Aims

The localization of necrotic areas has been reported to impact the prognosis and treatment strategy for osteonecrosis of the femoral head (ONFH). Anteroposterior localization of the necrotic area after a femoral neck fracture (FNF) has not been properly investigated. We hypothesize that the change of the weight loading direction on the femoral head due to residual posterior tilt caused by malunited FNF may affect the location of ONFH. We investigate the relationship between the posterior tilt angle (PTA) and anteroposterior localization of osteonecrosis using lateral hip radiographs.

Treatment of the femoral head necrosis with severe extensive collapse in young adults and adolescents are still challenging. We thought preserve the joint and bone stock were important factor for the treatment of femoral head necrosis in young patients. We reviewed the posterior rotational osteotomy for younger patients with severe osteonecrosis. The advantages of posterior rotational osteotomy are; the necrotic area is moved to non-weight bearing portion. The posterior column artery is shifted medially without vascular damage by rotation. Postoperative uncollapsed anterior viable areas are moved to the loaded portion below the acetabular roof in flexed positions. Eighty five hips of 66 young adults (less than 50 years old, mean age; 31 years) with extensive necrosis treated by posterior rotational osteotomy were reviewed with more than 5 year follow up with a mean of 9 years. Results of 13 hips of 12 adolescents (mean age; 14 years) with extensive collapsed necrosis treated by this procedure were also studied with a mean of 6.5 years. A mean degree of posterior rotation was 121. Recollapse was prevented in 77 hips (91%) of adults, and all 13 hips of adolescents on final AP radiographs. Collapsed lesion was remodeled well and resphericity of the postoperative transferred medial collapsed femoral head on final AP radiographs was observed. However, some of the cases were out of indication of the joint preserving procedure showing extensive lesion. In these cases, we performed the MAYO conservative stem for preserving bone stock. Radiological results of 26 hips with osteonecrosis treated by MAYO stem (mean age 42 years, minimum 5 year follow-up. mean; 6.7 years) showed that 2 mm subsidence in one, osteointegration of zone 2, 6 in 93%, no entire lucent line. No hips were revised for late loosening associated with osteolysis. CT imaging indicated that spot welds of zone 2, 6 were found in 100ï¼ï¿½, stress shielding of zone 1, 5 (23.5ï¼ï¿½). These operations were useful particularly for younger patients.

Introduction: We studied resphericity of the collapsed femoral head moved medially after posterior rotational osteotomy for osteonecrosis at a mean of 8.5 years follow-up.

Materials and Methods: Twenty-eight hips in 24 patients with osteonecrosis with apparent collapse treated by this operation were studied. All hips had no recollapse at final follow-up. The mean age of patients was 26 years. Twenty-two hips were non-traumatic, 6 were traumatic. The resphericity was studied by ratio (%, medial area of collapse/hip center to superior viable joint surface) at less than 6 months, 3years, and at final follow-up on postoperative antero-posterior radiographs. Disappearance of the subchondral fracture was also observed.

Results and Discussion: The mean ratio of the medial collapse area was 18.4% at less than 6 months, 8.3% at 3years, and 3.4% at final follow-up. Subchondral fracture was seen in 25 of 28 hips at less than 6 months, subchondral fractures disappeared in 17 hips at 3 years, and in 23 hips at final follow-up. We thought that remodeling of the postoperative medial collapsed lesion occurred after this operation.

Introduction: To investigate the presence or absence of osteonecrosis of femoral head (ONFH) in patients undergoing massive corticosteroid therapy, we have performed magnetic resonance imaging (MRI) early after administration. In some patients, MRI revealed an increase in hip fluid. In this study, we evaluated retention of hip fluid early after massive steroid therapy by MRI.

Materials and Methods: The subjects were 14 patients (28 joints) in whom oral administration of prednisolone at an initial dose of 40 mg/day or more or pulse therapy was performed. They consisted of 3 men (6 joints) and 11 women (22 joints). Ages ranged from 17 to 72 years, with a mean of 38.2 years. We evaluated retention of hip fluid in T2-weighted MRI images or T2 fat-suppressed images within 3 months after massive steroid therapy according to the joint fluid grading established by Mitchell et al and evaluated volume of hip fluid by integrating an area (by using Mac scope ver 2.58).

Results: Average volume of all joints was 7.18 cm³. Eleven joints were evaluated as Grade 1, in which a small amount of joint fluid is noted, and their average volume was 3.98 cm³. Fifteen joints were evaluated as Grade 2, in which retention involves the entire femoral neck, and their average volume was 8.96 cm³. Two joints were evaluated as Grade 3, in which marked retention involves the excavation of the cupsula articularis, and their average volume was 11.45 cm³. No joint was evaluated as Grade 0, in which no joint fluid is detected.

Discussion: The pathogenesis of corticosteroid-related ONFH is multifactorial; various hypotheses have been proposed, suggesting the involvement of arteriosclerosis, thrombosis, fat embolization, vascular endothelial disorder, venous return disorder, enhanced blood coagulation, fibrinolytic abnormalities, and bone tissue apoptosis. However the detailed mechanism remains to be clarified. In this survey, when regarding Grade 2 or higher joints as showing a significant increase in hip fluid, the increase was noted in 17 joints (60.7%). We understood objectively by an increase in hip fluid by estimating its volume. An increase in hip fluid early after massive steroid therapy may persistently increase intraarticular pressure, affecting influx of nutrient vessels in the femoral neck or venous return, which is considered to be a tamponade effect. This may be an etiological factor involved in ONFH.