musculoskeletal and connective tissue disorders
Acute Infectious Arthritis
Pathophysiology of Acute Infectious Arthritis
Infecting organisms multiply in the synovial fluid and synovial lining. Some bacteria (eg,S. aureus) produce virulence factors (adhesins), which allow bacteria to penetrate, remain within, and infect joint tissues. Other bacterial products (eg, endotoxin from gram-negative organisms, cell wall fragments, exotoxins from gram-positive organisms, immune complexes formed by bacterial antigens and host antibodies) augment the inflammatory reaction. Neutrophils migrate into the joint and phagocytose the infecting organisms. Phagocytosis of bacteria also results in neutrophil autolysis with release of lysosomal enzymes into the joint, which damage synovia, ligaments, and cartilage. Therefore, neutrophils are both the major host defense system and the cause of joint damage. Articular cartilage can be destroyed within hours or days. Inflammatory synovitis may occasionally persist even after the infection has been eradicated by antibiotics. Particularly in gonococcal cases, persistent antigen debris from bacteria or infection may alter cartilage, causing it to become antigenic, and—together with the adjuvant effects of bacterial components and immune complexes—immune-mediated, “sterile,” chronic inflammatory synovitis may develop. 