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Radiology Review

Arthritides

Jeffrey R. Thompson, DC
Professor Diagnostic Imaging
Texas Chiropractic College
The Arthritides
Degenerative
z Osteoarthritis
z Primary
z Secondary
z Post-traumatic
z Neuropathic arthropathy
z Diffuse Idiopathic Skeletal Hyperostosis
Inflammatory
z Rheumatoid
z Seronegative Spondyloarthropathies

z Septic arthritis
The Arthritides
Connective Tissue arthropathies
z LE (Lupus erythematosis)
z PSS (Progressive systemic sclerosis)

Crystal Deposition Arthropathies


z HADD
z CPPD

z Gout
Degenerative joint disease
AKA “osteoarthritis” or “osteoarthrosis”
A “wear and tear” type of arthritis
Confusing terminology in the spine
z Intervertebral osteochondrosis
z Spondylosis deformans

z Discogenic spondylosis

z (Please, no “spurs”- unless you’re from


Texas)
Osteoarthritis- Idiopathic localized
forms
Hands Knee
z Heberdens and z Medial compartment
Bouchards nodes (nodal) z Lateral compartment
z Patellofemoral compartment
z Erosive (non-nodal)
interphalangeal joints Hip
z Eccentric (superior)
z Carpal-1st metacarpal
z Concentraic (axial, medial)
Feet z Diffuse (coxae senilis)
z Hallux Valgus or rigidus Spine
z Contracted toes (hammer z Apophyseal joints
or cock-up toes) z Intervertebral discs
z Talonavicular joint z Spondylosis (osteophytes)
z Ligmentous (DISH)
Other isolated joints
z SI, TMJ, glenohumeral,
tibiotalar, etc.
Osteoarthritis- Secondary
Trauma Metabolic (continued)
z Acute z Wilson’s disese
z Chronic (occupation, sports) z Gaucher’s disease
z Frostbite Endocrine
z Caisson disease z Acromegaly
z Hemoglobinopathies z Hyperparathyroidism
Congenital or development z Diaetes
z Localized: Legg-Calve-Perthes, z Obesity
DDH, SFCE z Hypothyroidism
z Mechanical factors Calcium deposition
z Varus/valgus
disease
z Unequal leg length
z Hypermobility syndromes
z CPPD
z Bone dysplasias z Apatite arthropathy
Metabolic disorders Neuropathic
z Ochronosis
z Hemachromatosis
Osteoarthritis- Risk factors
Trauma
z Occupatational
z Kneeling/squatting, bending and heavy lifting all assoc. with inc.
incidence knee OA
z Sports
z Professional level athletes have inc. incidence of OA
z 2-3x risk OA knees/hips in former long distance runners and tennis
players
z Higher incidence in athletes with hx of joint injury
z 3x inc. risk of knee OA in soccer athletes with ACL tear compared to
athletes with intact ACL
Osteoarthritis- Risk factors
Obesity
z Marked inc. incidence of knee OA with increased body mass
z Obesity as young adult is strong predictor of later OA (Framingham
study)
z Elimination of obesity would reduce knee OA by an estimated 25-50%;
25% or more for hip.

Genetics- Heberden’s nodes


z DIP OA in females appears to related to autosomal recessive trait; in
males, the mechanism appears to be autosomal recessive
z Genetically controlled collagen abnormalities identified in animal models
lead to premature OA
z No definite heritable abnormality of collagen or other matrix
macromolecules has been identified in humans.
Osteoarthritis- Risk factors
Risk factors for progression (not onset) of knee OA
z Female
z Older age
z Overweight
z Heberdenl’s nodes
z ?low dietary vit. C
z ?low dietary vit. D

