Fig. 1
HFD accelerates the onset of OA. The onset of OA was determined by the irregular surface and the disappearance of surface layer cells from tissues stained with H&E and reduced Safranin O. Scale bars, 20 μm. a Mice fed an SD or an HFD for 12 weeks were subjected to surgery for experimental OA, and after 4 weeks (n = 10 for each diet), 6 weeks (n = 10 for each diet) and 8 weeks (n = 10 for each diet), the cartilage was observed. Representative histologic findings show that characteristic OA findings were observed 6 weeks after surgery in mice fed an HFD but not in mice fed an SD. The graph shows the occurrence of the onset of OA among mice fed an SD or an HFD during three different weeks. The dietary variable showed a significant difference between SD and HFD groups based on the likelihood ratio test (P < 0.01) from Poisson regression analysis. OA was more severe in HFD-fed mice compared to SD-fed mice as determined by OARSI scoring. **P < 0.01 according to Scheffe’s test. b Mice were fed an SD or an HFD for 25 weeks, and the cartilage was observed. Characteristic OA findings were observed in all mice fed an HFD (n = 10) but not in mice fed an SD (n = 10). The graph shows the occurrences of the onset of OA among 10 mice for the SD and HFD groups. There was a significant difference between SD and HFD feeding (P < 0.01) according to the chi-squared test. OA was more severe in HFD-fed mice compared to SD-fed mice as determined by OARSI scoring. **P < 0.01 according to Scheffe’s test
