AJR 2003; 181:199-202
© American Roentgen Ray Society
MR Imaging of Calcification of the Lateral Collateral Ligament of the Knee: A Rare Abnormality and a Cause of Lateral Knee Pain
S. E. Anderson1,
C. Bosshard2,
L. S. Steinbach3 and
F. T. Ballmer4
1 Department of Radiology, University Hospital of Bern, Inselspital, Bern CH
3010, Switzerland.
2 Department of Orthopedic Surgery, Spital Bern, Tiefenau, Bern CH 3010,
Switzerland.
3 Department of Radiology, University of California at San Francisco, San
Francisco, CA 94143.
4 Department of Orthopedic Surgery, University Hospital of Bern, Inselspital,
Bern CH 3010, Switzerland.
Received October 24, 2002;
accepted after revision December 6, 2002.
Presented at the closed scientific session of the International Skeletal
Society, Geneva, September 2002.
Address correspondence to S. E. Anderson
(suzanne.anderson{at}insel.ch).
Abstract
OBJECTIVE. Our objective was to describe the radiologic appearances
of calcification of the lateral collateral ligament (LCL) of the knee in four
patients who presented with acute atraumatic lateral knee pain. This rare
abnormality has not, to our knowledge, been previously shown on MR
imaging.
CONCLUSION. Calcification of the LCL of the knee is a rare cause of
lateral knee pain and is thought to reflect underlying hydroxyapatite
deposition. On MR imaging, calcification of the LCL may be associated with an
aggressive appearance that can be mistaken for other knee abnormalities.
Introduction
Calcification of the lateral collateral ligament (LCL) of the knee is
clinically rare and has not, to our knowledge, been previously reviewed on MR
imaging. We present four patients who had acute atraumatic lateral knee pain
associated with calcification in the region of the LCL on radiographs. The
precise location of the calcification in the proximal portion of an intact LCL
was visualized on MR imaging. To our knowledge, no reports about calcification
have been published in the radiology literature; however, in the orthopedics
literature, a few reports of calcific tendinosis of the popliteal tendon and
calcification in an iliotibial tract cyst at the lateral aspect of the knee
have been published.
Materials and Methods
Four patients with no history of trauma to the knee presented with acute
lateral knee pain of an inflammatory nature that worsened at night. The
patients ranged in age from 38 to 46 years, with a mean age of 42.5 years.
Three of the patients were drawn from a patient population of 785 consecutive
knee MR imaging examinations performed between May 1998 and June 2002 at the
primary institution. The fourth patient presented to the secondary
institution, which has a large population referred for treatment of knee
pain.
Sixteen radiographs, which were obtained in the anteroposterior and lateral
projections, of the four patients and MR images, all of which were obtained
with contrast material, of three of the four patients were reviewed
prospectively by a musculoskeletal radiologist and retrospectively by two
musculoskeletal radiologists by consensus. Investigation was performed with
imaging for clinical provisional diagnoses of infection, meniscus or lateral
ligament abnormality, and tumor.
The MR imaging protocol included coronal short tau inversion recovery
(STIR), T1-weighting, sagittal proton density, and T2-weighting. After IV
gadolinium was administered, contrast-enhanced T1-weighted fat-saturated
images were obtained in three planes. The studies were performed on one of the
following MR units: 1.5-T Magnetom (General Electric Medical Systems,
Milwaukee, WI), 1.0-T Harmony (Siemens, Erlangen, Germany), or 1.5-T Vision
(Siemens). The region of the LCL complex on MR imaging was enlarged, and
details of anatomy were reviewed. The location of any calcifications, the
status of the LCL, and adjacent soft-tissue findings were documented. Clinical
notes and laboratory results were reviewed.
Results
A calcification in the region of the LCL was seen on radiographs of all
four patients. Pain resolved between 10 days and 2 weeks after presentation in
all patients. Resorption of the calcification was evident on follow-up
radiographs obtained 4–6 weeks later after conservative treatment.
