BACKGROUND: Studies have confirmed that Atorvastatin drugs can increase the number of endothelial progenitor cells significantly in vitro, as well as the content of vascular endothelial growth factor(VEGF). OBJECTIVE: To investigate the effect of Atorvastatin on VEGF expression in necrotic femoral heads of rabbits. DESIGN, TIME AND SETTING: The randomized controlled animal experiment was performed at the Department of Orthopedic Surgery, Renmin Hospital of Wuhan University, from September 2007 to November 2008. MATERIALS: Forty-five male and female healthy New Zealand white rabbits weighing 2.5-3.5 kg were randomly divided into normal control group, model control group and AtorvastaUn group, 15 rabbits in each group. METHODS: Nitrogen refrigeration was used to develop femoral head necrosis models of rabbits in the model control and Atorvastatin groups. Two weeks after modeling, the animals in the Atorvastatin group were administered intragastically with Atorvastatin, normal control and model control group were treated with the same volume of normal saline. MAIN OUTCOME MEASURES: Each five rabbits were sacrificed at the 4th, 8th, and 12th weeks respectively for general observation, X-ray and histological observation. VEGF protein expression was assessed by immunohistochemistry method and VEGF mRNA level was assessed by reverse transcription - polymerase chain reaction method. RESULTS: The VEGF protein and mRNA levels in the model control and Atorvastatin groups were obviously lower than those in the normal control group, while the VEGF protein and mRNA levels in the Atorvastatin group were much higher than those in the model control group at the 8th and 12th weeks alter the treatment with Atorvastatin (P < 0.05). CONCLUSION: Atorvastatin can significantly upregulate the expression of VEGF, which is probably an effective clinical treatment to avascular necrosis of the femoral head.

Clinical data of twenty-six patients with primary tumors involving hip ioint treated surgically in Renmin Hospital of Wuhan University between March 1999 and May 2005 were retrospectively analyzed.The diagnosis of all patients was confirmed by pathohistology.There were 3 cases of chondrosarcomas.6 osteosarcomas,1 synovial sarcoma,14 giant cell tumors and 2 aneurysmal bone cysts.Seventeen cases were treated with custom-made total hip replacement prosthesis,7 with custom-made dipolar femoral head prostheses and 2 with saddle prostheses.They were followed up for 18 months to 6 years with an average of 4 years and 3 monts.Local relapse rate and final limb salvage rate was 40%and 60% in 10 patients with malignant bone tumors:125%and 875%in 16 patients with low-grade malignant bone tumors.According to Enneking(MSTS)evaluation criteria.the average score was 19 with an excellent and good rate of 76.9%.Custom-made artificial hip prosthesis is a satisfactory method in limb salvage operations for patients with malignant or low-grade malignant bone tumors jn hip joint.

BACKGROUND; Previous studies have shown that various miRNAs play a role in bone formation. miR-335-5p can protect osteoblasts from oxidative stress and protect osteoblasts under induction with ferric ammonium citrate, but the effect of miR-335-5p on osteoblast proliferation and apoptosis in high glucose environments is unknown. OBJECTIVE: To investigate the effect of miR-455-3p targeting HIPK2 on proliferation and apoptosis of osteoblasts induced by high glucose. METHODS; Dual luciferase reporter assay was used to verify the targeting of miR-455-3p to HIPK2. MC3T3-E1 cells were induced by high glucose in vitro, and MC3T3-E1 cells were treated as follows: Blank group, high glucose group, high glucose+miR-control group, high glucose+miR-455-3p group, high sugar+si-control group, high sugar+si-HIPK2 group, high glucose+miR-455-3p+pcDNA group and high glucose+miR-455-3p+pcDNA-HIPK2 group. The expression of miR-455-3p and HIPK2 mRNA was detected by qRT-PCR, cell viability was detected by MTT assay, apoptosis was detected by flow cytometry, and the expression of HIPK2, p-STAT3 and STAT3 protein was detected by western blot. RESULTS AND CONCLUSION: HIPK2 was a target gene of miR-455-3p, and miR-455-3p negatively regulated the expression of HIPK2. High glucose treatment inhibited the expression of miR-455-3p and promoted the expression of HIPK2. The over-expression of miR-455-3p or the inhibition of HIPK2 promoted MC3T3-E1 survival and inhibit cell apoptosis after high glucose treatment. The over-expression of HIPK2 partially reversed the survival promotion and apoptosis inhibition of miR-455-3p on osteoblasts induced by high glucose. miR-455-3p inhibited the expression of p-STAT3 in osteoblasts by regulating HIPK2. To conclude, miR-455-3p inhibits the apoptosis and promotes the proliferation of osteoblasts induced by high glucose via down-regulating HIPK2, which may be related to the inhibition of STAT3 signaling pathway.