Study On Steroid-induced Avascular Necrosis Of Femoral Head In The Early Days And Apoptosis And The Experimeantal Study On Bcl-2 And P53

Objective: with the increasing of incidence of Steroid-induced Avascular Necrosis of Femoral Head(SANFN), it's becoming the number-one fast developing disease, which is well over that of femoral neck fracture. But its exact mechanism is not quite clear today, which affects the dinical prevention and the treatment. As a new"Form of the death of cells", apoptosis provides a completely new research apporach to research on Steroid-induced Avascular Necrosis of Femoral Head. But there is little study on the controlling genes of apoptosis. According to the study of the rabbit modle, which is Steroid-induced Avascular Necrosis of Femoral Head, this subject works as a test of its histomorphology, apoptosis and immunohistochemistry in order to study the apoptosis and the function played by the Steroid-induced Avascular Necrosis of Femoral Head's controlling genes in the earty days. It helps to find a new cure to treat the Steroid-induced Avascular Necrosis of Femoral Head in its early days, and will lay a solid foundation of treating the Steroid-induced Avascular Necrosis of Femoral Head at the level of genes.Method: 30 healthy rabbits at the age of 6 months weighing 2-3 kg. Divide the rabbits into 2 groups, 15 for experimental group and 15 for control group. Test the histomorphology, apoptosis, immunohistochemistry after the models are finished.Result:1. Get rid of the dead animals including the rabbits which are Steroid-induced Avascular Necrosis of Femoral Head in the early days. 12 for experimental group and 15 for control group. The success rate of models reachs 80%.2. The result of histomorphology:General organization observation: The bone's sueface is light red in experimental group while the bone's surface is red in control group.Observation under microscpo (HE) : Compared with the control group, bone lamella thin at the cartilage,bone trabecula in experimental group becomes skarce, and empty bone lacune increases. The number fat cells in medullary cavity of bone increases and they become bigger, and the red bone marrow reduces.3. Some yellow granules which emerge in bone cells are masculine cells, and much more apoptosis emerges in experimental group, about (20.93±1.37)%, more than(1.51±0.24)% in control group.4. The result of immunohistochemistry:Bcl-2: cytolymph is covered with yellow granules, the rate of masculine cells is (9.10±0.67)%, which is lower than (11.13±1.80)%(P<0.01) in control group.P53: The nucleus ear yellow granules. The rate of masculine cells is (14.42±3.06)%, this rate is much higher than that of control group:(6.04±0.63)%(P<0.01).Conclusion: This animal model has made it possible to create the model of Steroid-induced Avascular Necrosis of Femoral Head successfully; The glucocorticoid may cause the death of bone cells in femoral head. The death of bone cells and apoptosis lead to the Steroid-induced Avascular Necrosis of Femoral Head in the early days. The proteinum Bcl-2 is restrained by too much bormone, while the hormone advances proteinum p53, so proteinum Bcl-2 and proteinum p53 both control the apoptosis.