Pain/disability risk factors


z Most individuals with x-ray demonstrable OA do not have joint symptoms
z Anxiety, depression and muscle weakness may all be important
z Disability (similar severity of OA)
z Women > men
z Welfare > working
z Divorced > married
Osteoarthritis
Gross pathology
z Softening, fibrilllation and loss of articular cartilage
z Eburnation of exposed bone \bone remodeling
z Osteophytes
z Subchondral cysts
z Synovitis
z Thickening of joint capsule
z Meniscus degeneration
z Periarticular muscle atrophy
Osteoarthritis- cartilage
changes
Target tissue is cartilage- however OA is a failure of the
entire joint, not just the cartilage
Early OA characterized by a healing response
z thickening of the articular cartilage
z increased water content
z increased rate of proteoglycan synthesis
Progression of disease
z Decreased proteoglycan conc.
z Cartilage thinning
z Vertical clefts (fibrillation) in cartilage
z Irregular fibrillated cartilage is worn away
Osteoarthritis- cartilage
changes
Normal articular cartilage is avascular and separated from
underlying bone by layer of calcified cartilage (tidemark)
z OA allows blood vessel penetration from bone thru calcified layer,
providing route for cytokines, growth factor, etc. to effect
remodeling
Fibrocytes may migrate into fissures in cartilage and
produce fibrocartilage
z Fibrocartilage is not as durable as hyaline cartilage
Osteoarthritis- bone changes
Remodeling and hypertrophy of subchondral bone occurs
z Sclerosis seen radiographically
“eburnation” = smooth, polished appearance of exposed
subchondral bone after articular cartilage has worn away
Microfractures of the bone allows synovial fluid to
penetrate subchondral bone = subchondral cyst formation
Combined growth of cartilage and bone at joint margins
results in osteophytes
Osteoarthritis- synovial
changes
Chronic, patchy synovitis occurs with lining cell hyperplasia,
lymphocytic infiltration and perivascular lymphoid aggregates
Villous formation may occur (reminescent of RA), but no
pannus formation and no erosion of cartilage.
Fragments of articular cartilage and bone may become
embedded in synovial membrane and surrounded by
macrophages and local inflammatory cells
Intervertebral
Osteochondrosis
Target tissue = the nucleus pulposis
Dessication of nucleus leads to :
z Vacuum phenomenon in IVD space
z Decreased intervertebral disc height
Intervertebral Osteochondrosis
Primarily affecting the nucleus
pulposis
Dessication of nucleus leads to :
z Vacuum phenomenon in IVD space
z Decreased intervertebral disc height
Intervertebral
Osteochondrosis
Spondylosis Deformans
Target tissue = annular fibers of disc
Key findings = osteophytes on vertebral
endplates
A rose by another name is still a rose, but…
An osteophyte on an endplate is a
spondylophyte
z NOTE! Don’t confuse this with syndesmophyte,
which typically implies an inflammatory arthritide
Spondylosis Deformans
Marginal location typical
Horizontal orientation
Spine DJD - puzzler
“Pseudo-fracture” appearance in cervical spine
Spine DJD - puzzler
Hypertrophic change of uncinate processes
Spine DJD - puzzler
Uncinate
hypertrophy
creates
horizontal
lucency
Not sure?
Take obliques!
Spine DJD
Sclerosis and osteophyte formation of
zygoaphyseal articulations and uncovertebral joints

Continues next slide…


Spine DJD (same case)
Intervertebral foraminal encroachment posteriorly
and anteriorly
DJD- Lumbar
Spondylosis, osteochondritis dissecans and
osteophyte formation of the posterior joints
Degenerative spondylolisthesis
Pars interarticularis is intact
Vertebra moves forward secondary to degenerative
remodeling of the posterior joints
Spine DJD - puzzler
Note the
increased
radiopacity of
vertebral bodies
L-2 and L-3
What’s does the
d/dx include for
blastic lesions in
vertebral bodies?
Hemispherical sclerosis
Type III Modic
changes
Reactive sclerosis of
vertebral body
adjacent to
degenerative disc,
often with a Schmorl’s
node
Type I and II Modic
changes visible on MR
Spinal Stenosis
Congenital and Aquired
Aquired most often due
to degenerative joint
disease
Other causes include
z Pagets
z Compression Fx
z Neoplasm (bone or s.t)
z Congenital anomaly
Spinal Stenosis
Stenosis here is
combination of bony
overgrowth (spondylosis)
and soft tissue (lig.
flavum hypertrophy)
Note narrowing of cord
Spinal Stenosis
Potential for chronic
vascular compromise
in spinal stenosis of
cervical spine
Myelomalacia may
result
Anterior spinal artery
supplies anterior 2/3
of cord
Spinal Stenosis
Soft tissue elements often as important (or more
important) than osseous
z Ligamentum flavum thickening
z Capsular thicking of zygopophyseal joints
z Synovial cyst of zygopophyseal joints

