Apoptosis Of Osteocyte In Rabbit Avascular Necrosis Of The Femoral Head Induced By Glucocorticoids

Objective: The pathogeny and mechanism of the avascular necrosis of the femoral head(ANFH) are still in nubibus and were considered to be one of the major problems in medical field. With the emerge of a new way of cell death, apoptosios, the programmed cell death, brought new methods for research of the avascular necrosis of the femoral head. Close relationship between them was demonstrated in some researches. To find the relationship between apoptosis and ANFH, we used a rabbit model of glucocorticoid excess. In this research, we evaluated the histological appearance and molecular biology changes to demonstrate ANFH is necrosis so called traditionally or cell apoptosis, yet make foundation for further study. Methods: forty-eight mature rabbits having a mean body weight of 2.5kg were randomly divided into two groups while A is control group and B is test group. While model was established, evaluations were made every two weeks including commonly status, X ray appearance, HE staining and TUNEL labeling. Results: group B had changes in commonly status four weeks after experiment starting, X ray stage was Ficat II, bone trabecula narrowing, cellula adipose increasing can been seen under light microscope. TUNEL labeling difference contrasted with group A has statistical significance (P<0.05). With experiment process, up to week twelve, the X ray showed femoral head shape was changed and collapsed, poor density uniformity and the joint space was narrowing as well in group B with a Ficat stage III-IV. 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. In some of the trabeculas, there was newly formed bone can be seen covered on necrotic bones. The bone lacunas were some of vacuities. The blood vessels of osteoepiphysis were scarce, bone marrow of the distal end of femoral head became adipose degeneration, a great quantity adipose cell can be seen. The quantities of positive TUNEL cell and empty bone lacunas had increased, but the amplitude of TUNEL was higher than that of empty bone lacunas, and most of them were laid under subcartilage zone and surrounding bone trabeculas. Conclusions: When avascular necrosis of the femoral head occurred, tiny fractures are also happens in the area of subcartilage zone of the formal head, under the affect of the glucocorticoids, numerous of the osteocytes become apoptotic, thus induced disorders of the bone regenerate function and accumulation of tiny fractures of this area. So the reason why glucocorticoids induced avascular necrosis of the femoral head still is developing even when the glucocorticoids take out of service can be explained. The relationship between the main glucocorticoids dose and the rate of avascular necrosis of the femoral head also can be explained. Apoptotic osteocytes in early and middle period of glucocorticoids 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 middle-late stage of the avascular necrosis of the femoral head, and also affect the balance of the bone development and regeneration, as to decide this disease's genesis and development.