Arthritis

Description of arthritis in comprehensive manner

1. Sushil Paudel, MS Orthopaedics (AIIMS)
TUTH

2. Types of arthritis
Symptoms of arthritis
Signs of arthritis
Treatment of arthritis

3. Rheumatoid arthritis (RA)
Osteoarthritis (OA)
Sero-negative arthritis

Ankylosing spondylitis
Psoriatic arthritis

Reactive arthritis

Enteropathic arthritis
Crystal arthropathies

4. stands for :
A: ALIGNMENT
B: BONY MINERALIZATION
C: CARTILAGE SPACE
D: DISTRIBUTION
S: SOFT TISSUE

5. Normal joint structure

6. NORMAL
SUBCHONDRAL BONE DESTRUCTION

7. 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

8. Primary or idiopathic
Secondary

Infection

Dysplasia
 Perthes
 SCFE
 Trauma
 AVN

9. Genetic
Metabolic
Hormonal
Mechanical
Ageing

10. Disparity between:-
stress applied to articular cartilage
and
strength of articular cartilage

11. Increased stress (F/A)
Increased load eg BW or activity
Decreased area eg varus knee or dysplastic hip

12. Weak cartilage
age
stiff eg ochronosis
soft eg inflammation
abnormal bony support eg AVN

14. Joint space narrowing
Osteophytosis
Subchondral cysts
Subchondral sclerosis

16. 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

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

20. OA Affecting Foot

21. Vacuum Phenomenon
Accumulation of Nitrogen
Degenarative etiology
Better seen in Extension
Excludes infective etiology
In peripheral joints
physiological

22. SPGR
T1W

23. SPGR
T2 FATSAT

24. pain
swelling
stiffness
deformity
instability
loss of function

25. Analgesia
Oral viscosupplements
Intrarticular steroids
Intrarticular viscosupplements
Altered activity
Walking aids
Physiotherapy

26. arthroscopy
osteotomy
arthrodesis
excision arthroplasty
replacement arthroplasty

29. Bilateral symmetry
Periarticular soft
tissue swelling
Uniform joint space loss
Marginal erosions
Juxta-articular osteoporosis
Joint deformity

34. Inflammation
◦Swollen
◦Stiff
◦Sore
◦Warm
Fatigue
Potentially Reversible

37. RA

38. Boutonniere deformity :
flexion deformity at PIP jt & hyperextension at
DIP
• Swan neck deformity :
combination of flexion at DIP
and extension at PIP

39. B/L KNEE ANKYLOSIS
RA

42. RA-foot deformity

43. Atlantodental interspace > 3.0mm
Odontoid erosions
Subluxation
Pseudo basilar invagination
Reduced disc space
Apophyseal joint: erosion, sclerosis, ankylosis
Sharpened pencil spinous process

44. ADI > 3.0mm

45. Soft tissue swelling
Rotator cuff rupture
Head erosions
Tapered distal clavicle due to
erosions
Irregular coracoid process

47. 
Enlarged Olecranon bursa
 Fat pad sign
 Supinator notch sign: erosion at
proximal ulna

48. RA-ELBOW

49. Uniform bicompartmental joint
space loss
Patellofemoral joint also involved
Soft tissue swelling
Baker’s cyst
Subchondral cysts

51. T1W
T1GRE

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

54. Unicompartmental Bicompartmental

55. 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!

56. NSAIDS
Steroids
Oral
Intra-articular
DMARDS
Synthetic
Methotrexate
Hydroxychloroquine
Leflunomide
Sulfasalazine

57. Monoclonal Antibodies to TNF
◦Infliximab
◦Adalimumab
Soluble Receptor Decoy for TNF
◦Etanercept
Receptor Antagonist to IL-1
◦Anakinra
Monoclonal Antibody to CD-20
◦Rituximab

58. Cyclo-oxygenase inhibitors
Do not slow the progression of the disease
Provide partial relief of pain and stiffness

60. Disease Modifying Anti-Rheumatic Drugs
Reduce swelling & inflammation
Improve pain
Improve function
Have been shown to reduce radiographic
progression (erosions)

62. Dihydrofolate reductase inhibitor
↓ thymidine & purine nucleotide synthesis
“Gold standard” for DMARD therapy
7.5 – 30 mg weekly
Absorption variable
Elimination mainly renal

63. Hepatotoxicity
Bone marrow suppression
Dyspepsia, oral ulcers
Pneumonitis
Teratogenicity
Folic acid reduces GI & BM effects
Monitoring
◦FBC, ALT, Creatinine