Normal
vs
thickened
Degenerative
Spondylolisthesis
Posterior elements
not separated from
body (no
spondylolysis)
Secondary to DJD
of posterior joints
Most common level
L4/5
Typically mild
displacement
z Usually <5-6mm
Degenerative
Spondylolisthesis
DJD- hip
Most common pattern causes narrowing of the superolateral
portion of the joint
Unilateral or bilateral (this case bilat)
DJD- hip
Most common joint for large subchondral cyst formation to
occur
z “geode” is term sometimes used to identify large subchondral cyst
Note marked involvement of superior joint space
Secondary DJD- hip
What condition predisposes this patient to DJD?
Secondary DJD- hip
DJD is present bilaterally, but more marked on left
Secondary
DJD
Note the sclerosis,
irregularity and joint
space narrowing on the
(reading) right hip
Note the atypical number
of coccygeal sements
z (“roht ro!)
DJD AC jnt
Osteophyte formation here can create impingement
on the available space for the supraspinatous
tendon (impingement syndrome)
Secondary DJD wrist
Wrist is not a common location for primary DJD
Ligamentous injury may predispose
Volar intercalated segment instability (VISI) indicated by volar
rotation of lunate and abnormal scapho-lunate angle and
capitolunate angle
Hands
Heberden’s nodes (DIP)
Bouchard’s nodes (PIP)
DJD-Knee
Narrowing, subchondral cysts and sclerosis, medial side of rt.
knee.
Tibial osteotomy may redistribute weightbearing for (temporary)
improvement of symptoms
DJD-Knee
Marked asymmetrical joint narrowing with osteophyte
formation and sclerosis.
D.I.S.H. – Clinical
Diffuse Idiopathic Skeletal Hyperostosis

Age= typically 5-6th Associated clinical


decade onset; zDiabetes mellitus (20-50%)
increased incidence
zApprox 1/3 + HLA B-27
with age
zApprox 40% + HLA B-8
Clinical / radiographic
zESR inc. in 22% pts.
mismatch is common
z Often minimal zPeripheral joint complaints

symptoms, other than include “heel spurs” and


“stiffness” despite tennis elbow.
marked x-ray change zOPLL may result in
z Dysphagia (20%) may symptoms of cord
result if c-spine involved compression
D.I.S.H. - X-ray characteristics

At least 4 contiguous levels


involved
Thick, flowing anterior
and/or lateral calcification or
ossification
No posterior joint ankylosis
Relative preservation of IVD
height and no other
associated signs of
degenerative disc disease
No SI joint erosion, sclerosis
or ankylosis
D.I.S.H.
X-ray characteristics
Diffuse, thick
calcification of
the ALL

Involvement of
thoracic spine
may be thinner
and mimic
ankylosing
spondylitis
D.I.S.H.
Peripheral involvement

Calcaneal hyperostosis =
“heel spur
D.I.S.H.
Hypertrophic change along
margin of glenoid fossa
(next slide same case)
D.I.S.H.
Characteristic changes in cervical and lumbar spine, but 4 contiguous
levels are not involved; diagnosis is still clearly DISH
D.I.S.H.
Characteristic change of cervical spine; mild change in lumbar spine
OPLL
Ossification of Posterior Longitudinal Lig.

May be isolated
phenomenon or
associated with DISH
Cervical spine most
often involved
z Thoracic > lumbar
May see on plain film
Multiplanar imaging
necessary for
assessment of cord
Arrow shows flattened cervical cord
space
(Lamina and spinous removed)
OPLL
Ossification of Posterior Longitudinal Lig.
Cervical cord
compression may result
in upper motor neuron
findings
z +Hoffman sign in hand
z +Babinski sign (“upgoing”
toes)
z “Clumsiness” of hand
z Pt. may have difficulty
walking on uneven
ground due to leg
spasticity
OPLL
Ossification of Posterior Longitudinal Lig.
CT slice- NO contrast!
OPLL
Ossification of Posterior Longitudinal Lig.
MR shows thick, low signal PLL
Osteitis Condensans Illi
CLINICAL FINDINGS
z May/not have symptoms
z Typically uni- or multi-
parous female patient
z childbearing age range
z Self-limiting condition that
resolves with age
z May be uni- or bi-lateral
z More often bilateral
Osteitis Condensans Illi
Affects the iliac side of SI
joints, usually bilateral
Affects lower ½ of joint
Triangular pattern of
reactive sclerosis
SI joint will not be fused!
No need for referral
Unusual to see in elderly
Osteitis Condensans Illi
Affects the iliac side of
SI joints, usually
Same case next slide..
bilateral
Affects lower ½ of joint
Triangular pattern of
reactive sclerosis
SI joint will not be
fused!
No need for referral
Unusual to see in
elderly
Osteitis Condensans Illi

