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7.6 Psoriasis and Psoriatic Arthritis 273
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7.6
Psoriasis and Psoriatic Arthritis
Psoriasis is an idiopathic genetic, multifactorial disease characterized by the formation of large, sharply
defi ned, sliver-white scaly cutaneous plaques on the
extensor surfaces of the knees and elbows, genitalia,
scalp, and lumbosacral area. Psoarisis comes from the
Greek word “spora,” which means itch.
Psoriasis can present as erythematous plaques (psoriasis vulgaris), or pustules (psoriasis pustulosa). The
psoriatic skin lesions are characterized by hyperproliferation of the epidermal keratinocytes, and infl ammatory cell cutaneous infi ltration in which neutrophils
and lymphocytes predominate. The earliest psoariatic
lesion is an erythematous papule surmounted by a fi ne
scale, and is characteristically sharply demarcated
from surrounding normal skin. If the scale of psoriasis
is lifted, multiple, minute areas of bleeding will form
( Auspitz sign ).
Predisposing factors of psoriasis include: emotional
trauma, infections (e.g., b -hemolytic streptococci),
sunlight, hormonal changes (e.g., pregnancy), medications (e.g., antimalaria drugs), and cigarette smoking.
Many patients experience worsening symptoms in
winter. Köbner’s phenomenon is a term used to describe
the formation of psoriatic lesions in an area of previous
trauma. Inverse psoriasis is a term used to describe a
condition in which the psoriasis involves the fl exor
surfaces rather than the extensor surfaces.
Psoriatic arthritis ( PsA ) is an infl ammatory, rheu-
matoid factor-negative arthritis that is associated with
psoriasis. PsA is found in 5–7% of patients with psoriasis. PsA can occur in up to 40% of severe psoriasis
cases. Up to 60% of PsA patients are HLA-B27 positive, and they are young adults aged 35–55 years.
Skin psoriasis precedes PsA in 70% of cases, and
occurs concomitantly with PsA in 15% of cases.
However, PsA may precede psoriasis skin lesions in
10–30% of cases.
PsA is characterized by bone erosions with new
bone formation, which is the most distinguishing character of PsA differentiating it from other seronegative
spondyloarthritis disorders. PsA is characterized by
the formation of periostitis, enthesitis, and distal joint
distribution in the extremities. Moreover, PsA arthritis
can be symmetrical mimicking rheumatoid arthritis,
asymmetrical, and affecting the axial skeleton mimicking ankylosing spondylitis. Because of these reasons, the history of psoriasis plus the absence of
serological tests for rheumatoid factor are essential criteria to establish the diagnosis of PsA.
Hyperuricemia may be found in association with
PsA as a result of increased purine metabolism due to
high cell turnover. However, gout arthropathy is rarely
developed in association with PsA.
Enthesitis is the infl ammation at the site of attachment of a tendon or a ligament to the joint capsule
(e.g., plantal fasciitis). The concept of an “enthesis
organ” states that the enthesis together with the adjacent fi brocartilage, periosteium, synovial and bursal
membrane should be viewed as a unique “organ.” PsA
is considered as a disease affecting the enthesis organ,
unlike rheumatoid arthritis which is a disease essentially affecting the synovium. Entheses may be fi brous
(located at the metaphyses or diaphyses of long bones),
or fi brocartilaginous (located at the apophyses and epiphyses of long bones). Both types are found in the
spine.
Sinus tarsi syndrome may occur in patients with
PsA. The sinus tarsi is a bony compartment bounded
by the talus, the calcaneus, the talonavicular and posterior subtalar joints, and is continuous with the tarsal
canal medially. The sinus tarsi contains fat, nerve endings, vessels, and ligaments (cervival and interosseus
ligaments). Sinus tarsi syndrome is a clinical condition
characterized by pain and paresthesia in the lateral side
of the ankle. The causes of sinus tarsi syndrome include
hemorrhage or infl ammation of the synovial recesses
of the sinus tarsi. Other causes include ganglion cyst
formation within the sinus tarsi.