64. Sulphapyridine + 5-aminosalicylic acid
Remove toxic free radicals
Remission in 3-6 month

65. Elimination hepatic
Dyspepsia, rashes, BM suppression

66. Mechanism unknown
◦Interference with antigen processing ?
◦Anti- inflammatory and immunomodulatory
•For mild disease

67. Side effects
Irreversible Retinal toxicity, corneal deposits
Ophthalmologic evaluation every 6 months

68. Competitive inhibitor of dihydroorotate
dehydrogenase (rate-limiting enzyme in de novo
synthesis of pyrimidines)
Reduce lymphocyte proliferation

69. Oral
T ½ - 4 – 28 days due to EHC
Elimination hepatic
Action in one month
Avoid pregnancy for 2 years

70. Hepatotoxicity
BM suppression
Diarrhoea
rashes

73. Triple Therapy
◦Methotrexate, Sulfasalazine, Hydroxychloroquine
Double Therapy
◦Methotrexate & Leflunomide
◦Methotrexate & Sulfasalazine
◦Methotrexate & Hydroxychloroquine

74. •Complex protein molecules
•Created using molecular biology methods
• Produced in prokaryotic or eukaryotic cell cultures

75. 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)

76. Trans-Membrane
Bound TNF
Soluble TNF
Strategies
for Reducing
Effects of
TNF
Macrophage
Monoclonal Antibody (Infliximab & Adalimumab)

77. Infection
◦Common (Bacterial)
◦Opportunistic (Tb)
Demyelinating Disorders
Malignancy
Worsening CHF

78. 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)

79. 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.

80. 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.

82. 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)

83. 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.

84. 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

85. 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.

86. 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.

87. 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.

88. 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.

89. 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.

90. 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.

91. 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

92. ANA (antinuclear antibody)
RF (Rheumatoid factor )
CRP (C-reactive protein)
ESR (erythrocyte sedimentation rate)
CCP (Cyclic Citrullinated Peptide
Antibody) test

93. 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%.

94. 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

95. Medication
s
Doses
(mg/kg)
Side effects
Aspirin 50-120
Stomack pain, vomiting,
gastrointestinal
bleedings, headache,
blood in the urine, fluid
retention, thinning and
scarring of the skin
(especially with
naproxen), stomach
ulcer (aspirin).
Ibuprofen 10-30
Tolmentin 10-15
Naproxen 5-20

96. Medications Doses
(mg/kg)
Side effects
Hydroxychlo-
roquine
(Plaquenil)
5-7
Upset stomach, skin
rash and a eye
damage. A child who
takes this drug should
have his/her eyes
examined at least
every six months by
an ophthalmologist
Sulfasalazine
(Azulfadine)

97. Medication
s
Doses(weekly,
depending
from body
weight )
Side effects
Auranofin,
Ridaura,
Myochrysine
Solganol
20 kg – 10 mg
30 kg – 20 mg
40 kg – 30 mg
50 kg – 40 mg
> 50 kg – 50 mg
Skin rash,
mouth sores,
kidney
problems, a low
blood count or
anemia

98. Medication
s
Doses Side effects
Methotrexate
(Rbeumatrex)
Azathioprine
(Imuran)
Cyclophospha
mide
(Cytoxan)
Typically 7.5 to
25 mg a week
Loss of appetite,
nausea or
vomiting, skin
rash, unusual
bleeding or
bruising,
tiredness or
weakness,
sterility.

99. 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])

101. Therapeutic exercises
Sports and Recreational Activities
Splints

102. Morning Stiffness Relief
Diet
Eye Care
Dental Care
Surgery

103. .

104. 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

105. Prevalence increasing
May be signal for
unrecognized comorbidities :
( Not to point of searching)
Obesity (Duh!)
Metabolic syndrome
DM
HTN
CV disease
Renal disease

106. ORGAN MEATS
WILD GAME
SEAFOOD
LENTILS
PEAS
ASPARAGUS
YEAST
BEER
Rich foods have a higher
concentration of protein. This could
cause major problems for a person
afflicted with gout.

107. Urate: end product of purine metabolism
Hyperuricemia: serum urate > urate solubility (>
6.8 mg/dl)
Gout: deposition of monosodium urate crystals
in tissues

108. Hyperuricemia caused by
Overproduction
Underexcretion
No Gout w/o crystal deposition

109.  Urate
Oevrproduction Underexcretion

Hyperuricemia
________________________________________
SilentGout Renal Associated
Tissue manifestationsCV events &
Deposition mortality

110. Purines are not
properly processed
in our body
Excreted through
kidneys and urine
Hyperuricemia-
build-up of uric acid
in body and joint
fluid

111. Asymptomatic hyperuricemia
Acute Flares of crystallization
Intervals between flares
Advanced Gout & Complications

112. Abrupt onset of severe joint inflammation, often
nocturnal;
Warmth, swelling, erythema, & pain;
Possibly fever
Untreated? Resolves in 3-10 days
90% 1
st
attacks are monoarticular
50% are podagra

