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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2690_Библиотеки_им_академика_М_И_Перельмана
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7.3 Gout Arthritis 263
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Fig. 7.3.2. Plain radiograph of a fi nger shows bony erosion with
sclerotic rim in the middle phalanges ( arrowhead )
Fig. 7.3.4. Coronal T1W ( a ), STIR ( b ), and T1W postcontrast
foot MRI of a patient investigated for gout with foot pain localized to the big toe show hypointense signal intensity due to
edema of the fi rst metatarsal head in ( a ), hyperintense T2 signal
Fig. 7.3.3. Plain radiograph of the foot of a patient with chronic gout
shows marginal erosion of the proximal phalanges ( arrowhead )
intensity in ( b ), and marked contrast enhancement of the fi rst
metatarsal head and the surrounding soft tissues due to active
infl ammatory process ( arrowhead )
264 Chapter 7 Rheumatology
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D i ff erential Diagnoses and Related Diseases
Lesch–Nyhan syndrome ( LNS ) is an X-linked recessive
metabolic disease characterized by defective purine
7.3
metabolism that results in uric acid overproduction.
The disease arises due to genetic absence or near
absence of the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRT). Patients with LNS
present with involuntary movements in a combination
of chorea and athetosis (choreoathetosis), spasticity,
and psychiatric abnormalities in the form of compulsive self-mutilation. Recurrent formation of renal uric
acid stones is commonly encountered in LNS due to
hyperuricemia. Laboratory fi ndings show increased
levels of uric acid in the urine, cerebrospinal fl uid, and
serum. Plain radiographs can show GA. Renal ultrasound can be used to screen for renal stones in these
patients. Brain MRI may show caudate nuclei head
atrophy with widening of the anterior lateral horns of
the lateral ventricles (Fig. 7.3.5 ). Furthermore, very
prominent prepontine cisterns with mild to moderate
midbrain atrophy have been reported in some patients.
For Further Reading
1 . Monu JUV et al Gout: a clinical and radiological review.
Radiol Clin North Am. 2004;42:169–84
2 . Jacobson JA et al Radiographic evaluation of arthritis:
infl ammatory conditions. Radiology. 2008;248:378–89
3 . Chang PC et al Tophaceous gout of the fi rst costochondral
junction in a heart transplant patient. Skeletal Radiol.
2006;35:684–6
4 . Agarwal K et al Fine needle aspiration cytology of gouty
tophi with review of the literature. J Cytol. 2007;24:142–5
Fig. 7.3.5. Axial T1W brain MR illustration demonstrates bilateral caudate nucleus atrophy in a patient with Lesch–Nyhan syndrome (LNS)
5 . Cabot J et al Tophaceous gout in the cervical spine. Skeletal
Radiol. 2005;34:803–6
6 . J a j i ć I et al Gout in the spine and sacro-iliac joints: radio-
logical manifestations. Skeletal Radiol. 1982;8:209–12
7 . Rosenfeld DL et al Serial renal songraphic evaluation in
patient with Lesch-Nyhan syndrome. Pediatr Radiol. 1994;
24:509–12
8 . Harris JC et al Craniocerebral magnetic resonance imaging
measurments and fi ndings in Lesch-Nyhan syndrome.
Arch Neurol. 1998;55:547–53
7.4 CPPD and HADD 265
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7.4
CPPD and HADD
Calcium pyrophosphate dihydrate crystal deposition disease (CPPD) and hydroxyapatite crystal deposition disease (HADD) are diseases characterized by deposition
of insoluble crystals within the joints and periarticular
soft tissues, initiating infl ammatory destructive reaction.
Other clinically important calcium-containing crystals
deposition diseases include tricalcium phosphate (TCP)
and octacalcium phosphate (OCP) diseases.
Calcium Pyrophosphate Dihydrate Crystal
Deposition Disease
CPPD, also known as pseudo-gout and chondrocal-
cinosis , is a disease characterized by calcium pyro-
phosphate crystals deposition within the articulating
cartilage , leading to cartilage infl ammation and later to
joint destruction in a similar fashion to gout arthritis.
