Atlas is capable for screw fixation via its posterior arch and lateral mass.

Atlas is capable for screw fixation via its posterior arch and lateral mass.

Steroid-induced osteonecrosis of the femoral head (ONFH) is a severe orthopedic disease caused by the long-term administration of glucocorticoids. The main pathological feature of ONFH is the gradually progressive necrosis of bone cells and the bone marrow, ultimately resulting in structural changes or even complete collapse of the femoral head. However, the exact pathogenic mechanism of ONFH remains unknown. Noncoding RNAs (ncRNAs) have emerged as very powerful regulators of gene expression, functioning at both transcriptional and posttranscriptional levels in the pathogenesis of ONFH. Here, we review the current knowledge of the role of ncRNAs, including microRNAs, long noncoding RNAs, and circular RNAs, in the pathogenesis of steroid-induced ONFH. Further focus and validation of these associations can provide new insight into the pathogenic mechanisms at the molecular level to suggest targets for treatment and prevention.

Activation of nuclear-factor-E2-related factor 2 (Nrf2) cascade can alleviate dexamethasone (DEX)-induced oxidative injury and death of human osteoblasts. A recent study has shown that phosphoglycerate kinase 1 (PGK1) inhibition/depletion will lead to Kelch-like ECH-associated protein 1 (Keap1) methylglyoxal modification, thereby activating Nrf2 signaling cascade. Here, in OB-6 osteoblastic cells and primary human osteoblasts, PGK1 silencing, by targeted shRNA, induced Nrf2 signaling cascade activation, causing Nrf2 protein stabilization and nuclear translocation, as well as increased expression of ARE-dependent genes (HO1, NQO1, and GCLC). Functional studies demonstrated that PGK1 shRNA largely attenuated DEX-induced oxidative injury and following death of OB-6 cells and primary osteoblasts. Furthermore, PGK1 knockout, by the CRISPR/Cas9 method, similarly induced Nrf2 signaling activation and protected osteoblasts from DEX. Importantly, PGK1 depletion-induced osteoblast cytoprotection against DEX was almost abolished by Nrf2 shRNA. In addition, Keap1 shRNA mimicked and nullified PGK1 shRNA-induced anti-DEX osteoblast cytoprotection. At last we show that PGK1 expression is downregulated in human necrotic femoral head tissues of DEX-taking patients, correlating with HO1 depletion. Collectively, these results show that PGK1 depletion protects human osteoblasts from DEX via activation of Keap1-Nrf2 signaling cascade.

Background The present study aims to investigate the incidence and risk factors associated with postoperative delirium in patients undergoing spine surgery. Methods PubMed, EMBASE, Cochrane Library, and Science Citation Index were searched up to August 2019 for studies examining postoperative delirium following spine surgery. Incidence and risk factors associated with delirium were extracted. Odds ratios (OR) and 95% confidence intervals (CI) were calculated for outcomes. The Newcastle–Ottawa Scale (NOS) was used for the study quality evaluation. Results The final analysis includes a total of 40 studies. The pooled analysis reveals that incidence of delirium is 8%, and there are significant differences for developing delirium in age (OR 1.07; 95% CI 1.04–1.09), age more than 65 (OR 4.77; 95% CI 4.37–5.16), age more than 70 (OR 15.87; 95% CI 6.03–41.73), and age more than 80 (OR 1.91; 95% CI 1.78–2.03) years, male (OR 0.81; 95% CI 0.76–0.86), a history of alcohol abuse (OR 2.11; 95% CI 1.67–2.56), anxiety (OR 1.74; 95% CI 1.04–2.44), congestive heart failure (OR 1.4; 95% CI 1.21–1.6), depression (OR 2.5; 95% CI 1.52–3.49), hypertension (OR 1.12; 95% CI 1.04–1.2), kidney disease (OR 1.41; 95% CI 1.16–1.66), neurological disorder (OR 4.66; 95% CI 4.22–5.11), opioid use (OR 1.86; 95% CI 1.18–2.54), psychoses (OR 2.77; 95% CI 2.29–3.25), pulmonary disease (OR 1.81; 95% CI 1.27–2.35), higher mini-mental state examination (OR 0.7; 95% CI 0.5–0.89), preoperative pain (OR 1.88; 95% CI 1.11–2.64), and postoperative urinary tract infection (OR 5.68; 95% CI 2.41–13.39). Conclusions A comprehensive understanding of incidence and risk factors of delirium can improve prevention, diagnosis, and management. Risk of postoperative delirium can be reduced based upon identifiable risk factors.