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.

We performed superselective angiography in 28 hips in 25 patients with Perthes’ disease in order to study the blood supply of the lateral epiphyseal arteries (LEAs). Interruption of the LEAs at their origin was observed in 19 hips (68%). Revascularisation in the form of numerous small arteries was seen in ten out of 11 hips in the initial stage of Perthes’ disease, in seven of eight in the fragmentation stage and in five of nine in the healing stage. Penetration of mature arteries into the depths of the epiphysis was seen in four of nine hips in the healing stage. Vascular penetration was absent in the weight-bearing portion of the femoral head below the acetabular roof. Interruption of the posterior column artery was seen where it passed through the capsule in seven hips when they lay either in internal rotation or in abduction with internal rotation.

We suggest that in Perthes’ disease the blood supply of the LEAs is impaired at their origin and that revascularisation occurs from this site by ingrowth of small vessels into the femoral epiphysis. This process may be the result of recurrent ischaemic episodes.