D i ff erential Diagnoses and Related Diseases
SAPHO syndrome is a disease characterized by
S ynovitis, A cne, P ustulosis the palmar and plantar skin
surface (psoriasis vulgaris), H yperostosis of bones
(e.g., sterno-clavicular joint), and O stitis. SAPHO syn-
drome can occur with PsA in 2% of cases.
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7.6
Signs on Radiographs (In General, the
Radiographic Features Are Either Erosive or
Proliferative Changes)
Osteoporosis is mild or absent in spite of severe bone erosions.
Erosions typically start at the margins then progress toward
the center.
Bone erosions start from the periphery of the joint and extend
to the articular surface. The distal interphalangeal joints
(DIPJs) of the hands and feet are commonly aff ected.
The sacroiliac joint is aff ected in a unilateral or bilateral
pattern (sacroiliitis occurs in up to 40%).
Periosteal reaction is seen at the aff ected bones as fuzzy
appearance, which is characteristic for the bony proliferation
associated with psoriatic arthritis (Fig. 7.6.1 ).
Sausage fi ngers or toes : soft tissue swelling of the aff ected
fi ngers or toes due to tenosynuvitis. It is seen in 40% of
psoriatic patients (Fig. 7.6.2 ).
Ivory phalanx is a characteristic lesion of PsA that most often
occurs in the distal phalanx of the great toe. It is seen as a
dense appearance of the distal interphalangeal joint due to
sclerosis plus periosteal and endosteal new bone formation.
Pencil and cup deformity : this deformity is seen in a severe
form of marginal erosion, with one end of the joint forming
the cup and the other a pencil that projects into this cup. It is
mostly seen in the DIP joints of the fi ngers. The pencil tip is
represented by the distal end of the metatarsal or metacarpal
bone with the cup represented by the eroded articular surface
of the apposing phalanx.
Non-marginal bridging
: this is seen in the axial skeleton as
excess bone formation that usually begins toward the
vertebral bodies and curves upward. In contrast, syndesmophytes in ankylosing spondylitis begin at the corner of the
vertebral body and extend vertically.
Fig. 7.6.1. Plain radiograph of the distal fi ngers in a patient with
psoriasis shows narrowing of the DIP joints and marginal new
bone formation ( arrowheads )
Fig. 7.6.2. Plain radiograph of the fi ngers in a patient with psoriasis shows soft tissue swelling ( arrowheads ) of the PIP joints
(sausage fi ngers)
7.6 Psoriasis and Psoriatic Arthritis 275
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Signs on MRI
Tenosynovitis is defi ned as high T2 signal intensity surround-
ing a low T2 intensity tendon (Fig. 7.6.3 ).
In the foot, PsA can develop Achilles tendinitis, which is seen
as thickened Achilles’ tendon with high signal intensity within
the tendon (Fig. 7.6.3 ).
Plantal fasciitis is seen as a T2 high signal intensity at the site
where the plantar fascia is inserted into the calcaneus
(enthesitis) (Fig. 7.6.3 ).
In sinus tarsi syndrome, there are low T1 and high T2 signal
intensities within the sinus tarsi, with or without loss of the
cervical or the interosseus ligaments (Figs. 7.6.3 and 7.6.4 ).
Fig. 7.6.3. Sagittal STIR ankle MR illustration demonstrates
types of foot pathologies seen in psoriatic arthritis: ( 1 ) synovitis,
( 2 ) sinus tarsi syndrome, ( 3 ) tenosynovitis, ( 4 ) Achilles periten-
dinitis, ( 5 ) Achilles tendonitis, ( 6 ) retrocalcaneal bursitis, and
( 7 ) plantar fasciitis
Fig. 7.6.4. Sagittal T1W ( a ) and STIR ( b ) ankle MRI of a patient
with chronic sinus tarsi syndrome show mild hyperintense signal
within the sinus tarsi with disruption of the interosseus ligament
( arrowhead )
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7.6
For Further Reading
1 . Baden HP et al Psoriasis. Dis Mon. 1973;19:1–45
2 . Prasad PVS et al A clinical study of psoriatic arthropathy.
