Rheumatoid arthritis Dr Jaskaran sandhu MS orthopaedics

1. SEMINAR ON
RHEUMATOID ARTHRITIS
PRESENTED BY DR.JASKARAN SINGH
MODERATOR BY DR.SAURABH SAHU

2. RHEUMATOID ARTHRITIS
• It is a systemic auto immune
disease of chronic polyarticular
inflammation that leads to joint
swelling, joint deformity, loss of
joint function, and early
death(mainly due to ischaemic
heart disease).

3. • Characterised by
Hyperplasia of synovial
lining cells
,angiogenesis,mononuclea
r cells infiltrate which
leads to pannus formation
,then cartilage erosion &
joint destruction .
• Most common cause of
chronic inflammatory joint
disease.
• Symmetrical involvement
of peripheral joints .

4. EPIDEMIOLOGY
• RA occurs in 1 to 3% of the white adult
population, but prevalence varies depending on
age, race, and classification criteria used
• Peak incidence in 4th or 5th decade
• WOMEN : MEN Ratio is 3:1
• More common in caucasians.

5. Factors responsible for RA
Genetic Susceptibility
Immunological reaction
Inflammatory reaction in joints & tendon
sheath
Appearance of RF & anti CCP in blood &
synovium
Perpetuation of inflammatory process
Articular cartilage destruction

6. Genetic Susceptibility
 Associated with specific HLA loci (HLA-DR4 ,CHR 6)
 HLA Class II molecules appear as surface antigens on cells
of immune system(B-lymphocytes ,macrophages,
dendritic cells) which act as Antigen preseneting cells.
 In immune reactions ,process starts when the antigenic
peptide(special affinity for synovial tissue) presented in
association with specific HLA allele.

7. Inflammatory reaction
 Infectious cause like Mycoplasma, mycobacteria, rubella,
Ecoli,EBV ,CMV,Parvovirus etc are believed to induce auto
immune response against joints by exhibiting molecular
mimicry.
 Once APC /T-cells interaction starts,various local factors like
TNF ,IL 1 , IL 6 acts as chemotactic agents
 It leads to marked proliferation of synovium with
neoangiogenesis.
 Resulting synovitis in joints & in tendon sheath is hallmark
of RA.

8. Rheumatoid Factor
• B cells activation leads to anti – IgG
autoantibodies(RF) production
Sensitivity 71.6%
Specificity 80.3%
• Presence of anti CCP is more specific for RA
Sensitivity 66.0%
Specificity 90.4%

9. CHRONIC SYNOVITIS & JOINT
DESTRUCTION
 Chronic synovitis is associated with production of
proteolytic enzymes , prostaglandins & cytokins TNF &
IL 1 .
 Deposition of immune complex in synovial joints
 It leads to cartilage matrix depletion ,eventually
damage to cartilage & underlying bone.
 Vascular proliferation , osteoclastic activity contribute
to cartilage destruction and periarticular bone erosion.

10. PATHOLOGY
• Antigen mediated activation of T cells in an immunogenetically
susceptible host
• Infiltration of CD4 T cells around capillaries , microvascular injury ,
neovascularisation & hyperplasia & hypertrophy of synovial
endothelium
• Infiltration of B cells ,plasma cells & macrophages
• Release of Inflammatory cytokines & chemokines (IL1 , TGF BETA
,TNF ALPHA ,IFN GAMMA ) which accounts for pathologic & clinical
manifestation of RA
• Bony & Cartilage destruction caused by activation of collagenases &
other degrading enzymes released from inflammatory pannus by
cytokines.

11. STAGES OF RHEUMATOID ARTHRITIS
• PRE CLINICAL STAGE :
Raised ESR,CRP & RF may be detectable years before
clinical syptoms
• SYNOVITIS :
Vascular congestion , neoangiogenesis , synovial
proliferation ,infiltration by polymorphs
,lymphocytes , plasma cells
• DESTRUCTION :
Persistent inflammation causes joint destruction &
tendon destruction due to proteolytic enzymes
and granuation tissue invasion into articular
cartilage
• DEFORMITY :
Combination of articular destruction , capsular
stretching & tendon rupture leads to progressive
instability & joints deformity

12. EXTRA ARTICULAR TISSUE
INVOLVEMENT
 Rheumatoid Nodules : Occur under skin ,in synovium,on tendon,in
sclera etc
 Lymphadenopathy : Draining & distant nodes can be involved ,
spleenomeagly
 Vasculitis : Involvement of nailfold infarcts is common
 Muscle Weakness: May be due to myopathy or neuropathy. So,
spinal cord disease ,nerve intrapement should be checked
 Visceral disease: Lungs ,heart (ischaemic heart disease), kidneys ,GI
tract , Brain are sometimes affected.

