pannus

In rheumatoid arthritis, pannus formation begins with synovial hyperplasia triggered by chronic autoimmune inflammation (anti-CCP antibodies, rheumatoid factor, and immune complex deposition). Activated synovial fibroblasts and macrophages proliferate, forming a thickened, hypervascular synovial membrane infiltrated by lymphocytes (especially CD4+ T cells), plasma cells, and neutrophils. This tissue, called pannus, extends over and invades the articular cartilage and subchondral bone, releasing matrix metalloproteinases, cytokines (TNF-α, IL-1, IL-6), and RANKL, which promote cartilage degradation and osteoclast-mediated bone erosion. Over time, pannus leads to joint space narrowing, bony erosions (seen on X-ray as juxta-articular osteopenia and marginal erosions), and eventually fibrous or bony ankylosis, causing deformities such as ulnar deviation, swan-neck, and boutonniere deformities. Pannus is a hallmark of RA pathology and differentiates it from osteoarthritis, which lacks significant inflammatory synovial proliferation. The term "pannus" can also refer to vascularized fibrous tissue overlying the cornea (corneal pannus), seen in trachoma or chronic contact lens wear, representing a different but analogous process of inflammatory tissue overgrowth. Clinically, pannus formation correlates with the chronicity and severity of RA, and its presence underlies the rationale for early aggressive treatment with DMARDs and biologics (e.g., TNF-α inhibitors) to prevent irreversible joint damage.