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Backgrounds: Intervertebral disc degeneration (IDD) is a major cause of low back pain, however its underlying pathogenesis is complicated and remains extensively illumination. Here we investigate the role of sirtuin 2 (SIRT2) in human IDD. Methods: We compared the RNA and protein levels of SIRT2 in non-degenerate and degenerate human tissues and assessed their relationship with clinical features. After isolated the intervertebral disc cartilage endplate (CEP) cells, the cell proliferation and apoptosis were tested. Further underlying mechanisms were explored from molecular levels. Findings: We found that the CEP cell proliferation and apoptosis was not changed during IDD. However, the CEP collagen synthesis and secretion were attenuated in IDD patients compared with healthy individuals. Moreover, the SIRT2 expression was downregulated in the CEP cells isolated from IDD patients. Overexpressing SIRT2 can significantly rescue the capacity of collagen II synthesis. Upon SIRT2 overexpression, the NF-κB was deacetylated and subsequently modulate collagen gene transcription, therefore preventing IDD development. Interpretation: SIRT2 downregulation is one of the possible causes of IDD during aging. Overexpressing SIRT2 will attenuate IDD progression via deactivating NFκB. Funding Statement: This work is supported by the National Natural Science Foundation of China (NSFC #81601957) Declaration of Interests: The authors state: "None declared." Ethics Approval Statement: The work was approved by the Ethics Committee of the China–Japan Union Hospital (Changchun, China). Written informed consent was obtained from patients or relatives before tissue collection. All procedures are complied with the principles outlined in the Declaration of Helsinki.

Background context Bulging of ligamentum flavum can happen with the aging process and can lead to compression of the spinal cord and nerves. However, the distribution and the risk factors associated with a missed ligamentum flavum bulge (LFB) are unknown. Purpose The aim was to evaluate the distribution and risk factors associated with missed LFB in the cervical spine. Study design This was a retrospective analysis of kinematic magnetic resonance images (kMRI). Patient sample Patients diagnosed with symptomatic neck pain or radiculopathy between March 2011 and October 2012 were included. Outcome measures The outcome measures were missed LFB and degenerative factors. Methods A total of 200 patients (1,000 cervical segments) underwent upright kMRI in neutral, flexion, and extension postures. The LFB, sagittal cervical angles, disc herniation, disc degeneration, disc height, angular motion, translational motion, age, and gender were recorded. After excluding segments with LFB in neutral and flexion position, Pearson and Spearman correlation coefficients were used to evaluate the relation between the risk factors and missed LFB in the extension position. Results The average depth of LFB was 0.24±0.71 mm at C2–C3, 1.02±1.42 mm at C3–C4, 1.65±1.48 mm at C4–C5, 2.13±1.37 mm at C5–C6, and 1.05±1.54 mm at C6–C7. The distribution of LFB was the most frequent at C5–C6 level (76.58%) followed by C4–C5 (63.06%). Disc herniation, disc degeneration, angular variation, and translational motion were significantly correlated with missed LFB at C4–C5 andC5–C6. Disc degeneration was the only factor significantly correlated with missed LFB at all cervical segments. Conclusions Occurrence and depth of missed LFB was the highest at C4–C5 and C5–C6 compared with other cervical levels. Disc degeneration, disc herniation, angular variation, and translational motion could play a role in the development of LFB at C4–C5 andC5–C6.