Diagnosis is made on MRI scans and confirmed on
F. Lintz (&)
N. Pujol
P. Boisrenoult
P. Beaufils
Andre Mignot Hospital of Versailles, 177 route de Versailles,
78150 Le Chesnay, France
e-mail: francoislintz@gmail.com
K. Bargoin
University Hospital of Nantes, 1 place Alexis Ricordeau,
44000 Nantes, France
D. Dejour
Clinique de la sauvegarde, 480 avenue Ben Gourion,
69009 Lyon, France
123
•
histopathological samples. Current treatment involving
ACL arthroscopic resection is efficient on pain and range
of motion but is not a benign procedure and causes knee
laxity.
Conclusions Anterior cruciate ligament mucoid degen-
eration needs to be more broadly known and properly
diagnosed so that progress can be made in its management.
Further research will be necessary to confirm the current
trends in the literature, which suggest being less aggressive
with ACL arthroscopic resection when dealing with
mucoid degeneration and making more use of conservative
measures such as notchplasty.
Level of evidence Systematic review, Level IV.
Keywords Knee
Anterior cruciate ligament
Mucoid
degeneration
Myxoid degeneration
Ganglion
Cyst
Introduction
Historically, mucoid degeneration was not described in the
skeletal system. Initial literature in the 1950s related to the
cardiovascular system. The first report in a limb, in 1974,
concerned striated muscle [18]. The first ligament case in a
patellar ligament [55] was in fact histologically a mucoid
cyst (MC). This illustrates the main downside of anterior
cruciate ligament (ACL) mucoid degeneration literature,
being that it is intermingled with ACL MC literature,
making it difficult to identify evidence specifically related
to mucoid degeneration.
The first case of ACL mucoid degeneration was described
by Kumar et al. [35] in 1999. Since then, twelve articles [19,
20, 22, 24, 36, 41–44, 47, 48] have been published on ACL
mucoid degeneration. Mucoid cysts have been more
Knee Surg Sports Traumatol Arthrosc (2011) 19:1326–1333
regularly reported in the ACL in 24 articles [2, 3, 8, 10, 11,
14, 16, 17, 21, 23, 26–31, 39, 40, 46, 49, 51–53, 56] since
1988 [10] and PCL since 1965 [7, 15, 46, 58].
The term itself by which this pathological entity is
described does not seem to be unanimously accepted by
authors. Kumar et al. paper was entitled ‘‘Mucoid Cystic
Degeneration of the ACL.’’ Mc Intyre et al. [42] and
Bergin et al. [6] specifically addressed mucoid degenera-
tion as opposed to MC. Kim et al. [33] entitled the lesion
‘‘Mucoid Hypertrophy.’’
One of the explanations for this hesitation around
mucoid degeneration nosology in the midst of mucoid
pathology of the knee is the lack of available patients for
studies. Being in the first place, a rare condition and not
well known by physicians, it is probably clinically under-
diagnosed or mistaken for ACL tear [42]. Thus, much of
the previous literature were case reports.
Epidemiology
This was summed up in 2004 by Bergin et al. [6], who per-
formed a retrospective study on 4,221 consecutive knees
referred for MRI which they screened systematically for
ACL mucoid lesions. They found 74(1
8%) knees con-
cerned, 24% of which were mucoid degeneration and 76%
MC, which makes mucoid degeneration a more frequent
condition than previously thought although asymptomatic in
a majority of cases. Mean age of mucoid degeneration
patients was 42 years old and sex ratio was one. Further-
more, a third (35%) of knees had MRI criteria for both MC
and mucoid degeneration suggesting common pathogenesis,
as previous literature had done. The MC concerned in 50%
cases, only the proximal or distal insertion of ACL, whereas
mucoid degeneration concerned the entire length of ACL in
93%. Bilateral situations were not found by Bergin but have
been reported by others [20, 38].
A recent publication by Salvati et al. [54] in a similar
population of 44 years mean age seems to confirm Bergin’s
findings. Salvati et al. analyzed 1,251 knee MRI examin-
ations. The sex ratio was 1
28 male to one female. They
found 5
3% of ACL mucoid degeneration, all of which then
received arthroscopic assessment to confirm diagnosis.
Salvati et al. described a «segmental» lesion (limited to a
single ACL bundle—mostly posterior lateral) in 17% cases
and a «diffuse» lesion in 83% cases, with femoral or tibial
bony infiltration by mucoid substance.
