Q Zhou1, Q Li, L Yang, F Liu. 1. Department of Orthopaedics, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
Abstract
OBJECTIVE: To evaluate the effects of fatty tamponade in medullary cavity (serious intramedullary fatty infiltration) on the changes of blood vessels in femoral heads during the pathological process of glucocorticoid (GC)-induced avascular necrosis (AVM) of the femoral heads. METHODS: The animal model of AVN was established with injection of dexamethasone (DEX) at a high dose of 2.5 mg x kg(-1) x d(-1) in rabbits. Histopathological and morphological changes of blood vessels in the femoral heads were investigated during GC-treatment and after the cessation scanning electron microscope, light microscope, and image analysis. RESULTS: At the 2nd week of DEX-treatment, the fatty tamponade in the medullary cavity appeared in the femoral heads. Intramedullary vascular sinusoids were pressed by an excess of lipocytes and became narrow. The impressions of lipocytes on the surface of vascular sinusoids were definitely displayed on the vascular casts and ink-perfused slides of the femoral heads. These changes were pronounced with the prolongation of the treatment and the vascular sinusoids gradually lost their characteristics. Image analysis showed that the vascular area in the femoral heads continuously decreased. At the 8th week, the effects of fatty tamponade were the most marked. Intramedullary vessels became very sparse and the vascular area decreased to 1/4 of the controls. At the 6th week after the GC-treatment cessation, intramedullary fatty infiltration still existed. The blood vessels were fine and sparse, and the structural features of vascular sinusoids disappeared in the load-bearing regions of the femoral heads. At the 4th week, typical osteonecrosis focuses appeared in the femoral heads. The focuses became larger and the degree of osteonecrosis was increasing with the time of experiment. CONCLUSION: The fatty tamponade in the medullary cavity is one of the important pathological factors causing ischemic damage to the femoral heads, and plays an important role in the early stage of GC-induced AVN.
OBJECTIVE: To evaluate the effects of fatty tamponade in medullary cavity (serious intramedullary fatty infiltration) on the changes of blood vessels in femoral heads during the pathological process of glucocorticoid (GC)-induced avascular necrosis (AVM) of the femoral heads. METHODS: The animal model of AVN was established with injection of dexamethasone (DEX) at a high dose of 2.5 mg x kg(-1) x d(-1) in rabbits. Histopathological and morphological changes of blood vessels in the femoral heads were investigated during GC-treatment and after the cessation scanning electron microscope, light microscope, and image analysis. RESULTS: At the 2nd week of DEX-treatment, the fatty tamponade in the medullary cavity appeared in the femoral heads. Intramedullary vascular sinusoids were pressed by an excess of lipocytes and became narrow. The impressions of lipocytes on the surface of vascular sinusoids were definitely displayed on the vascular casts and ink-perfused slides of the femoral heads. These changes were pronounced with the prolongation of the treatment and the vascular sinusoids gradually lost their characteristics. Image analysis showed that the vascular area in the femoral heads continuously decreased. At the 8th week, the effects of fatty tamponade were the most marked. Intramedullary vessels became very sparse and the vascular area decreased to 1/4 of the controls. At the 6th week after the GC-treatment cessation, intramedullary fatty infiltration still existed. The blood vessels were fine and sparse, and the structural features of vascular sinusoids disappeared in the load-bearing regions of the femoral heads. At the 4th week, typical osteonecrosis focuses appeared in the femoral heads. The focuses became larger and the degree of osteonecrosis was increasing with the time of experiment. CONCLUSION: The fatty tamponade in the medullary cavity is one of the important pathological factors causing ischemic damage to the femoral heads, and plays an important role in the early stage of GC-induced AVN.