Fig. 6

Inhibition of COX-2 attenuates spontaneous OA progression in STR/ORT mice. a Top: safranin O and fast green staining of the subchondral bone of STR/ORT mice and CBA control mice treated with vehicle or a COX-2 inhibitor. Proteoglycan (red) and bone (blue). Scale bar, 200 μm. Middle: representative images of TRAP staining in the subchondral bone of STR/ORT and CBA mice treated with vehicle or a COX-2 inhibitor. Scale bars, 50 μm. Bottom: trichrome staining of the subchondral bone of STR/ORT and CBA mice treated with vehicle or a COX-2 inhibitor. Scale bars, 50 μm. b OARSI scores of STR/ORT mice and CBA control mice treated with vehicle or a COX-2 inhibitor. N = 5 mice in each group from three independent experiments. c Quantitative analysis of TRAP⁺ cells on the bone surface in STR/ORT mice and CBA control mice treated with vehicle or a COX-2 inhibitor. N = 5 mice in each group from three independent experiments. d Serum PGE2 levels in STR/ORT mice and CBA control mice treated with vehicle or a COX-2 inhibitor. N = 5 mice in each group from three independent experiments. e–g Representative images of calcein double labeling of subchondral bone e and the quantification of the mineral apposition rate (MAR) f and bone formation rate (BFR) per bone surface (BS) g in STR/ORT mice treated with vehicle or a COX-2 inhibitor. Scale bar, 25 μm. h and i Quantitative analysis of the bone volume (BV)/tissue volume (TV) ratio h and trabecular pattern factor (Tb.Pf) i in subchondral bone, as determined by μCT analysis. N = 5 mice in each group from three independent experiments. j Quantitative analysis of mechanical allodynia in STR/ORT mice treated with vehicle or a COX-2 inhibitor, as measured by the foot-lift response frequency to stimulation with a 0.008-g von Frey filament. N = 5 mice in each group from three independent experiments. All data are shown as the mean ± standard deviation. *P < 0.05. Statistical significance was determined by Student’s t-test