113. 90% of gout
patients eventually
have podagra : 1st
MTP joint

116. Can occur in other
joints, bursa &
tendons

118. Asymptomatic
If untreated, may advance
Intervals may shorten
Crystals in asx joints
Body urate stores increase

120. Chronic Arthritis
X-ray Changes
Tophi Develop
Acute Flares continue

121. Chronic Arthritis
Polyarticular acute
flares with upper
extremities more
involved

122. Solid urate deposits
in tissues

123. Irregular &
destructive

124. Long duration of hyperuricemia
Higher serum urate
Long periods of active, untreated gout

127. Hx & P.E.
Synovial fluid analysis
Not Serum Urate

128. Not reliable
May be normal with flares
May be high with joint Sx from other causes

129. Male
Postmenopausal
female
Older
Hypertension
Pharmaceuticals:
Diuretics, ASA,
cyclosporine

130. Transplant
Alcohol intake
Highest with beer
Not increased with wine
High BMI (obesity)
Diet high in meat & seafood

131. The Gold standard
Crystals intracellular during attacks
Needle & rod shapes
Strong negative birefringence

133. 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.

134. Similar Acute attacks
Different crystals under Micro;
Rhomboid, irregular in CPPD

136. Both have polyarticular, symmetric arthritis
Tophi can be mistaken for RA nodules

138. 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.

139. 139
•Treat acute flare rapidly with anti-
inflammatory agent
•Initiate urate-lowering therapy to
achieve sUA <6
•Use concomitant anti-inflammatory
prophylaxis for up to 6 mo to prevent
mobilization flares
INITIATE
(acute flare)
RESOLVE
(urate-lowering therapy)
139
•Continue urate lowering therapy
to control flares and avoid crystal
deposition
•Prophylaxis use for at least 3-6
months until sUA normalizes
MAINTAIN
(treatment to control sUA)

140. 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

141. 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

142. NSAIDS
Colchicine
Corticosteroids

143. Colchicine- reduces pain, swelling, and
inflammation; pain subsides within 12 hrs and
relief occurs after 48 hrs
Prevent migration of neutrophils to joints

144. Side effects
Nausea
Vomiting
Diarrhea
Rahes

145. 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

146. 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
146Kanna D, et al. Arthritis Care Res (Hoboken). 2012 Oct;64(10):1447-61

147. 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

148. 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!
148

149. 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

150. 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

151. Lower urate to < 6 mg/dl : Depletes
Total body urate pool
Deposited crystals
RX is lifelong & continuous
MED choices :
Uricosuric agents
Xanthine oxidase inhibitor

154. Probenecid, (Losartan & fenofibrate for mild
disease)
Increased secretion of urate into urine
Reverses most common physiologic abnormality
in gout ( 90% pt.s are underexcretors)

155. 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

157. Allopurinol :
Blocks conversion of hypoxanthine to uric acid
Effective in overproducers
May be effective in underexcretors
Can work in pt.s with renal insufficiency

158. 158
hypoxanthine urate xanthine
XO XO
XO=xanthine oxidase
Allopurinol and febuxostat inhibit
xanthine oxidase and block uric acid
formation
Markel A. IMAJ, 2005.
158

159. 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
allopurinol oxypurinol
Xanthine
Oxidase
Stevens-
Johnson
Syndrome
Allopurinol
Hypersensitivity
Syndrome
Toxic Epidermal
Necrolysis
159

160. 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.

161. 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).

162. 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.

163. 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, 13
th
ed. 2008.
163

164. 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)

165. AllopurinolUricosuric
Issue in renal disease X X
Drug interactions X X
Potentially fatal hypersen-
sitivity syndrome X
Risk of nephrolithiasis X
Mutiple daily dosing X

166. RX gaps :
Can’t always get urate < 6
Allergies
Drug interactions
Allopurinol intolerance
Worse Renal disease

167. 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.
.

168. 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

169. 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
169
Khanna D, et al. Arthritis Care Res . 2012 Oct;64(10):1431-46

170. 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

171. Calcium pyrophosphate Crystal Deposition
Disease (CPPD) is the syndrome secondary to the
calcium pyrophosphate in articular tissues.
This includes: Chondrocalcinosis, Chronic CPPD
and Pseudogout.

172. 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.

174. 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.

175. Disease Associations: hyperthyroidsm,
hypocalciuria, hypercalcemia, hemochromatosis,
hemosiderosis, hypophosphatasia,
hypomagnesemia, hypothyroidsm, gout,
neuropathic joints, amyloidosis, trauma and OA.

176. 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.

177. 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.

178. 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.

179. 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.

180. Differential Diagnosis: Includes septic arthritis,
gout, inflammatory OA, Rheumatoid Arthritis,
neuropathic arthritis and Hypertrofic
Osteoarthropathy.

182. 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.