35 yr. Old female with


chronic, low grade
sacroiliac joint pain
Seronegative
Spondyloarthropathies
Seronegative?
z Serologically negative for Rheumatoid arthritis
z Used to be called “rheumatoid variants”; not a
currently used term
Spondyloarthropathy
z Spondylo” = spine
z Arthropathy = Abnormal findings in the joints
Seronegative
Spondyloarthropathies
Group of disorders including
z Ankylosing spondylitis
z Psoriatic arthropathy

z Reactive arthritis
z Previously known as “Reiter’s disease”- eponym
currently out of favor
z Enteropathic arthropathy
Seronegative
Spondyloarthropathies
The HLA-B27 antigen (Human Leucocyte Antigen)
z The major function of HLA molecules is to present
antigen fragments for recognition by T cells
z Ankylosing spondylitis – 90% +

z Psoriatic arthropathy – 50% +

z Reactive arthritis - 75% +


Ankylosing Spondylitis
Age onset 15 –35 yrs
z Only 10% begin > 39 yrs of age
Sex: Males > Females by 10 or 15:1 ratio
Race: Caucasian > Black by 4:1
50% will have radiating pain to lower
extremities at some point – d/dx sciatica
10 – 50% have extremity joint pain at
presentation
z Large extremity joints (hips and shoulders)
predilicted over small joints
z Hip involvement est. at 17 – 35%
Ankylosing Spondylitis
Clinical Diagnostic Criteria
Lumbar pain/stiffness for > 3mos., not
relieved by rest
Limited lumbar ROM
Pain/stiffness of thoracic area
Limited chest expansion
History of iritis and iridocyclitis
Sacroillitis with any 2 of the above criteria
Ankylosing Spondylitis
extraskeletal
Up to 18% of patients with ulcerative colitis
or Crohn’s Disease will develop ankylosing
spondylitis
Aortitis
Iritis in 25%- may be presenting symptom
Pulmonary fibrosis may occur
Up to 80% reported to have chronic
prostatitis
Ankylosing Spondylitis
Variable degree of
progression
z Inflammation may be
limited to SI joints
z Widespread spinal
involvement and
disability may occur
Classic forward posture
and exaggerated
kyphosis
Ankylosing Spondylitis
Bilateral sacroiliac
involvement almost
always seen
Early changes are
widening of joint
space, erosions and
predilection of the
lower portion of the
joint.
More change on
iliac side- thinner
cartilage
Ankylosing Spondylitis
Later changes involve
bony fusion of SI joints
“Star sign” may be seen
at iliolumbar lig. Insertion
About 50% patients will
have complete, bilateral
SI joint fusion

Classic “star sign”


and fused SI joints
Ankylosing Spondylitis
Early changes in the
spine often at the
thoraco-lumbar junction
Syndesmophytes
z Thin, vertical and bilateral
calcific/ossific density
z Attach to joint margin
(“marginal”)
z Bridging the IVD space,
resulting in ankylosis
Ankylosing Spondylitis
Close-up previous case
Ankylosing Spondylitis
Enthesopathy =
inflammation of
ligamentous and
tendinous insertions
“Shiny corner sign” in
spine- precedes
syndesmophyte
May result in “squared
off” appearance of
vertebral bodies
Ankylosing Spondylitis
“Squared off”
appearance of vertebral
bodies
Sclerotic SI joints
Ankylosing Spondylitis
“Bamboo spine” is late
stage, but does not
always result
Ankylosing Spondylitis
Always check for
atlantoaxial instability
in ANY patient with an
inflammatory
arthropathy!
z Est. 2% of AS patients
develop spontaneous
Cl/C2 instability
Ankylosing Spondylitis
Predisposition to
“carrot-stick” spinal
fracture, or advanced
degenerative change in
spinal joints with
residual mobility
z “Anderson lesion”
Ankylosing Spondylitis
Peripheral joint
symptoms at
presentation in up to
50% of patients
Large extremity joints
predilected (hip and
knee)
Changes resemble
rheumatoid arthritis
Psoriasis- clinical
Dry, scaly
erythematous
patches
z May bleed if scales
removed
Skin lesions
common on extensor
surfaces of
arms/hands, in
eyebrows and
gluteal fold
Psoriasis- clinical
Nail changes seen in up
to 80% patients
Hyperkeratosis, pitting
and discoloration
HLA B-27 factor in
approx. 75%, if SI joints
are involved
HLA B27 factor in 30%
of those with only small
joint changes
Psoriatic Arthropathy
Arthritis is seen in approx. 7% of patients
with psoriasis; 25% in those with severe
disease
Stronger association of sacroiliitis in patients
with nail involvement
Arthritis predilicts peripheral joints, but may
be seen on spine (spondyloarthropathy) as
well.
In up to 20% of cases, arthritis may precede
skin changes
Psoriatic Arthropathy
Patterns of involvement (Resnick)
z Peripheral arthritis with DIP predilection
z Pattern similar to rheumatoid

