Focal adhesion kinase depletion does not reduce synovial fibroblast invasion into cartilage and bone or clinical arthritis in murine tumor necrosis factor α-induced arthritis. TNF+CreER+FAKf/f mice were treated with tamoxifen at 6 weeks of age (FAK-/-). For each experimental mouse, there was a littermate control (FAKf/f) that was either a TNF+CreER+FAKf/f mouse treated with vehicle or a TNF+CreER-FAKf/f mouse treated with tamoxifen. Spleen lysates from FAKf/f and FAK-/- mice at 5 months of age were subjected to Western blot analysis to detect focal adhesion kinase (FAK) and tubulin. A representative blot is presented in (A). (B) Densitometry was performed, and the average ± SEM data for FAK levels normalized to tubulin are presented in the graph (n = 3, *P < 0.05 by t-test). (C) Synovial fibroblasts derived from the tibiotalar joints of a 5-month-old FAK-/- mouse and a FAK+/+ mouse were expanded to passage 3. Lysates from these synovial fibroblasts were subjected to Western blot analysis for FAK and tubulin. (D) Arthritis was clinically scored in FAK-/- and littermate control FAKf/f mice based on hind foot deformity, swelling and grip strength on a scale of 0 to 3. Average ± SEM data are presented in the graph (n = 12 sex-matched pairs at 2, 3 and 4 months and n = 8 pairs at 5 months). The tibiotalar joint was fixed, decalcified, embedded and sectioned for hematoxylin and eosin staining when the mice were 5 months of age. Representative images are shown in (E). Inset shows areas of pannus invading cartilage (arrows) and bone (arrowheads). Bar represents 200 μm. (F) Joints were scored for severity of synovitis, cartilage erosion and bone erosion on a scale of 0 to 4, with average ± SEM data presented in the graph (n = 6 pairs).