CPPD is classifi ed based on its etiology into hereditary, idiopathic, or secondary to metabolic disorders
(e.g., vitamin D intoxication). The disease is age-related,
with an incidence of 5% in patients >70 years, and
nearly 50% in patients >90 years. Many patients present
with gout-like arthritic episodes characterized by joint
synovitis, malaise, and fever that lasts from 1 day to
4 weeks. Up to 50% of patients develop progressive
degeneration of multiple joints. The most frequently
involved joints are the knees, wrists, metacarpophalangeal joints, and the hips.
Pyrophosphate deposition involves both hyaline
cartilage and fi brocartilage joints like symphysis pubis,
annulus of the spine, triangular fi brocartilagenous
complex (TFCC) of the wrist, and menisci. CPPD can
occur in high incidence with other diseases like gout,
hyperparathyroidism and hemochromatosis.
CPPD diagnosis is established by identifying the
pyrophosphate crystals within the synovial fl uid after
aspiration. Plasma and uric acid levels of pyrophosphate
are typically not elevated (differential point from gout).
Signs on Plain Radiograph
Chondrocalcinosis : cartilage calcifi cation is the hallmark of
CPPD. Chondrocalcinosis is usually observed in medial and
lateral compartments of the knee, wrist TFCC, and the
symphysis pubis (Fig. 7.4.1 ).
Pseudo-charcot’s joint
: severe joint destruction that mimics
Charcot’s joint may be observed occasionally.
Normal bone density with occasional subchondral cysts.
SLAC wrist deformity : S capho- L unate A dvanced C ollapse is a
pathological situation characterized by loss of the cartilage
between the scaphoid bone and the radius, causing the
scaphoid to indent the radius, and the capitate to collapse,
thus disturbing the scapholunate joint articulation (Fig. 7.4.2 ).
is a pathological condition
Generalized chondrocalcinosis
characterized by involvement of more than one group of joints
with cartilage calcifi cation (e.g., knees, wrists, plus vertebral
discs).
Fig. 7.4.1. Anteroposterior knee radiograph shows calcifi cation of the lateral meniscus due to CPPD chondrocalcinosis
( arrowhead )
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7.4
Fig. 7.4.2. Plain hand radiograph shows scaphoid indenting the
distal radius with sclerosis ( arrowhead ) and collapse of the capi-
tate from its normal position ( arrow ) (SLAC wrist deformity)
Hydroxyapatite Crystal Deposition Disease
HADD, also known as calcifi c periarthritis and peri-
tendinitis calcarea , is characterized by hydroxyapatite
crystal deposition in the soft tissues, especially the
tendons.
The most characteristic feature of this disease is
tendon calcifi cation within the body, especially around
the shoulder. Moreover, crystal deposition and calcifi cation tend to occur characteristically around the joints
(periarticular). HADD can be sporadic, or associated
with long-term hemodialysis for renal insuffi ciency.
Patients with HADD can be asymptomatic, or present with recurrent attacks of arthritis in the area of
crystal deposition. Shoulder pain is the commonest
complaint since supraspinatus tendon calcifi cation is
common in HADD.
HADD is characterized by three pathological
phases: silent, mechanical, and adhesive. The silent
phase is characterized by crystal deposition that is
completely within the tendon. The mechanical phase
is characterized by enlargement of the deposits with
starting of impingement-like symptoms (e.g., bursitis).
The adhesive phase is characterized by generalized
disability and limitation of motion. When the adhesive
phase occurs in the shoulder, the condition is called
adhesive capsulitis or frozen shoulder . Hydroxyapatite
crystals are commonly deposited in damaged tissues
(dystrophic calcifi cation).
HADD calcifi cation is often monoarticular, although
it can be polyarticular. Involvement of the joints of the
feet and toes are rare (<1%). There are two syndromes
associated with HADD due to crystal deposition
around the joints: calcifi c periarthritis with bone
resorption (acute HADD arthritis), and rapid destructive arthritis of the shoulder (Milwaukee shoulder
syndrome).
Calcifi c periarthritis with bone resorption is char-
acterized by infl ammation of the calcifi ed focus with
resorption of the bone beneath it. The condition mimics bone sarcoma, especially if perisotitis develops.