Clinical findings
The symptoms may have been ongoing for a number of
weeks or months [22, 24, 52]. An initiating knee injury is
1327
reported by some, but its relationship to subsequent mucoid
degeneration is debated. Scranton and Farrar [55], who
described mucoid degeneration in the patellar ligament,
report an initiating trauma or sport-related overuse in all
cases. As far as the ACL is concerned, cases are reported
[29] which appeared after a minor trauma to the knee
followed by a gradually increasing pain and limitation of
range of motion. Other authors, such as Narvekar and
Gajjar [47] however, reported about 5 cases without any
known injury.
Posterior pain is the most consistent finding [15, 19, 35,
52]. The intensity of pain is affected by flexion or climbing
up stairs; some patients also describe painful limitation of
extension [33]. The mechanisms by which mucoid degen-
eration causes pain are discussed in previous publications,
although many agree on the fact that this is difficult to
assess considering the important proportion of patients in
which other lesions are associated which can by themselves
cause pain. In Bergin et al.’s. [6] study, eight patients
received an arthroscopic examination that found in half of
them another lesion (chondral or meniscal) possibly
explaining painful symptoms, and in Kim et al. [33] older
patients, this proportion was 95%. For Kumar et al. [35]
and Hansen et al. [22], pain is caused by extrusion of the
hypertrophic ACL into the posterior lateral compartment of
the knee. Fealy et al. [19] reported in the case of smaller
lesions that pain could be mediated through intratendinous
pain receptors during increased ACL fiber tensioning in
flexion. This is, according to Fealy et al. supported by the
efficiency of ACL resection on pain relief.
Clinical examination demonstrates a limited range of
motion toward flexion, around 100° [19, 35]. Joint effusion
might be noted [6, 42]. The ACL is competent and dem-
onstrates no anterior drawer, with a firm Lachman end
point [35]. The grinding test to investigate menisci may be
positive, and patients may report intermittent catching or
grinding symptoms [52]. In this case, care must be taken to
rule out an unstable meniscal or chondral lesion, a loose
body or plica synovialis. The reported number of associ-
ated lesions [38] is in that respect a source for misdiagnosis
and may result in unnecessary meniscectomy which have
shown to be deleterious with regards to the evolution of
osteoarthritis [5, 50].
Imaging
Standard radiographs are performed to search for osteoar-
thritic lesions and notch stenosis but show no specific signs
of ACL mucoid degeneration.
The gold standard for diagnosis is MRI, demonstrating
intermediate [6, 19, 35] signal in T1-weighed and increased
[6, 15] signal in T2-weighed images diffuse within the
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ACL (Fig. 1). Many authors have described ACL mucoid
degeneration aspects on MRI scans as the ‘‘celery stalk’’
sign [20, 22, 24]. Bergin et al. [6] listed the MRI diagnostic
criteria of ACL mucoid degeneration and differentiated
them from ACL MC, based on their 2004 publication and
previous findings [42] reported in the literature (Table 1).
Differential diagnosis can be an ACL tear [42] or a
malignant process [35, 57]. In a significant number of
cases, ACL mucoid degeneration was described as asso-
ciated with an erosion of the lateral condyle [11, 35, 43].
The better acknowledged ACL MC [15] is different in that
it sits near to or on the ACL, often near an insertion area
whereas mucoid degeneration signal is seen within the
substance of the ACL, dividing its fibers into a large
fusiform bulb-like structure bulging inside the interc-
ondylar notch. The mucoid substance is seen intermingled
with the collagen fibers, dissecting between them but not
interrupting them [20, 42, 47]. Fernandes et al. [20] added
that, unlike MC, mucoid degeneration signal was always
inferior to joint fluid. Moreover, MC is often multilocular
on MRI scans, which is never the case for mucoid degen-
eration. These findings are particularly consistent with
clinical and arthroscopic findings.
Fig. 1 MRI aspect of anterior
cruciate ligament mucoid
degeneration. a T1-weighed
sagital view. b T2-weighed
sagital view. c T2-weighed
coronal view
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Knee Surg Sports Traumatol Arthrosc (2011) 19:1326–1333
Arthroscopic findings
Although diagnosis can be initially based on MRI assess-
ment, it must be confirmed with pathologic examination of
histological samples [36, 41]. Arthroscopy, however, can-
not be self-sufficient as a diagnostic tool for it might miss
an interstitial lesion [6] that will be seen on MRI scans.
Arthroscopy is also carried out for treatment, unless a
doubt exists as to the possible malignant nature of the
lesion [35, 57]. However uncommon this occurrence might
be, biopsy should be considered prior to treatment in the
case of associated erosive bony lesions.
