[Effect of Quantitative indicators of ilium height on approach of percutaneous endoscopic lumbar discectomy treatment in patients with L 5, S 1 lumbar disc herniation].

OBJECTIVE: To identify effect of quantitative indicators of ilium height on approach of percutaneous endoscopic lumbar discectomy (PELD) treatment in patients with L 5, S 1 lumbar disc herniation. METHODS: A retrospective study between May 2014 and March 2016 was conducted, including 100 patients with disc herniation at L 5, S 1, who were initially enrolled for the PELD treatment. Among them, 66 patients were successfully treated with PELD (group A), and the other 34 patients failed to perform puncture, catheterization, or microscopical operation due to the influence of iliac bone and other peripheral bone structures and treated with alternative surgical plans. By analyzing the X-ray films of lumbar vertebrae (including bilateral ilium) of the two groups before operation, the concept of ilium height rate and ilium angle rate was put forward innovatively. The ilium height rate and ilium angle rate of the two groups were measured and compared, and the diagnostic critical points of ilium height rate and ilium angle rate were determined by ROC curve analysis. RESULTS: The ilium height rate was 0.61±0.09, 0.74±0.05 and the ilium angle rate was 0.66±0.08, 0.80±0.08 in groups A and B, respectively, showing significant differences between the two groups ( F=69.729, P=0.000; F=65.165, P=0.000). ROC curve analysis showed that the critical point of ilium height rate was 0.71 (area under ROC curve was 0.927, P=0.000), and the critical point of ilium angle rate was 0.75 (area under ROC curve was 0.965, P=0.000). CONCLUSION: PELD is not recommended for patients with L 5, S 1 intervertebral disc herniation, when the ilium height rate is greater than 0.71 and/or the ilium angle rate is greater than 0.75. Other surgical plans such as transpedicular approach, transpedicular approach, or open surgery, should be recommended to reduce the risk of surgery and the pain of patients.

Aquaporin 1 contributes to chondrocyte apoptosis in a rat model of osteoarthritis.

Aquaporins (AQPs) have been found to be associated with a number of diseases. However, the role of AQP­1 in the pathogenesis of osteoarthritis remains unclear. We previously found that AQP­1 expression was upregulated in osteoarthritic cartilage and strongly correlated with caspase­3 expression and activity. The aim of this study was to further investigate the association of AQP­1 expression with chondrocyte apoptosis in a rat model of osteoarthritis, using RNA interference to knock down AQP­1. For this purspose, 72 male Sprague­Dawley rats were randomly assigned to 3 groups as follows: the control group not treated surgically (n=24), the sham­operated group (n=24), and the osteoarthritis group (n=24). Osteoarthritis was induced by amputating the anterior cruciate ligament and medial collateral ligament and partially excising the medial meniscus. Chondrocytes from the rats with osteoarthritis were isolated and cultured. shRNAs were used to knock down AQP­1 expression in the cultured chondrocytes. The expression of AQP­1 and caspase­3 was determined by reverse transcription-quantitative polymerase chain reaction. Caspase­3 activity was measured using a caspase­3 colorimetric assay. The rats in our model of osteoarthritis exhibited severe cartilage damage. The knockdown of AQP­1 decreased caspase­3 expression and activity in the cultured chondrocytes. In addition, the expression of AQP­1 positively correlated with caspase­3 expression and activity. Thus, the findings of our study, suggest that AQP­1 promotes caspase­3 activation and thereby contributes to chondrocyte apoptosis and to the development of osteoarthritis.

Effects of osteoprotegerin, RANK and RANKL on bone destruction and collapse in avascular necrosis femoral head.

Avascular necrosis of femoral head (AVFH) is a clinically recalcitrant disease of hip that leads to joint destruction. Osteoprotegerin (OPG), receptor activator of nuclear factor kappa-B (RANK) and RANK ligand (RANKL) regulates the balance, maturation and function of osteoclast and bone remodeling. This study aims to investigate molecular pathways which leads to AVN by studying expression profile of OPG, RANK and RANKL genes. Quantitative Real Time-PCR is used to evaluate mRNA expression of OPG, RANK and RANKL. mRNA and protein level in normal and necrotic tissue from 42 samples of ANFH specimens were analyzed. OPG and RANKL protein levels are estimated by western blotting. The results indicated that OPG mRNA levels are higher but not significantly different in necrotic tissue than that in normal tissue (P>0.05). Although expression of RANK and RANKL is significantly lower than that of OPG, RANK and RANKL mRNA levels are higher in necrotic tissue than normal tissue (P<0.05). Protein levels of OPG and RANKL show no significant difference. In conclusion, OPG, RANK and RANKL play important role in progress of bone remodeling in necrotic area and in disturbance of bone homeostasis, which might have an effect on bone destruction and subsequent collapse of hip joint.