MR imaging showed the calcification to lie in the intact but thickened LCL
(Figs. 1A,
1B,
1C,
2A,
2B,
2C,
2D,
3A,
3B,
3C), with adjacent soft-tissue
reaction on T2-weighted and STIR sequences in three patients who underwent MR
imaging. Marked contrast enhancement was seen in this area on
gadolinium-enhanced T1-weighted fat-saturated images.
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Fig. 1A. —38-year-old man with acute atraumatic knee pain of 48-hr
duration that feels worse at night and provisional clinical diagnosis of
lateral collateral ligament (LCL) tear, lateral meniscus tear, or fracture.
Radiograph shows calcification (arrows) in region of LCL. Ten days
later, patient was asymptomatic, and within 4 weeks, calcium had resorbed on
follow-up conventional radiographs (not shown).
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Fig. 1B. —38-year-old man with acute atraumatic knee pain of 48-hr
duration that feels worse at night and provisional clinical diagnosis of
lateral collateral ligament (LCL) tear, lateral meniscus tear, or fracture.
Coronal STIR image (TR/TE, 180/30; flip angle, 180°) shows thickening of
intact LCL (arrows) and focus of low signal (asterisk) that
corresponds to region of calcification on radiograph. Bone marrow signal is
normal.
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Fig. 1C. —38-year-old man with acute atraumatic knee pain of 48-hr
duration that feels worse at night and provisional clinical diagnosis of
lateral collateral ligament (LCL) tear, lateral meniscus tear, or fracture.
Axial contrast-enhanced T1-weighted fat-saturated MR image (780/14) shows LCL
thickening and calcification (arrow). Popliteal recess and tendon are
normal.
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Fig. 2A. —39-year-old man who presented with acute pain of 3 days'
duration, joint effusion, and clinical provisional diagnosis of infection.
Radiograph shows calcification (arrows) in region of lateral
collateral ligament (LCL).
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Fig. 2B. —39-year-old man who presented with acute pain of 3 days'
duration, joint effusion, and clinical provisional diagnosis of infection.
Coronal STIR image (TR/TE, 4500/30; inversion time, 180 sec) that was obtained
after patient reported sudden unexplained decrease in pain shows thickening
and calcification of LCL (thick arrows) and additional calcification
between LCL and biceps femoris tendon (thin arrows), possibly
representing rupture of LCL calcific tendinitis into LCL—biceps femoris
bursa. Normal popliteal tendon (asterisk) is noted. Other images (not
shown) showed moderate-sized effusion and Baker's cyst.
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Fig. 2C. —39-year-old man who presented with acute pain of 3 days'
duration, joint effusion, and clinical provisional diagnosis of infection.
Axial contrast-enhanced T1-weighted fat-saturated MR image (646/20) shows
focal calcification in LCL (arrow) and adjacent additional
calcification (asterisk), possibly in LCL—biceps femoris
bursa.
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Fig. 2D. —39-year-old man who presented with acute pain of 3 days'
duration, joint effusion, and clinical provisional diagnosis of infection.
Axial contrast-enhanced T1-weighted MR image shows additional calcifications,
possibly within LCL—biceps femoris bursa (asterisk) and medial
to LCL (short arrow). Biceps femoris tendon (long arrow) and
popliteal tendon (arrowhead) are normal.
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Fig. 3A. —46-year-old man who presented with acute knee pain.
Radiograph shows calcification (arrows) in region of lateral
collateral ligament (LCL). Calcification and pain resolved 4 weeks later.
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Fig. 3B. —46-year-old man who presented with acute knee pain. Coronal
STIR image (TR/TE, 3740/18; inversion time, 90 msec) shows thickened proximal
LCL with focal calcification in LCL (arrow) and marked adjacent
soft-tissue reaction (arrowheads). Popliteal tendon is normal.
