The Study About Pathogenesy Of Alcohol-Induced Avascular Necrosis Of The Femoral Head

Background:The disease related to alcohol grows day by day with the increase of average consumption of alcohol,and the number of alcohol-induced avascular necrosis of femoral head (AIANFH) presents a growth trend,at present it's a hotspot to probe into the pathogenesy of AIANFH.Purpose: To study the relationship between different doses of alcohol intake and femoral head avascular necrosis in rats,to establish an ideal and practical animal model which might investigate the pathogenesis of femoral head avascular necrosis.Method: 120 rats were randomly divided into 3 groups, each group consists of 40 rats. experimental group A(EG A) was administered the wine containing 45% of alcohol at dosage of 8ml.kg~-1 .d~-1(equal to 4g.kg~-1.d~-1), experimental group B(EG B) was administered the wine containing 45% of alcohol at dosage of 6ml.kg~-1.d~-1(equal to 3g.kg~-1.d~-1), and control group conducted the same amount of NS respectively. All animals were killed in 8 weeks, 16 weeks, 24 weeks respectively after the start of the procedure. Detected indexes as followed: the conditions of rats, the changes of histology in the femoral head,electron microscope analysis, the items of lipid metabolism, hemorheology, oxygenfree radical(OFR), endothelin(ET) and nitric oxide(NO), radioisotope scanning.Results: 1.The conditions of rats:the in control group was better than in other groups;most of the rats of the control group's weight didn't change,their shapes of femoral head were normal. In experimental groups(EG A and EG B), the weight increased slowly and the cartilage of the femoral head were destroyed,or there were stases of veins,or the femoral heads caved in.Pathological changes of EG A was more obvious than those of EG B.2.Histology:the contrlo group was normal;there was no difference between them after 8,16 weeks(p>0.05);there was significant difference between their quantities of empty osteocyte lacuna after 24 weeks(p<0.05 or p<0.01).In experimental groups, empty osteocyte lacuna increased and trabecula of bone decreased, ruptured. Pathological changes of EG A was more obvious than those of EG B.3.Electron microscope analysis:the control group was normal;osteocytes and osteoblasts in experimental groups decreased,nucleolus shrunk,and osteocytes had degeneration signs or fatty drips appeared in osteocytes, and intramedullary lipocytes became larger in experimental groups. Pathological changes of EG A was more obvious than that of EG B.4.Lipid metabolism: there was no difference between them after 8,16 weeks(p>0.05); TC,TG,LDL increased significantlyin EG A,HDL decreased significantly in EG A after 24 weeks;there was significant difference between EG A and the control group(p<0.05 or p<0.01).5.Hemodynamics:there was no difference between them after 8,16 weeks(p>0.05);whole blood viscosity(low-shear and high-shear), plasma viscosity and whole blood relative viscosity at low-shear rate;RBC aggregation index of EG A increased sigificantly in the 24th week;there was significant difference between EG A and the control groupafter 24 weeks(p<0.05 or p<0.01).6.Levels of MDA: there was no difference between EG A and the control group after 8,16 weeks(p>0.05).EG A's Level of SOD decreased in the 24th week significantly,and there was significant difference between EG A and the control group(p<0.05).EG A's level of MDA increased significantly,and there was significant difference between EG A and the control group(p<0.05);there was significant difference between EG B and the control(p<0.05).7.The level of serum NO: there was no difference between them after 8,16 weeks(p>0.05);the level of serum NO in EG A decreased after 24 weeks.There was significant difference between EG A and the control group(p<0.05);there was no difference between EG B and the control group(p>0.05).8.The level of plasma ET: there was no difference between them after 8,16 weeks(p>0.05);the level of plasma ET increased significantly.There was significant difference while each group was compared with another(p<0.05 or p<0.01).9.Radioisotope scanning:EG B and the control group were normal.The radioisotope of blood stream picture was sluggish in the femoral head of EG A after 24 weeks,and there was concentration phenomenon of blood pond radioisotope.There was concentration phenomenon of radioisotope in the femoral head of the whole body picture. Conclusion:1 .the high dose of alcohol intake can induce the disorder of lipid metabolism,and came into being hyperlipemiaJt's because of the cumulative effect of fat embolism in bone,the high pressure in marrow,the hindering of the vein refluence and the accroching fatty degeneration in bone cell,et al,so the blood supply of femoral head was discontinued,and the necrosis formed.2. the high dose of alcohol intake can induce the change of hemorheology, its viscosity enhanced; it's because of the blood stasis,the defilade of microcirculation,the present of thrombus, the blood supply of femoral head was discontinued,and the necrosis formed.3. the high dose of alcohol intake can induce the OFR metabolic disorder.Lipid over-oxidation accelerated the pathological changes of microvascular,aggravated the barrier of micrcirculation of the femoral head,accelerated AIANFH.4. the high dose of alcohol intake can induce plasma ET increased and serum NO decreased,which can induce the contraction of blood vessel. and the presentation of thrombus,then the blood supply of femoral head was discontinued,and the necrosis formed.5.the detection of ECT showed that the distribution of nuclide in blood film was retarded;the distribution of nuclide in blood pool film concentrated;the concentration of nuclide in femoral head can be found in femoral head image of all over the body.which is cue that there was blood stasis in bone, pathological tissue is presented in segment,or new bone formed.So ECT is significant to the early diagnosis of AIANFH.