The arthroscopic aspect of ACL mucoid degeneration is
unequivocally described as a large, tensed ACL bulging
anteriorly from the intercondylar notch. Mucoid degener-
ation itself is described as a yellow or brown substance
which can be either seen through the most anterior fibers of
the ACL or found by probing between them [19, 35]
(Fig. 2). In that case, mucoid degeneration can be extruded
from the ligament and will be removed in the saline flow.
ACL fibers are found to be continuous and normally oriented.
In a small number of cases, the lesion is situated posteriorly
and has to be reached through a posterior-medial
Knee Surg Sports Traumatol Arthrosc (2011) 19:1326–1333
Table 1 MRI criteria for anterior cruciate ligament mucoid lesions, according to Bergin [6]
Mucoid cyst Common criteria
Ligament liquid signal 2 of the 3 ACL collagen fibers uninterrupted
following from tibial to femoral insertion
for both bundles
Ligament signal stronger than joint Possibly associated with joint
fluid effusion or bony cysts
Mass effect on ACL
Round, lobulated, with septa
arthroscopic portal [6, 19]. The literature shows that
missing a mucoid degeneration diagnosis can lead to sup-
plementary meniscectomies in an attempt to solve
impingement-type symptoms [38].
The ACL tension, consistently with clinical findings, is
described during arthroscopic probe examination as either
normal or increased [47]. Impingement of the large ACL
into the lateral compartment can also be demonstrated by
arthroscopic examination, which provides a reasonable
explanation for the meniscal-type symptoms advocated by
some, as well as lateral condyle erosions [47]. Anterior
impingement may also be seen and explains that patients
may show limited extension [33]. This is also consistent
with descriptions by Cha et al. [9] of notch anatomy and
particularly vertical notch plafond angles colliding with the
anterior aspect of the ACL.
Many authors have also described the absence of
synovial lining [6, 22, 36, 38, 42] normally covering the
anterior aspect of the ACL. Mc Intyre et al. [42] found this
in their ten patients and included it in their arthroscopic
diagnostic criteria for ACL mucoid degeneration which
sum up the most important findings in previous literature:
1. ACL fibers intact, competent
2. Increased ACL diameter
3. Yellow substance found by probing
4. Loss of synovial lining
Fig. 2 Arthroscopic aspect of anterior cruciate ligament mucoid
degeneration
1329
Mucoid degeneration
Ligament fibers not well seen on
T1-weighed images
Ligament bundles and fibers better
seen on T2-weighed images
Mucoid degeneration seen as T1
and T2 increased signal, but less
than that of joint fluid in T2
Other elements are reported in a study by Kim et al.
[33], such as associated osteoarthritic changes in 96% cases
(anterior tibial insertion osteophyte and posterior capsular
retraction) or the presence in 80% cases of notch stenosis
due to the presence of voluminous osteophyte buildup
around the anterior and lateral ridge of the notch.
Pathophysiology
A number of theories exist to explain intra-articular MC
formation [15, 52]. One of those is the ‘‘synovial’’ theory,
in which they form by accumulation of synovial fluid
inside a pouch of synovial lining which has herniated.
Another is the ‘‘traumatic’’ theory. Concerning the ACL,
glycosaminoglycan that account for the best part of mucoid
substance is known to be secreted by ACL fibroblasts in
response to traumatic injury. Others consider the ‘‘degen-
erative’’ theory, in that the mucoid tissue could result from
aging degeneration of normal tissues [20, 34]. Another
theory is based on the hypothesis that ectopic synovial
tissue could exist inside the ACL and account for the
presence of interstitial joint fluid cyst [22, 25]. Lancaster
et al. [36] advocate that mucoid degeneration is in fact an
earlier stage of MC in that micro cysts form following a
number of minor or more significant trauma and with time
can grow together into larger mucoid formations. In fact,
mucoid degeneration is a different problem in that it is not
contained within a cyst but intermingled with the ACL
fibers.
According to the latter theory, the creation of minor
interstitial ACL lesions, following either acute injury or
repeated micro trauma, is the primum movens of any ACL
mucoid lesion, either cystic or interstitial. A strong argu-
ment toward the common pathogenesis of MC and mucoid
degeneration is brought by Bergin et al.’s study [6], who
found one-third of mucoid degeneration patients also
having criteria for MC and two-thirds demonstrating cri-
teria for bony cysts deep to the tibial and femoral insertions
areas of the ACL [22]. Other studies (Rolf and Watson
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1330
[52], Lintz et al. [38]) also report on the coexistence in the
same patient of ACL mucoid degeneration with small MCs
and bony cysts. Considering the consistency of this previ-
ous literature, it seems very likely that a pathogenetic
continuum exists between mucoid degeneration and MC
and also bony cysts. The article by Kim et al. [33] also
supports this hypothesis. It shows that ACL mucoid
degeneration is frequent in osteoarthritic knees. In these
patients, mucoid degeneration may be related to continuous
impingement between the ACL and an osteoarthritic
intercondylar notch tightened by a rim of prominent
osteophytes.
