Fig. 5.

OA-like phenotype was decelerated when either the Mmp13 or the Adamts5 gene was deleted in β-catenin(ex3) ^Co12ER mice. Tamoxifen was administered into 2-week-old mice (0.1 mg/g body weight, i.p., daily for 5 d). TMJ samples were harvested from 3- or 6-month-old mice and Alcian blue/H&E and SO/FG staining were performed. Alcian blue/H&E staining (A) and SO/FG staining (B) showed decelerated TMJ defect progression and more aggrecan contents in double mutant mice compared to those in β-catenin(ex3)^Co12ER mice. (C) Total TMJ cartilage area was quantified by tracing the Alcian blue-positive area. Cartilage areas were 8 and 13 % decreased in 3-month-old (β-catenin(ex3)/Mmp13)^Co12ER and β-catenin(ex3)^Co12ER/Adamts5^−/− double mutant mice, and were 22 and 27 % decreased in 6-month-old (β-catenin(ex3)/Mmp13)^Co12ER mice and β-catenin(ex3)^Co12ER/Adamts5^−/− mice compared to the same age control mice (*p < 0.05, compared to Cre-negative control group; **p < 0.05, compared to β-catenin(ex3) ^Co12ER group; one-way ANOVA followed by Dunnett’s test, n = 5). (D) Total cartilage thickness was quantified by tracing the Alcian blue-positive thickness in the centre of the TMJ cartilage. Total cartilage thickness was decreased 6 and 25 % in 3-month-old double mutant mice and 30 and 34 % decreased in 6-month-old double mutant mice compared to the same age control mice (*p < 0.05, compared to Cre-negative control group; **p< 0.05, compared to β-catenin(ex3)^Co12ER group; one-way ANOVA followed by Dunnett’s test, n = 5).