Sushil Paudel, MS Orthopaedics (AIIMS)

TUTH

Types of arthritis


Symptoms of arthritis


Signs of arthritis


Treatment of arthritis

Rheumatoid arthritis (RA)

Osteoarthritis (OA)


Sero-negative arthritis
 Ankylosing spondylitis
 Psoriatic arthritis
 Reactive arthritis
 Enteropathic arthritis


Crystal arthropathies
 stands for :
 A: ALIGNMENT
 B: BONY MINERALIZATION
 C: CARTILAGE SPACE
 D: DISTRIBUTION
 S: SOFT TISSUE
Normal joint structure
NORMAL SUBCHONDRAL BONE DESTRUCTION
 A chronic joint disorder in which there is
progressive softening and disintegration of
articular cartilage accompanied by new
growth of cartilage and bone at the joint
margins (osteophytes) and capsular fibrosis

Primary or idiopathic


Secondary

Infection
 Dysplasia
 Perthes
 SCFE
 Trauma
 AVN

Genetic


Metabolic


Hormonal


Mechanical


Ageing
Disparity between:-

stress applied to articular cartilage

and
strength of articular cartilage
Increased stress (F/A)


Increased load eg BW or activity
Decreased area eg varus knee or dysplastic
hip
Weak cartilage

age

stiff eg ochronosis

soft eg inflammation

abnormal bony support eg AVN
 Joint
space narrowing
 Osteophytosis
 Subchondral cysts
 Subchondral sclerosis
 Femoral neck buttressing
 Tilt deformity ( flattening of head surface

with osteophyte at anteroinferior aspect)

 Superior >medial migration
 Secondary OA due to previous trauma or

inflammatory arthritis
 Erect weight-bearing AP film
 Unicompartmental
 Sharpening of tibial prominence
 Loose bodies
 Varus deformity
 Patellar tooth sign – irregular anterior patellar

surface
OA Affecting Foot
 Vacuum Phenomenon
 Accumulation of Nitrogen
 Degenarative etiology
 Better seen in Extension
 Excludes infective etiology
 In peripheral joints

physiological
SPGR

T1W
SPGR

T2 FATSAT

pain

swelling

stiffness

deformity

instability

loss of function

Analgesia

Oral viscosupplements

Intrarticular steroids

Intrarticular viscosupplements

Altered activity

Walking aids

Physiotherapy

arthroscopy

osteotomy

arthrodesis

excision arthroplasty

replacement arthroplasty
 Bilateral symmetry
 Periarticular soft

tissue swelling
 Uniform joint space loss
 Marginal erosions
 Juxta-articular osteoporosis
 Joint deformity
 Inflammation
◦ Swollen
◦ Stiff
◦ Sore
◦ Warm
 Fatigue
 Potentially Reversible
RA
 Boutonniere deformity :
flexion deformity at PIP jt & hyperextension
at DIP

• Swan neck deformity :

combination of flexion at DIP
and extension at PIP
 RA

B/L KNEE ANKYLOSIS

RA-foot deformity
 Atlantodental interspace > 3.0mm
 Odontoid erosions
 Subluxation
 Pseudo basilar invagination
 Reduced disc space
 Apophyseal joint: erosion, sclerosis, ankylosis
 Sharpened pencil spinous process
ADI > 3.0mm
 Soft tissue swelling
 Rotator cuff rupture
 Head erosions
 Tapered distal clavicle due to

erosions
 Irregular coracoid process

Enlarged Olecranon bursa
 Fat pad sign
 Supinator notch sign: erosion

at proximal ulna
RA-ELBOW
 Uniform bicompartmental joint
space loss
 Patellofemoral joint also

involved
 Soft tissue swelling
 Baker’s cyst
 Subchondral cysts
T1W

T1GRE
◦ Rheumatoid arthritis is a synovial disease
-Osteoarthritis is a disease of the cartilage.
-Volar subluxation never in osteoarthritis

Normal joint
Unicompartmental Bicompartmental
 Most of the disability in RA is a result of the
INITIAL burden of disease
 People get disabled because of:

◦ Inadequate control
◦ Lack of response
◦ Compliance
 GOAL: control the disease early on!
NSAIDS
Steroids
Oral
Intra-articular
DMARDS
Synthetic
Methotrexate
Hydroxychloroquine
Leflunomide
Sulfasalazine
 Monoclonal Antibodies to TNF
◦ Infliximab
◦ Adalimumab
 Soluble Receptor Decoy for TNF
◦ Etanercept
 Receptor Antagonist to IL-1
◦ Anakinra
 Monoclonal Antibody to CD-20
◦ Rituximab
 Cyclo-oxygenase inhibitors

 Do not slow the progression of the disease

 Provide partial relief of pain and stiffness

Disease Modifying Anti-Rheumatic Drugs

 Reduce swelling & inflammation

 Improve pain
 Improve function
 Have been shown to reduce radiographic

progression (erosions)
 Dihydrofolate reductase inhibitor

 ↓ thymidine & purine nucleotide synthesis

 “Gold standard” for DMARD therapy

 7.5 – 30 mg weekly

 Absorption variable
 Elimination mainly renal
 Hepatotoxicity
 Bone marrow suppression
 Dyspepsia, oral ulcers
 Pneumonitis
 Teratogenicity

 Folic acid reduces GI & BM effects

 Monitoring

◦ FBC, ALT, Creatinine

 Sulphapyridine + 5-aminosalicylic acid

 Remove toxic free radicals

 Remission in 3-6 month

 Elimination hepatic

 Dyspepsia, rashes, BM suppression

 Mechanism unknown
◦ Interference with antigen processing ?
◦ Anti- inflammatory and immunomodulatory

• For mild disease

Side effects

 Irreversible Retinal toxicity, corneal deposits

 Ophthalmologic evaluation every 6 months

 Competitive inhibitor of dihydroorotate
dehydrogenase (rate-limiting enzyme in de novo
synthesis of pyrimidines)

 Reduce lymphocyte proliferation

 Oral
 T ½ - 4 – 28 days due to EHC
 Elimination hepatic

 Action in one month

 Avoid pregnancy for 2 years
 Hepatotoxicity

 BM suppression

 Diarrhoea

 rashes
 Triple Therapy
◦ Methotrexate, Sulfasalazine, Hydroxychloroquine

 Double Therapy
◦ Methotrexate & Leflunomide
◦ Methotrexate & Sulfasalazine
◦ Methotrexate & Hydroxychloroquine
• Complex protein molecules

• Created using molecular biology methods

• Produced in prokaryotic or eukaryotic cell cultures

 TNF is a potent inflammatory cytokine

 TNF is produced mainly by macrophages

and monocytes

 TNF is a major contributor to the

inflammatory and destructive changes that
occur in RA

 Blockade of TNF results in a reduction in a

number of other pro-inflammatory
cytokines (IL-1, IL-6, & IL-8)
Strategies for Monoclonal Antibody (Infliximab & Adalimumab)
Reducing
Effects of
TNF
Trans-Membrane
Bound TNF

Macrophage

Soluble TNF
 Infection

◦ Common (Bacterial)
◦ Opportunistic (Tb)
 Demyelinating Disorders
 Malignancy
 Worsening CHF
 Potent anti-inflammatory drugs
 Serious adverse effects with long-term use
 To control the diaseas
 Indications

◦ As a bridge to effective DMARD therapy

◦ Systemic complications (e.g. vasculitis)

 Most common childhood chronic disease
causing disability.

