Rheumatoid Arthritis

Definition
• RA is a chronic inflammatory, autoimmune progressive symmetrical polyarthropathy
and systemic disease of unknown aetiology.
 1-2% populations – monozygotic twins: 12-15%
 Chief age of onset : 40-50 years
 M:F = 1:3
 Important factors in the evolution of RA
1. Genetic susceptibility
2. Immunological reaction
3. Inflammatory reaction in joint and tendon sheaths
4. Appearance of antibodies
5. Anti-CCP antibodies
6. Perpetuation of inflammatory process
7. Articular cartilage destruction
Genetic Susceptibility
 HLA-DR4: in 70% people in RA ; encoded in MHC region of chr. 6
 ‘shared epitope’
Immunological reaction
 After the immune reaction has been initiated, various local factors come in to play and
there is progressive enhancement of the immune response.
 Marked proliferation of synovium with appearance of new blood vessels
 Cytokines, namely TNF-alpha, IL-1 and IL-6 are secreted
 Hallmark of early RA: synovitis both in joints and in tendon sheath linings
 Rheumatoid Factor are anti-IgG antibodies formed due to B-cell activation. RF also
positive in SLE, and Sjogren’s Sydrome.
 Anti-CCP (cyclic citrullinated peptide)
Chronic Synovitis and Joint Destruction
 Production of proteolytic enzymes, prostaglandins and cytokines TNF and IL-1

PATHOLOGY
 Though RA is a systemic disease most characteristic lesion are seen in the synovium
or within the rheumatoid nodules.
 The pathological changes in joints, if unchecked, progress in four stages
1. Preclinical :
 Raised ESR, RA and CRP may be detectable years before the
diagnosis
2. Synovitis and joint swelling:
 Vascular congestion with new blood vessel formation.
 Proliferation of synoviocytes
 Infiltration of synovial layers by polymorphs, lymphocytes and plasma
cells
 There is joint swelling due to thickening of the capsular structures,
villous formation of synovium, cell rich effusion into joints and
tendon sheaths,
3. Destruction: of joint and tendon and erosion of articular cartilage
 Articular cartilage is eroded by
 Proteolytic enzymes
 Vascular tissue in folds of synovium
  Direct invasion of cartilage by pannus
 Joint margins eroded by
 Tissue invasion
 Osteoclastic resorption
 Tendon sheaths: Tenosynovitis  invasion of collagen bundles 
partial or complete rupture of tendons
 Synovial effusion causes swelling of the joints, tendons and bursae
4. Deformity: progressive instability and deformity of joints. Progressive
inflammation continues
Rheumatoid Arthritis in the hand
1. Early stage: Synovitis of the joint and tendon sheaths
2. Progressive stage: joint and tendon erosion and mechanical derangements
3. Late stage: joint destruction, attenuation of ligament, tendon ruptures -- > instability
and progressive deformity
Clinical features:
1. Early stage:
a. stiffness and swelling of fingers
b. features of carpal tunnel syndrome
c. on Examination:
i. swelling of MCP and PIP joints
ii. spindle shaped fingers
iii. bilateral affection
iv. swelling of tendon sheaths usually on the dorsum of the wrist and
along the ulnar border. Thickened flexor tendons on the volar aspects
of proximal phalanges.
v. Tender joints, crepitus, diminished joint mobility and grip strength
2. Progressive stage:
a. Radial deviation of the wrist and ulnar deviation of fingers.
b. Swan neck, buotonniere, drop finger, mallet thumb
Why ulnar deviation of MCP?
1. palmar grip and thumb pressure naturally tend to push the index finger
ulnarwards
2. weakening of the collateral ligaments and the first dorsal interosseous
muscle reduces the normal resistance to this force
3. the wrist is usually involved and, as it collapses into radial deviation, the
MCP joints automatically veer in the opposite direction (the so-called
‘zigzag mechanism’)
4. once ulnar drift begins, it becomes self-perpetuating due to tightening of
the ulnar intrinsic muscles and stretching of the radial intrinsics and the
adjacent capsular structures.
5. As the sagittal bands fail, the extensor tendon slips ulnarwards and
palmarwards, accentuating the deformity even further.
 3. Late stage
a. Inflammation subsides
b. Deformities are established
i. Carpus settles into radial tilt and volar subluxation
ii. Market ulnar drift of fingers and volar dislocation of MCP joints
iii. Multiple swan neck and buotonniere deformities
c. When deformities become fixed, patients cannot dress or feed themselves due
to functional loss
General features
1. Rheumatoid hands are weak because of
a. Generalized muscular weakness
b. Pain inhibition
c. Tendon malalignment or rupture
d. Joint stiffness and nerve compression
2. Rheumatoid nodules in pressure areas (pulps of fingers and radial side of index
finger)
3. Z-collapse: if one of two adjacent joints change direction, then the overlying tendons
will pull the other joint in opposite direction. E.g., radial tilt of wrist with ulnar drift
of MCP joints, buotonniere and swan neck.
X-Rays:
1. Early: soft tissue swelling and osteopenia
2. Progressive: joint space narrowing, peri-articular erosions (MCP joints and ulnar
styloid)
3. Late: marked articular destruction, joint deformity and dislocation
Treatment

