Figure 3
Diminished joint pathology within the knees of Fib
– mice immunized with CII.
(A–H) Representative hematoxylin and eosin–stained knee joint sections prepared from unchallenged (A and B) and CII-immunized (C–H) Fib+ and Fib– mice. At 40 days after initial challenge, the knee joints collected from Fib+ mice exhibited extensive destruction of the joint, characterized by widespread synovial hyperplasia (C, arrow), and considerable erosion, if not obliteration, of cartilage on articular surfaces (C and E, arrowheads) and within the meniscus. Neutrophil-rich inflammatory exudates were frequently observed within the synovial fluid of knees collected from Fib+ mice with CIA (E and G). In contrast, knee joints collected in parallel from CII-immunized Fib– mice typically displayed more normal architecture with intact and smooth articular surfaces (D, F, and H). (I–K) Immunohistochemical detection of fibrin(ogen) within knee sections prepared from Fib+ mice (brown stain). Note the strong fibrin(ogen) deposition on eroding articular surfaces (I, arrowheads) and as a component of neutrophil-rich rice bodies within the joint space (J and K). Scale bar: 200 μm (A–F, I, and J); 10 μm (G, H, and K).