 About 7/100,00 newly diagnosed children with

JIA per year.

 Prevalence about 1/1,000 children = 1,000

children in BC with JIA.

 7 subtypes.

 Disease begins at any time during childhood or

adolescence.
  To be considered JIA, onset must occur before 16 years of
age.
 JIA is heterogeneous: the presentation of the disease and
its natural history vary among individuals and over time.
 The disease is typically classified into categories based on
the symptoms displayed and their severity.
 Systemic arthritis
 Oligoarthritis
 Rheumatoid-factor positive (RF+) polyarthritis
 Rheumatoid-factor negative (RF-) polyarthritis
 Enthesitis-related arthritis
 Psoriatic arthritis
 Undifferentiated

G.ahrq.gov/dmardsjia.cfm.
 Child under 16 years old

 At least one joint with objective signs of arthritis:

› Swelling, or two of the following: pain with movement, warmth of

the joint, restricted movement, or tenderness

 Duration of more than 6 weeks

 Other causes have been excluded (ex. Infections, Lupus and other
connective tissue diseases, malignancies)
 All kids with JIA have fevers.

 All kids with JIA have rashes.

 A child with joint pain (but no arthritis) must have JIA.

 All arthritis is painful.

 If a child has a positive rheumatoid factor, they must have arthritis.

 If x-rays are normal, there is no arthritis.

 Heterogeneous group of diseases characterized by
chronic inflammatory processes involving the synovial
membrane, cartilage, and bone

 The classification of JIA subgroups based on clinical and

laboratory characteristics including the number of affected
joints and the presence of autoimmune markers

 Th1 cell-mediated disorder, driven by a population of T

cells producing inflammatory cytokines and chemokines
 Joint pain, stiffness, and swelling:
These are the most common
symptoms of JRA, but many children
do not recognize, or do not report,
pain. Stiffness and swelling are likely
to be more severe in the morning.
 Loss of joint function: Pain, swelling,
and stiffness may impair joint
function and reduce range of
motion. Some children are able to
compensate in other ways and
display little, if any, disability.
Severe limitations in motion lead to
weakness and decreased physical
function and sometimes to
invalidization.
 Limp: A limp may
indicate a particularly
severe case of JRA,
although it also may
be due to other
problems that have
nothing to do with
arthritis, such as an
injury. In JRA, a limp
often signals knee
involvement.
 Eye irritation, pain, and
redness: These symptoms are
signs of eye inflammation. The
eyes may be sensitive to light.
In many cases, however, eye
inflammation has no
symptoms. If the inflammation
is very severe and not reversed,
it can cause loss of vision. The
most common types of eye
inflammation in JRA are uveitis
and iritis. The names refer to
the part of the eye that is
inflamed.
 Recurrent fevers: Fever is
high and comes and
goes with no apparent
cause. Fever may “spike”
(go high) as often as
several times in one day.

 Rash: A light rash may

come and go without
explanation.
 Myalgia (muscle
aches): This is similar
to that achy feeling
that comes with the
flu. It usually affects
muscles throughout
the whole body, not
just one part.
 Lymph node swelling. Swollen lymph nodes are
noticed most often in the neck and under the
jaw, above the clavicle, in the armpits, or in the
inguinal region.
 Weight loss. This is common in children with
JRA. It may be due to the child’s simply not
feeling like eating.
 Growth problems:
Children with JRA often
grow more slowly than
average. Growth may be
unusually fast or slow in
an affected joint, causing
one arm or leg to be
longer than the other.
General growth
abnormalities may be
related to having a chronic
inflammatory condition
such as JRA or to the
treatment, especially
glucocorticoids
 ANA (antinuclear antibody)
 RF (Rheumatoid factor )
 CRP (C-reactive protein)
 ESR (erythrocyte sedimentation rate)
 CCP (Cyclic Citrullinated Peptide

Antibody) test
 The goals: eliminate active disease, normalize
joint function, preserve normal growth,
prevent long-term joint damage, and prevent
patient disability
 The American College of Rheumatology

Pediatric 30 criteria (ACR Pedi 30) defines

improvement as involving at least 3 of 6 core
set variables, with no more than 1 of the
remaining variables worsening by > 30%.
 The 6 core set includes
◦ Physician global assessment

◦ active joint count

◦ number of joints with limited range of motion

◦ Inflammatory markers

◦ patient or parent assessments

 Medications Doses Side effects
(mg/kg)
Aspirin 50-120 Stomack pain, vomiting,
gastrointestinal
Ibuprofen 10-30 bleedings, headache,
blood in the urine, fluid
retention, thinning and
Tolmentin 10-15
scarring of the skin
(especially with
Naproxen 5-20 naproxen), stomach
ulcer (aspirin).
 Medications Doses Side effects
(mg/kg)
Hydroxychlo- 5-7 Upset stomach, skin
roquine rash and a eye
(Plaquenil) damage. A child who
takes this drug should
Sulfasalazine have his/her eyes
(Azulfadine) examined at least
every six months by
an ophthalmologist
 Medications Doses(weekly, Side effects
depending from
body weight )
Auranofin, 20 kg – 10 mg Skin rash,
Ridaura, 30 kg – 20 mg mouth sores,
Myochrysine 40 kg – 30 mg kidney
Solganol problems, a low
50 kg – 40 mg blood count or
> 50 kg – 50 mg anemia
 Medications Doses Side effects

Methotrexate Typically 7.5 to Loss of appetite,

(Rbeumatrex) 25 mg a week nausea or
vomiting, skin
Azathioprine rash, unusual
(Imuran) bleeding or
Cyclophospha bruising,
mide tiredness or
(Cytoxan) weakness,
sterility.
 Biologic Agents, which blocks the protein
TNF
Etanercept (Enbrel)
Infliximab (Remicade)
 Glucocorticoid Drugs (Dexamethasone,
Methylprednisolone, Cortef, Prednisolone
and Prednisone)
 Analgesics (acetaminophen [Tylenol,
Panadol], tramadol [Ultram])
 Therapeutic exercises
 Sports and Recreational Activities
 Splints
 Morning Stiffness Relief
 Diet
 Eye Care
 Dental Care
 Surgery
.
 Identify diagnostic criteria for gout

 Identify 3 treatment goals for gout

 Name the agents used to treat the acute

flares of gout and the chronic disease of gout
 Prevalence increasing
 May be signal for
unrecognized
comorbidities : ( Not to
point of searching)

Obesity (Duh!)
Metabolic syndrome
DM
HTN
CV disease
Renal disease
 Rich foods have a higher
concentration of protein. This could
cause major problems for a person
afflicted with gout.

