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A sandwich vertebra is formed after multiple osteoporotic vertebral fractures treated by percutaneous vertebroplasty, which has a risk of developing new fractures. The purpose of our study was to (i) investigate the occurrence of new fractures in sandwich vertebra after cement augmentation procedures and to (ii) evaluate the clinical outcomes after prophylactic vertebral reinforcement applied with resorbable bone cement.From June 2011 to 2014, we analysed 55 patients with at least one sandwich vertebrae and treated with percutaneous vertebroplasty. Eighteen patients were treated by prophylactic vertebroplasty with a resorbable bone cement to strengthen the sandwich vertebrae as the prevention group. The others were the non-prevention group. All patients were examined by spinal radiographs within 1 day, 6 months, 12 months, 24 months and thereafter.The incidence of sandwich vertebra is 8.25% (55/667) in our study. Most sandwich vertebrae (69.01%, 49/71) are distributed in the thoracic–lumbar junction. There are 24 sandwich vertebrae (18 patients) and 47 sandwich vertebrae (37 patients) in either prevention group or non-prevention group, respectively. No significant difference is found between age, sex, body mass index, bone mineral density, cement disk leakage, sandwich vertebrae distribution or Cobb angle in the two groups. In the follow-up, 8 out of 37 (21.6%) patients (with eight sandwich vertebrae) developed new fractures in non-prevention’ group, whereas no new fractures were detected in the prevention group. Neither Cobb angle nor vertebral compression rate showed significant change in the prevention group during the follow-up. However, in the non-prevention group, we found that Cobb angle increased and vertebral height lost significantly (P < 0.05).Prophylactic vertebroplasty procedure applied with resorbable bone cement could decrease the rate of new fractures of sandwich vertebrae.

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Disruption of lysosomal homeostasis contributes to the tubulopathy of diabetic nephropathy; however, its underlying mechanisms remain unclear. Herein, we report that decreased activity of transcription factor EB (TFEB) is responsible for the disturbed lysosome biogenesis and clearance in this pathological process. This was confirmed by the findings that insufficient lysosomal replenishment and damaged lysosomal clearance coincided with TFEB inactivation, which was mediated by mTOR hyperactivation in the renal tubular epithelial cells (TECs) of diabetic nephropathy. Furthermore, either TFEB overexpression or pharmacological activation of TFEB enhanced lysosomal clearance via promoting lysosomal biogenesis and protected TECs by reducing apoptosis in vitro. In addition, pharmacological activation of TFEB attenuated renal tubule injury, apoptosis, and inflammation in db/db mice. In conclusion, diabetes-induced mTOR activation represses TFEB function, thereby perturbing lysosomal homeostasis through impairing lysosomal biogenesis and clearance in TECs. Moreover, TFEB activation protects TECs from diabetic injuries via restoring lysosomal homeostasis.