Rheumatoid Arthritis

[Blood vessels, skin, heart, lungs, nerves and eyes may also be affected.]

Rheumatoid arthritis is thought to be initiated by an arthritogenic microbial agent in an immunogenetically susceptible host (associated with HLA-DR4). After initial injury, a continuing autoimmune reaction ensues, in which T cells (CD4+) release cytokines and inflammatory mediators that ultimately destroy the joint.

Pathological changes of rheumatoid arthritis: laboratory and biopsy findings…

Rheumatoid synovitis:

• Neutrophils (rheumatoid arthritis cells) can be present in synovial fluid

• The synovium demonstrates chronic inflammation (intense lympho-plasmacytic and histiocytic synovial infiltrate)

• Hypertrophy and hyperplasia (swollen – villous pattern) frequently with fibrinous exudates at the surface.

• Exuberant synovium known as a pannus eventually fills the joint space
  

Articular cartilage destruction:

• Due to release of destructive enzymes (proteases and collagenase), cytokines (IL-1 & TNF-) and pannus formation across articular surfaces.

• Changes reminiscent of DJD but with fibrous and bony ankylosis (fusion of joint)

• The capsule and periarticular structures are also destroyed; this can lead to instability in the joint, with subluxation and dislocation

Focal destruction of bone:

• Osteolytic destruction of bone occurs at the edges of the joint; with little reparative activity

• Bone ‘erosions’ can be seen on radiography, and they are associated with joint deformity.

Clinical aspects:

• Typically polyarticular, bilateral and symmetric

• Any joint can be affected; most common are small joints of the hands and fee

• Presents with: general malaise, pain and stiffness in the joints (most marked in the morning)

• On examination: hot, woollen and tender joint

Other investigative findings are:

• Radiology: osteoporosis, erosion

• Serology: rheumatoid factor (70%)

• Synovial fluid analysis: milky and turbid

Category: Orthopedics Notes , Pathology Notes