z Asymmetrical oligoarthritis or monoarthritis

z Arthritis mutilans

z Sacroillitis.
Psoriatic Arthropathy
More prominent
features:
z Asymmetrical
z Joint swelling
z Enthesopathy and
periostitis
z Bony ankylosis of
interphalangeal joints
Psoriatic Arthropathy- spine
Syndesmophytes
z Asymmetrical
z Coarse
z Non-marginal
z May be“comma-
shaped”
z Not as vertical as AS
z Indistinguishable from
Reactive arthritis
z Often begin T-L
junction
Psoriatic Arthropathy- hands
“Ray pattern” =
involvement of all
three joints is
common
IP joint ankylosis
almost
pathognomonic

Same case next slide…


Psoriatic Arthropathy- hands
Extensive periostitis
and hypertrophic
enthesopathy
Psoriatic Arthropathy
“mouse-ear” erosions
DIP joints predilicted
Psoriatic Arthropathy SI
Bilateral and
asymmetrical most
common
Wide, hazy joints-
ankylosis is NOT
common
30-50% involvement in
pts. with psoriatic
arthropathy
Strong assoc. of SI
involvement in pts with
nail disease
Psoriatic Arthropathy
Atlanto-axial instability
may occur
Reactive Arthritis
Previously “Reiter’s Syndrome”
z Reiter was not the first to describe the syndrome
z Reiter is said to have been a Nazi sympathizer

HLA factor on 80-90% patients


z People with HLA B-27 factor are more at risk, but
most HLA B-27 positive individuals do not get
disease
Uncommon in black pop. and males
predilected over females approx. 5:1
Reactive Arthritis
Involvement of eyes, urinary tract and prediliction
for lower extremity involvement
z Clinical mnemonic “Can’t see, can’t pee, can’t dance with
me”
Conjunctivitis or iritis
History of previous urinary tract or GI tract infection
is common
z May/not be SID
z Shigella of GI tract reported
Age of onset typically late teens to mid thirties
Reactive Arthritis
Lower extremity
prediliction
z Knee > Ankle > Forefoot >
Calcaneus
Most cases are self-
limiting
Est. 60-80% of pts.
Eventually show x-ray
changes
z Only about 5% cases
result in residual disability
Reactive Arthritis
“Lover’s heels”
Calcaneal osteophyte and/or periostitis
z Subtle periostitis on inf. aspect of calcaneus (left photo)
Reactive Arthritis
Inflammatory erosions of
small joints of feet may
be seen

Same case next slide


Reactive Arthritis
Syndesmophyte
formation in spine and
sacroiliitis.
SI joint fusion NOT
common
Erosive changes seen
in up to 50%
z Bone scan shows up to
70% patients have
involvement

Close-up next slide


Reactive Arthritis
Syndesmophyte formation in spine in approx. 15%
Indistinguishable from psoriatic arthropathy
z Thick, non-marginal and asymmetrical
Rheumatoid Arthritis
Dx criteria include
z Morning stiffness >/= 1 hr. duration
z 3 or more joints simultaneously involved
z Joint swelling (fluid, not bony overgrowth)
z MCP, PIP, MTP, ankle, wrist, knee or elbow

z Bilateral and symmetrical involvement


z Rheumatoid nodules on extensor surfaces or bony
prominences
z RA factor +

z X-ray changes (erosions and demineralization)


Rheumatoid Arthritis
Periarticular
osteopenia
Marginal erosions
Diffuse joint
narrowing
ST swelling
Rheumatoid Arthritis
Rheumatoid Arthritis
Rheumatoid Arthritis
•Erosive joint disease in both upper
and lower extremities- same patient
as previous slide of hands
R.A. - advanced
Misalignment of joints
z Ulnar drift of MCs
z “Swan-neck” deformity
Rheumatoid Arthritis -hips
Uniform joint space loss
Protrusio acetabuli may occur
z “Otto’s pelvis” = bilateral protrusio acetabuli
Secondary DJD may create confusing appearance
Rheumatoid Arthritis -hips
Uniform joint space loss and erosions
Rheumatoid Arthritis
Spine
z Most common
location C-spine
z Esp. C1/C2
z Always check
atlantoaxial stability
with flex/ext views!
Rheumatoid Arthritis
Spine
z Pannus formation
may stenose canal!
Rheumatoid Arthritis
Journal case (AJR) showing pannus formation
Multiple calcifications in joint
Synovial
chondrometaplasia
Condition of unknown etiology
Syovial tissue begins to produce
osteochondral bodies that may calcify
Age: 3rd to 5th decade predilected
Sex: 2:1 male > females
Synovial chondrometaplasia
Sites: Large joints predilected
z hips, knees and shoulders and elbows most
commonly affected
May involve joint capsule or other synovial
lined structures
z bursae and tendon sheaths also synovial lined!
Almost always monoarticular
Treated with resection, but recurrence
common.
Synovial chondrometaplasia