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In one patient, additional calcification was evident on MR imaging between
the LCL and the biceps femoris tendon, possibly within the LCL—biceps
femoris bursa. In all three of the patients who underwent MR imaging,
popliteal tendon calcification was absent, and bone marrow signal intensity
was normal. The iliotibial tract was also intact. A medial meniscus tear was
found in one patient, but the tear was considered to be unrelated clinically
to the lateral knee pain. The lateral meniscus in each of the three patients
who underwent MR imaging appeared normal.
The clinical histories of the patients revealed that none had a history of
systemic diseases, such as gout, systemic sclerosis, dermatomyositis, or
sarcoidosis, or of metabolic or endocrine disorders, such as kidney failure.
Calcium and phosphate levels were normal. At the time of this study, the
abnormality was monoarticular, although one patient presented 2 years later
with the typical clinical findings and radiologic appearances of rotator cuff
calcific tendinitis and calcification in the supraspinatus tendon. All
patients had a slightly elevated WBC value and erythrocyte sedimentation rate
during their episodes of acute pain. In the patient who underwent joint
aspiration because infection was suspected, the aspirate was sterile with an
increased WBC. All patients requested conservative treatment with nonsteroidal
anti-inflammatory medication and local heat and cold therapy.
Discussion
We describe four patients who presented with acute and severe atraumatic
lateral knee pain with calcification of the LCL, with an emphasis on imaging
findings. MR imaging performed in three of the patients showed that lateral
knee calcification seen on radiography was lying within the intact LCL. LCL
calcification presents with inflammatory pain and thus may mimic other
abnormalities associated with inflammation, such as joint infection, or can be
so painful that it may mimic acute knee trauma, such as meniscal or ligament
tear or fracture.
In 1955, Holden [1]
described a 64-year-old man and a 60-year-old woman who presented with acute
lateral knee pain and evidence of calcification in the popliteal tendon that
disappeared on resolution of pain. One patient underwent exploratory surgery.
The popliteal tendon was edematous and contained material that was chiefly
acellular collagen with a low calcium content. The other patient's pain
resolved after 6 weeks of bed rest, as did the calcification on conventional
radiographs.
In 1966, McCarty and Gatter
[2] described two patients with
histories of multiarticular calcific tendinitis due to hydroxyapatite
deposition disease. Both patients presented with acute atraumatic bilateral
knee pain and calcification at the lateral aspect of the knees in the region
of the LCL. In the first patient, a 67-year-old woman with presumed gout,
joint aspiration showed shiny coinlike bodies with an X-ray diffraction powder
pattern characteristic of apatite crystals. The second patient was a
39-year-old man who had focal swelling and redness 2 inches (5 cm) proximal to
the lateral joint margin with an effusion. Joint aspiration revealed negative
findings for crystals. Surgery showed an area of calcification beneath the
iliotibial tract in a cystlike structure that microscopically stained positive
for calcium and phosphate and was stated to represent focal hydroxyapatite
crystal deposition.
In 1999, Werlich [3]
described a 72-year-old woman who presented with acute atraumatic lateral knee
pain. No evidence of swelling, increased skin warmth, blue skin, or joint
effusion was present. Radiography showed a 5 x 20 mm calcification at
the lateral aspect of the knee. Four days after admission, a joint effusion
had developed; the effusion was aspirated. The aspirate was sterile with an
increased number of WBC. The erythrocyte sedimentation rate at this time was
slightly elevated. Subsequently, with a decrease in pain, radiography showed
wide dispersion of the calcification over the lateral epicondyle, and at day
10 the patient was asymptomatic. The effusion and the calcification were no
longer visible on radiography. Hydroxyapatite deposition disease was suggested
as an underlying mechanism.
Surgically proven calcific tendinitis of the distal tendon of the vastus
lateralis muscle at the level of the superolateral patella has been described
in a 40-year-old male athlete
[4], and calcification of the
bursae of the knee joint has been described
[5] with clinical presentations
associated with acute pain, absence of trauma, and calcification on
radiography.
