PATHOPHYSIOLOGY

Auto immunity theory suggest,

Antigen triggers the formation of an abnormal immunoglobulin G(IgG)

RA characterised by
Presence of auto antibodies against abnormal igG
Auto antibodies are known as rheumatoid factor RF

RF combines with IgG to form immune complex

Initially deposit on synovial membrane or superficial articular cartilage in joints

Immune complex activates T and B cells proliferation (Angiogenesis in synovial lining}

Inflammation and Neutrophills get attracted to the site

Release proteolytic enzymes that can damage articular cartilage and

 causes the synovial lining to thicken

Invades the surrounding cartilage ligaments, tendons, joint capsule

T –helper CD4 cells (primary orchestrates of

Pannus {highly vascular granulation tissue} forms within joint
cell mediated immune response)

Eventually covers and erodes the entire surface of articular

Activated CD4 cells stimulate cartilage
Monocytes, macrophages and synovial
Fibroblast to secrete (Production of inflammatory cytokines at the Pannus- cartilage

Junction)

Further cartilage destruction

pro inflammatory cytokines

Interleukin-1 Interleukin -6 and Tumor Necrotising factor
 Pannus also scars and shortens supporting structures
These cytokines are primary factors that drive
Inflammatory response in R A
Joint laxity sublaxation, contracture

Joint changes from chronic inflammation begins

When the hypertrophied synovial membrane invades the
Surrounding cartilage ligaments tendons and joint
capsule
clinical manifestations