Synopsis
Several
crystals (urate, CPPD and hydroxyapatite) can deposit in tissues of the
musculoskeletal system in asymptomatic individuals. I in some cases, those
deposits can be associated with diseases such as Gout, Pseudogout and Calcific
Tendinitis. MRI examination can be very useful in the diagnosis of such
entities, differential diagnosis and help treatment decisions.
Several crystals can
deposit in tissues of the muscle skeletal system in asymptomatic individuals, and
in some cases, be associated with diseases. There are various imaging features
for common crystal-related deposition entities including monosodium urate, calcium
pyrophosphate dihydrate as well as hydroxyapatite.
Magnetic resonance
imaging (MRI) examination features associated with crystal deposition diseases
include: a) location (hyaline cartilage and fibrocartilage, tendons, ligaments,
bone, synovial membrane), b) morphology (size, soft-tissue signal
characteristics), c) surrounding tissue signal alteration, d) arthritic changes
(bone, synovial membrane), leading to a deferential diagnosis among those
crystal-related deposition entities and other diseases.
Monosodium urate monohydrate crystals or uric acid deposits into tissues can cause a disease named Gout. It happens
when hyperurecimia is above 6 to 7 mg/dL. Gout is the most common inflammatory
arthritis in men over the age of 30 years.
Radiographic findings of gout do not occur until the disease has been
present for at least 6 or more years. In acute phase MRI findings of the joint
effusion and synovial thickening are nonspecific. Gouty tophi are mostly of
low- or intermediate-signal intensity on T1W images with variable gadolinium
enhancement. The imaging findings of tophi on T2W images are variable. Calcification,
fibrosis, or hemosiderin can occur within the tophi. With dual source computed
tomography, the uric acid deposits can be differentiated with high accuracy and
high imaging contrast.
Calcium pyrophosphate
dihydrate (CPPD) crystal deposit can be found with a high frequency in older
people in the hyaline cartilage, fibrocartilage, tendons and ligaments. Calcification
in the spinal ligaments specifically around the odontoid process is common in
this entity. Focal calcifications forming conglomerates around joints like
tophaceous gout may be also seen. When CPPD crystal deposits become symptomatic
it receives the name of Pseudogout, most commonly occurring in knee and wrist.
It is often seen in women >80 years old (``disease of octogenarians´´). The
shoulder is a non-weight-bearing joint and degenerative changes and narrowing
and loss of articular cartilage seen in this joint with the absence of prior
injury raises the possibility of CPPD. CPPD deposit may cause arthritis with
severe inflammation or may present as destructive joint disease, which may
mimic neuropathic joint. The appearance of scapholunate advanced collapse
(SLAC) in the wrist is an example of destructive features of pseudogout. Intervertebral disk CPPD crystal deposits can
be found in asymptomatic individual but in some more rare cases can cause destructive
disc disease.
Calcium hydroxyapatite
(HA) deposits also can be found in asymptomatic individuals, are often periarticular
or intratendinous. Although CPPD is the most common cause of radiographic signs
in chondrocalcinosis, both CPPD and calcium hydroxyapatite can be present. On
MR imaging, HA deposits are of low signal. Moreover, there is often overlying
inflammation and edema, which the radiologist may misinterpret as tenosynovitis
or joint synovitis with infection or injury. At high calcium concentrations
(above 30% to 40%) susceptibility effects and decreases in proton density
dominate, leading to signal intensity loss. However, T1 shortening effects
resulting in hyperintensity on T1-weighted images are also present. They have
been attributed to surface interaction of protons with calcified tissue. At
lower concentrations of calcium, T1 shortening effects dominate, resulting in
isointensity or even hyperintensity. Gradient echo sequences best show these
calcific foci. The deposition of HA may
mimic an acute inflammation. For those patients that are symptomatic, trauma or
acutely increased use of the joint seem to be initiating factors. Calcific tendinosis is most commonly seen in
the shoulder in the distal supraspinatus tendon insertion at the greater
tuberosity of the humerus. Less common locations may include tendons of
infraspinatus, subscapularis, and deltoid, wrist, elbow, gluteus maximus, knee,
and neck. Rarely erosion of bone adjacent to calcification at the insertion
site of the tendons can be visualized. Acknowledgements
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