Early Stage:
1. Control systemic disease and local synovitis
2. Splints to rest the inflamed joints and tendons
3. Local injection of corticosteroids with local anesthetic
a. 0.5 ml for MCP joint / flexor tendon sheath
b. 1 ml for wrist
4. Synovectomy, carpal tunnel release
Progressive stage:
1. Operative synovectomy + physiotherapy
2. Reconstruction of soft tissues on the ulnar side of wrist
3. Tightening of capsular structures
4. Repair of isolated tendon ruptures
5. Surface replacement for MCP joints destruction without ulnar drift
Late Disease
1. Arthrodesis
2. Joint replacement with Silastic spacers
Treatment of rheumatoid thumb
1. Ruptured FPL
a. Painless: leave alone
b. Painful: tendon graft, FDS transfer, IP fusion
 2. Buotonniere deformity
a. Passively correctible: corticosteroid injection + splintage
b. Fixed MCP, passively correctible IP and mobile CMC: MCP fusion
c. Fixed MCP and IP joints: fuse IPj, fuse or replace MCP joint
d. With CMC failure: Trapeziectomy + CMC joint stabilization
3. Arthritis mutilans
a. Arthrodesis with interposition bone graft
4. Swan neck deformity: adduction contracture of thumb base and MCP hyperextension
a. Trapeziectomy + soft tissue reconstruction +MCP fusion
b. Swan neck with MCP and CMC preserved: palmar plate advancement + MCP
fusion
5. Gamekeeper’s thumb
a. Ligament reconstruction + MCP joint fusion

Clinical Features
1. PIP joints -- > wrist -- > knee -- > shoulder
2. Tenosynovitis -- > extensor compartment of wrist and flexor sheaths of fingers. Seen
by passive movement
3. Valgus knees, valgus feet and clawed toes
4. Rheumatoid nodules
a. Pathognomonic, but only in 25%
b. Subcutaneous, rubbery
c. Back of elbow, tendons, viscera, eye
d. Muscle wasting, skin ulceration, vasculitis, sensory neuropathy
X-Rays
1. Erosions within 2 years

Blood
- Normocytic, hypochromic anemia
- RF – 80%
 - ANA – 30%
Diagnosis
A rapid diagnosis is vital so that early treatment can be started with DMARDs.
1. Clinical – bilateral symmetric arthritis or proximal joints of hands and feet persisting
for at least 6 weeks.
a. Subcutaneous nodules
2. X-Ray: periarticular erosions
3. Importance of RF:
a. Prognosis -- > persistently higher titres herald more serious disease
4. D/D:
a. Seronegative inflammatory polyarthritis
b. AS
c. Reactive arthritis: larger joints and LS spine
d. Polyarticular gout: Both RA and gout don’t occur in the same patient
e. CPPD
f. Sarcoidosis: Acute, chronic, no bone
involvement, ESR, SACE, non-caseating
granuloma
g. Lyme disease
i. Asymmetrical inflammatory
polyarthritis affecting larger joints
h. Viral arthritis
i. Parvovirus B-19
i. Polymyalgia rheumatica
i. Pectoral and pelvic girdles. Joints not
tender, muscles are. Predisposed to giant cell arteritis
j. Polyarticular osteoarthritis
Treatment
- There is no cure
- Medical treatment – rapid and aggressive reduction of inflammation
- Principles of medical management
o Steroids (prednisolone 30 mg or 120mg im methylprednisolone)
o Methotrexate (10-25 mg/week)
o Sulfasalazine, hydroxycholoroquine
o If methotrexate untolerated, use leflunomide
o If no satisfactory response to DMARDs, biological therapies must be used
 TNF- inhibitors- infliximab, etanercept, adalimumab
 Inhibitors of T-cell costimulation – abatacept
 IL-6 inhibitor – tocilizumab
 B-cell depleting – rituximab
- Surgical management
o Synovectomy
o Osteotomy, arthrodesis, arthroplasty for late stages
- Methotrexate can be used during orthopaedic surgery. But doses of prednisolone must
be low and TNF inhibitors must be discontinue prior.
- Complications
1. Fixed deformities
2. Muscle weakness
3. Joint rupture
4. Infection
5. Spinal cord compression
6. Systemic vasculitis
7. Amyloidosis