抄録
It is well known that steroids and alcohol are major factors possibly involved in the onset of idiopathic osteonecrosis of the femoral head (INFH) . The etiology of this disease has already been studied considerably with respect to steroids. However, as about one-third of the patients with INFH suggest an involvement of alcohol, this disease should be studied also in relation to it. In the present study, blood examinations, histological analyses and histochemical examination for lactate dehydrogenase (LDH) were carried out following long-term alcohol treatment in a rabbit model.
The aberration of fat metabolism (hyperlipidemia, relative decrease of HDL cholesterol and lecithin cholesterol acyltranseferase (LCAT) ) and increase of the serum cortisol level were disclosed following alcohol dosing. Histologically, fatty liver and deposition of lipid in osteocytes of the femoral head were observed. These findings became more severe with time. Histochemically, the positive-stained deposition in osteocytes, which showed LDH activity and indicated viability of the osteocytes, disappeared in the subchondral area of the femoral head 3 months after the commencement of alcohol dosing.
The hyperlipidemia and the elevation of cortisol level may help to increase the inflow of lipid into the osteocytes. On the other hand, the depression of viability of osteocytes and relative decrease of lipid clearance agents (HDL cholesterol and LCAT) may reduce the outflow of lipid from the osteocytes. It is thus suggested that alcohol dosing brings about the accumulation of lipid in the osteocytes by these mechanisms, and that the serum cortisol level should be examined clinically as a pathogenic factor of INFH.
