Fat-cell changes as a mechanism of avascular necrosis of the femoral head in cortisone-treated rabbits

The effect of long‐term methylprednisolone treatment on the femoral head in growing pigs

“…Long-term steroid treatment has shown to cause increased IOP of the F H [39] and decreased FH blood flow in mature rabbits [38]. These studies suggested that growth of fat cells causes a rise in IOP, and thereby to compress the thin-walled sinusoids, with subsequent decrease in bone blood flow [41]. The lower trabecular bone volume found in the CS treated pigs in the present study might counteract an increase in IOP.…”

Effects of pulse methylprednisolone on bone and marrow tissues. Corticosteroid‐induced osteonecrosis in rabbits

“…In our study, a single dose was used, and the dosage (20 mg/kg of body weight) was much higher than that used in previous animal studies (15,16,22,24,25). Abeles et a1 (1) suggested that the high initial corticosteroid dosage in patients with systemic lupus erythematosus may be apt to induce osteonecrosis of the femoral head.…”

“…Since the relationship between the occurrence of ON and the systemic administration of corticosteroids was first reported in 1957 (4), there have been several experiments that demonstrated many steroid-related histopathologic and pathophysiologic alterations in the bone tissue, such as fat embolism (21,22), an increased pressure of bone marrow in the femoral head (24), an enlargement of the fat cell size (15), and an accumulation of lipid within the osteocytes (1 6). However, no histopathologically definitive ON has been described in those steroid-treated animals.…”

“…First, ON-prone sites may differ in mammalian species, and thus the distribution of ON should be characterized by examining all parts of the bonc. Most previous studies have mainly examined the femoral head, expecting a collapsed lesion (15,16,22,24,25). However, Matsui et a1 (28) reported that ON was recognized in only the metaphysis and diaphysis in rabbit models of ON produced by serum sickness with horse serum and corticosteroid treatment.…”

“…Many experimental studies using corticosteroids have suggested the possible pathogenesis of corticosteroid-induced ON, such as an enlargement of the size of fat cells (15), an accumulation of lipid within the osteocytes (16), and fat emboli (12,13,15,17). However, to our knowledge, the studies have never succeeded in developing histologically definitive ON (18)(19)(20) in animals by the injection of corticosteroids alone (15,16,(21)(22)(23)(24)(25). Perhaps the studies were focusing exclusively on the epiphyseal regions of the femoral and humeral heads that result in subchondral collapse, and were not thoroughly evaluating the metaphyseal and diaphyseal regions.…”