Inhibitory effect of zinc on the advanced glycation end product-induced apoptosis of mouse osteoblastic cells.

Osteoporosis and diabetes have become serious health problems worldwide. Previous studies have suggested that diabetes is associated with osteoporosis and increased fracture risk. However, the mechanism underlying diabetes­induced osteoporosis remains to be elucidated. Therefore, the present study aimed to examine the mechanism underlying diabetes­induced osteoporosis, and determine the protective effects of zinc, which is known to be closely associated with osteoporosis and diabetes. The results of the present study demonstrated that zinc inhibited advanced glycation end product (AGE)­induced MC3T3­E1 cell apoptosis by attenuating the production of reactive oxygen species, inhibiting caspase­3 and caspase­9 activation, and inhibiting the release of cytochrome c from between the mitochondria and the cytosol. Furthermore, zinc was found to protect cells against AGE­induced apoptosis via the mitogen­activated protein kinase/extracellular signal­regulated kinase and phosphoinositide 3­kinase/AKT signaling pathways. In conclusion, these findings enable a better understanding of the mechanism underlying diabetes­induced osteoporosis, and may indicate a novel target for its prevention and treatment.

[Correlation between expression of aquaporins 1 and chondrocyte apoptosis in articular chondrocyte of osteoarthritis].

OBJECTIVE: The changes of the aquaporins 1 (AQP-1) expression may be related to the chondrocyte apoptosis. To explore the correlation between the expression of AQP-1 and chondrocyte apoptosis by observing the expression of the AQP-1 and the Caspase-3, so as to provide experimental evidence for the further study in the pathogenesis of osteoarthritis (OA). METHODS: Seventy-two 8-week-old clean grade male Sprague Dawley rats, weighing 286-320 g (mean, 300 g), were randomly divided into the operated group (n = 24), the sham-operated group (n = 24), and the control group (n = 24). OA models were made by amputating the anterior cruciate ligament and medial collateral ligament, and partial excision of medial meniscus in operated group; the articular cavity was exposed only in sham-operated group; and no treatment was given in control group. The general condition of the rat was observed after model was established. At 1, 2, 4, and 8 weeks, the specimens of knee joints were harvested to perform the gross and histological observations; the mRNA expressions of AQP-1 and Caspase-3 were determined by real-time fluorescent quantitative PCR; and the activity of the Caspase-3 protease was detected. The correlations between the expression of AQP-1 mRNA and the expressions of Caspase-3 mRNA and protease were analyzed. RESULTS: Totally 6 rats died after operation, and the rats were supplied immediately; the other rats survived to the end of experiment. The appearance and structure of knee articular cartilage were normal in control group and sham-operated group. While in operated group, the cartilage had a rough surface with fissure and vegetation, and fibrosis and irregular cell arrangement were seen on the surface of cartilage. There were significant differences in the Mankin score between the operated group and sham-operated group, control group at 2, 4, and 8 weeks (P < 0.05). There was no significant difference in expressions of the AQP-1 mRNA and Caspase-3 mRNA, and the activity of the Caspase-3 protease among 3 groups at 1 week after operation (P > 0.05); while the expressions of the AQP-1 mRNA, Caspase-3 mRNA, and the activity of the Caspase-3 protease in operated group were significantly higher than those in sham-operated group and control group at 2, 4, and 8 weeks after operation (P < 0.05), and there was an increased trend over time. There was significantly positive correlation (r = 0.817, P = 0.000) between the expressions of AQP-1 mRNA and Caspase-3 mRNA, and the regression equation was y = 0.426 7x(2) + 0.051 5x; meanwhile, there was also significantly positive correlation (r = 0.945, P = 0.000) between the expression of AQP-1 mRNA and the activity of Caspase-3 protease, and the regression equation was y = 15.423 0x + 4.392 8. CONCLUSION: The up-regulation of AQP-1 expression in OA cartilage may be related to the chondrocyte apoptosis, and the changes of AQP-1 expression may involve in the pathogenesis of OA.