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1.
World Neurosurg ; 160: e430-e435, 2022 04.
Article in English | MEDLINE | ID: mdl-35051635

ABSTRACT

OBJECTIVE: To study the relationship between distribution of bone cement and intravertebral cleft of patients with Kummell disease on the clinical effect of percutaneous kyphoplasty (PKP). METHODS: According to the relationship between the distribution of bone cement and the cleft in the vertebrae, a total of 92 patients with Kummell disease who underwent PKP in our hospital were divided into 2 groups. Specifically, the bone cement of patients in group A was localized in the cleft of the vertebrae and did not infiltrate around the cleft, while that of group B patients not only filled the cleft of the vertebrae, but also distributed diffusely around the cleft of the vertebrae. The amount of bone cement injected, leakage rate, visual analogue scale (VAS) score, Oswestry Disability Index (ODI), and vertebral imaging changes before operation, and 2 days and 1 year after operation were compared between the 2 groups. RESULTS: The amount of bone cement injected and the permeability of bone cement in group B were higher than those in group A (P < 0.05). The scores of VAS and ODI in both groups were significantly improved after operation, but the two scores in group B were better than those in group A one year after operation. The height of anterior vertebral body and Cobb's angle of kyphosis in the 2 groups were significantly improved after operation, but 1 year after operation, those in group B were better than those in group A. CONCLUSIONS: PKP was an effective method for treating Kummell disease. At the same time, the relationship between the distribution of bone cement and the cleft in the vertebral body was an important factor affecting the curative effect after PKP. The effect of the distribution pattern of bone cement filled with intravertebral cleft and diffusely distributed around the fissures was better than that of bone cement confined in the vertebral cleft.


Subject(s)
Fractures, Compression , Kyphoplasty , Osteoporotic Fractures , Spinal Fractures , Bone Cements/therapeutic use , Fractures, Compression/surgery , Humans , Kyphoplasty/methods , Osteoporotic Fractures/surgery , Retrospective Studies , Spinal Fractures/surgery , Treatment Outcome
2.
J Gene Med ; 24(3): e3395, 2022 03.
Article in English | MEDLINE | ID: mdl-34668273

ABSTRACT

BACKGROUND: This study was designed to verify whether enhancer of zeste homolog 2 (EZH2) affects intervertebral disc degeneration (IVDD) development through regulation of microRNA (miR)-129-5p/MAPK1. METHODS: Initially, we collected lumbar nucleus pulposus (NP) tissue samples from patients with juvenile idiopathic scoliosis (n = 14) and IVDD (n = 34). We measured the expression of related genes in clinical IVDD tissues and a lipopolysaccharide (LPS)-induced NP cell model. After loss- and gain-of-function assays, NP cell proliferation and senescence were examined. The targeting relationship between miR-129-5p and MAPK1 was explored by dual luciferase reporter gene and RNA immunoprecipitation (RIP) assays. The enrichment of EZH2 and H3K27me3 in miR-129-5p promoter was verified by chromatin immunoprecipitation (ChIP). Finally, an IVDD rat model was established to test the effects of transduction with lentiviral vector carrying miR-129-5p agomir and/or oe-EZH2 in vivo. RESULTS: miR-129-5p was underexpressed, and EZH2 and MAPK1 levels were overexpressed in lumbar nucleus pulposus from human IVDD patients and in LPS-induced NP cells. miR-129-5p overexpression or silencing of MAPK1 promoted proliferation of NP cells, while inhibiting their senescence. EZH2 inhibited miR-129-5p through H3K27me3 modification in the miR-129-5p promoter. miR-129-5p could target the downregulation of MAPK1 expression. EZH2 overexpression increased the release of inflammatory factors and cell senescence factors, which was reversed by miR-129-5p agomir in vivo. CONCLUSIONS: Taken together, EZH2 inhibits miR-129-5p through H3K27me3 modification, which upregulates MAPK1, thereby promoting the development of IVDD.


Subject(s)
Intervertebral Disc Degeneration , MicroRNAs , Animals , Apoptosis/genetics , Enhancer of Zeste Homolog 2 Protein/genetics , Enhancer of Zeste Homolog 2 Protein/metabolism , Histones , Humans , Intervertebral Disc Degeneration/genetics , Lipopolysaccharides , MicroRNAs/genetics , MicroRNAs/metabolism , Mitogen-Activated Protein Kinase 1/metabolism , Rats
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