The Study Of Cell Apoptosis In Rabbit Steroid-induced Avascular Necrosis Of The Femoral Head

Objective: The mechanism of the steroid-induced avascular necrosis of the femoral head(SANFH) are still in nubilous and were considered to be one of the major problems in medical field. With the emerge of a new way of cell death, apoptosis, the programmed cell death, brought new methods for research of the SANFH. Some study from nation or overseas have opened out the close relationship between them. we used a rabbit model of glucocorticoid excess to find the relationship between apoptosis and SANFH,. In this research, we evaluated the histological appearance and molecular biology changes to demonstrate SANFH is necrosis so called traditionally or cell apoptosis, and make foundation to treat and prevent SANFH.Methods: Thirty mature six-month rabbits having a mean body weight of 2.5kg were randomly divided into two groups which are the test group(twenty) and the control group(ten). The test group were injected Prednisolone Acetate Injection of 7.5mg/kg biweekly, and the control group were injected same 0.9% Sodium Chloride Injection biweekly for ten weeks. While model was established, We execute four test rabbits and two control rabbits every two weeks .We take out both femoral head ,one for histological appearance ,another for molecular biology .Results: The test group had changes in commonly status four weeks after experiment starting, X ray stage was Ficat I, bone trabecula narrowing, cellula adipose increasing can been seen under light microscope. TUNEL labeling difference contrasted with the control group has statistical significance (P<0.05). With experiment process up to week six , the X ray showed femoral head density was poor, part are heighten , bone trabecula illegibility and transfiguration. X ray stage was Ficat II . With experiment process up to week eight ,we find the femoral head changed and collapsed, and the joint space was narrowing with a Ficat stage III. The shape and the cartilage surface of the femoral head were uneven when observing with bare eyes. The femoral head was easy to cut, and the blood supply was poor. In histological examining, bone trabeculas had tiny focus of infections, also became narrowing and discontinuing. The bone lacunas were some of vacuities. bone marrow of the distal end of femoral head became adipose degeneration, a great quantity adipose cell can be seen. The quantities of apoptotic cell and empty bone lacunas had increased, but the amplitude of apoptotic cell was higher than that of empty bone lacunas, and most of them were laid under subcartilage zone and surrounding bone trabeculas.Conclusions: Under the affect of the glucocorticoids, a great quantity osteocytes become apoptotic, thus induced disorders of the bone regenerate function and accumulation of tiny fractures of this area. So the reason why glucocorticoid induced avascular necrosis of the femoral head still is developing even when the glucocorticoid take out of service can be explained. The relationship between the main glucocorticoid dose and the rate of avascular necrosis of the femoral head also can be explained. Apoptotic cell in early and middle period of glucocorticoid induced avascular necrosis of the femoral head can be detected, the quantity increasing with experimental time and the increasing amplitude is higher than that of empty bone lacunas, and the difference has statistical significance contrasted with control group. So we think apoptosis occurred and played a very important role in the avascular necrosis of the femoral head, and also affect the balance of the bone development and regeneration, as to decide this disease's occurrence and development.