Our four patients represent a younger age group (mean age, 42.5 years) with
lateral knee joint calcification than the patients who have been described in
the literature. In our patients, the pain was more inflammatory in nature,
with increased pain at night. In addition, another anatomic site, the LCL
[6–8],
was involved in our patients as opposed to the popliteal tendon or iliotibial
tract. This different site of involvement suggests that the knee pain in these
two patient groups may result from a different cause than that in our patient
group. In both groups, the pain resolved and the calcification was no longer
visible on radiography. Radiographic and MR imaging features suggest that the
calcifications represent hydroxyapatite crystal deposition disease. We believe
that hydroxyapatite deposition in the LCL was the primary mechanism of
causation of this entity in our patients; however, the exact cause remains
unknown because all the patients requested conservative treatment. Also highly
suggestive of hydroxyapatite deposition is that one of our patients presented
2 years later with rotator cuff calcific tendinitis.
Hydroxyapatite deposition disease usually affects men and women between the
ages of 40 and 70 years [6].
Patients present with atraumatic pain that is initially monoarticular,
although it may be multiarticular. The most common site of involvement is the
shoulder, although other sites such as the wrist and hand, foot, elbow, hip,
and spine are well described. Clinical findings include acute pain with local
tenderness and swelling at the joint, some restriction of movement, and mild
fever. Laboratory results are usually within the normal limits except the
erythrocyte sedimentation rate, which may be elevated during an episode of
pain. Hydroxyapatite crystals may deposit in tendons, ligaments, joint
capsules, bursae, or soft tissues. The calcific deposits are cheesy or
milklike in appearance on imaging. The microspheres are small, ranging from
0.1 to 0.2 µmm. Crystal deposits are often heterogeneous, with a variety of
calcium phosphate crystals present. The radiographic appearance of the crystal
deposits reflects the duration of disease: initially, the crystals appear
poorly defined and cloudlike, but as the disease progresses, they appear
denser and homogeneous with a linear or circular configuration. The cause
remains unclear, and proposed mechanisms include calcification in regions of
tendon degeneration or in hypoxic or necrotic tissue with or without
antecedent trauma, a congenital condition, and a genetic predisposition with
influential metabolic factors.
MR imaging in one patient showed calcification medial to the LCL, possibly
in the LCL—biceps femoris bursa
[9,
10] (Figs.
2A,
2B,
2C,
2D). The patient had a clinical
history of abrupt and otherwise unaccounted-for change in pain. Presumably
some of the calcification from the LCL ruptured into what is thought to
represent the LCL—biceps femoris bursa. In one of their patients,
McCarty and Gatter [2]
described calcification in a cystlike structure located beneath the iliotibial
tract to be associated with acute lateral knee pain and calcification on
radiography. Hydroxyapatite deposition disease with teardrop-shaped radiodense
areas in the subacromial and supracoracoid bursae of the shoulder
[11] and layering fluid levels
[12] have been described.
The radiologic differential diagnosis for periarticular calcifications
includes posttraumatic changes and articular disorders such as calcium
pyrophosphate deposition disease and gout. Calcification due to posttraumatic
changes cannot be completely differentiated from hydroxyapatite deposition
disease on imaging alone; however, in our series, none of the patients had a
history of trauma. Calcifications associated with articular disorders usually
occur in patients who are older than the patients in our patient group and
usually have associated features on imaging such as chondrocalcinosis and
pyrophosphate arthropathy. Further differential diagnoses include septic
arthritis; collagen vascular diseases, such as scleroderma and
dermatomyositis; hyperparathyroidism and renal osteodystrophy; idiopathic
tumoral calcinosis; hypothyroidism; hypervitaminosis D; milk-alkali syndrome;
and sarcoidosis. Because of its aggressive MR appearance, LCL calcification
may mimic other abnormalities, especially infection or trauma, particularly
when radiographs are not available at the time of MR reporting.
In conclusion, LCL calcification is a rare cause of lateral knee pain
presumably due to hydroxyapatite deposition and can have an aggressive
appearance on MR imaging.
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Abstract
Introduction