187. HLA B-27
Enthesitis
Synovitis
Osteitis

188. Spondyloarthropathies
Axial and Peripheral
AMOR criteria (1990)
ESSG criteria (1991)
Axial Spondyloarthritis
ASAS classification 2009
Ankylosing spondylitis
Prototype of axial spondylitidis
Modified New York criteria 1984
Peripheral Spondyloarthritis
ASAS classification 2010
Psoriatic arthritis
From Moll & Wright 1973 to CASPAR criteria 2006
Sieper et al. Ann Rheum Dis 2009;68:ii1-ii44
Taylor et al. Arthritis & Rheum 2006;54:2665-73
Van der Heijde et al. Ann Rheum Dis 2011;70:905-8
ESSG: European Spondyloarthropathy Study Group
ASAS: Assessment of Spondyloarthritis International Society
CASPAR: Classification criteria for psoriatic arthritis
Infliximab (IFX) and Golimumab (GLM)
indications

189. 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 sites
1
◦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.

190. Normal interspace 2-5mm
B/L symmetric
Lower two third
Rosary bead appearance
Reactive sclerosis
Bony ankylosis
osteoporosis
SACROILITIS

197. Romanus lesion(erosion)
Squaring, Osteoporosis
Shiny corner sign
Marginal Syndesmophytes
Bamboo spine
Trolley-track sign
Dagger sign
SPINE

199. •Mortality figures parallel RAMortality figures parallel RA
6,7,86,7,8

““Rare”Rare”

““Not” a serious disease, functional limitation is Not” a serious disease, functional limitation is
mildmild

““Rarely shortens life”Rarely shortens life”
•Burden of disease significant in pain, sick leave, early retirementBurden of disease significant in pain, sick leave, early retirement
3,4,53,4,5
•0.1-0.9%0.1-0.9%
1,21,2
11
Sieper J et al. Sieper J et al. Ann Rheum Dis. Ann Rheum Dis. 2002; 61 (suppl 3);iii8-18. 2002; 61 (suppl 3);iii8-18.
2 2
Lawrence RC., Arthritis Rheum 1998; 41:778-99. Lawrence RC., Arthritis Rheum 1998; 41:778-99.
33
Zink A., et al., Zink A., et al., J RheumatolJ Rheumatol 2000; 27:613-22. 2000; 27:613-22.
4 4
Boonen A. Boonen A. Clin Exp RheumatolClin Exp Rheumatol. 2002;20(suppl 28):S23-S26.. 2002;20(suppl 28):S23-S26.
55
Gran JT, et al. Gran JT, et al. Br J RheumatolBr J Rheumatol. 1997;36:766-771.. 1997;36:766-771.
66
Wolfe F., et al. Arthritis Rheum. 1994 Apr;37(4):481-94. Wolfe F., et al. Arthritis Rheum. 1994 Apr;37(4):481-94.
77
Myllykangas-Luosujarvi R, et al. Myllykangas-Luosujarvi R, et al. Br J Rheumatol.Br J Rheumatol. 1998;37:688-690. 1998;37:688-690.
88
Khan MA, et al. Khan MA, et al. J Rheumatol.J Rheumatol. 1981;8:86-90. 1981;8:86-90.
99
Braun J., Pincus T., Clin Exp Rheumatol. 2002; 20(6 Suppl 28):S16-22. Braun J., Pincus T., Clin Exp Rheumatol. 2002; 20(6 Suppl 28):S16-22.

200. The incidence of AS may be underestimated
due to unreported cases
1

HLA-B27 gene is associated with AS
6
Age of onset typically between 15 and 35
years
1,2,3
2-3 times more frequent in men than in women
6
1
The Spondylitis Association of America. Available at: www.spondylitis.org. Accessed December
2,2004. 61(suppl 3);iii8–18.
6
Khan MA. Ann Intern Med. 2002;136:896–907.

201. Axial manifestations:
•Chronic low back pain
•With or without buttock pain
•Inflammatory characteristics:
–Occurs at night (second part)
–Sleep disturbance
–Morning stiffness
•Limited lumbar motion
•Onset before age of 40 years
Sengupta R & Stone MA.
Inflammatory back
pain (IBP) =
Characteristic symptom
MRI sacro-iliac joint

202. AS: Characteristic Pathologic FeaturesAS: Characteristic Pathologic Features
Sieper J. Arthritis Res Ther 2009;11:208
Elewaut D & Matucci MC. Rheumatology 2009;48:1029-1035
• 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

203. Most striking feature of AS = New bone
formation in the spine with:
Spinal syndesmophytes
Ankylosis
Both can be seen on conventional
radiography
Bamboo spine and
bilateral sacroiliitis
X-ray showing
syndesmophytes
Even in patients with longer-
standing disease, syndesmophytes
are present in ～50% patients and
a smaller percentage will develop
ankylosis
Sieper J. Arthritis Res Ther 2009;11:208

