Understanding the Complex Pathogenesis of Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by inflammatory arthritis and extra-articular involvement. It represents a chronic inflammatory disorder often resulting from the interaction between genetic predispositions and environmental factors, such as tobacco exposure. This condition predominantly involves synovial joints and typically begins in small peripheral joints, presenting symmetrically.

The pathogenesis of RA is multifaceted, involving a range of genetic, environmental, immunologic, and other contributing factors. While the exact etiology remains unclear, it is understood that environmental and genetic influences can interact, triggering adaptive immune responses. This complexity is further illustrated by the broad heterogeneity among patients diagnosed with rheumatoid arthritis based on the 1988 American College of Rheumatology Classification Criteria.

Iain B. McInnes, F.R.C.P., Ph.D., and others have contributed significantly to the understanding of RA’s pathogenesis, highlighting the intricate interplay between various factors. RA is more frequently observed in females than males and is commonly seen in the elderly. Reports from 2002 indicate a prevalence rate ranging from 0.5% to 1% of the population, with regional variations. The disease primarily affects the lining of synovial joints, leading to significant morbidity, decreased quality of life, increased mortality, and substantial economic costs.

For further insights into the pathogenesis of rheumatoid arthritis, refer to these comprehensive sources:

StatPearls – NCBI Bookshelf
The American Journal of Medical Sciences
UpToDate
The New England Journal of Medicine
Cell Press
NEJM
PubMed
PMC