Steroid-associated osteonecrosis: Epidemiology, pathophysiology, animal model, prevention, and potential treatments (an overview)

Xie, Xin-Hui; Wang, Xin-Luan; Yang, Hui-Lin; Zhao, De-Wei; Qin, Ling

The recent advance in understanding the pathophysiological mechanism of the inadequate repair at the early stage of SAON is on a decreased activity of BMSCs pool [13e15]. Steroids can induce differentiation of BMSCs into adipocytes linage by upregulating adipocytes transcription factor gene expression (Peroxisome proliferator-activated receptor gamma adipose-specific 422 and adipsin) and inhibit their osteogenic differentiation by downregulating osteoblast transcription factor gene expression [Cbfa1/Runx2, type I collagen, bone morphogenetic protein (BMP-2), osteocalcin, osteopontin, and osteonectin, and osteocalcin], thus resulting in increased lipid deposition including larger fat cells number and its area fraction. Clinically, Gangji and Hernigou reported decreased number and osteogenic differentiation ability of BMSCs pool in iliac or femora in patients with SAON, which resulted in the inadequate lesion repair at early stage of ON [13e15]. The authors' group also demonstrated significantly increased lipid deposition including larger fat cells number and fat deposition area at the early stage of SAON in an animal model [9, 11, 16, 17] .