Biopsy can be avoided if the location of the osteolytic
lesion is characteristic of HADD (near a tendon insertion), and other manifestations of HADD exist in the
body.
Milwaukee shoulder syndrome is a disease charac-
terized by destructive shoulder arthropathy, bloodstained joint effusion (80%), and chronic tears of the
rotator cuff tendon. Patients are typically elderly
women with a mean age of 72 years. Symptoms range
from none to severe shoulder pain with joint effusion.
Most patients have symptoms dating from several
years back. Bilateral shoulder involvement is common,
and knees arthropathy is found in 50% of patients.
Diff erential Diagnoses and Related Diseases
Crowned dens syndrome ( CDS ) is a rare clinical condi-
tion characterized by deposition of pyrophosphate or
calcium hydroxyapatite crystals around the odontoid
process of the axis vertebra and its ligaments, especially ligamentum fl avum. Infl ammatory signs and
high erythrocyte sedimentation rate (ESR) are present
in up to 30% of cases.
The patients often present with acute attack of neck
pain, neck rigidity, and fever, mimicking acute meningitis or spondylodiscitis. CDS affects mostly females,
with up to 45% of cases found in patients above 85
years of age.
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Signs on Radiographs
Calcifi cation of the supraspinatus and infraspinatus tendons
are a very characteristic feature of HADD (Figs. 7.4.3 and
7.4.4 ). The calcifi cation typically starts in the site of tendon
insertion, or the critical zone. The critical zone is the part of the
supraspinatus tendon 1 cm proximal to its insertion into the
greater tubercle of the humerus.
Areas of calcifi cations are noticed in the periarticular soft
tissues.
Calcifi cation within the carpal bones, ligaments, and wrist
tendons are commonly seen.
Always suspect HADD in a calcifi cation that is observed near a
joint, at tendon insertion, near muscular attachment, or after
trauma (dystrophic).
In Milwaukee shoulder syndrome , there is glenohumeral joint
destruction, narrowing, and sclerosis. Upward sublaxation of
the humeral head can be seen indicating long-standing
rotator cuff tendon disruption. Periarticular calcifi cation is
noticed in 40% of cases. Pseudo-arthrosis between the
humeral head, coracoid, and acromion is common. Knees
involvement is similar to that of CPPD arthropathy.
Fig. 7.4.3. Plain radiograph of the shoulder shows calcifi cation in
the area of the supraspinatus tendon due to HADD ( arrowhead )
In crown dens syndrome , radio-opaque calcifi cations with
diff erent sizes and shapes are seen around and above the
superior part of the odontoid process, giving the shape of a
“crown on a head” appearance. CDS can be mistaken with
cervical block vertebra (Klipple-Feil anomaly type 1).
Fig. 7.4.4. Plain radiograph
of the shoulder ( a ) and T1W
shoulder MRI ( b ) show
calcifi cation area within the
infraspinatus tendon due to
HADD ( arrowheads )
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7.4
For Further Reading
1 . Curtis W et al Calcium hydroxyapatite deposition disease.
RadioGraphics. 1999;10:1031–48
2 . Fam AG et al Hydroxyapatite pseudopodagra. A syndrome
of young women. Arthritis Rheum. 1989;32:741–7
3 . Vargas A et al Calcium pyrophosphate dihydrate crystal
deposition disease presenting as a pseudotumor of the
temporomandibular joint. Eur Radiol. 1997;7:1452–3
4 . Nguyen VD. Rapid destructive arthritis of the shoulder.
Skeletal Radiol. 1996;25:107–2
5 . Hayashi M et al Idiopathic widespread calcium pyrophos-
phate dihydrate crystal deposition disease in young patient.
Skeletal Radiol. 2002;31:246–50
6 . Baysal T et al The crown dens syndrome: a rare form of
calcium pyrophosphate dihydrate crystal deposition disease. Eur Radiol. 2000;10:1003–5
7 . Steinbach LS. Calcium pyrophosphate dihydrate and cal-
cium hydroxyapatite crystal deposition disease: imaging
perspectives. Radiol Clin North Am. 2004;42:185–205
8 . Talbott JH. Gout. Dis Mon. 1957;3:1–39
9 . Till G et al Calcium pyrophosphate dihydrate crystal depo-
sition disease: a report of a case. JCCA 1988;32:23–7
7.5 Osteoarthritis 269
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7.5
Osteoarthritis
Osteoarthritis (OA) is a clinical condition that arises primarily from cartilaginous defect in the joint, which leads
to cartilage degeneration and bone-to-bone friction
resulting in joint destruction and osteophytes formation.