 ORGAN MEATS
 WILD GAME
 SEAFOOD
 LENTILS
 PEAS
 ASPARAGUS
 YEAST
 BEER
 Urate: end product of purine metabolism

 Hyperuricemia: serum urate > urate

solubility (> 6.8 mg/dl)

 Gout: deposition of monosodium urate

crystals in tissues
 Hyperuricemia caused by
Overproduction
Underexcretion

 No Gout w/o crystal deposition

 Urate
 Oevrproduction Underexcretion

 Hyperuricemia

 ________________________________________

 Silent Gout Renal Associated

 Tissue manifestations CV events &
 Deposition mortality
 Purines are not
properly processed
in our body
 Excreted through

kidneys and urine

 Hyperuricemia-

build-up of uric
acid in body and
joint fluid
 Asymptomatic hyperuricemia

 Acute Flares of crystallization

 Intervals between flares

 Advanced Gout & Complications

 Abrupt onset of severe joint inflammation,
often nocturnal;
Warmth, swelling, erythema, & pain;
Possibly fever
 Untreated? Resolves in 3-10 days
 90% 1st attacks are monoarticular
 50% are podagra
 90% of gout
patients
eventually have
podagra : 1st MTP
joint
 Can occur in
other joints,
bursa & tendons
 Asymptomatic

 If untreated, may advance

 Intervals may shorten

 Crystals in asx joints
 Body urate stores increase
 Chronic Arthritis

 X-ray Changes

 Tophi Develop

 Acute Flares continue

 Chronic Arthritis
 Polyarticular

acute flares with

upper extremities
more involved
 Solid urate
deposits in
tissues
 Irregular &
destructive
 Long duration of hyperuricemia

 Higher serum urate

 Long periods of active, untreated gout

 Hx & P.E.

 Synovial fluid analysis

 Not Serum Urate

 Not reliable

 May be normal with flares

 May be high with joint Sx from other causes

 Male
 Postmenopausal

female
 Older
 Hypertension
 Pharmaceuticals:

Diuretics, ASA,
cyclosporine
 Transplant
 Alcohol intake

Highest with beer

Not increased with wine
 High BMI (obesity)
 Diet high in meat & seafood
 The Gold standard

 Crystals intracellular during attacks

 Needle & rod shapes

 Strong negative birefringence

 Acute Gout: septic arthritis, pseudogout,
Reactive arthritis, acute rheumatic fever and
other crystalline arthropathies.
 Chronic tophaceus gout: Rheumatoid

Arthritis, Pseudogout, seronegative

spondyloarthropathies and erosive
osteoarthritis.
 Similar Acute attacks

 Different crystals under Micro;

Rhomboid, irregular in CPPD
 Both have polyarticular, symmetric arthritis

 Tophi can be mistaken for RA nodules

 Diet is usually impractical, ineffective and
rarely adhered to in clinical practice.
 Indications for pharmacological therapy

includes: inability to reverse secondary

causes, tophaceus gout, recurrent acute gout
and nephrolithiasis.
 INITIATE •Treat acute flare rapidly with
(acute flare) anti-inflammatory agent

•Initiate urate-lowering therapy to

RESOLVE achieve sUA <6
•Use concomitant anti-inflammatory
(urate-lowering therapy) prophylaxis for up to 6 mo to prevent
mobilization flares

•Continue urate lowering therapy

MAINTAIN to control flares and avoid crystal
(treatment to control sUA) deposition
•Prophylaxis use for at least 3-6
months until sUA normalizes 139

139
 Rapidly end acute flares
Protect against future flares
Reduce chance of crystal inflammation

 Prevent disease progression

Lower serum urate to deplete total body urate pool
Correct metabolic cause
 Control inflammation & pain & resolve the
flare
 Not a cure
 Crystals remain in joints
 Don’t try to lower serum urate during a flare
 Choice of med not as critical as alacrity &
duration
 NSAIDS

 Colchicine

 Corticosteroids
Colchicine- reduces pain, swelling, and
inflammation; pain subsides within 12 hrs
and relief occurs after 48 hrs

Prevent migration of neutrophils to joints

Side effects

 Nausea
 Vomiting
 Diarrhea
 Rahes
 Colchicine :
Not as effective “late” in flare
Drug interaction : Statins, Macrolides,
Cyclosporine
Contraindicated in dialysis pt.s
Cautious use in : renal or liver dysfunction;
active infection, age > 70
  The choice of pharmacologic agent depends on severity of
the attack
◦ Monotherapy for mild/moderate attack
◦ Combination therapy for severe attack or those refractory
to monotherapy
 Acceptable combination therapy approaches include
◦ Colchicine and NSAIDS
◦ Oral steroids and colchicine
◦ Intra-articular steroids with all other modalities
 Continue current therapy during flare
 Patient education on signs of flare for self treatment

Kanna
146 D, et al. Arthritis Care Res (Hoboken). 2012 Oct;64(10):1447-61
 Rapidly end acute flares
Protect against future flares
Reduce chance of crystal inflammation
 Prevent disease progression
Lower serum urate to deplete total body
urate pool
Correct metabolic cause
 Hyperuricemia ≠ Gout
 Goal sUA < 6
 Use prophylaxis for at least 3 months after

initiating gout therapy

 Do not stop gout medication unless patient is

showing evidence of drug toxicity or adverse

reaction
 Ask your friendly rheumatologist for help!

14
8
 Colchicine : 0.5-1.0 mg/day
 Low-dose NSAIDS

 Both decrease freq & severity of flares

 Prevent flares with start of urate-lowering RX
Best with 6 mos of concommitant RX

 Won’t stop destructive aspects of gout

 Rapidly end acute flares
Protect against future flares
Reduce chance of crystal inflammation
 Prevent disease progression
Lower serum urate to deplete total body
urate pool
Correct metabolic cause
 Lower urate to < 6 mg/dl : Depletes
Total body urate pool
Deposited crystals

 RX is lifelong & continuous

 MED choices :

Uricosuric agents
Xanthine oxidase inhibitor
 Probenecid, (Losartan & fenofibrate for mild
disease)

 Increased secretion of urate into urine

 Reverses most common physiologic

abnormality in gout ( 90% pt.s are
underexcretors)
 Patients taking uricosuric agents are at risk
for urolithiasis. This can be decreased by
ensuring high urinary output and by adding
sodium bicarbonate 1 gram TID.
 The available agents include: probenecid (1-2

g/day) and sulfinpyrazone (50-400 mg BID).

 Dose should be increased to decrease uric

acid < 6.0 mg/ml

 Allopurinol :
 Blocks conversion of hypoxanthine to uric

acid
 Effective in overproducers
 May be effective in underexcretors
 Can work in pt.s with renal insufficiency
 XO XO
hypoxanthine xanthine urate

XO=xanthine oxidase

Allopurinol and febuxostat inhibit

xanthine oxidase and block uric acid
formation
158

Markel A. IMAJ, 2005.

15
8
 Allopurinol
Hypersensitivity
Syndrome
Xanthine
Oxidase Toxic Epidermal
allopurinol oxypurinol
Necrolysis

Stevens-
Johnson
Syndrome

 Oxypurinol, allopurinol metabolite, cleared by

kidney and accumulates in patients with renal
failure
 Oxypurinol inhibits xanthine oxidase
 Increased oxypurinol related to risk of allopurinol
hypersensitivity syndrome

15
9
 Allopurinol decreases uric acid in
overproducers and underexcreters; it is also
indicated in patients with a history of
urolithiasis, tophaceus gout, renal
insufficiency and in prophylaxis of tumor
lysis syndrome.
 Allopurinol: usual dose is 300 mg/day.
Maximal recommended dose is 800 mg/day.
 In renal insufficiency dose should be

decreased to 200 mg/day for creatinine

clearance < 60ml/min and to 100 mg/day if
clearance < 30 ml/min).
 Start with small doses of allopurinol to reduce
the risk of precipitating an acute gout attack.
 Most common side effects are rash (2% of

patients) but rarely patients can develop

exfoliative dermatitis that can be lethal.
 Chronic use of colchicine (0.6-1.2 mg/day) is

used as prophylaxis for acute attacks.