Indian J Dermatol Venerol Leprol. 2007;73:166–70
3 . Jacobson JA et al Radiographic evaluation of arthritis:
infl ammatory conditions. Radiology. 2008;248:378–89
4 . Zuhal Erdem C et al MR imaging features of foot involve-
ment in patients with psoriasis. Eur J Radiol. 2008;67: 521–5
5 . Tan AL. Imaging of seronegative spondyloarthritis. Best
Pract Res Clin Rheumatol. 2008;22:1045–59
6 . Leung YY et al Psoriatic arthritis as a distinct disease entity.
J Postgrad Med. 2007;53:63–71
7 . Zelickson BD et al Generalized pustular psoriasis in child-
hood. Report of thirteen cases. J Am Acad Dermatol. 1991;
24:186–94
8 . Vun YY et al Generalized pustular psoriasis of pregnancy
treated with narrowband UVB and topical steroids. J Am
Acad Dermatol. 2006;54:S28–30
9 . Bellet JS et al Intertriginous pustular psoriasis. J Am Acad
Dermatol. 2009;60:679–83
10 . Herbst RA et al Guttate psoriasis triggered by perianal
streptococcal dermatitis in a four-year-old boy. J Am Acad
Dermatol. 2000;42:885–7
11 . Jiaravuthisan MM et al Psoriasis of the nail: anatomy,
pathology, clinical presentation, and a review of the literature on therapy. J Am Acad Dermatol. 2007;57:1–27
12 . Lee Bennett D et al Spondyloarthropathies: ankylosing
spondulitis and psoriatic arthritis. Radiol Clin North Am.
2004;42:121–34
13 . Benjamin M et al Magnetic resonance imaging of entheses.
Part 1. Clin Radiol. 2008;63:691–703
7.7 Baastrup’s Disease (Spinout Process Impingement Syndrome) 277
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7.7
Baastrup’s Disease (Spinout Process
Impingement Syndrome)
Baastrup disease (BD) is a pathological condition
characterized by close approximation and contact of
adjacent spinout processes, an appearance known as
“kissing spines,” leading to reactive bone and cartilage
formation in the spinous processes causing sclerosis,
enlargement, and fl attening of the involved spines,
with calcifi cation of the interspinous and supraspinous
ligaments (Fig. 7.7.1 ).
BD most commonly occurs in the lumbar spines.
Cervical spines can be affected rarely. Patients typically present with back pain exacerbated on spine
extension, which is relieved by fl exion. The pain arises
due to irritation of the periosteum or adventitial bursae
between abutting spinous processes.
Signs on Plain Radiograph
There is close approximation of the spinous processes with
sclerosis, osteophytes formation, and hyperlordosis (Fig. 7.7.2 ).
Signs on MRI
There is approximation of the spinous processes, usually in the
lumbar spines. Bone marrow edema is often seen in active
disease, typically located in the spinous processes.
Fig. 7.7.1. An illustration of the thoracic vertebrae demonstrates
the gross appearance of the kissing spines and the calcifi cation of
the interspinous and supraspinous ligaments in Baastrup’s disease
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7.7
Fig. 7.7.2. Lateral and anteroposterior plain radiograph of the
vertebral column in the thoracolumbar region shows fl attened
spinous processes of the lumbar vertebrae with sclerosis and
For Further Reading
1. Lin E. Baastrup’s disease (kissing spine) demonstrated by
FDG/PET CT. Skeletal Radiol. 2008;37:173–5
2. Pinto PS et al Spinous process fracture associated with
Baastrup disease. J Clin Imaging. 2004;28:219–22
3. Hui C et al Two unusual presentations of Baastrup’s disease.
Clin. Radiol. 2007;62:495–7
close approximation ( arrowheads ), typical fi ndings in Baastrup’s
disease of the spines
7.8 Scheuermann’s Disease (Juvenile Kyphosis Dorsalis) 279
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7.8
Scheuermann’s Disease
(Juvenile Kyphosis Dorsalis)
Scheuermann’s disease (SD) is a disease characterized
by juvenile thoracic kyphosis with minimal deformity
and few clinical symptoms (Fig. 7.8.1 ). The disease
has an autosomal dominant pattern of inheritance, with
an incidence of 1% of population.