The hallmarks of OA are:
Joint space narrowing : due to loss of the cartilagi-
nous surface of the joint.
Osteophytes formation : osteophytes are small extra
bony growths commonly seen at the margins of the
affected joint. Osteophytes formation is the body’s
palliative attempt to increase the articular surface
area. They are formed in the areas of low stress, classically at the margins of the joint, because vascularization of the subchondral bone is high.
Subchondral sclerosis : new bone (callus) formation
at the areas of articular cartilage loss due to bone-tobone friction and trabecular bone micro-fractures.
Subchondral cysts ( geodes ): cystic lesions formed in
the subchondral bone due to trabecular bone microfractures with deposition of hemorrhagic, myxoid,
and adipose material within these fractured trabeculae. Later, a cyst forms in these fractured trabeculae
instead of bone healing.
abnormalities (e.g., ochronosis), and bleeding into
joints (hemoarthrosis) are common causes of secondary OA. The incidence of OA increases with age, but it
is not a natural outcome of it (not every old person
develops OA).
Erosive OA is a severe form of primary OA that
presents clinically with an acute infl ammatory process
of swelling, erythema of the joint, and limitation in
function. Erosive OA is predominantly seen in the
hands of postmenopausal women, and it can be confused with rheumatoid arthritis. It has the same distribution as primary OA (bilateral and symmetrical), but
is associated with severe osteoporosis and erosions in
the hands (it occurs only in hands). Erosions of erosive
OA affect the central portion of the articular surface,
unlike rheumatoid arthritis which affects margins of
the articular surface.
Rapid destructive osteoarthritis ( Postel’s osteoar-
thritis ) is an uncommon type of hip OA where destruction of the bone and cartilage occurs within a matter of
weeks to months. The cause of this disorder is unknown.
Cases might be seen with disorders like ochronosis,
hemochromatosis, and drug-induced arthropathy (especially indomethacin). Patients are usually women presenting with severe progressive pain classically in a
single hip joint.
Signs on Plain Radiographs and MRI
Primary OA is a term used when OA develops with no
predisposing factor (e.g., trauma), and it can be classifi ed into three subtypes: genetically determined OA
(type 1), estrogen-hormone-dependent OA (type 2),
and aging-related OA (type 3). Genetically determined
OA is commonly seen in middle-aged women and
occurs almost exclusively in the hands. It affects the
distal and proximal interphalangeal (DIP and PIP)
joints, and the base of the thumb in bilateral symmetrical fashion. Primary OA must be bilaterally symmetrical to be diagnosed. Estrogen-dependent OA is seen in
females after menopause, or patients with hysterectomy due to loss of the effect of estrogen on the cartilage, bone, synovium, ligaments, and muscles. It affects
mostly the knees, and is seen perimenopausally or
within 5 years of natural menopause or hysterectomy.
Secondary OA is the most common form, which
develops after a pathological event that violates the
articular cartilage integrity. Joint trauma, metabolic
The radiological hallmarks for OA are its four main signs:
narrowing of joint space, bone sclerosis, subchondral cysts,
and osteophytes formation (Fig. 7.5.1 )
Normal bone density (no osteoporosis): this diff erentiates OA
from rheumatoid arthritis which is characteristically
associated with osteoporosis of the aff ected joint due to
hyperemia and synovial infl ammation.
( geodes ) are seen as cystic lesions located
Subchondral cysts
below the articular cartilage. On MRI, the cysts show fl uid
signal intensity on T2W images (high signal) (Fig. 7.5.2 ).
Heberden’s nodes are osteophytes that are seen at the DIP
joints. They are commonly seen in primary OA, mainly in the
index and the middle fi ngers (Fig. 7.5.3 ).
