Non-traumatic osteonecrosis of the femoral head (ONFH) is believed to be avascular necrosis. Certainly, a disruption of a supplying artery induces necrosis in the supplying artery-dominant region. However, when an abn...Non-traumatic osteonecrosis of the femoral head (ONFH) is believed to be avascular necrosis. Certainly, a disruption of a supplying artery induces necrosis in the supplying artery-dominant region. However, when an abnormality such as cell apoptosis, or another reason, is developed in the supplying artery-dominant region, it induces a disruption of the supplying artery. Therefore, to prove that ONFH is avascular necrosis, it is necessary to demonstrate the disruption of the supplying artery prior to histological osteonecrosis development. Here we investigate histologically, using a rat model, whether disruption of the supplying artery occurs before the initial development of ONFH following corticosteroid treatment. Rats were given imiquimod and methylprednisolone, and were sacrificed 1, 2, 3, 7 or 14 days after the last injection. At the sacrifice, the rat was perfused with 20 ml black Indian ink through the left ventricle. ONFH was observed in the Imiquimod + Methylprednisolone group at 7 and 14 days. The osteonecrotic area was not stained with perfused black Indian ink. However, the lateral portion of the femoral head near the superior retinacular artery was stained with the ink. In conclusion, the present study shows that the superior retinacular artery did not occlude before the initial development of ONFH histologically in rats.展开更多
文摘Non-traumatic osteonecrosis of the femoral head (ONFH) is believed to be avascular necrosis. Certainly, a disruption of a supplying artery induces necrosis in the supplying artery-dominant region. However, when an abnormality such as cell apoptosis, or another reason, is developed in the supplying artery-dominant region, it induces a disruption of the supplying artery. Therefore, to prove that ONFH is avascular necrosis, it is necessary to demonstrate the disruption of the supplying artery prior to histological osteonecrosis development. Here we investigate histologically, using a rat model, whether disruption of the supplying artery occurs before the initial development of ONFH following corticosteroid treatment. Rats were given imiquimod and methylprednisolone, and were sacrificed 1, 2, 3, 7 or 14 days after the last injection. At the sacrifice, the rat was perfused with 20 ml black Indian ink through the left ventricle. ONFH was observed in the Imiquimod + Methylprednisolone group at 7 and 14 days. The osteonecrotic area was not stained with perfused black Indian ink. However, the lateral portion of the femoral head near the superior retinacular artery was stained with the ink. In conclusion, the present study shows that the superior retinacular artery did not occlude before the initial development of ONFH histologically in rats.
