scholarly journals Fatty disc: An unusual pattern of disc degeneration

2021 ◽  
Vol 0 ◽  
pp. 1-3
Author(s):  
Neha Choudhary ◽  
Paramjeet Singh ◽  
Vikas Bhatia ◽  
Mahesh Prakash

The intervertebral disc is the fibrocartilaginous structure between the endplates of adjacent vertebral bodies, providing support and mobility to the spine. Normally, the disc is isointense on the T1 weighted image (T1WI) and hyperintense on the T2 weighted image (T2WI). Degenerating disc shows loss of hyperintensity on T2WI due to disc dehydration. The development of hyperintensity on T1WI in degenerating disc is unusual. Causes of discal hyperintensity on T1WI include calcification, hemorrhage, melanin, mucin, or fat within the disc. Fat contents in the disc may be rarely seen in degeneration and appear as hyperintense signal on T1WI and T2WI. We, hereby report a case of discal hyperintensity on T1WI and T2WI due to fatty degeneration of the disc.

Author(s):  
Saeeda Baig

During the recent past focus has shifted from identifying intervertebral disc degeneration as being caused by physical exposure and strain to being linked with a variety of genetic variations. The objective of this review is to provide an up to date review of the existing research data regarding the relation of intervertebral disc degeneration to structural protein genes and their polymorphisms and thus help clearly establish further avenues where research into causation and treatment is needed. A comprehensive search using the keywords “Collagen”, “COL”, “Aggrecan”, “AGC”, “IVDD”, “intervertebral disc degeneration”, and “lumbar disc degeneration” from PubMed and Google Scholar, where literature in the English language was selected spanning from 1991 to 2019. There are many genes involved in the production of structural components of an intervertebral disc. The issues in production of these components involve the over-expression or under-expression of their genes, and single nucleotide polymorphisms and variable number of tandem repeats affecting their structures. These structural genes include primarily the collagen and the aggrecan genes. While genetic and environmental factors all come into play with a disease process like disc degeneration, the bulk of research now shows the significantly larger impact of hereditary over exposure. While further research is needed into some of the lesser studied genes linked to IVDD and also the racial variations in genetic makeup, the focus in the near future should be on establishment of genetic testing to identify individuals at greater risk of disease and deliberation regarding the use of gene therapy to prevent disc degeneration.


2019 ◽  
Author(s):  
Takashi Ohnishi ◽  
Katsuhisa Yamada ◽  
Koji Iwasaki ◽  
Takeru Tsujimoto ◽  
Hideaki Higashi ◽  
...  

2020 ◽  
Author(s):  
Jialiang Lin ◽  
Xuanqi Zheng ◽  
Zengjie Zhang ◽  
Zhenxuan Shao ◽  
Chongan Huang ◽  
...  

2021 ◽  
Vol 29 ◽  
pp. 123-133
Author(s):  
Xian-Fa Du ◽  
Hai-Tao Cui ◽  
He-Hai Pan ◽  
Jun Long ◽  
Hao-Wen Cui ◽  
...  

Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 4320-4330
Author(s):  
Ming Lei ◽  
Kangcheng Zhao ◽  
Wenbin Hua ◽  
Kun Wang ◽  
Shuai Li ◽  
...  

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Xue-Lin Lin ◽  
Zhao-Yun Zheng ◽  
Qing-Shan Zhang ◽  
Zhen Zhang ◽  
You-Zhi An

Abstract Objective To investigate the expression of miR-195 and its target gene Bcl-2 in intervertebral disc degeneration (IVDD) and its effect on nucleus pulposus (NP) cell apoptosis. Methods The expressions of miR-195 and Bcl-2 in NP tissues of IVDD patients were quantified by qRT-PCR and western blotting, respectively. NP cells were divided into blank group, TNF-α group, TNF-α + miR-NC group, TNF-α + siBcl-2 group, and TNF-α + miR-195 inhibitors + siBcl-2 group. Cell proliferation was detected by MTT assay, cell apoptosis evaluated by flow cytometry, and mitochondrial membrane potential (MMP) tested by JC-1 staining. Moreover, the function of miR-195 on IVDD in vivo was investigated using a puncture-induced IVDD rat model. Results IVDD patients had significantly increased miR-195 expression and decreased Bcl-2 protein expression in NP tissues. The expression of miR-195 was negatively correlated with the expression of Bcl-2 in IVDD patients. Dual-luciferase reporter gene assay indicated that Bcl-2 was a target gene of miR-195. In comparison with blank group, TNF-α group showed decreased cell proliferation and MMP, increased cell apoptosis, upregulated expression of miR-195, Bax, and cleaved caspase 3, and downregulated Bcl-2 protein, while these changes were attenuated by miR-195 inhibitors. Additionally, siBcl-2 can reverse the protective effect of miR-195 inhibitors on TNF-α-induced NP cells. Besides, inhibition of miR-195 alleviated IVDD degeneration and NP cell apoptosis in the rat model. Conclusion MiR-195 was significantly upregulated in NP tissues of IVDD patients, and inhibition of miR-195 could protect human NP cells from TNF-α-induced apoptosis via upregulation of Bcl-2.


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