  2% of all allopurinol users develop cutaneous rash
 Frequency of hypersensitivity 1 in 260
 DRESS syndrome
◦ Drug Reaction, Eosinophilia, Systemic Symptoms
 20% mortality rate
 Life threatening toxicity: vasculitis, rash,
eosinophilia, hepatitis, progressive renal failure
 Treatment: early recognition, withdrawal of drug,
supportive care
◦ Steroids, N-acetyl-cysteine, dialysis prn

Markel A. IMAJ, 2005.

Terkeltaub RA, in Primer on the Rheumatic Disease , 13th ed. 2008.
16
3
 Base choice on above considerations &
whether pt is an overproducer or
underexcretor : Need to get a 24-hr. urine for
urate excretion:
< 700 --- underexcretor
(uricosuric)
> 700 --- overproducer
(allopurinol/ febuxostat)
 Allopurinol Uricosuric
Issue in renal disease X X
Drug interactions X X
Potentially fatal hypersen-
sitivity syndrome X
Risk of nephrolithiasis X
Mutiple daily dosing X
 RX gaps :
 Can’t always get urate < 6
 Allergies
 Drug interactions
 Allopurinol intolerance
 Worse Renal disease
 Non-purine selective inhibitor of xanthine oxidase
 Lowers serum uric acid levels more potently than allopurinol while having
minimal effects on other enzymes associated with purine and pyrimide
metabolism
 Frequent adverse events reported in clinical trials liver function abnormalities,
nausea, arthralgias, and rash
 Available as 40- and 80-mg tablets
 Recommended starting dosage is 40 mg orally once daily. If serum uric acid
concentrations are not less than 6 mg/dL after two weeks, the dosage can be
increased to 80 mg orally once daily
 Dosage adjustments are not needed in elderly patients or patients with mild or
moderate renal or hepatic impairment.

.
  Therapeutic goal of urate-lowering therapy
is sUA <6.0 mg/dL
 Urate lowering therapy indications:

◦ Recurrent gout attacks

◦ Tophi and/or radiographic changes on initial
presentation
 Address associated risk factors and
comorbidities – tailor to the individual
168

Zhang W, et al. Ann Rheum Dis. 2006; 65: 1312-1324.

168
  Lifestyle Modification for all patients with gout

 Xanthine Oxidase Inhibitor (XOI) first-line urate-

lowering pharmacologic therapy

 Target sUA <6 at minimum, sUA <5 better

 Starting dose of allopurinol should be 100mg, less in

CKD with titration above 300mg prn if needed (even in
CKD)

 Continue prophylaxis for 3 (no tophi) – 6 months (tophi)

after achieving target sUA

Khanna
169 D, et al. Arthritis Care Res . 2012 Oct;64(10):1431-46
 Gout is chronic with 4 stages
 Uncontrolled gout can lead to severe

disease
 Separate RX for flares & preventing

advancement
 Many meds for flares
 Treating the disease requires lowering urate
 Get a 24-hr urine for urate excretion
 Calcium pyrophosphate Crystal Deposition
Disease (CPPD) is the syndrome secondary to
the calcium pyrophosphate in articular
tissues.
 This includes: Chondrocalcinosis, Chronic

CPPD and Pseudogout.

 Etiology: It is unknown, but can be secondary
to changes in the cartilage matrix or
secondary to elevated levels of calcium or
inorganic pyrophosphate.
 Pathology: CPPD crystals are found in the

joint capsule and fibrocartilaginous

structures. There is neutrophil infiltration
and erosions.
 Demographics: It is predominantly a disease
of the elderly, peak age 65 to 75 years old. It
has female predominance (F:M, 2-7:1).
 Prevalence of chondrocalcinosis is 5 to 8% in

the general population.

 Disease Associations: hyperthyroidsm,
hypocalciuria, hypercalcemia,
hemochromatosis, hemosiderosis,
hypophosphatasia, hypomagnesemia,
hypothyroidsm, gout, neuropathic joints,
amyloidosis, trauma and OA.
 Clinical Manifestations
 Pseudogout: Usually presents with acute

self-limited attacks resembling acute gout.

The knee is involved in 50% of the cases,
followed by the wrist, shoulder, ankle, and
elbow.
 In 5% of patients gout can coexist with
pseudogout.
 The diagnosis is confirmed with the synovial

fluid analysis and/or the presence of

chondrocalcinosis in the radiographs.
 Acute Pseudogout primarily affects men.
 Chondrocalcinosis: Generally is an incidental
finding in XRays.
 Diagnostic Tests: Inflammatory cell count in

the synovial fluid. Rhomboidal or rodlike

intracellular crystals. Imaging studies reveal
chondrocalcinosis usually in the knee, but
can be seen in the radial joint, symphisis
pubis and intervertebral discs.
 Chronic CPPD: predominately affects women;
it is a progressive, often symmetric,
polyarthritis.
 Usually affects the knees, wrists, 2nd and 3rd

MCP’s, hips, spine, shoulders, elbows and

ankles.
 Chronic CPPD differs from pseudogout in its

chronicity, involvement of the spine and

MCP’s.
 Differential Diagnosis: Includes septic
arthritis, gout, inflammatory OA, Rheumatoid
Arthritis, neuropathic arthritis and Hypertrofic
Osteoarthropathy.
 Therapy: It is similar to gout and includes
intrarticular corticosteroids. Colchicine can
be used in acute attacks and also in
prophylaxis. There is no specific treatment
for chronic CPPD. It is important to treat
secondary causes and colchicine could be
helpful.
 HLA B-27
 Enthesitis
 Synovitis
 Osteitis
 Spondyloarthropathies
Axial and Peripheral
AMOR criteria (1990)
ESSG criteria (1991)

Axial Spondyloarthritis Peripheral Spondyloarthritis

ASAS classification 2009 ASAS classification 2010

Ankylosing spondylitis
Prototype of axial spondylitidis Infliximab (IFX) and Golimumab (GLM)
Modified New York criteria 1984 indications

Psoriatic arthritis
From Moll & Wright 1973 to CASPAR criteria 2006

ESSG: European Spondyloarthropathy Study Group Sieper et al. Ann Rheum Dis 2009;68:ii1-ii44
ASAS: Assessment of Spondyloarthritis International Taylor et al. Arthritis & Rheum 2006;54:2665-73
Society Van der Heijde et al. Ann Rheum Dis 2011;70:905-8
 AS is a chronic, progressive immune-mediated
inflammatory disorder that results in ankylosis of
the vertebral column and sacroiliac joints 1
 The spine and sacroiliac joints are the common
affected sites1
◦ Chronic spinal inflammation (spondylitis) can lead
to fusion of vertebrae (ankylosis) 1

1
Taurog JD. et al. Harrison‘s Principles of Internal Medicine, 13 th Ed. 1994: 1664-67.
 SACROILITIS
Normal interspace 2-5mm

