Steroid-associated osteonecrosis animal model in rats

Zheng, Li-Zhen; Wang, Jia-Li; Kong, Ling; Huang, Le; Tian, Li; Pang, Qian-Qian; Wang, Xin-Luan; Qin, Ling

Besides bone tissue, we also used DXA to test the fat/lean composition in the SAON rat model for the first time for studying soft tissues around the SAON region. The ROI was chosen at the low limb because the fat percent in the normal control group was low, i.e., 1.5% from the result that provided reference data to study their alterations in the SAON group. There is muscleebone crosstalk that they may modulate each other mechanically and metabolically [38] , especially in the metabolic syndrome affected by excess corticosteroid [39] . Inflammation, oxidative stress and hormonal modification could be the common causes involved in development of decreased muscle mass and decreased osteoblast activity [38] . In our SAON rat model, we found significantly lower lean mass from DXA results and lower bone mass from micro-CT at week 6 that shared similar clinical features [39] . DXA results in this study also showed significantly increased fat percentage in the lower limb in the SAON group at week 6, whereas the body weight for rats from the SAON group did not increase from week 2 to week 6, suggesting that corticosteroid treatment changed the tissue composition, i.e., increased fat tissue and decreased bone and skeletal muscle, but not body weight in this rat SAON model. The excess corticosteroid treatment could affect differentiation potential of both adipocytes and osteoblasts by activating peroxisome proliferator-activated receptor gamma (PPARg) of the precursor cells of adipocytes and osteoblasts to increase adipogenesis and meanwhile decrease osteogenesis to induce osteonecrosis [40, 41] .