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Related Concept Videos

Degenerative Disc Disease I: Introduction01:27

Degenerative Disc Disease I: Introduction

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Degenerative disc disease is a chronic condition in which intervertebral discs gradually lose structure and function. It is not infectious or autoimmune; rather, it results from age-related biochemical and mechanical changes, influenced by genetic, metabolic, and environmental factors.Structure and Function of DiscsThe spine contains 23 intervertebral discs that absorb load, distribute forces, maintain spacing, and allow flexibility. Each disc consists of a nucleus pulposus, a gel-like core...
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Degenerative Disc Disease ll: Pathophysiology01:23

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The symptoms of degenerative disc disease arise from a combination of mechanical compression, vascular compromise, and biochemical inflammation, which together disrupt nerve function and produce pain.Mechanical CompressionDisc degeneration reduces height and elasticity, predisposing to herniation of the nucleus pulposus, a major cause of radicular pain. Herniations may be protrusion (bulging with intact annulus), extrusion (nucleus extends beyond disc but remains connected), or sequestration...
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Gene Expression Changes Precede Elevated Mechanical Sensitivity in the Mouse Intervertebral Disc Injury Model.

Zuozhen Tian1, Ken Chen2, Frances S Shofer3

  • 1Department of Physical Medicine & Rehabilitation Perelman School of Medicine, University of Pennsylvania Philadelphia Pennsylvania USA.

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Intervertebral disc (IVD) injury triggers significant gene expression changes, particularly in inflammation and repair pathways. These molecular alterations correlate with the development of persistent mechanical pain after injury.

Keywords:
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Area of Science:

  • Biomedical research
  • Molecular biology
  • Pain research

Background:

  • Back pain following intervertebral disc (IVD) injury is a prevalent clinical issue.
  • Prior investigations into early molecular changes post-IVD injury primarily employed a candidate marker strategy.

Purpose of the Study:

  • To comprehensively analyze early molecular changes in injured intervertebral discs (IVDs) using a nonbiased approach.
  • To correlate gene expression profiles with subsequent pain behavior following IVD injury.

Main Methods:

  • Induced mouse tail IVD injury via needle puncture.
  • Performed whole transcriptome analysis using RNASeq on injured and intact murine IVDs.
  • Utilized bioinformatic methods for transcriptome comparison and assessed mechanical allodynia with the Von Frey method.

Main Results:

  • Out of 17,722 genes, 7242 were differentially expressed (P.adj < 0.01) post-injury.
  • Upregulated genes were enriched in leukocyte migration; TNF-alpha showed the most protein-protein interactions.
  • Downregulated pathways were associated with pattern specification; mechanical allodynia persisted for 4 weeks.

Conclusions:

  • RNASeq identified numerous early genes involved in inflammation and repair post-IVD injury.
  • Observed mechanical allodynia was temporally linked to these gene expression changes.