The normal disc space is composed of two end
plates, central nucleus pulposus, and an outer annulus
fi brous tissue (annulus fi brosus) surrounding the
nucleus pulposus. Due to age process or repetitive
trauma, the nucleus pulposus loses its watery content
and the annulus fi brosus develops cracks and fi ssures.
When this occurs, the nucleus pulposus extrudes
through the annulus fi brosus fi ssures. Extrusion of the
nucleus pulposus into the vertebral end plates results in
Schmorl node and limbus vertebra, while extrusion
through the annulus fi brosus results in disc degenerative disease (disc hernia). Schmorl node is nucleus pul-
posus extrusion into the end plates and then into the
vertebral body. In contrast, limbus vertebra is extrusion
of the nucleus pulposus below the ring apophysis separating it from the body of the vertebra. SD is characterized by the presence of Schmorl node and multiple end
plate irregularities due to nucleus pulposus extrusion.
Although the etiology of SD is unknown, Scheuermann proposed that the kyphosis resulted from avascular necrosis of the vertebral body’s apophysis ring,
but it is now generally believed to be a form of disc
degeneration. Kyphosis is a term used to describe poste-
rior convex curvature of the spine. Normal vertebral
kyphosis is located in the cervico-lumbar areas and does
not exceed 25–45°. Any kyphosis exceeding this range
is considered pathologic. Kyphosis is classifi ed into:
Arcuate kyphosis : kyphosis with long arc. This type is
seen in SD, osteoporosis, and ankylosing spondylitis.
Angular kyphosis : kyphosis with short arc. This type
is seen in vertebral pathologic or compressive fractures, and spondylities.
SD can be associated with scoliosis in 15% of cases.
Scoliosis is defi ned as an abnormal lateral curvature of
the vertebral column. It can be classifi ed into:
Rotoscoliosis : scoliosis with rotation of the vertebra
in the axial plane (Fig. 7.8.2 ).
Kyphoscoliosis : scoliosis plus kyphosis
S-shaped scoliosis : double lateral deviation of the
vertebral column (Fig. 7.8.3 ).
C-shaped scoliosis : single lateral curve of the verte-
bral column.
Fig. 7.8.1. An illustration
demonstrates thoracic
kyphosis in a young patient
with Scheuermann’s disease
(SD)
Fig. 7.8.2. A plain abdominal radiograph of a patient shows
right rotoskoliosis
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7.8
Signs on Radiographs, CT, and MRI
Increased thoracic kyphosis with compensatory lumbar
hyperlordosis (Fig. 7.8.4 ).
Wedging of at least three consecutive vertebrae (>5°) with
end plate irregularities (Fig. 7.8.4 ).
End plate irregularities, loss of disc space height, and Schmorl
nodes. Schmorl node is defi ned as localized depression of the
superior or inferior end plates >3 mm in diameter (Fig. 7.8.5 ).
Limbus vertebra is visualized as separation of the ring
apophysis from the vertebral body (Fig. 7.8.6 ).
Scoliosis in 15% of cases.
Fig. 7.8.3. A plain abdominal radiograph of a patient with
Marfan’s syndrome shows right S-shaped skoliosis
Neurological symptoms of SD are rare in general, and
usually arise due to spinal cord compression. There are
three types of neural compression reported in SD:
Extradural spinal cyst.
Compression of the cord at the apex of the kyphos.
Disk hernia at the apex of the kyphos.
Criteria for Scheuermann’s
Disease Diagnosis
More than 5° of wedging of at least three adjacent
vertebrae at the apex of the kyphosis.
End plate irregularities.
A thoracic kyphosis of more than 45°.
Fig. 7.8.4. Lateral plain radiograph of the thoracic spine of an
18-year-old girl with SD shows marked thoracic kyphosis with
wedging of more than three adjacent vertebrae
7.8 Scheuermann’s Disease (Juvenile Kyphosis Dorsalis) 281
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Fig. 7.8.5. Sagittal ( a ) and
axial ( b ) T2W image MRI of
a patient with SD shows
Schmorl’s node seen as
localized depression of the
superior end plates >3 mm in
diameter due to extrusion of
the nucleus pulposus into the
end plates ( arrowheads )
Fig. 7.8.6. Sagittal T1W ( a )
and T2W ( b ) MRI of a patient
with vertebral column
osteochondrosis shows L2
limbus vertebra ( arrowheads )
and L4/L5 grade 1 (<25%)
spondylolisthesis ( arrows ).