Other authors have addressed the issue of the relation
between the ACL and the intercondylar notch. Many report
impingement assessed during arthroscopic procedures and
perform a debridement of the extra bone [47]. The anatomy
of the notch was addressed by Cha et al. [9] in relation to
ACL mucoid degeneration hypertrophy. He compared the
‘‘sagittal notch angle’’ (notch plafond sagittal slope) and
the ‘‘notch area’’ in 47 patients with ACL mucoid degen-
eration versus a paired control group. He found that ACL
mucoid degeneration was significantly related to smaller
and more vertical intercondylar notches. These findings
support the ‘‘traumatic’’ pathogenetic hypothesis in that
tighter notches will impinge on the ACL resulting in
repeated micro trauma. Similarly, more vertical notch
plafonds will impinge onto the anterior aspect of the ACL
during terminal knee extension. Should the ACL’s size be
increased in the first place by the presence of mucoid
degeneration or should the latter appear secondary to this
mechanism remains unclear. However, a tight intercondy-
lar notch certainly favors ACL overuse. Further, authors
[19, 35, 42] have reported cases of ACL mucoid degen-
eration in younger and more active patients in which an
initial trauma was definitely identified, underlying the fact
that the injury to ACL could be either due to repeated
micro trauma or initiated by a single trauma to the ACL
itself or the synovial lining. Interestingly, Lancaster et al.
[36] hypothesized that the primum movens of mucoid
degeneration formation could be a synovial lining injury or
atrophy, supported by the report of absent, atrophic
(or seldom inflammatory) synovial lining during arthro-
scopic examination of ACLs for mucoid degeneration.
These clinical findings are supported by research on the
role and anatomy of the ACL synovium. Amiel et al. [1]
showed the protective role of the synovial sheath by
looking at collagenase activity in an animal model of ACL
synovectomy. He showed that synovial injury may result in
exposure of the ligament substance to the degradative
effects of joint fluid and hemarthrosis. Furthermore, Deie
et al. [12] demonstrated in human ACL culture models that
intrinsic healing capabilities were diminished in ACLs with
resected synovium. This was further addressed by Lee et al.
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Knee Surg Sports Traumatol Arthrosc (2011) 19:1326–1333
[37], who demonstrated that the ACL was included in an
intrasynovial space which does not normally allow joint
fluid to enter the substance of the ligament. On a molecular
scale, matrix-degrading enzymes such as cathepsin K and
tartrate-resistant acid phosphatase (TRAP) have been
shown in dogs [45] to induce progressive ACL degenera-
tion, and Barrett et al. [4] more recently showed similar
changes in human ACLs implicating the same enzymes.
Synovial injury therefore does seem to be the first patho-
genetic step toward mucoid degeneration.
Histology
Mucoid lesions contain a brown or yellow basophilic
substance, described as thick or dense. It contains a high
density of glycosaminoglycan such as hyaluronic acids,
which are detectable in histochemistry by reaction with the
Alcian blue stain [33, 35, 38].
Microscopically, ACL mucoid degeneration differs from
ACL MC by the following characteristics: (Fig. 2).
1. Mucoid degeneration is a diffuse, interstitial ACL
lesion.
2. Collagen fibers are observed, dissected by the mucoid
substance, and they appear thin and displaced but
healthy and uninterrupted.
3. No cystic envelope with any lining can be found
around mucoid degeneration lesions. The substance is
free between collagen fibers.
4. No communication can be found with the joint space.
5. Focal neovascularization may also be seen, as well as
diffuse edema, hemosiderin deposits, witnessing focal
bleeding and giant cell macrophage reactions.
6. The synovial lining of the ACL has been described
most often as absent or atrophic, seldom inflammatory.
In spite of these differences, histological findings tend to
support the theory of a common pathophysiological path-
way for MC and mucoid degeneration, through the pres-
ence in each of mucoid substance and micro cysts inside
mucoid degenerative ACL samples.
Treatment
In most cases, patients are referred after failure of symp-
tomatic management based on nonsteroidal anti-
inflammatory drugs and physiotherapy sessions, during
2–6 months [24, 35, 47]. Two publications [3, 8] have
reported the treatment of ACL MC by aspiration under CT
scan guidance, and a third during arthroscopy [6], but it has
never been described in mucoid degeneration and is not
relevant in this case, given its interstitial nature.
