Objectives To evaluate hidden blood loss (HBL) and its possible risk factors among patients following expansive open-door laminoplasty (EOLP) for multilevel, cervical spondylotic myelopathy. Methods This was a retrospective analysis of data from patients over 18 years of age who underwent posterior cervical EOLP (from C3-C6) in our department from January 2017 to July 2018. HBL was calculated by deducting the observed perioperative blood loss from the calculated total blood loss (TBL) based on the fall in haematocrit level. Results 45 patients (35 men and 10 women) were identified. Mean ± SD HBL was 337.2 ± 187.8 ml, which was 46.8% of the total perioperative blood loss (705.2 ± 269.6 ml). Twenty-three patients developed postoperative anaemia. Posterior cervical soft tissue was positively correlated with both TBL and hidden blood loss (HBL) and hypertension was positively correlated with TBL. Conclusions HBL following cervical EOLP was significant and should be recognised as a detrimental factor to patient safety during the perioperative period, especially in patients with thick posterior cervical soft tissue.

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BackgroundCartilaginous endplate (CEP) degeneration is considered as one of the major causes of intervertebral disc degeneration (IVDD) which causes low back pain. Recent studies have proved that epigenetic alteration is involved in a variety of diseases. This work explored the role of histone methyltransferase enhancer of zeste homologue 2 (EZH2) in CEP degeneration, as well as its underlying epigenetic mechanisms, and confirmed the effect of EZH2 knockdown on delaying IVDD development.MethodsWestern blotting, immunofluorescence staining, and ChIP assay were applied to demonstrate the molecular mechanism of EZH2 in CEP tissue. The therapeutic potential of EZH2 was investigated using puncture-induced rat models.FindingsThe EZH2 expression was upregulated in human and rat CEP tissue. It was also found that the overexpression of EZH2 suppressed the expression of Collagen II, aggrecan and Sox-9, and promoted the expression of ADTAMTS5 and MMP13 in rat endplate chondrocytes (EPCs), which could be reversed by EZH2 silencing. The correlation between EZH2 and Sox-9 was further explored, while overexpression of Sox-9 could reverse the effect of EZH2 in rat EPCs. Moreover, inhibition of EZH2 upregulated the level of Sox-9 by demethylating H3K27me3 at Sox-9 promoter sites, revealing the regulatory mechanism of EZH2 on Sox-9. Meanwhile, puncture-induced rat models showed that EZH2 knockdown exerted a protective effect on CEP and disc degeneration.InterpretationThis study reveals that EZH2 inhibition is a promising strategy for mitigating the symptoms and progression of IVDD.Funding: This study was funded by the Natural Science Foundation of Zhejiang Province (Y16H060034). Authors declare that the funders had no involvement in the study design, data analysis and interpretation of the results.