Notice the active bone
marrow edema around the
bone fragment of the anterior
superior end plate of L2 in ( b )
For Further Reading
1. Swischunk LE et al Disk degeneration in childhood:
Scheuermann’s disease, Schmorl’s nodes, and the limbus vertebra: MRI fi ndings in 12 patients. Pediatr Radiol. 1998;28:334–8
2. Arlet V et al Scheuermann’s kyphosis: surgical manage-
ment. Eur Spine J. 2005;14:817–27
3. Kapetanos GA et al Thoracic cord compression caused by
disk herniation in Scheuermann’s disease. A case report
and review of the literature. Eur Spine J. 2006;15(suppl. 5):
S553–8
4. Alexander CJ. Scheuermann’s disease. Skeletal Ardiol. 1977;
1:209–21
5. Paajanen H et al Disc degeneration in Scheuermann disease. Skeletal Radiol. 1989;18:523–6
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7.9
7.9
Sjögren Syndrome
(Myoepithelial Sialadenitis)
Sjögren syndrome (SS) is a chronic, systemic autoimmune disease characterized by infi ltration of the acinar
cells of the salivary and lacrimal glands by lymphocytes, causing dry eye ( xeropthalmia ), dry mouth
( xerostomia ), and infl ammation of the cornea and the
conjunctiva ( keratoconjunctivitis ).
SS is classifi ed as secondary ( Sicca syndrome )
when it is associated with other connective tissue disorders (e.g., rheumatoid arthritis), and primary when it
occurs without any manifestation of other connective
tissue disorders.
Criteria to Diagnose SS Include
Symptoms and signs of ocular dryness (e.g., positive
Schrimer’s test).
Symptoms and signs of mouth dryness.
Evidence of autoimmune disease (e.g., positive rheu-
matoid factor).
Exclusion of lymphoma, sarcoidosis, and acquired
immunodefi ciency syndrome.
meningoencephalitis and multiple sclerosis-like symptoms (25% of cases). Psychiatric manifestations
include Alzheimer-type dementia, poor attention and
concentration, and memory defi cits. Rarely, neuromyelitis optica may coexist in patients with SS. In children, although it is rare, SS is characterized by bilateral
parotid enlargement. Very rarely, SS may be associated with amyloidosis.
Laboratory investigation reveals high titer of SS-A
antibodies and SS-B antibodies plus rheumatoid factor
in 50% of cases.
Signs on Sialography
On both conventional and MR-sialography, the aff ected salivary
gland shows mottled appearance with cystic changes due to
destruction of the gland parenchyma (sialectasia). Four stages of
sialectasia are classically described:
Stage 1 ( punctuate ): multiple dots <1 mm in size (Fig. 7.9.1 ).
Stage 2 ( globular ): multiple dots 1–2 mm in size.
Stage 3 ( cavitary ) : multiple dots >2 mm in size.
Stage 4 ( destructive ) : multiple irregular and widened ducts due
to gland infl ammation ( sialodochitis ).
SS causes salivary glands infl ammation ( sialeadenitis )
that leads to parenchymal destruction and salivary
gland dilatation ( sialectasia ).
Patients with SS are commonly perimenopausal
women who often develop multiple systemic manifestations that include mouth dryness, which affects eating, speaking, and may lead to teeth decay; extreme
fatigue occurs in 50% of patients, which is more troublesome than the exocrine symptoms; intermittent polyarthritis affecting the small joints in asymmetrical
fashion; dry skin (50%), esophageal dysmotility (up to
90%), vaginal atrophy and dyspareunia, and interstitial
nephritis. Patients with SS have risk for developing
lymphoma, and they should be closely monitored.
Patients with SS may also develop neuropsychiatric
manifestations. Brain manifestations include aseptic
Fig. 7.9.1. Lateral conventional sialography radiograph in a
patient with submandibular sialectasis grade 1-2 seen as diffuse
multiple punctuated dots between 1-2 mm in diameter
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