B/L symmetric
Lower two third
Rosary bead appearance
Reactive sclerosis
Bony ankylosis
osteoporosis
 SPINE
 Romanus lesion(erosion)
 Squaring, Osteoporosis
 Shiny corner sign
 Marginal Syndesmophytes
 Bamboo spine
 Trolley-track sign
 Dagger sign
  “•Rare”
0.1-0.9% 1,2

 “Not” a serious disease, functional

limitation is mild
• Burden of disease significant in pain, sick leave, early retirement3,4,5

 “Rarely shortens life”

• Mortality figures parallel RA6,7,8

1
Sieper J et al. Ann Rheum Dis. 2002; 61 (suppl 3);iii8-18.
2
Lawrence RC., Arthritis Rheum 1998; 41:778-99. 6
Wolfe F., et al. Arthritis Rheum. 1994 Apr;37(4):481-94.
3
Zink A., et al., J Rheumatol 2000; 27:613-22. 7
Myllykangas-Luosujarvi R, et al. Br J Rheumatol. 1998;37:688-690.
4
Boonen A. Clin Exp Rheumatol.
Rheumatol. 2002;20(suppl 28):S23-S26.
8
Khan MA, et al. J Rheumatol. 1981;8:86-90.
5
Gran JT, et al. Br J Rheumatol.
Rheumatol. 1997;36:766-771.
9
Braun J., Pincus T., Clin Exp Rheumatol. 2002; 20(6 Suppl 28):S16-22.
  The incidence of AS may be
underestimated due to unreported cases1
 HLA-B27 gene is associated with AS6
 Age of onset typically between 15 and 35

years1,2,3
 2-3 times more frequent in men than in

women6

1
The Spondylitis Association of America. Available at: www.spondylitis.org. Accessed December
2,2004. 61(suppl 3);iii8–18. 6Khan MA. Ann Intern Med. 2002;136:896–907.
 Axial manifestations:
• Chronic low back pain
• With or without buttock pain
• Inflammatory characteristics:
MRI sacro-iliac joint
– Occurs at night (second part)
– Sleep disturbance
– Morning stiffness
• Limited lumbar motion
Inflammatory back • Onset before age of 40 years
pain (IBP) =
Characteristic symptom

Sengupta R & Stone MA.

AS: Characteristic Pathologic Features
• Chronic inflammation in:
– Axial structures (sacroiliac joint, spine, anterior chest
wall, shoulder and hip)
– Possibly large peripheral joints, mainly at the lower limbs
(oligoarthritis)
– Entheses (enthesitis)

• Bone formation particularly in the axial joints

Sieper J. Arthritis Res Ther 2009;11:208

Elewaut D & Matucci MC. Rheumatology 2009;48:1029-1035
 Most striking feature of AS = New
bone formation in the spine with:
Spinal syndesmophytes
Ankylosis

Both can be seen on conventional

X-ray showing radiography
syndesmophytes

Even in patients with longer-

standing disease, syndesmophytes Bamboo spine and
are present in ～ 50% patients and bilateral sacroiliitis
a smaller percentage will develop
ankylosis

Sieper J. Arthritis Res Ther 2009;11:208

Marginal erosions and new bone formation
Unilateral sacroiliitis
Peripheral manifestations

Enthesitis Peripheral arthritis Dactylitis

1
Cruyssen BV et al. Ann Rheum Dis 2007;66:1072-1077
2
Sidiropoulos PI et al. Rheumatology 2008;47:355-361
Likelihood of erosions is higher The first abnormality to appear in swollen
for digits with dactylitis than joints associated with
those without1 spondyloarthropathies is an enthesitis2

1
Brockbank. Ann Rheum Dis 2005;62:188-90;
2
McGonagle et al. The Lancet 1998;352.
 EAM Prevalence in AS
Patients (%)
Anterior uveitis 30-50
IBD 5-10
Anterior uveitis Subclinical inflammation of the gut 25-49
Cardiac abnormalities
Conduction disturbances 1-33
Aortic insufficiency 1-10
Psoriasis 10-20 Terminal ileitis
Renal abnormalities 10-35
Lung abnormalities 40-88
Airways disease 82
Interstitial abnormalities 47-65
Cardiac Emphysema 9-35
abnormalities
Bone abnormalities
Osteoporosis 11-18
Osteopenia 39-59
Elewaut D & Matucci MC. Rheumatology 2009;48:1029-1035
 Bad QoL1 ASAS=23.7
mean duration:
years 23.7 yr
1

Percentage of Patients (%)

100
◦ Pain 90.2
83.1
◦ Sleep problems 80
◦ Fatigue 62.4
60 54.1
◦ Loss of mobility and
dependency 40
◦ Loss of social life
20
 Effectemployability 1

 Higher rate of 0
Stiffness Pain Fatigue Poor
mortality2 N=175 Sleep

High socio-economic consequences

 100
First symptoms
Percentage of Patients (%)

80 First diagnosis

60
Average delay in diagnosis: 8.8
years
40 B27(+) 8.5 vs B27(-) 11.4

20 Males (n=920)
Females (n=476)

0
0 10 20 30 40 50 60 70 Age in years
Delay  Worse clinical outcomes contributing to both physical and
work-related disability
Adapted from Feldtkeller E et al. Rheumatol Int 2003;23:61–66
Sengupta R & Stone MA. Nat Clin Pract Rheumatol 2007;3:496-503
 Modified New York Criteria for AS1
◦ Low back pain > 3 months (improved by exercise and not relieved
by rest)
◦ Limitation of lumbar spinal motion in sagittal and frontal planes
◦ Chest expansion decreased relative to normal
◦ Bilateral sacroilitis grade 2-4 or unilateral sacroilitis grade 3 or 4
 Detection of sacroilitis via X-ray or MRI1
◦ MRI can be used for earlier detection of inflammation (enthesitis) at
other sites.
 There is no specific laboratory test for AS1
◦ ESR and CRP can indicate inflammation
 50-70% of active AS patients will have increased ESR and CRP2
◦ Rheumatoid factor is not associated with AS
◦ HLA-B27

1
Khan M, Ankylosing Spondylitis-the facts; 2002:Oxford University Press:94-98.
2
Sieper J, et al. Ann Rheum Dis. 2002;61(Suppl 8).
Diagnostic Standard for AS: Modified NY
Classification Criteria (1984)1
• Clinical components:
– Low back pain and stiffness for more than 3 months which
improves with exercise, but is not relieved by rest
• Old criteria
– Limitation of motion of the lumbar spine in both the sagittal
• Defined before TNF blockers
and frontal planes
• Sacroiliitis detectable by X-ray occurs
– lately expansion relative to normal values
Limitation of chest
correlated for• age and sex resonance imaging (MRI)
No magnetic
• • Used for clinical trial
Radiological component:
– Sacroiliitis Grade >2 bilaterally or Grade 3-4 unilaterally

Definite AS if the radiological criterion is associated with at least one clinical

criterion2
Probable AS if three clinical criteria present or radiologic criteria present
without clinical criteria2 1
Linden VD et al. Arthritis Rheum 1984;27:361-368
2
Rudwaleit M et al. Arthritis Rheum 2005;52:1000-1008
Diagnostic Standard for AS: Modified NY
Classification Criteria (1984) (Cont’d)
Radiographic stage
(Ankylosing Spondylitis)

Back Pain
Radiographic
Back Pain
Syndesmophytes
sacroiliitis

Modified NY criteria (1984)

Time (years)

The greatest problem in the management of AS was the lack of effective

treatments. In recent years, NSAIDs and TNF-blockers have been shown to
have good efficacy in the treatment of AS.

