This document provides an overview of rheumatoid arthritis (RA), including its epidemiology, pathogenesis, clinical manifestations, diagnostic criteria, and management. RA is a chronic autoimmune disorder causing symmetrical polyarthritis, most commonly affecting the small joints of the hands and feet. It results from a breakdown of self-tolerance and cytokine-mediated inflammation that leads to joint destruction. Diagnosis is based on symptoms, serology tests, and x-ray findings. Treatment involves NSAIDs, corticosteroids, and disease-modifying drugs to suppress symptoms and prevent long-term joint damage.

1. Presented By-
Paridhi Jain
Batch- 2017-18

2. Index
 Introduction
 Epidemiology
 Normal Structure
 Etiology
 Pathogenesis
 Morphology & Clinical Manifestation
- Articular
- Extra articular
 Variants
 Score
 Laboratory Investigation
 Differential Diagnosis
 Management

3. Introduction
 Rheumatoid Arthritis is a chronic auto immune
disorder causing a symmetrical polyarthritis.
 Though the most prominent manifestation of
RA is inflammatory arthritis of peripheral joints,
usually with symmetrical distribution , its
symmetrical manifestation include
haematologic , pulmonary, neurological and
cardiovascular abnormalities.

4. Epidemiology
• Prevalence of 1%
• More common in women than men (female:
male ratio of 3:1)
• Peak onset is in the third or fourth decade for
women and the fifth to eighth decades for men
• 40% of RA patients are registered as disabled
within 3 years of onset, and around 80% are
moderately to severely disabled within 20 years

5. Normal Structure

6. Etiology
Causes of RA remains unknown. Following three
factors play important role:
• Genetic Factor : Genetic susceptibility is major factor
in pathogenesis of RA
HLA gene : HLA-DRB1
Non- HLA gene: Polymorphism in PTPN22
• Environmental arthritogen : Smoking & Microbial
agents
• Immunological Derangement

7. Pathogenesis
 Break down of self tolerance : RA is initiated in genetically susceptible
individual by an exposure to arthitogenc agent which results in break down of
self tolerance.
 Cytokine- mediated inflammation:
loss of self tolerance
activation of CD4+ cells( TH1 &TH17 and interferon)
recruit macrophages & other inflammatory cell
tissue injury
activation of synovial cells( synoviocytes)

8.  Activation of B lymphocytes : produce 2 types
of antibodies
- Anti – CCPs : antibodies against cyclic citrulinated peptides
(CCPs).
Antibodies against CCPs form immune complex and deposit in
various tissues.
-Rheumatoid Factor : RF is serum immunoglobin M (IgM) auto
antibody that binds to Fc portion of own/self IgG.
Rheumatoid factor form immune complex with self IgG & can
produce damage to joints and other tissues.

9.  Production of proteolytic enzymes:
inflammation causes tissue injury
activaton of synoviocytes
produce proteolytic enzyme(collagenase , elastase)
enzymes along with antigen antibody complex
destroys articular cartilage, ligaments & tendons
TNF family of cytokines may cause increased activity of
osteoclast & produce destruction of bone

10. Consequences : above actions bring out
- edema
- hyperplasia of synoviocytes
- inflammatory inflammation in synovium
- formation of pannus
- destruction of cartilage
- erosion of adjacent subchondral bone

12. Morphologic Features
Articular Lesion
Joints Involved : -symmetrical and bilateral joints
- diarthordial joints
Joints Lesion : - chronic non supprative
proliferative polyarthritis
-destruction of articular cartilage

13. Histologically
 Synovial Hyperplasia : Hyperplastic synoviocytes
may form villus or finger like structure.
 Dense inflammatory
infiltration : consisting 0f
lymphocytes, B cells &
macrophages.

14.  Pannus Formation : mass of synovium and
synovial stroma consisting of inflammatory cell ,
granulation tissue & synovial fibroblast . Pannus
grows over the articular cartilage and destroys
it.
Ankylosis : After the destruction of cartilage ,
pannus bridges the opposite bones to form
fibrous ankylosis , which may result in bony
ankylosis. Destruction of joint followed by fusion
is termed as ankylosis.

16. Skin : Rheumatoid nodules are the common
cutaneous nodules

17. Clinical Feature
• Onset of pain
• Early-morning stiffness (lasting more than 30
minutes)
• Swelling in the small joints of the hands and feet
• As the disease progresses there is weakening of
joint capsules
– joint instability
– Subluxation
– deformity

18. Hammer toe

19. Non-articular manifestations of
RA
•Systemic – Fever, Fatigue, Weight loss
•Eyes- Scleritis, Scleromalacia perforans
(perforation of the eye)
•Neurological- Carpal tunnel syndrome,
Atlantoaxial subluxation, Cord compression
•Hematological- Lymphadenopathy, Felty’s
syndrome (rheumatoid arthritis, splenomegaly,
neutropenia), Anaemia (chronic disease,
NSAIDinduced, gastrointestinal blood loss,
haemolysis, hypersplenism), Thrombocytosis

20. • Pulmonary - Pleural effusion, Lung fibrosis,
Rheumatoid nodules, Rheumatoid
pneumoconiosis
• Heart and peripheral vessels – Pericarditis,
Pericardial effusion, Raynaud’s syndrome
• Vasculitis - Leg ulcers, Nail fold infarcts,
Gangrene of fingers and toes
• Kidneys - Amyloidosis causes the nephrotic
syndrome and renal failure

21. Variants of RA
 Juvenile RA : Found in adolescent patient.
 Felty’s syndrome : Consist of polyarticular RA
associated with splenomeagly & hypersplenism.
 Ankylosing Spondylitis or Rheumatoid spondylitis :
Rheumatoid involvement of spine particularly sacro
iliac joint. This condition has a strong HLA-B27
association & may have association with other
inflammatory disorder.

22. *Criteria for Diagnosis of Rheumatoid
Arthritis2,7
Criterion Score
• Joints affected
1 large joint 0
2–10 large joints 1
1–3 small joints 2
4 -10 small joints 5
• Serology
Negative RF and ACPA 0
Low positive RF or ACPA 2
High positive RF or ACPA 3

23. • Duration of symptoms
< 6 wks 0
> 6 wks 1
• Acute phase reactants
Normal CRP and ESR 0
Abnormal CRP or ESR 1
Patients with a score ≥ 6 are considered to have definite RA.
*European League Against Rheumatism/American College of Rheumatology 2010 Criteria.

24. Investigation
•Blood count- usually a normochromic, normocytic
anemia, ESR and CRP are raised
•Serum autoantibodies - Anti-CCP has high
specificity (90%) and, Rheumatoid factor is
positive in 70% of cases sensitivity (80%) for RA.
•X-ray- joint narrowing, erosions at the joint
margins
•Synovial fluid - high neutrophil count in
uncomplicated disease

29. Complications of RA
• Ruptured tendons
• Ruptured joints (Baker's cysts)
• Joint infection
• Spinal cord compression (atlantoaxial or upper
cervical spine)
• Amyloidosis (rare)
• Side-effects of therapy

30. Management
• No treatment cures RA
• Goals are
–Remission of symptoms
–Return of full function
–Maintenance of remission with disease-
modifying agents
• Effective management of RA requires a
multidisciplinary approach

31. • NSAIDs and coxibs- effective in relieving the joint pain and
stiffness of RA
• Corticosteroids - suppress disease activity
• Disease-modifying anti-rheumatic drugs (DMARDs)- act
mainly through inhibition of inflammatory cytokines (6
weeks to 6 months of disease onset)
–Sulfasalazine, Methotrexate