Also called synovial


osteochondromatosis
Crystal deposition
arthropathies
Gout
Calcium Pyrophosphate Dihydrite
Deposition Disease (CPPD)
Hydroxyapatite Dihydrite Deposition
Disease (HADD)
Gouty Arthritis
Primary gout Secondary gout
z Renal disease
z Idiopathic
z Hypertension
z Myeloproliferative
disease (eg, multiple
myeloma)
z Inherent metabolic
disorder
z Hemolytic disease
z Drug induced
z obesity
Gouty Arthritis

Gout = “gutta” = to drop


z Evil humors were thought to drop into the
joint and cause pain
“Podagra”
Gr. “pous” = foot + “agra” = to attack
Gouty Arthritis- Clinical
Age: typically 5th decade onset
Sex: Males > females 20:1
z Estrogen appears to have protective effect,
promoting excretion of XS uric acid
Familial occurrence in about 20% cases
z 25% of 1st degree relatives of gout pts have
hyperuricemia
Most common cause of inflamatory arthritis in
men over the age of 30
Probably the 2nd most common of all inflamm.
arthropathy
Gouty Arthritis- Clinical
Typically acute onset of monoarticular pain
z Patient may think bitten by insect
z D/dx infection! Get joint aspiration

Usually exacerbation/remission pattern


Very painful with associated swelling and
redness
1st MTP joint involved classically
Gouty Arthritis- Clinical
Serum
z Elevated serum uric acid may be seen in acute
stage
z Note: Asymptomatic hyperuricemia may occur
z Est. only 1 in 5 hyperuricemic individuals will develop
clinically apparent urate crystal deposition
Joint fluid microscopy = major criterion of Dx
z Joint aspiration yields needle shaped crystals
z Polarized light microscopy shows negative bi-
refringence of crystals
Gouty Arthritis – X-ray
Radiographic
manifestations not
common
z Most cases medically
controlled
z Repeated episodes
necessary for x-ray
changes to be seen
Predilicts lower
extremity
Spine, hips, shoulders
not commonly affected
Gouty Arthritis – X-ray
Joint spaces typically
not compromised early
Classic large erosion of
joint margin or even
away from joint edge
Overhanging edge
Sharp definition of
erosion
Gouty Arthritis – X-ray
Periarticular soft
tissue calcifiction may
result from tophi (uric
acid crystals
deposited in soft
tissues)
CPPD- many clinical
patterns
“Pseudogout” affects approx. 10-20% with
acute joint pain/swelling
Pseudo-rhematoid pattern seen in approx. 2-
3%
Chronic arthritic pain with superimposed
acute inflammatory episodes seen in 35-60%
May mimic DJD in approx. 10–35%
Asymptomatic in significant number
z Cart. Ca++ seen in approx. 25% by 9th decade
Neuropathic appearance in 1-2%
CPPD clinical
Calcium pyrophosphate Hereditary occurrence
dihydrate deposition in may be seen with
articular cartilage or autosomal dominant
other periarticular tissue pattern
z Dicalcium phosphate Other conditions
dihydrate, octocalcium
phosphate and other associated with CPPD
orthophosphates may include:
cause cartilage z Hyperparathyroidism
calcification as well z Gout
Age: typically middle- z DJD
aged to elderly z Trauma
Sex: men and women z Ochronosis
both affected- studies z Wilson’s disease
vary on predominance z Others….
CPPD- clinical
Clinical evaluation of patient with CPPD crystal
deposition should include serological tests for:
z Calcium
z Magnesium
z Phosphorus
z Alkaline phosphatase
z Feritin/iron and iron-binding capacity
z Glucose
z TSH
z Uric acid
CPPD – x-ray findings
Deposition of calcium
pyrophosphate dihydrate in
hyaline cartilage of joint may
result in cartilage calcification
(“chondrocalcinosis”)
CPPD – x-ray findings
Favorite sites
z Triangular
fibrocartilage of wrist
z Knee (esp. menisci)
z 1st and 2nd MCP
Involvement
typically bilateral,
but not always
symmetrical
Cloud-like ca++ of
synovium may occur
as well

