Diagnosis and Discussion
Calcium pyrophosphate dihydrate deposition disease (CPPD)
Though there are degenerative changes in the knee, the finding
of chondrocalcinosis, or calcification of the cartilage sets
this apart from simple DJD. Though gout can produce chondrocalcinosis
it is extremely rare in the knee. Also, the lack of hyperuricemia
speaks against gout. Gout will typically produce marginal,
periarticular, or intraosseous erosions.
Calcium pyrophosphate dihydrate deposition disease is a
crystal induced arthropathy similar to gout. Calcium pyrophosphate
crystals deposit in cartilage and produce chondrocyte death,
then cartilage thinning. Minor trauma may cause the crystals
to "shed" or break out of cartilage into the joint producing
an acute synovitis. The mechanism of how the crystals deposit
in cartilage is not known. There is some thought that local
tissue damage, either age-related or secondary to trauma,
leads to susceptibility for crystal deposition.
CPPD affects both men and women, middle-aged and elderly.
The most common presentation resembles degenerative joint
disease with the onset occurring after 30 years of age. The
symptoms can mimic gout, rheumatoid arthritis, and degenerative
joint disease. There are three manifestations of CPPD that
may occur alone or together:
a: Crystal Induced Acute Synovitis.These acute attacks, also
known as pseudogout, may last one day to several weeks. The
patient may find relief from colchicine.
b: Cartilage Calcification. Calcification of the cartilage,
or chondrocalcinosis, is classic for CPPD though it may be
seen with other conditions such as hyperparathyroidism, hemochromatosis,
acromegaly, gout, and Wilson's disease. Some people may have
asymptomatic chondrocalcinosis that is never associated with
CPPD arthropathy. The crystals may deposit in fibrocartilage
such as in the meniscus of the knee, triangular fibrocartilage
of the wrist, acetabral labra, symphysis pubis, or anulus
of the intervertebral disc. These deposits look thick, and
irregular. When deposits are in hyaline cartilage they appear
thin, linear, and they parallel the cortical surface of the
bone. Calcification may also occur in the synovium where it
may resemble synovial osteochondromatosis. Capsular calcifications
are linear and fine in their appearance. When deposits occur
in tendons, bursae, or ligaments, they resemble calcium hydroxyapatite
crystal deposition disease (HADD) though they should appear
more linear and thin. Many times, however, patients do have
a mixed crystal arthropathy with both calcium pyrophosphate
and calcium hydroxyapaptite crystal deposition.
Joint Abnormalities The degenerative changes seen with CPPD
are termed pyrophosphate arthropathy. Though these changes
are similar in appearance to degenerative joint disease there
are some distinct differences. The distribution of CPPD arthropathy
is at sights not common for DJD, including the wrist, elbow,
and shoulder. When CPPD does affect joints, it produces a
pattern of degeneration unlike DJD.
In the knee, CPPD will produce degenerative changes at the
patellofemoral joint and in the medial and lateral joint spaces.
DJD typically affects the medial joint space, as this is the
weightbearing portion of the joint. Advanced patellofemoral
joint space narrowing may result in a pressure erosion of
the anterior surface of the distal femur. Pyrophosphate arthropathy
produces more prominent subchondral cysts, subchondral collapse,
and loose bodies than are seen with DJD. The osteophyte formation
In the wrist, CPPD produces calcification of the triangular
fibrocartilage, and the hyaline cartilage of the radiocarpal
and midcarpal joints. The radiocarpal joint is involved most
often, especially the scapholunate articulation. Proximal
displacement of the scaphoid and distal displacement of the
lunate result in a classic "stepladder" appearance. Disruption
of the scapholunate ligament results in widening of the distance
between the two bones.
In the shoulder, CPPD produces glenohumeral joint space narrowing,
capsular, tendinous, and bursal calcifications. Again, large
subchondral cyst formation and subchondral sclerosis are common.
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Introduction to Unknown Cases
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