N. Shabaldin, A. V. Shabaldin, N. E. Popova, A. V. Postnikova, L. Bogdanov, A. Tsepokina
{"title":"Modeling of femoral head aseptic necrosis in Wistar rats","authors":"N. Shabaldin, A. V. Shabaldin, N. E. Popova, A. V. Postnikova, L. Bogdanov, A. Tsepokina","doi":"10.23946/2500-0764-2022-7-3-23-30","DOIUrl":null,"url":null,"abstract":"Aim. To develop an animal model of femoral head aseptic necrosis for studying Legg–Calvé–Perthes disease.Materials and Methods. To induce the development of aseptic necrosis, we used Wistar rats (n = 8) which suffered from combined hypoperfusion of the femoral head and increased intra-articular pressure in the hip joint. Having employed isoflurane anesthesia, we performed an incision (≈ 3 cm length) on the outer surface of the thigh in the projection of the hip joint and then excised periosteum in the proximal third of the femur. A dense vicryl ligature was applied around the femoral neck to reduce blood perfusion of the femoral head. Further, 1.5 mL 2% rheopolyglucinum solution (10% isotonic dextran, 30-40 kDa molecular weight) was injected into the hip joint cavity to increase intra-articular pressure. Rats were sacrificed upon 8-week follow-up with subsequent X-ray and histological examination.Results. Our animal model of femoral head aseptic necrosis includes two main components of Legg–Calvé–Perthes disease: an increase in the intra-articular pressure and insufficient blood perfusion of the femoral head. In all (8/8) cases, aseptic necrosis of the femoral head was achieved. Eight weeks post intervention, the condition of the proximal femur 8 was similar to impression fracture.Conclusion. Our model of femoral head aseptic necrosis fully reflects the pathogenesis of LeggCalve-Perthes disease and can be therefore used in experimental studies.","PeriodicalId":12493,"journal":{"name":"Fundamental and Clinical Medicine","volume":"77 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Fundamental and Clinical Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.23946/2500-0764-2022-7-3-23-30","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Aim. To develop an animal model of femoral head aseptic necrosis for studying Legg–Calvé–Perthes disease.Materials and Methods. To induce the development of aseptic necrosis, we used Wistar rats (n = 8) which suffered from combined hypoperfusion of the femoral head and increased intra-articular pressure in the hip joint. Having employed isoflurane anesthesia, we performed an incision (≈ 3 cm length) on the outer surface of the thigh in the projection of the hip joint and then excised periosteum in the proximal third of the femur. A dense vicryl ligature was applied around the femoral neck to reduce blood perfusion of the femoral head. Further, 1.5 mL 2% rheopolyglucinum solution (10% isotonic dextran, 30-40 kDa molecular weight) was injected into the hip joint cavity to increase intra-articular pressure. Rats were sacrificed upon 8-week follow-up with subsequent X-ray and histological examination.Results. Our animal model of femoral head aseptic necrosis includes two main components of Legg–Calvé–Perthes disease: an increase in the intra-articular pressure and insufficient blood perfusion of the femoral head. In all (8/8) cases, aseptic necrosis of the femoral head was achieved. Eight weeks post intervention, the condition of the proximal femur 8 was similar to impression fracture.Conclusion. Our model of femoral head aseptic necrosis fully reflects the pathogenesis of LeggCalve-Perthes disease and can be therefore used in experimental studies.