The effect of lipid peroxide on osteoblasts and vascular endothelial cells--the possible role of ischemia-reperfusion in the progression of avascular necrosis of the femoral head.

Many patients undergo operations of the hip joint for avascular necrosis of the femoral head (ANF). Abnormal lipid metabolism in thought to play a certain role in the pathogenesis of ANF. In the present study we have detected the abnormal lipid from the necrotic area of the femoral heads suffering from ANF by gas chromatography-mass spectrometry (GC/MS). This abnormal lipid was supposed to be cholesterol epoxide, because its peak was observed at one oxygen molecular weight larger position than that of cholesterol. However, this abnormal lipid was not found in the femoral heads with osteoarthritis (OA). We also investigated the effect of the lipids (cholesterol and cholesterol epoxide) and corticosteroid (prednisolone) on proliferation of osteoblastic cell line (MC3T3-E1) cells and vascular endothelial cells (EC) derived from human umbilical vein using 3H-thymidine (3H-TdR) incorporation. Cholesterol has no effect on osteoblast proliferation up to 100 micrograms/ml, while cholesterol epoxide inhibited the 3H-TdR incorporation in a dose dependent fashion and a significant suppression was attained at the concentration of 10 micrograms/ml. In contrast, both cholesterol and cholesterol epoxide had suppressive effect on the EC proliferation. DNA synthesis of the osteoblasts was suppressed by prednisolone and additive inhibitory effect was observed in the combination of cholesterol epoxide and prednisolone. None of the free radical scavengers such as mannitol, dimethylsulfoxide (DMSO), super oxide dismutase (SOD) and catalase had significant recovery effect on the suppressed 3H-TdR incorporation of both MC3T3-E1 cells and EC. Only alpha-tocopherol restored the suppressed incorporation of 3H-TdR. These results suggest that lipid peroxide has an important role in the progression of ANF by suppressing the proliferation of osteoblasts and EC.

Cultured osteoblast synthesize nitric oxide in response to cytokines and lipopolysaccharide.

Nitric oxide (NO) is generated from L-arginine by NO synthase. NO has been reported to be produced by a variety of cell types such as vascular endothelial cells, macrophages, neutrophils and articular chondrocytes. A recent report demonstrated that NO inhibits osteoclast (OC) function and, in this way, is critically associated with bone metabolism. In the present study we have studied NO synthesis by osteoblasts (OBs). OB cell line, MC3T3-E1, was cultured with the various cytokines for 72 hrs. Nitrite, a stable endproduct of cell-generated NO, in the culture supernatant was then determined by using a spectrophotometric method based on Griess reaction. IL-1 alpha increased nitrite release in a dose-dependent fashion and a significant enhancement (p < 0.01) was attained at 10 U/ml. OBs released 14.2 nmol/4.0 x 10(4) cells of nitrite after 72 hrs stimulation by 100 U/ml IL-1 alpha. In contrast IL-1 beta, TNF-alpha and INF-gamma failed to affect NO synthesis by MC3T3-E1. The results suggest that OBs produce NO in response to IL-1 alpha and OB-induced NO may play a role in OB-OC interaction in the inflammatory process.

[Reconstruction using non-vascularized fibula of an aneurysmal bone cyst of the humerus in a child]. / Reconstruction par Fibula non Vascularisee d'un Kyste Osseux Anevrysmal de L'Humerus Chez L'Enfant.

Aneurysmal bone cyst is a pseudotumoral bone dystrophy which accounts for 1.5 to 4% of benign bone tumours. We report the case of a bulky aneurismal cyst of the left superior humeral metaphysis in a seven year old child revealed by a repeated pathologic fracture. Exeresis of the cyst was performed with reconstruction by a non vascularized fibula. After a follow up of one year the patient recovered safely with normal range of motion and anatomically. The cystic exeresis sparing the growth cartilage with fibula graft is indicated in the management of active and aggressive aneurismal cyst of long bones.