Adapted from Rudwaleit M et al. Arthritis Rheum 2005;52:1000-1008

Brandt HC et al. Ann Rheum Dis 2007;66:1479-84
Diagnostic Standard for AS: Modified NY
Classification Criteria (1984) (Cont’d)
Pre-radiographic stage Radiographic stage
(Axial undifferentiated SpA) (Ankylosing Spondylitis)

Back Pain Back Pain

Radiographic
Back Pain
IBP
Syndesmophytes
MRI active sacroiliitis sacroiliitis

Modified NY criteria (1984)

Time (years)
• Recent application of MRI techniques has demonstrated (and confirmed) that ongoing
active (“acute”) inflammation in fact does occur in the sacroiliac joints and/or spine
prior to the appearance of changes detectable radiographically
• The presence and absence of radiographic sacroiliitis in patients with SpA represent
different stages of a single disease continuum
Adapted from Rudwaleit M et al. Arthritis Rheum 2005;52:1000-1008
In patients with back pain ≥3 months and age at onset <45 years
Sacroiliitis* on imaging HLA-B27
plus OR plus
≥1SpA feature** ≥2 other SpA features**
*Sacroiliitis on imaging: **SpA features:
•Inflammatory back pain
•Active (acute) inflammation on
•Arthritis
MRI highly suggestive of •Enthesitis (heel)
sacroiliitis associated with SpA •Uveitis
or •Dactylitis
•Psoriasis
•Definite radiographic sacroiliitis •Crohn’s disease/ulcerative colitis
according to modified New York •Good response to NSAIDs
criteria •Family history for SpA
•HLA-B27
•Elevated CRP
Rudwaleit M et al. Ann Rheum Dis 2009;68(6):770-6
 Patients will be categorized as an ASAS 20 responder if the
patient achieves the following:
◦ >20% improvement from baseline and absolute baseline
improvement of >10 (on a 0-100mm scale) in at least 3 of the
following 4 domains:
 Patient global assessment
 Spinal pain
 Function (BASFI)
 Inflammation
 Average of the last 2 BASDAI questions concerning level
and duration of morning stiffness
◦ No deterioration from baseline (>20% and absolute change of
at least 10 on a 0-100 mm scale) in the potential remaining
domain

Anderson JJ, et al. Arthritis Rheum. 2001;44(8):1876–1886.

 Chronic progressive, inflammatory disorder of the joints and
skin1
◦ Characterized by osteolysis and bony proliferation1
◦ Clinical manifestations include dactylitis, enthesitis,
osteoperiostitis, large joint oligoarthritis, arthritis
mutilans, sacroiliitis, spondylitis, and distal
interphalangeal arthritis1
 PsA is one of a group of disorders known as the
spondyloarthropathies2
 Males and females are equally affected3
 PsA can range from mild nondestructive disease to a severely
rapid and destructive arthropathy3
◦ Usually Rheumatoid Factor negative3
 Radiographic damage can be noted in up to 47% of patients
at a median interval of two years despite clinical
improvement with standard DMARD therapy 4
Taylor WJ. Curr Opin Rheumatol. 2002;14:98–103.
1

Mease P. Curr Opin Rheumatol. 2004;16:366–370.

2

Brockbank J, et al. Exp Opin Invest Drugs. 2000;9:1511–1522.

3

4
Kane D, et al. Rheumatology. 2003;42:1460–1468.
 Spondyloarthritis (SpA)
 The prevalence of SpA is comparable to that of RA (0.5–1.9%) 1,2
Undifferentiated
Psoriasis (Pso) SpA (uSpA)
 Psoriasis affects 2% of population
Juvenile SpA PsA
 7% to 42% of patients with Pso will develop arthritis 3 Ankylosing
spondylitis (AS)
Arthritis
Psoriatic Arthritis associated with Reactive
 A chronic and inflammatory arthritis in association with skinIBD psoriasis 4 arthritis
 Usually rheumatoid factor (RF) negative and ACPA negative 5

◦ Distinct from RA
 Psoriatic Arthritis is classified as one of the subtypes of spondyloarthropathies

◦ Characterized by synovitis, enthesitis, dactylitis, spondylitis, skin and nail

psoriasis4

Rudwaleit M et al. Ann Rheum Dis 2004;63:535-543; 2Braun J et al. Scand J Rheumatol 2005;34:178-90;
1
3
Fitzgerald “Psoriatic Arthritis” in Kelley’s Textbook of Rheumatology, 2009;
4
Mease et al. Ann Rheum Dis 2011;70(Suppl 1):i77–i84. doi:10.1136/ard.2010.140582;
RA: Rheumatoid arthritis 5
Pasquetti et al. Rheumatology 2009;48:315–325
 Affects men & women equally
 Occurs in 4-6% up to 30% of patients with

known psoriasis
◦ 60 – 70%: Skin psoriasis first
◦ 15%: Psoriatic arthritis first
◦ 15%: Skin and arthritis diagnosed at same time
 Epidemiological Evidence
 Prevalence of psoriasis in the general
population: 0.1-2.8%.
 Prevalence of psoriasis in arthritis
patients: 2.6-7.0%.
 Prevalence of arthritis in the general
population: 2-3%.
 Prevalence of arthritis in psoriatic patients:
6-42%.
 Morning stiffness lasting >30 min in 50% of patients 1
 Ridging, pitting of nails, onycholysis – up 90% of
patients vs nail changes in only 40% of psoriasis cases 2,3
 Patients may present with less joint tenderness than is
usually seen in RA1
 Dactylitis may be noted in >40% of patients 2,4
 Eye inflammation (conjunctivitis, iritis, or uveitis) — 7–
33% of cases; uveitis shows a greater tendency to be
bilateral and chronic when compared to AS 2
 Distal extremity swelling with pitting edema has been
reported in 20% of patients as the first isolated
manifestation of PsA5
1
Gladman DD. In: Up To Date. Available at: www.uptodate.com. Accessed December 3, 2004.
2
Taurog JD. In: Harrison's Online McGrawHill. Available at: http://www3.accessmedicine.com/popup.aspx?
aID=94996&print=yes. Accessed January 2,2005.
3
Gladman DD. Rheum Dis Clin N Amer. 1998;24:829–844.
4
Veale D, et al. Br J Rheumatol. 1994;33:133–38.
5
Cantini F, et al. Clin Exp Rheumatol. 2001;19:291–296.
*Low levels of RF and ACPA can be found in 5-16% of patients; **To a lesser degree than in RA
***Spinal disease occurs in 40-70% of PsA patients
Helliwell PS & Taylor WJ. Ann Rheum Dis 2005;64(2:ii)3-8
Fitzgerald “Psoriatic Arthritis” in Kelley’s Textbook of Rheumatology, 2009

