Large doses of cortisone were given to growing and adult rabbits over a
five-month period to produce avascular necrosis of the femoral head. The
cortisone caused an increase in the serum cholesterol, fatty metamorphosis
of the liver, and fat emboli visible in sections of the femur and humerus.
These emboli partially obliterated the microcirculation of the subchondral
vessels of both femoral and humeral heads. The average diameter of the
marrow fat cells also increased more than ten micrometers. This increase in
cell volume might be significant because in the closed chamber of the
femoral head it could increase tissue pressure, diminish perfusion, and be
the mechanism for avascular necrosis induced by cortisone.