Role of hypercoagulability in steroid-induced femoral head necrosis in rabbits

The pathogenesis of femoral head necrosis is still uncertain. Both steroid treatment and hypercoagulopathy are considered risk factors. To investigate possible changes in coagulability and histology during steroid-induced osteonecrosis, we used a combination of the Shwartzman reaction and corticoid injections in rabbits to develop an animal model of femoral head necrosis. We studied blood coagulability and histopathological characteristics of the femoral head and liver.

A total of 30 rabbits were divided into three groups. In group A, rabbits were given two injections of lipopolysaccharide (40 microg/kg) at an interval of 24 h and were then immediately given one injection of prednisolone acetate (20 mg/kg). In group B, 10 rabbits were given one injection of prednisolone acetate (20 mg/kg). In group C, 10 rabbits were given no treatment and served as controls. At 1, 3, 7, 14, and 21 days after prednisolone injection, coagulability, blood lipid levels, and blood platelet levels were measured; and the femoral head and liver were removed for histopathological examination.

At 24 h after the prednisolone injection in group A, coagulability and blood lipid levels were increased (P < 0.01), and blood platelet levels were decreased (P < 0.01). These abnormal levels were maintained throughout the entire observation period. Histologically, degeneration and necrosis of hepatocytes and osteocytes were found at day 21 after prednisolone injection in group A. In group B, coagulability and blood lipid levels were significantly increased by day 3 after treatment.

Abnormal hypercoagulability might potentiate the thrombotic status and induce thrombus formation in the presence of steroid-induced necrosis of the femoral head.