204. Marginal erosions and new bone formation

205. Unilateral sacroiliitis

206. 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
2

207. The first abnormality to appear in
swollen joints associated with
spondyloarthropathies is an enthesitis
2
Likelihood of erosions is higher
for digits with dactylitis than
those without
1

1
Brockbank. Ann Rheum Dis 2005;62:188-90;
2
McGonagle et al. The Lancet 1998;352.

208. EAM Prevalence in AS
Patients (%)
Anterior uveitis 30-50
IBD 5-10
Subclinical inflammation of the gut 25-49
Cardiac abnormalities
Conduction disturbances
Aortic insufficiency
1-33
1-10
Psoriasis 10-20
Renal abnormalities 10-35
Lung abnormalities
Airways disease
Interstitial abnormalities
Emphysema
40-88
82
47-65
9-35
Bone abnormalities
Osteoporosis
Osteopenia
11-18
39-59
Elewaut D & Matucci MC. Rheumatology 2009;48:1029-1035
Terminal ileitis
Anterior uveitis
Cardiac
abnormalities

209. Bad QoL
1
◦Pain
◦Sleep problems
◦Fatigue
◦Loss of mobility and
dependency
◦Loss of social life
Effect employability
1
Higher rate of mortality
2
High socio-economic consequences
AS=23.7 years
90.2
83.1
62.4
54.1
0
20
40
60
80
100
StiffnessPainFatiguePoor
Sleep
N=175
AS mean duration: 23.7 yr
P
e
r
c
e
n
t
a
g
e

o
f

P
a
t
i
e
n
t
s

(
%
)
1

210. Adapted from Feldtkeller E et al. Rheumatol Int 2003;23:61–66
Sengupta R & Stone MA. Nat Clin Pract Rheumatol 2007;3:496-503

First symptoms
First diagnosis
Age in years
Males (n=920)
Females (n=476)
0
0 10 20 30 40 50 60 70
20
40
80
60
100
P
e
r
c
e
n
t
a
g
e

o
f

P
a
t
i
e
n
t
s

(
%
)
Average delay in diagnosis: 8.8
years
B27(+) 8.5 vs B27(-) 11.4
Delay  Worse clinical outcomes contributing to both physical and
work-related disability

211. Modified New York Criteria for AS
1
◦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 MRI
1
◦MRI can be used for earlier detection of inflammation (enthesitis) at
other sites.
There is no specific laboratory test for AS
1
◦ESR and CRP can indicate inflammation
50-70% of active AS patients will have increased ESR and CRP
2

◦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).

212. Diagnostic Standard for AS: Modified NY Diagnostic Standard for AS: Modified NY
Classification Criteria (1984)Classification Criteria (1984)
11
•Clinical components:
– Low back pain and stiffness for more than 3 months which
improves with exercise, but is not relieved by rest
– Limitation of motion of the lumbar spine in both the sagittal
and frontal planes
– Limitation of chest expansion relative to normal values
correlated for age and sex
•Radiological component:
–Sacroiliitis Grade >2 bilaterally or Grade 3-4 unilaterally
Definite AS if the radiological criterion is associated with at least one clinical
criterion
2
Probable AS if three clinical criteria present or radiologic criteria present
without clinical criteria
2
1
Linden VD et al. Arthritis Rheum 1984;27:361-368
2
Rudwaleit M et al. Arthritis Rheum 2005;52:1000-1008
•Old criteria
•Defined before TNF blockers
•Sacroiliitis detectable by X-ray occurs
lately
•No magnetic resonance imaging (MRI)
•Used for clinical trial

213. Adapted from Rudwaleit M et al. Arthritis Rheum 2005;52:1000-1008
Brandt HC et al. Ann Rheum Dis 2007;66:1479-84
Time (years)
Back Pain
Syndesmophytes
Radiographic stage
(Ankylosing Spondylitis)
Back Pain
Radiographic
sacroiliitis
Modified NY criteria (1984)
Diagnostic Standard for AS: Modified NY Diagnostic Standard for AS: Modified NY
Classification Criteria (1984) (Cont’d)Classification Criteria (1984) (Cont’d)
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.

214. Adapted from Rudwaleit M et al. Arthritis Rheum 2005;52:1000-1008
Time (years)
Back Pain
IBP
MRI active sacroiliitis
Back Pain
Syndesmophytes
Radiographic stage
(Ankylosing Spondylitis)
Pre-radiographic stage
(Axial undifferentiated SpA)
Back Pain
Radiographic
sacroiliitis
Modified NY criteria (1984)
Diagnostic Standard for AS: Modified NY Diagnostic Standard for AS: Modified NY
Classification Criteria (1984) (Cont’d)Classification Criteria (1984) (Cont’d)
•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

215. In patients with back pain ≥3 months and age at onset <45 years
Sacroiliitis* on imaging
plus
≥1SpA feature**
HLA-B27
plus
≥2 other SpA features**
**SpA features:
•Inflammatory back pain
•Arthritis
•Enthesitis (heel)
•Uveitis
•Dactylitis
•Psoriasis
•Crohn’s disease/ulcerative colitis
•Good response to NSAIDs
•Family history for SpA
•HLA-B27
•Elevated CRP
*Sacroiliitis on imaging:
•Active (acute) inflammation on
MRI highly suggestive of
sacroiliitis associated with SpA
or
•Definite radiographic sacroiliitis
according to modified New York
criteria
Rudwaleit M et al. Ann Rheum Dis 2009;68(6):770-6
OR

216. 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.