DIP involvement (39%)2
Nail psoriasis (80%)4, 5
Enthesopathy (38%)2
DIP: Distal interphalangeal
Back involvement (50%)1
Skin Involvement
In nearly 70% of patients,
cutaneous lesions precede
the onset of joint pain, in
20% arthropathy starts
before skin manifestations,
and in 10% both are
concurrent. 6
Dactyilitis (48%)3
1
Gladman D et al. Arth & Rheum 2007;56:840; 2 Kane. D et al. Rheum 2003;42:1460-1468
3
Gladman D et al. Ann Rheum Dis 2005;64:188–190; 4Lawry M. Dermatol Ther 2007;20:60-67
5
Jiaravuthisan MM et al. JAAD 2007;57:1-27; 6Yamamoto Eur J Dermatol 2011;21:660-6
 Ocular inflammation1 Pso patients6-8
(Iritis/Uveitis/ Episcleritis) • Psychosocial burden
• Reactive depression
• Higher suicidal ideation
• Alcoholism

IBD2 
Metabolic Syndrome3-5
• Hyperlipidemia
• Hypertension
• Insulin resistent
• Diabetes
• Obesity
 Higher risk of
Cardiovascular disease (CVD)

Qieiro et al. Semin Arth Rheum 2002;31:264; 2Scarpa et al. J Rheum 2000;27:1241; 3Mallbris et al. Curr Rheum Rep 2006;8:355;
1

4
Neimann et al. J Am Acad Derm 2006;55:829; 5Tam et al. 2008;47:718; 6Kimball et al. Am J Clin Dermatol 2005;6:383-392;
7
Naldi et al. Br J Dermatol 1992;127:212-217; 8Mrowietz U et al. Arch Dermatol Res 2006;298(7):309-319
 P s o r i a t i c A r t h r i t is

D a c t y lit is E n t h e s i t is

Ritchlin C. J Rheumatol. 2006;33:1435–1438.

Helliwell PS. J Rheumatol. 2006;33:1439–1441.
• Diffuse swelling of a digit may be acute, with painful
inflammatory changes, or chronic wherein the digit remains
swollen despite the disappearance of acute inflammation1
• Also referred to as
“sausage digit”1
• Recognized as one
of the cardinal
features of PsA,
occurring in up
to 40% of patients1,2
• Feet most commonly
affected1
• Dactylitis involved
digits show more ACR Slide Collection on the Rheumatic Diseases; 3 rd edition. 1994.
radiographic damage1 1
Brockbank J, et al. Ann Rheum Dis. 2005;64:188–190.
2
Veale D, et al. Br J Rheumatol. 1994;33:133–38.
 Entheses are the regions at
which a tendon, ligament, or
joint capsule attaches to
bone1
 Inflammation at the entheses
is called enthesitis and is a
hallmark feature of PsA1,2
 Pathogenesis of enthesitis
has yet to be fully
elucidated2
 Isolated peripheral enthesitis
may be the only
rheumatologic sign of PsA in
a subset of patients3

McGonagle D. Ann Rheum Dis. 2005;64(Suppl II):ii58–ii60.

1

2
Anandarajah AP, et al. Curr Opin Rheumatol. 2004;16:338–343.
3
Salvarani C. J Rheumatol. 1997;24:1106–1140.
Achilles Tendon Spur Achilles Tendon Insertion Erosion
Plantar Spur
ACR Slide Collection on the Rheumatic Diseases; 3 rd edition. 1994.
Data on file, Centocor, Inc.


Oligoarthritis Distal Arthritis

Polyarticular Pattern
Arthritis Mutilans

 Periostitis

Tuft resorption
 Distal asymmetric distribution
 Ray pattern
 Soft tissue swelling( sausage/spindle)
 Preserved bone density
 Marginal erosions
 Fluffy periosteitis
 Pencil in cup deformity
 Mouse ear sign
 Arthritis mutilans
 Nonmarginal syndesmophytes
 Bilateral asymmetric involvenent of SI joint
  Including 5 clinical patterns:
◦ Asymmetric mono-/oligoarthritis (~30% [range 12-70%])1-4
◦ Symmetric polyarthritis (~45% [range 15-65%])1-4
◦ Distal interphalangeal (DIP) joint involvement (~5%)1
◦ Axial (spondylitis and Sacroiliitis) (HLA-B27) (~5%)1,3
◦ Arthritis Mutilans (<5%)1,3

• However patterns may change over time and are therefore not useful for
classification 5
HLA: Human leucocytes antigen References see notes
Clinical subgroups at baseline and follow-up:
Monoarthritis Monoarthritis

Oligoarthritis Oligoarthritis

DIP DIP

Polyarthritis Polyarthritis

Spondyloarthritis Spondyloarthritis

Mutilans Mutilans

No clinical evidence of
joint disease
McHugh et al. Rheum 2003;42:778-783
 Inflammatory articular disease (joint, spine, or
entheseal)
 With 3 points from following categories:
− Psoriasis: current (2), history (1), family history (1)
− Nail dystrophy (1)
− Negative rheumatoid factor (1)
− Dactylitis: current (1), history (1) recorded by a
rheumatologist
− Radiographs: (hand/foot) evidence of juxta-articular new
bone formation
 Specificity 98.7%, Sensitivity 91.4%

Taylor et al. Arthritis & Rheum 2006;54: 2665-73

 Spondyloarthropathies
Axial and Peripheral
AMOR criteria (1990)
ESSG criteria (1991)

Axial Spondyloarthritis Peripheral Spondyloarthritis

ASAS classification 2009 ASAS classification 2010

Ankylosing spondylitis
Prototype of axial spondylitidis Infliximab (IFX) and Golimumab (GLM)
Modified New York criteria 1984 indications

Psoriatic arthritis
From Moll & Wright 1973 to CASPAR criteria 2006

ESSG: European Spondyloarthropathy Study Group Sieper et al. Ann Rheum Dis 2009;68:ii1-ii44
ASAS: Assessment of Spondyloarthritis International Taylor et al. Arthritis & Rheum 2006;54:2665-73
Society Van der Heijde et al. Ann Rheum Dis 2011;70:905-8
 Rheumatoid  Ankylosing Spondylitis
Arthritis ◦ Strong HLA B27
◦ Symmetric association
◦ PIP, MCP, not ◦ Male predominance
distal ◦ Axial skeletal
◦ Ulnar deviation, involvement –
swan neck sacroilitis
deformities ◦ Bamboo spine
◦ Rheumatoid ◦ Schober test
nodules demonstrating limited
flexion

Uptodate.com
 Reactive Arthritis  Inflammatory Bowel
◦ LE arthritis Disease Associated
◦ 1-4 weeks after an ◦ Crohn’s
infection ◦ LE distribution
◦ Infectious agents:
 Shigella
 Salmonella
 Yersinia
 Campylobacter
 Chlamydia
◦ Triad: urethritis,
conjunctivitis, arthritis
◦ Keratoderma
Blennorhagicum

AAFP
 Bare area erosions
 Terminal tuft erosions
 Ray pattern
 Irregular periosteal bone apposition
 Feet more severely affected than hands’
 Severe bone destruction without regional

osteoporosis
 Subluxations
 1 – NSAIDS
 2 – DMARDS
◦ MTX
◦ Leflunomide
◦ Sulfasalazine
◦ Cyclosporine
◦ TNF α inhibitor
 Coordinate b/w Rheumatology and
Dermatology
Psoriatic Arthritis Response Criteria (PsARC)
 Clinical assessment of joint improvement, no skin
assessment
 Improvement in at least 2 of 4 criteria,
one of which must be tender or swollen-joint score
◦ Physician global assessment (> 1 unit)
◦ Patient global assessment (> 1 unit)
◦ Tender-joint score (> 30%)
◦ Swollen-joint score (> 30%)
 No worsening in any criterion

Clegg D.O. et al. Arthritis Rheum 1996;39:2013.

