[Inflammation and joint destruction during rheumatoid polyarthritis: what relation?]

Abstract

A QUESTION REVISITED: It is generally accepted that acute then chronic joint inflammation leads to the development of a synovial pannus and secondarily to characteristic degenerative joint disease en rheumatoid arthritis. However accumulating clinical and biological evidence would question the real relationship between inflammation and joint destruction, and suggest therapeutic strategies might need to be revisited. THE CAUSAL EVENTS: Synovial proliferation is the fundamental event in joint lesions. The contact between the synovial pannus and the cartilage leads to characteristic joint damage mediated by pro-inflammatory cytokines (TNF alpha and IL 1) and enzyme secretion, particularly metalloproteases. ROLE OF T CELLS: The role of T-lymphocytes is a question of much debate. Although it is generally accepted that T cells are crucial in the initial phases of rheumatoid arthritis, several arguments suggest that the process of synovial proliferation and joint destruction in advanced stage disease would be independent of T cell activity. Synovial macrophages and fibroblasts, and perhaps chondrocytes, play a central role at this phase.

Therapeutic implications: A direct mandatory relationship between inflammation and joint destruction appears to be excluded, although complex and poorly understood links exist between these events in rheumatoid arthritis. A better understanding of the mechanisms involved would be very useful for the development of more adapted therapeutic strategies in rheumatoid arthritis.