Skip to main content
. 2014 Jan 6;111(3):1072–1077. doi: 10.1073/pnas.1318685111

Fig. 2.

Fig. 2.

IL-1Rl–deficient mice are protected from developing cmo pathology. (A) Kaplan-Meier disease-free survival curves for cmo (n = 27), cmo.IL-1RI+/− (n = 48), and cmo.IL-1RI−I− (n = 49) mice. Test of equality over the three groups (log–rank P < 0.0001; Bonferroni-adjusted pairwise survival curve comparisons, each P < 0.0005). (B and C) Representative tail kinks and foot deformities in a 3-mo-old cmo.IL-1RI+/− mouse in comparison with a littermate cmo.IL-1RI−/− mouse by gross (B) and radiological (C) examination. (D) Representative fixed decalcified tail bone from WT, cmo, cmo.IL-1RI+/−, and cmo.IL-1RI−/− sectioned and stained with H&E. In the cmo and cmo.IL-1RI+/− sections there is loss of trabecular and cortical bone, with fibrosis and infiltration of macrophages, lymphocytes, and neutrophils (arrows). In contrast, the section from the cmo.IL-1RI−/− mouse shows normal bone with no inflammation. (Scale bars, Upper, 200 μm; Lower, 50 μm.) (E) Histological scoring for severity of inflammation and bone loss was performed on tail bones from cmo mice lacking IL-1Rl compared with heterozygous controls (n = 5 per group). (F) Histologic sections of tail vertebrae from WT, cmo, and cmo.IL-1RI−/− mice stained for TRAP, a marker for osteoclasts (arrows). (G) Number of osteoclasts per 400× field per mouse was scored using lmageJ software (n = 5 for cmo, n = 3 for cmo.IL-1RI−I−). *P = 0.033 by two-tailed Mann-Whitney test.