 Urethritis, conjunctivitis, arthritis
 Lower extremity
 Osteoporosis/soft tissue swelling
 Uniform joint space loss
 Marginal erosion/periosteitis
 Asymmetric broad based nonmarginal

syndesmophytes
 Bilateral asymmetric involvenent of SI joint
Reiter’s Disease
 Wave like hyperostosis
 Flowing ossification
 >4 contiguous vertebras
 Thoracic spine
 ossified anterior

longitudinal ligament
 Normal SI joint
 Normal disc space
 Calcification of cartilage, synovium, capsule,
tendon or ligaments
 More than one joint exclusive of the
intervertebral disks.
 Crystals aspirated from joints showing absent
or weakly positive birefringence
 Joint-space narrowing, sclerosis, cyst
formation
 Bony fragmentation, and osteophytosis
 Cartilage calcification
 Degenarative
 Gout, Pseudogout
 Hemochromatosis
 Wilson disease
 ochronosis
 Hypertrophic- weight bearing joints
 Disorganization
 Bone destruction
 Dislocation
 Debris
 Preserved bone density
 Atrophic- non weight bearing joints

 Amputated/lick candy stick

 Neuropathic joint
 Syringomyelia
 Syphilis
 Diabetes
 Leprosy
 Alcoholism
 Multiple sclerosis
 Trauma
Neuropathic
 Disc calcification
 Vaccum phenomenon
 Osteophytes
 Ankylosis
 Osteoporosis
 Key is disc changes with
advanced degenarative
changes in unexpected
locations
 Childbearing female
 Hands affected predominantly
 Bilateral symmetry
 Osteoporosis
 Normal joint spaces
 calcification
 Ulnar drifting/deformities
 Hitch-hiker’s deformity
 Soft tissue atrophy
SLE
 Recurrent attacks of rheumatic fever
 Deforning nonerosive peripheral arthropathy
 Normal joint space
 Juxta articular osteoporosis
 Soft tissue swelling
 Ulnar drifting
 Flexion at MCP
 Joint pain, swelling, and limitation of
motion
 3-5 th decade male
 Knee> hip
 Multiple intraarticular calcified nodules,

uniform in size
 Laminated to stippled appearance
 Promote early degenarative disease
 Chondrosarcoma in 5%
Synovial Osteochondromatosis
PD
PD
 Benign proliferative disorder of the synovium
 May affect the joints, bursae, or tendon

sheaths
 Preserved joint space
 No osteoporosis
PVNS
Haemophilic Arthropathy
 Resorption of distal tuft
 Retraction of fingertips <20%
 Soft tissue calcification
 Disuse osteoporosis
 Joints may be normal or erosive

arthropathy
SCLERODERMA
 Usually monoarticular
 Cartilage destruction
 Subchondral bone erosion
 Osteoporosis
 Effusion
 More aggressive
course & bone
destruction in pyogenic
 Bony ankylosis
 Monoarticular involvement
 Soft-tissue swelling
 Joint effusions
 Periarticular osteopenia
 Marginal erosions.
 Joint space narrowing is unusual
TIW

T2W

POSTGAD
 Bone erosion
 Marrow signal abnormalities
 Extra-articular extension
 Soft tissue abscess
Postgad
 Chronic hemodialysis
 Plasma cell dyscrasia
 Bilateral
 Juxtaarticular soft-tissue masses
 Periarticular osteopenia
 Subchondral cysts
 Joint effusions, erosions
 Preserved joint spaces
 Synovitis
 Acne
 Pustulosis
 Hyperostosis
 Osteitis
 Sternoclavicular joint>Flat bones
 Recurent osteomyelitis
 Hot on bone scan
 Gout
 Neuropathic
 CPPD
 PVNS
 Synovial Chondronatosis
 Postel’s arthritis
 JRA
 Psoriatic
 Reiter’s
 Hemophilia
 HPA
 Osteoarthritis
 Gout
 CPPD
 Psoriatic
 Anktlosing Spondylitis
 Neuropathic
 Reiter-chronic case
 Rheumatoid arthritis
 JRA
 Infective
 Haemophilia
 Scleroderma
 SLE
 CPPD
 GOUT
 Alkaptonuria
 Haemochromatosis
 Wilson
 Acromegaly
Increased joint space

Acromegaly
 DEGENRATIVE
 RA
 CPPD
 AVN
 Ankylosing Spondylitis
 Psoriasis
 Inflammatory Bowel Disease
 Primary OA
 Rheumatoid arthritis
DISTAL :
Psoriasis
Reiter’s syndrome
Osteoarthritis

PROXIMAL : RA
CPPD
 OA
 RA
 CPPD
 Ankylosing spondylitis
 Pigmented villonodular synovotis
 Synovial osteochondromatosis
 AS
 IBD
 PSORIASIS
 REITER’S SYNDROME
 OA
 INFECTION
 Certain questions to be answered
 1). It is a monoarticular / pauci/
polyarticular involvement
 2). It is synovial or chondropathic
 3).if polyarticular, specific distribution and
pattern
 4). Sacroiliac and CVJ etc.
 5). Clinical presentation (history)
 Any monoarticular synovial jt.
Involvement is assumed to be infective
unless proved otherwise.

 Any monoarticular chondropathic jt. is

considered as degenerative.

 Polyarticular jt. Involvement s/o

inflammatory noninfective etiology.
 Synovial arthropathy:
 1). Periarticular osteopenia

 2). Jt. Space effusion (soft tissue)

 3). Erosions

 4). Loss of jt. space (late feature)

 D/D of synovial arthritis

 Infection- >3month---tuberculous
acute onset— pyogenic
 RA
 Seronegative spondyloarthritis
 GOUT
 CHONDROPATHIC
ARTHROPATHY:
 Loss of jt. Space
 Sclerosis
 Osteophytes
 Subchondral cyst.
 D/D of chondropathic
arthritis
 OA
 GOUT
 CPPD
 HEMOCHROMATOSIS.
 If Polyarticular

 Distribution
 Ass. Findings
 Chondrocalcinosis.
 A R T H R IT I S

A L IG N M E N T BONY C A R T IL A G E D IS T R I B U T I O N S O F T T IS S U E
M IN E R A L IS A T I O N SPACE LO SS

P S O R I A S IS PRESERVED LO ST OA P IP D IP G E N E R A L IS E D L O C A L IS E D
R E I T E R 'S
RA; SLE CPPD RA O A ; R E IT E R ' S RA
N E U R O P A T H IC HEMOCHRO. CPPD P S O R I A S IS GOUT

RA RA
OA S U B C H O N D R A L JRA
G E N E RJRA
A L I Z E D J U X T A A R T IC U L A R IN C R E A S E D DECREASED
CPPD P yo g e n i c NFECTIVE
C T d iHEMOPHILIA
s o rd e rs RA
GOUT HEMOPHILIAINFECTIVE P S O R IA S I S SCLERO DERM A
SLE SLE R E I T E R 'S DERM ATO M YO
 ARTHRITS

Erosive Erosive+ Productive NO Erosion/

Productive Productive

RA Psoriasis OA SLE
Gout Reiter, AS DISH
Dermatomyositis
Erosive OA JRA, Neuropathic