Tuesday, May 25, 2010

Chemical mediators of pain due to disc injury



Authors such as McKenzie have emphasized distinct pain patterns attributable to mechanical & chemical origin within the scope of mechanical spinal disorders. It is easily understood that disc injury produces pain by mechanical effect. However, injured discs can produce chemical mediators of pain. Not only this, these chemical mediators can lead to degeneration of the disc itself. Interestingly biochemical events that occur with intervertebral disc degeneration and, in particular, the role of biochemical mediators of inflammation and tissue degradation have received sparse attention in the literature.

Kang et al obtained herniated lumbar & cervical disc specimens from patients undergoing surgical discectomy for persistent radiculopathy. They found biochemical mediators of inflammation due to tissue degradation play a role in intervertebral disc degeneration and in the pathophysiology of radiculopathy.

Herniated lumbar & cervical discs were producing spontaneously increased amounts of
1. matrix metalloproteinases,
2. nitric oxide,
3. prostaglandin E2, and
4. interleukin-6.
These products may be involved intimately in the biochemistry of disc degeneration and the pathophysiology of radiculopathy.

Interestingly, Interleukin 1 alpha, interleukin-1 beta, tumor necrosis factor-alpha, interleukin-1 receptor antagonist protein, and substance P were not detected in the culture media of either the herniated.

N.B. How the chemical mediators of inflammation produced from the disc affects the vertebra endplate & vertebra itself is again a less researched issue.

Reference:
1. Kang JD et al; Spine (Phila Pa 1976). 1996 Feb 1;21(3):271-7. (Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2)
2. Kang JD et al; Spine (Phila Pa 1976). 1995 Nov 15;20(22):2373-8. (Herniated cervical intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2)



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