13. CLINICAL FEATURES
Symptoms :
 insidious onset of morning stiffness
and polyarthropathy
 usually affects hands and feet ( DIP
joint of hand is usually spared )
 may also affect knees, cervical spine,
elbows, ankle and shoulder
Physical exam :
 subcutaneous nodules in 20% (strong
association with positive serum RF)
 ulnar deviation with
metacarpophalangeal (MCP)
subluxation, swan neck deformity
 hallux valgus, claw toes,
metatarsophlanageal (MTP)
subluxation
 joints become affected at later stage
in disease process
Early Features
(Synovitis)
Late Features
(Destructive)
More
later(Deformity)

14. EARLY FEATURES (SYNOVITIS)
Most commonly affected MCPJ &
PIPJ,wrist,tendon sheath around joints(wrist –
feet-knee-shoulder)
Bilateral symmetrical polsynovitis
Pain,fusiform swelling,stiffness,loss of mobility
Constitutional Symptom like loss of
weight,malaise,low grade fever,tenosynovitis

15. LATE FEATURES(DESTRUCTIVE)
• Spread to other joint :
Wrist,ankle,knee,should
er ( in order of
frequency)
• Morning Stiffness (more
than 30 min )
• Activity of daily living
will be affected

16. More later Features (Deformity )
• Pain,deformity,instability,
decreased ROM
• Joint deformity – moment
restricted and painful
• Thumb –Z deformity
• Finger –Swan neck
deformity/Boutonniere’s
deformities,ulnar
deviation

17. HAND INVOLVEMENT
• Z deformity :
Radial deviation of wrist , ulnar
deviation of digits
• Swann Neck Deformity :
 Hyperextension of PIP ,flexion of
DIP
 Cause : prolonged DIP flexion with
dorsal subluxation of lateral bands
.
• Boutonniere deformity :
 Flexion of PIP , Extension of DIP
 Cause : Central slip distruption
and lateral band volar subluxation

28. Diagnostic Criteria (1987 Revised
Criteria for Diagnosis of RA)
• Morning stiffness ≥ 1h
• Swelling in ≥ 3 joints
• Rheumatoid nodules
• Radiographic changes of the hand including bony
erosions and decalcification
• Symmetric arthritis
• Serum rheumatoid factor
• Arthritis of the hand (MCP, PIP) and wrist
≥4 of 7 criteria for a 6 week period

30. INVESTIGATION
• BLOOD EXAMINATION:
 RBC : Normocytic
hypochromic anaemia due
to abnormal erythropoiesis
from chronic inflammation
 Inflammatory markers : ESR
,CRP elevated
 Rheumatoid Factor(RF) :
Serum IgM anti IgG auto Ab
 Anti cyclic citrullinated
peptide ( CCP ) Ab

31. INVESTIGATION
• X RAY IMAGING :
Early stage (Synovitis) : Soft tissue swelling
,periarticular osteopenia
Later Stage(Destructive) : Bony erosion
,narrowing of joint space
Advance Stage (Deformity): Articular destruction
& joint deformity

32. Medical Management
• The group of drugs that are useful can be
grouped as NSAIDs , Corticosteroids , DMARDs
, Biological DMARDs
• Combined therapy :
 Triple therapy – Methotrexate , Sulfasalazine
Hydroxychloroquine
 Methotrexate and Leflunomide
 Methotrexate plus a biological

33. DMARDs
DMARDs Dose Serious
Adverse
Effect
Common
adverse effect
Initial
examination
Followup
Hydroxychlo-
roquine HCQ
200-400mg/d •Irreversible
retinal
damage
•Cardiotoxic
-ity
•Blood
Dyscrasia
•Nausea
•Diarrhea
•Headache
•Rash
Eye
examination >
40 yr old ,
Previous
ocular disease
Funduscopic
and visual
field testing
every 12
months
Sulfasalazine Initially 500
mg orally BD
Maintenance
1000 1500 mg
BD
•Granulocytop
-enia
•Hemolytican-
mia (G6PD )
•Nausea
•Diarrhea
•Headache
CBC , LFT
,G6PG levels
CBC every 2 –
4 weeks for
first 3 months
, then every 3
months
Methotrexate 10-25mg
/weekly orally
or subcutan-
eous , Folic
•Hepatotoxicit
iy
•Pneumonitis
•Infection
•Nausea
•Diarrhea
•Headache
CBC , LFT ,
Viral Hepatitis
,
CXR
CBC ,
S .creatinine ,
LFT every 2
months

34. Biological DMARDs
Infliximab : Monoclonal antibody against TNF –
alpha ( 3mg /kg i.v. at 0 , 2 , 6 then every 8 weeks
. Can be increased upto 10 mg /kg every 4 weeks
Etanercept : Recombinant antibody against TNF
alpha ( 25 mg s/c twice weekly )
Adalimumab : Human monoclonal antibody
against TNF alpha ( 40 mg s/c every 2 weeks , can
increased to weekly )

35. • Golilumab : Human monoclonal antibody
against TNF alpha ( 50 mg SQ monthly )
• Certolizumab : Human monoclonal antibody
against TNF alpha ( 400 mg SQ weeks 0 , 2 , 4
then 200 mg every week
• Anakinra : Monoclonal antibody to IL 1 ( 100
mg daily s/c )

36. • Rituximab : Monoclonal antibody Direct
against CD 20
• Abatacept : Inhibits the co stimulation of T
cells by blocking CD 28 – CD 80/86
• Tocilizumab : IL 6 receptor antibody .

37. Surgical Management
• Nodules are best left alone unless they cause
pain and functional loss . Local steroid
injection may be given
• Entrapment neuropathies require surgical
release
• Tendon rupture require surgical repair
• Recurrent Backer’s cyst requires excision
• Total joint replacement for arthritis

38. Complication of RA
Ruptured tendons
Ruptured joints(Baker’s cysts)
Joint infection
Spinal Cord Compression (atlantoaxial or
upper axial spine)
Amyloidosis