Same case next slide


CPPD – x-ray findings
Parallel calcifications along
articular margins
CPPD
Note the “halo” of
calcification that parallels
the subchondral bone
CPPD – x-ray findings
Prominent subchondral
cyst formation common
Unusual location
suggestive
z “Degenerative” change
isolated to non-weight
bearing joint such as
radiocarpal joint or
glenohumeral joint
z Isolated patellofemoral
joint involvement also
suggestive
z May cause DJD of the
2nd and 3rd MCP joints
Hydroxyapatite Dihydrite
Deposition Disease (HADD)
Sometimes called
“Calcific tendonitis”
Most common in
supraspinatous
tendon
Symptoms typically
intermittent
Calcification may Picture from Resnick/Niwayama Diagnosis of Bone and
Joint Disorders 2nd ed.
appear/disappear on
x-ray
Hydroxyapatite Dihydrite
Deposition Disease (HADD)
Calcification
develops in the
relatively avascular
area of tendon near
insertion- same
place tears
frequently occur

Picture from Resnick/Niwayama Diagnosis of Bone and


Joint Disorders 2nd ed.
HADD
Calcification typically more amorphous and “soft” than the nodular
densities of synovial chondrometaplasia
HADD
Dominant hand involvement more common, however may be
bilateral
HADD- gluteal
Clumpy, amorphous area of inc. density seen over proximal femur

Close-up AP
Frog-leg view
HADD -gluteal
Lateral view (right) shows
calcification along gluteal insertion

AP and Frog-leg view


shows faint inc.
density
Neuropathic Arthropathy
“Charcot joint”
z Charcot described initially in association with
neurosyphilis; other etiologies more common
z 5-10% of pts. With neruosyphilis develop neuropathic joint
Other etiologies include:
z Diabetes mellitus (est 1-5% pts with DM)
z Syringomyelia (est. 10-25% pts. with s-myelia)
z Cushing’s synd. or exogenous corticosteroids
Clinical
z Better described as “not as painful as anticipated” than
“painless”.
z Loss of trophic nerve function and desensitization of joint
to pain result in marked joint destruction
Neuropathic Arth.-
Mechanism
Similar mechanism to DJD; fibrillation and destruction
of cartilage, subchondral trabecular thickening,
osteophytosis, joint laxity and fragmentation.
Dispute over whether impaired trophic function of
nerves ("French theory” proposed by Mitchell and
Charcot) was cause or if abnormal mechanical
stresses and subclinical trauma on insensitive joint
("German theory proposed by Volkman and Virchow)
was actual cause of neuro-arthropathy.
Probably some combination of neurovascular change
and trauma is accurate.
Neuropathic Arthropathy
central neuropathy
z syphilis
z syringomyelia

z meningomyelocele

z Charcot-Marie-Tooth synd.

z cong. vascular anom.


Neuropathic Arthropathy
peripheral neuropathy
z diabetes mellitus
z alcoholism
z amyloidosis
z infection
z pernicious anemia
z trauma
z steriods (intra or extra-articualar)
z amyloidosis
z cong. insensitivity to pain
Neuropathic Arthropathy
Hypertrophic type Atrophic type
“D-words” describe x-ray May look like a surgical
findings resection
z Inc. Density
z Sharply demarcated,
z Debris around joint
smooth bone ends
z Destruction of bone
z Dislocation Possibly related to lack
z Disorganization of sympathetic vascular
z (Disaster?) control = hyperemia
Described as “DJD with a
More common in
vengence”
peripheral types
More common in central
types
Neuropathic arthropathy
Syringomyelia may cause neuropathic arthropathy
of the upper extremities
Neuropathic arthropathy
Paraplegic patient
Dense sclerotic
changes of the hips
and also in the lumbar
spine
Prominent heterotopic
bone formation at the
hips
Neuropathic arthropathy
Relatively rapid progression may occur
Case below shows 4 month progression
Neuropathic arthropathy
Diabetic patients (as below) are predisposed to
lower extremity neuroarthropathy
Forefoot > midfoot > ankle> knee > spine > upper ext.
Connective Tissue Disorders
Progressive Systemic Sclerosis (PSS)
z aka Systemic Sclerosis (SS) or Scleroderma
Dermatomyositis
Systemic lupus erythematosus (SLE)
Mixed connective tissue disorder
Scleroderma:
DFN: generalized multi-systemic inflammatory
conective tissue disease of unknown etiology.
z Underlying process is autoimmune
z Autoantibodies to nuclear elements and to Type I and IV collagen
Mechanism
z overproduction of collagen by fibroblasts appears to be
cause of the sclerotic changes of skin and viscera.
z Extensive proliferation of vascular intimal tissues and
deposition of extracellular matrix into pericapillary spaces