217. Chronic progressive, inflammatory disorder of the joints and skin
1
◦Characterized by osteolysis and bony proliferation
1
◦Clinical manifestations include dactylitis, enthesitis,
osteoperiostitis, large joint oligoarthritis, arthritis mutilans,
sacroiliitis, spondylitis, and distal interphalangeal arthritis
1
PsA is one of a group of disorders known as the
spondyloarthropathies
2
Males and females are equally affected
3
PsA can range from mild nondestructive disease to a severely
rapid and destructive arthropathy
3
◦Usually Rheumatoid Factor negative
3
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
1
Taylor WJ. Curr Opin Rheumatol. 2002;14:98–103.
2
Mease P. Curr Opin Rheumatol. 2004;16:366–370.
3
Brockbank J, et al. Exp Opin Invest Drugs. 2000;9:1511–1522.
4
Kane D, et al. Rheumatology. 2003;42:1460–1468.

218. Spondyloarthritis (SpA)
The prevalence of SpA is comparable to that of RA (0.5–1.9%)
1,2
Psoriasis (Pso)
Psoriasis affects 2% of population
7% to 42% of patients with Pso will develop arthritis
3
Psoriatic Arthritis
A chronic and inflammatory arthritis in association with skin psoriasis
4
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 psoriasis
4

1
Rudwaleit M et al. Ann Rheum Dis 2004;63:535-543;
2
Braun J et al. Scand J Rheumatol 2005;34:178-90;
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;
5
Pasquetti et al. Rheumatology 2009;48:315–325
Juvenile SpA
Reactive
arthritis
Arthritis
associated with
IBD
PsA
Undifferentiated
SpA (uSpA)
Ankylosing
spondylitis (AS)
RA: Rheumatoid arthritis

219. 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

220. 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%.
Epidemiological Evidence

221. 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 RA
1
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 PsA
5
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.

222. Helliwell PS & Taylor WJ. Ann Rheum Dis 2005;64(2:ii)3-8
Fitzgerald “Psoriatic Arthritis” in Kelley’s Textbook of Rheumatology, 2009
*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

223. 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;
4
Lawry M. Dermatol Ther 2007;20:60-
67
5
Jiaravuthisan MM et al. JAAD 2007;57:1-27;
6
Yamamoto Eur J Dermatol 2011;21:660-6
Enthesopathy (38%)
2
Dactyilitis (48%)
3
DIP involvement (39%)
2
Back involvement (50%)
1
Nail psoriasis

(80%)
4, 5

S
k
i
n

I
n
v
o
l
v
e
m
e
n
t
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
DIP: Distal interphalangeal

224. Pso patients
6-8
•Psychosocial burden
•Reactive depression
•Higher suicidal ideation
•Alcoholism

Metabolic Syndrome
3-5
• Hyperlipidemia
• Hypertension
• Insulin resistent
• Diabetes
• Obesity
Þ Higher risk of
Cardiovascular disease (CVD)
Ocular inflammation
1
(Iritis/Uveitis/ Episcleritis)
IBD
2


1
Qieiro et al. Semin Arth Rheum 2002;31:264;
2
Scarpa et al. J Rheum 2000;27:1241;
3
Mallbris et al. Curr Rheum Rep 2006;8:355;
4
Neimann et al. J Am Acad Derm 2006;55:829;
5
Tam et al. 2008;47:718;
6
Kimball et al. Am J Clin Dermatol 2005;6:383-392;
7
Naldi et al. Br J Dermatol 1992;127:212-217;
8
Mrowietz U et al. Arch Dermatol Res 2006;298(7):309-319

225. D a c t y l i t i s E n t h e s i t is
P s o r i a t i c A r t h r i t is
Ritchlin C. J Rheumatol. 2006;33:1435–1438.
Helliwell PS. J Rheumatol. 2006;33:1439–1441.