Knee Surg Sports Traumatol Arthrosc (2011) 19:1326–1333
Fig. 3 Microscopic aspect of anterior cruciate ligament mucoid degeneration. a Standard 9 20 view. b Standard 9 40 view. c Alcian blue stain
Standard anterior medial and lateral portals are used. If
required, a posterior medial portal can facilitate access to
the retroligamentary space [17, 19, 42]. A probe is used to
search for mucoid substance, directly or through a longi-
tudinal incision [48]. In some cases, the ACL will have to
be debrided.
The resection can be partial or complete [19, 35, 38, 47],
when the lesion concerns the whole ACL, from tibial to
femoral insertion and both bundles [36]. Adhesions
between ACL and PCL or the notch are also released.
A soft tissue resector is then used until a remaining healthy
ACL tissue is obtained. Fealy et al. [19] described a lesion
that concerned only the anterior medial bundle. Narvekar
et al. [47] described a similar procedure for a posterior
lateral bundle lesion. Nishimori et al. [48] described a
longitudinal incision of the ACL to preserve more of the
ACL. A notchplasty is used [33, 47] to suppress any con-
flict between the ACL and the notch.
The aggressive attitude toward the ACL is not defended
by all authors. There is no evidence in the literature of any
recurrence after treatment of mucoid degeneration by
incomplete resection of the ACL. Dejour et al. [13] have on
the other hand reported about 27 patients which demon-
strated postoperative positive anterior drawer tests in 36%
of patients and positive pivot-shift tests in 55%. Kim et al.
[33] treated their patients with ACL debridement and
notchplasty and report 87% of satisfactory results on pain
and 82% on range of motion. These findings in the more
1331
elderly and osteoarthritic patients back up previous
degenerative pathogenetic theories [20, 34] but seem
however to correspond to a different problem in younger,
more active patients who, as Diard et al. recall [15], present
with an isolated ACL lesion in 80% of cases. In any case, it
brings strong support for the efficiency of notchplasty when
an impingement exists between a hypertrophic ACL and
the intercondylar notch.
Postoperative knee stability
After arthroscopic treatment, mobilization is begun
immediately [47]. Short-term clinical results on range of
motion and pain are very good [35]. However, the issue of
instability after ACL resection is subject to debate. In most
cases, patients are satisfied and do not complain about
instability; these data do not seem to be reliable enough to
back up an evidence-based practice in ACL mucoid
degeneration. Moreover, patients reported to have regained
their previous level of activity were sedentary without
sporting habits and were thus less demanding from ACL
function. It is possible that in these cases the thinned ACL
will be functionally sufficient [8, 42, 48]. This has unfor-
tunately led to a general belief that ACL resection was
somehow without adverse effect on the operated knee.
Only one study [38] has been published, which used sys-
tematic Lachman test and TELOSTM dynamic radiographs
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postoperatively to assess ACL function after mucoid
degeneration resection, and showed 93% postoperative
anterior laxity and 2 subsequent ACL reconstructions. Rolf
and Watson [52] reported a secondary anterior instability
14 weeks post surgery. Mc Intyre et al. [42] report an
atraumatic acute instability accident in a patient at 1 year
post surgery. Other findings by Kannus and Jozsa [32]
show that mucoid degeneration weakens the ACL, and
Nishimori et al. [48] recommend for young and active
patients a systematic ACL reconstruction.
Conclusion
Mucoid degeneration of the ACL was considered a rare
entity, but recent publications show that it is more frequent
than previously thought. This infiltration of glycosamino-
glycan deposits between collagen bundles is a distinct
condition from mucoid cysts but can be found in associa-
tion with the latter. It is thought to arise from an initial
injury to the ACL synovial lining, secondary to acute
trauma or chronic impingement. Patients present with a
deep posterior knee pain and limitation of flexion. Diag-
nosis is initiated with MRI findings of a hypertrophic ACL
demonstrating mucoid hypersignal intermingled with
uninterrupted ligament bundles in T2-weighed images.
Definitive diagnosis is made on Alcian blue-stained path-
ologic samples. Treatment involves arthroscopic resection
of the yellow mucoid substance and is efficient on the relief
of symptoms. We recommend that this procedure be as
conservative as possible, using notchplasty as an alterna-
tive to ACL resection to avoid postoperative laxity. Further
clinical research is required which will be possible with
surgeons, radiologist and pathologists being more aware of
this pathology.
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