Bouchard’s nodes are osteophytes that are seen at the PIP
joints ( Fig. 7.5.3 ).
Gangelion cyst formation : a gangelion cyst is a myxoid,
tumor-like, cystic lesion that is surrounded by dense
connective tissue and fi lled with gelatinous material. It is
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typically located in the epiphysis of long bones. Gangelion
cysts are typically round or tubular, unilocular or multilocular
lesions with often sharply defi ned internal septa (Fig. 7.5.4 ).
They may show rim enhancement following contrast injection.
7.5
Gangelion cysts can be found juxta-articular, intra-osseus, and
periosteal in location. Sometimes they are diffi cult to
diff erentiate from synovial cysts based on imaging alone.
Gullwing sign describes wavy contours of the base of the distal
phalanx resembling the wings of a seagull due to small
osteophytes formation on both sides of the articular surface.
Thumb-base osteoarthritis ( rhizarthrosis ) is OA that occurs at
the trapeziometacarpal joint and the trapeziometacarpal joint
of the thumb. (Fig. 7.5.5 )
of the interphalangeal joints (characteristic of
Central erosions
erosive arthritis).
Hallux rigidus is a term used to describe OA of the fi rst
metatarsophalangeal joint (the big toe). The appearance of
accentuated transverse skin crease overlying the big toe at the
DIP joint is commonly associated with hallux rigidus (Fig. 7.5.6 ).
Rapid destructive osteoarthritis : the radiographic features may
mimic osteonecrosis of the hip joint. Septic arthritis must be
excluded by synovial fl uid aspiration before diagnosing rapid
erosive OA.
In OA of the hip joint, superior migration of the femoral head
may occur (Fig. 7.5.7 ).
Fig. 7.5.1. Plain shoulder radiograph shows the classical signs
of OA: narrowing of the joint space, sclerosis of the humeral
head and the glenoid fossa, and osteophyte formation at the base
of the humeral head ( arrow )
Fig. 7.5.2. Plain knee
radiograph ( a ) and coronal
T1W knee MRI of the same
patient shows subchondral
cysts ( black arrowheads ) and
marginal osteophyte in the
lateral tibial plateau ( white
arrows )
7.5 Osteoarthritis 271
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Fig. 7.5.3. Plain radiograph of the fi nger shows both Heberden’s
node ( arrow ) and Bouchard’s node ( arrowhead )
Fig. 7.5.4. Sagittal ( a ) and axial ( b ) PD knee MRI shows juxta-
articular intra-osseus gangelion cysts formation in the posterior
part of the tibia with bone marrow edema due to knee OA
( arrowheads ). A small Baker cyst can be seen as a secondary
fi nding ( arrow )
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7.5
Fig. 7.5.5. Plain radiograph of the hand shows OA of the base of
the thumb ( arrow )
Fig. 7.5.7. Anteroposterior
plain radiograph of the pelvis
shows severe OA of the left
hip joint with superior
displacement of the femoral
head. Notice the total right
hip joint replacement due to
previous OA of the right hip
joint
For Further Reading
1 . Gupta KB et al Radiographic evaluation of osteoarthritis.
Radiol Clin North Am. 2004;42:11–41
2 . Corrà T et al Ochronotic arthropathy: Rapid destructive
hip osteoarthritis associated with metabolic disease. Clin
Rheumatol. 1995;14:474–7
3 . Theiler R et al Reduced vitamin A tolerance in a hyperlipi-
demia patient with rapid destructive and hyperostotic
osteoarthritis of the hip. Clin Rheumatol. 1994;13:293–8
Fig. 7.5.6. An illustration demonstrates hallux rigidus with its
accentuated transverse skin crease
4 . Kijowski R et al Correlation between radiographic fi ndings
of osteoarthritis and arthroscopic fi ndings of articular cartilage degeneration within the patellofemoral joint. Skeletal
Radiol. 2006;35:895–902
5 . Weiss E et al Osteoarthritis revisited: A contemporary
review of aetiology. Int J Osteoarchaeol. 2007;17:437–50
6 . Beaman FD et al MR imaging of cysts, ganglia, and bursae
about the knee. Radiol Clin North Am. 2007;45:969–82
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