eCM (Eur Cell Mater / e Cells & Materials) Not-for-profit Open Access
Created by Scientists, for Scientists
 ISSN:1473-2262         NLM:100973416 (link)         DOI:10.22203/eCM

2015   Volume No 30 – pages 104-117

Title: Disc in flames: Roles of TNF-α and IL-1β in intervertebral disc degeneration

Author: ZI Johnson, ZR Schoepflin, H Choi, IM Shapiro, MV Risbud

Address: 1025 Walnut Street, Suite 511 College Building, Philadelphia, PA 19107, USA

E-mail: makarand.risbud at jefferson.edu

Key Words: Intervertebral disc, nucleus pulposus, cytokines, extracellular matrix, tumour necrosis factor, interleukin-1, Toll-like receptor.

Publication date: September 21st 2015

Abstract: The intervertebral disc is an important mechanical structure that allows range of motion of the spinal column. Degeneration of the intervertebral disc – incited by aging, traumatic insult, genetic predisposition, or other factors – is often defined by functional and structural changes in the tissue, including excessive breakdown of the extracellular matrix, increased disc cell senescence and death, as well as compromised biomechanical function of the tissue. Intervertebral disc degeneration is strongly correlated with low back pain, which is a highly prevalent and costly condition, significantly contributing to loss in productivity and health care costs. Disc degeneration is a chronic, progressive condition, and current therapies are limited and often focused on symptomatic pain relief rather than curtailing the progression of the disease. Inflammatory processes exacerbated by cytokines tumour necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) are believed to be key mediators of disc degeneration and low back pain. In this review, we describe the contributions of TNF-α and IL-1β to changes seen during disc degeneration at both cellular and tissue level, as well as new evidence suggesting a link between infection of the spine and low back pain, and the emerging therapeutic modalities aimed at combating these processes.

Article download: Pages 104-117 (PDF file)
DOI: 10.22203/eCM.v030a08