CLINICAL
z Age: 20-40 yrs. for 2/3 cases; peak in 5th and 6th decade
z Sex: Females>Males 3:1
z (female preponderance for both types)
Scleroderma: Diagnostic Criterion
Major criterion = symmetric thickening,
tightening and induration of skin proximal to
MCP or MTP joints.
Minor criterion
z Sclerodactyly (as above, limited to fingers)
z Pitting scars of fingertips or resorption of distal
soft tissues of fingers due to ischemia
z Bilateral basilar pulmonary fibrosis on chest
radiograph
*If 1 major or two minor criterion are met,
then dx can be made.
Scleroderma: Two clincal types
Diffuse Cutaneous SSc
z more generalized and involves trunk and face as
well as acral changes
z Poorer prognosis

z Tend to have abrupt onset with swollen hands and


legs and rapid progression of skin thickening
z Early and significant incidence of interstitial lung
disease,oliguric renal failure, diffuse GI disease
and myocardial involvement
Scleroderma: Diffuse
These patients have more skin thickening proximally
(trunk and proximal extremities) and greater incidence
of renal, GI pulmonary and cardiovascular
complications
Nailfold capillary dilation and capillary destruction
Absence of anti-centromere antibodies
Frequent antiopoisomerase (anti-Scl-70) antibodies
z high specificity, but low (20-30%) sensitivity
z Presence of anti-bodies do not seem to predict severity of
disease or mortality
anti-RNA polymerase III is an autoantibody with the
highest sensitivity- 45% of diffuse scleroderma
patients were found to have this
Diffuse vs limited forms

DIFFUSE FORM LIMITED FORM


Age <40 at 35% 50%
onset

Female sex 75% 85%


Duration S/S 3.0 8.5
before Dx
Survival >10 55% 75%
yrs
Diffuse vs limited
DIFFUSE FORM LIMITED FORM
Skin thickening 100% 95%
Telangiectasia 30% 80%
Calcinosis 5% 45%
Raynaud’s 80% 60%
Tendon friction rub 65% 5%
Arthralgia/-itis 80% 60%
Jnt. Contracture 85% 45%
Myopathy 20% 10%
Esophageal hypomotility 75% 75%
Renal crisis 15% 1%
Pulmonary fibrosis 35% 35%
Scleroderma: Limited
Usually, cutaneous involvement confined to
face and distal extremities of fingers
Typically a prolonged interval (one or more
decades) before onset of visceral involvement
CREST syndrome is characteristic
z Calcinosis
z Raynaud’s phenomenon

z Esophageal dysmotility

z Sclerodactyly

z Telangiectasia
Scleroderma
Flexion contracture, distal resorption
Lack of normal soft tissue contour
Scleroderma
Flexion contracture, and calcinosis
Diffuse pulmonary fibrosis
Scleroderma
Calcinosis cutis
Scleroderma
Resorption with distal tapering of the clavicles
may occur with PSS
Pigmented Villonodular
Synovitis (PVNS)
Rare, proliferative disorder of ?? etiology
3 forms
z Isolated lesion of tendon sheath = tendon sheath
giant cell
z Solitary intra-articular nodule = localized PVNS

z Diffuse villous and pigmented synovial lesion

Typically monoarticular
Predilicts lower extremity
z Knee affected in 80% cases
PVNS- clinical
20-40 age range
May follow trauma
Pain, warmth and stiffness may occur
z Joint locking may result, especially if a large
pedunculated lesion is present
Lab studies (CBC, ESR, etc) WNL
Arthroscopic findings
z lobulated, yellow pedunculated mass in localized
form
z Diffuse form shows redundant villous or
pedunculated brown-orange masses of synovium
z Hemosiderin deposition causes brownish color
PVNS- x-ray
Soft tissue mass/swelling
z May have generalized increased radiopacity, but
does not calcify
Pressure erosions of bone may occur
z More likely in tightly compartmented joints (eg, hip
rather than knee)