226. ACR Slide Collection on the Rheumatic Diseases; 3
rd
edition. 1994.
1
Brockbank J, et al. Ann Rheum Dis. 2005;64:188–190.
2
Veale D, et al. Br J Rheumatol. 1994;33:133–38.
•Diffuse swelling of a digit may be acute, with painful
inflammatory changes, or chronic wherein the digit remains
swollen despite the disappearance of acute inflammation
1
•Also referred to as
“sausage digit”
1
•Recognized as one
of the cardinal
features of PsA,
occurring in up
to 40% of patients
1,2
•Feet most commonly
affected
1
•Dactylitis involved
digits show more
radiographic damage
1

227. Entheses are the regions at
which a tendon, ligament, or
joint capsule attaches to
bone
1
Inflammation at the
entheses is called enthesitis
and is a hallmark feature of
PsA
1,2
Pathogenesis of enthesitis
has yet to be fully
elucidated
2
Isolated peripheral
enthesitis may be the only
rheumatologic sign of PsA
in a subset of patients
3

1
McGonagle D. Ann Rheum Dis. 2005;64(Suppl II):ii58–ii60.

2
Anandarajah AP, et al. Curr Opin Rheumatol. 2004;16:338–343.
3
Salvarani C. J Rheumatol. 1997;24:1106–1140.

228. Achilles Tendon Insertion Erosion
Plantar Spur
Achilles Tendon Spur

229. ACR Slide Collection on the Rheumatic Diseases; 3
rd
edition. 1994.
Data on file, Centocor, Inc.

230. Oligoarthritis Distal Arthritis



231. Polyarticular Pattern

232. Arthritis Mutilans

234. Tuft resorption
Periostitis

235. Distal asymmetric distribution
Ray pattern
Soft tissue swelling( sausage/spindle)
Preserved bone density
Marginal erosions
Fluffy periosteitis

236. Pencil in cup deformity
Mouse ear sign
Arthritis mutilans
Nonmarginal syndesmophytes
Bilateral asymmetric involvenent of SI joint

237. 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
References see notes
•However patterns may change over time and are therefore not useful for
classification
5
HLA: Human leucocytes antigen

238. McHugh et al. Rheum 2003;42:778-783
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

239. Inflammatory articular disease (joint, spine, or
entheseal)
With ³3 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

240. Spondyloarthropathies
Axial and Peripheral
AMOR criteria (1990)
ESSG criteria (1991)
Axial Spondyloarthritis
ASAS classification 2009
Ankylosing spondylitis
Prototype of axial spondylitidis
Modified New York criteria 1984
Peripheral Spondyloarthritis
ASAS classification 2010
Psoriatic arthritis
From Moll & Wright 1973 to CASPAR criteria 2006
Sieper et al. Ann Rheum Dis 2009;68:ii1-ii44
Taylor et al. Arthritis & Rheum 2006;54:2665-73
Van der Heijde et al. Ann Rheum Dis 2011;70:905-8
ESSG: European Spondyloarthropathy Study Group
ASAS: Assessment of Spondyloarthritis International Society
CASPAR: Classification criteria for psoriatic arthritis
Infliximab (IFX) and Golimumab (GLM)
indications

241. Rheumatoid Arthritis
◦Symmetric
◦PIP, MCP, not distal
◦Ulnar deviation,
swan neck
deformities
◦Rheumatoid nodules
Ankylosing Spondylitis
◦Strong HLA B27
association
◦Male predominance
◦Axial skeletal
involvement – sacroilitis
◦Bamboo spine
◦Schober test
demonstrating limited
flexion
Uptodate.com

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

243. 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

244. 1 – NSAIDS
2 – DMARDS
◦MTX
◦Leflunomide
◦Sulfasalazine
◦Cyclosporine
◦TNF α inhibitor
Coordinate b/w Rheumatology and Dermatology

245. Psoriatic Arthritis Response Criteria (PsARC)Psoriatic Arthritis Response Criteria (PsARC)
Clegg D.O. et al. Arthritis Rheum 1996;39:2013.
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

246. 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

247. Reiter’s Disease

249. Wave like hyperostosis
Flowing ossification
>4 contiguous vertebras
Thoracic spine
ossified anterior
longitudinal ligament
Normal SI joint
Normal disc space

250. 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

251. Cartilage calcification
Degenarative
Gout, Pseudogout
Hemochromatosis
Wilson disease
ochronosis

253. Hypertrophic- weight bearing joints
 Disorganization
 Bone destruction
 Dislocation
 Debris
 Preserved bone density
Atrophic- non weight bearing joints
 Amputated/lick candy stick

254. Syringomyelia
Syphilis
Diabetes
Leprosy
Alcoholism
Multiple sclerosis
Trauma
Neuropathic joint

257. Neuropathic

258. Disc calcification
Vaccum phenomenon
Osteophytes
Ankylosis
Osteoporosis
Key is disc changes with
advanced degenarative
changes in unexpected
locations

259. Childbearing female
Hands affected predominantly
Bilateral symmetry
Osteoporosis
Normal joint spaces
calcification
Ulnar drifting/deformities
Hitch-hiker’s deformity
Soft tissue atrophy

