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

Ischaemia is a very important pathomechanism of SAON ( Fig. 2) . Abnormality of lipid metabolism and clotting disorders of blood are the major events which lead to ischaemia. High-dose MPSL could induce multifocal ON in conjunction with thrombocytopenia, hypofibrinogenemia, and hyperlipaemia, which resulted in increased blood glutinousness followed by decreased blood flow. The altered fat metabolism could increase serum lipid levels (triglyceride and cholesterol) and a fat embolism resulted in vascular occlusion which accelerated the ischaemia. The intravascular thrombosis resulting from clotting disorders was also the key pathogenic pathway to cause ischaemia in SAON found by others and our own studies [7, 10, 17, 28] . A study from our group showed that the inhibition of both thrombosis and lipid deposition could reduce the incidence of SAON [11, 16] , which proved that the abnormality of lipid metabolism and clotting disorders were indeed important mechanism for SAON. It was found that hypercoagulability of plasma happened after 24 hours of high-dose MPSL treatment, which might be the pathogenetic factors contributing to the early stage of SAON and therefore to be used as an index of early risk factor to predict later SAON occurrence.