260. SLE

261. Recurrent attacks of rheumatic fever
Deforning nonerosive peripheral arthropathy
Normal joint space
Juxta articular osteoporosis
Soft tissue swelling
Ulnar drifting
Flexion at MCP

262. 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%

264. Synovial Osteochondromatosis

265. PD

266. PD

267. Benign proliferative disorder of the synovium
May affect the joints, bursae, or tendon sheaths
Preserved joint space
No osteoporosis

268. PVNS

271. Haemophilic Arthropathy

272. Resorption of distal tuft
Retraction of fingertips <20%
Soft tissue calcification
Disuse osteoporosis
Joints may be normal or erosive
arthropathy

273. SCLERODERMA

274. Usually monoarticular
Cartilage destruction
Subchondral bone erosion
Osteoporosis
Effusion
More aggressive
course & bone
destruction in pyogenic
Bony ankylosis

275. Monoarticular involvement
Soft-tissue swelling
Joint effusions
Periarticular osteopenia
Marginal erosions.
Joint space narrowing is unusual

276. TIW
T2W
POSTGAD

277. Bone erosion
Marrow signal abnormalities
Extra-articular extension
Soft tissue abscess

279. Postgad

280.  Chronic hemodialysis
 Plasma cell dyscrasia
 Bilateral
 Juxtaarticular soft-tissue masses
 Periarticular osteopenia
 Subchondral cysts
 Joint effusions, erosions
 Preserved joint spaces

281. Synovitis
Acne
Pustulosis
Hyperostosis
Osteitis
Sternoclavicular joint>Flat bones
Recurent osteomyelitis
Hot on bone scan

282. Gout
Neuropathic
CPPD
PVNS
Synovial Chondronatosis
Postel’s arthritis

283. JRA
Psoriatic
Reiter’s
Hemophilia
HPA

284. Osteoarthritis
Gout
CPPD
Psoriatic
Anktlosing Spondylitis
Neuropathic
Reiter-chronic case

285. Rheumatoid arthritis
JRA
Infective
Haemophilia
Scleroderma
SLE

286. CPPD
GOUT
Alkaptonuria
Haemochromatosis
Wilson
Acromegaly

287. Acromegaly
Increased joint spaceIncreased joint space

288. DEGENRATIVE
RA
CPPD
AVN

289. Ankylosing Spondylitis
Psoriasis
Inflammatory Bowel Disease

290. Primary OA
Rheumatoid arthritis

291. DISTAL :
Psoriasis
Reiter’s syndrome
Osteoarthritis
PROXIMAL : RA
CPPD

292. OA
RA
CPPD
Ankylosing spondylitis
Pigmented villonodular synovotis
Synovial osteochondromatosis

293. AS
IBD
PSORIASIS
REITER’S SYNDROME
OA
INFECTION

294. 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)

295. 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.

296. Synovial arthropathy:
1). Periarticular osteopenia
2). Jt. Space effusion (soft tissue)
3). Erosions
4). Loss of jt. space (late feature)

297. D/D of synovial arthritis
Infection- >3month---tuberculous
acute onset— pyogenic
RA
Seronegative spondyloarthritis
GOUT

298. CHONDROPATHIC
ARTHROPATHY :
Loss of jt. Space
Sclerosis
Osteophytes
Subchondral cyst.

299. D/D of chondropathic arthritis
OA
GOUT
CPPD
HEMOCHROMATOSIS.

300. If Polyarticular
Distribution
Ass. Findings
Chondrocalcinosis.

301. P S O R I A S I S
R E I T E R ' S
R A ; S L E
N E U R O P A T H I C
A L I G N M E N T
O A
C P P D
G O U T
P R E S E R V E D
S U B C H O N D R A L
P y o g e n i c
G E N E R A L I Z E D
C T d i s o r d e r s
J U X T A A R T I C U L A R
R A
L O S T
B O N Y
M I N E R A L I S A T I O N
O A
C P P D
H E M O C H R O .
C A R T I L A G E
S P A C E L O S S
P I P
R A
C P P D
D I P
O A ; R E I T E R ' S
P S O R I A S I S
D I S T R I B U T I O N
I N C R E A S E D
P S O R I A S I S
R E I T E R ' S
D E C R E A S E D
S C L E R O D E R M A
D E R M A T O M Y O
G E N E R A L I S E D L O C A L I S E D
R A
G O U T
S O F T T I S S U E
A R T H R I T I S
RA
JRA
NFECTIVE
HEMOPHILIA
SLE
RA
JRA
HEMOPHILIA
INFECTIVE
SLE

302. ARTHRITS
Erosive Erosive+ Productive NO Erosion/
Productive Productive
RA Psoriasis OA SLE
Gout Reiter, AS DISH Dermatomyositis
Erosive OA JRA, Neuropathic