New Immune System Clue to Low Back Pain

Researchers Identify Substance That May Trigger Inflammatory Process for Herniated, Degenerated Discs

By Kathleen Doheny
WebMD Health News

Reviewed By Laura J. Martin, MD

June 29, 2010 -- An immune system substance may contribute to causing the low back pain associated with herniated and degenerated discs, according to a new study.

"We have identified an immune substance that could start the inflammatory process for disc herniation and disc degeneration," says researcher William J. Richardson, MD, professor of orthopaedic surgery at Duke University Medical Center in Durham, N.C.

The substance, interleukin-17 or IL-17, was found in more than 70% of surgical tissue samples taken from patients with degenerated or herniated disc disease, but rarely in healthy disc tissue samples, the researchers found.

The discovery is believed to be a first, Richardson tells WebMD. "This is the first paper to identify IL-17 in patients with disc herniation and disc degeneration. It suggests that IL-17 may be a mediator for disc herniation and the inflammatory pain associated with that, and also with disc degeneration."

While there is no immediate benefit for those suffering from low back pain due to disc problems, "it opens up new avenues to deal with the problem down the road," he says. One possibility: a drug that blocks IL-17. Such drugs are in development for rheumatoid arthritis, Richardson says, but he has not begun a study for disc patients.

The study is published in the July issue of Arthritis & Rheumatism.

Your Immune System and Your Discs

Low back pain is among the most frequent reasons people seek medical care, the researchers note, with the economic burden of acute low back pain estimated at $200 billion a year in the U.S.

Disc problems are a common cause of that low back pain.

Discs act as cushions between vertebrae, the shock absorbers for your spine. When a disc becomes herniated, sometimes called a slipped or ruptured disc, part of its soft inner layer pushes out through a tear in the tough outer layer. The result is often back pain that shoots down your leg, called sciatica.

"There appear to be two components to sciatica; one is mechanical compression [when the disc pushes out through the tear], the other is inflammatory," Richardson says.

"What wasn't clearly understood was what substances were involved in the inflammatory component."

His team obtained tissue samples from patients, looking at 25 samples of degenerated disc tissue and 12 samples of herniated disc tissue, and compared them with eight samples of healthy tissues.

In looking for specific inflammatory substances, they found IL-17 was found in more than 70% of the diseased tissues but rarely or modestly in healthy tissues.

Disc Degeneration, Herniation: Second Opinion

The research adds valuable new information to what is known about disc problems, says Theodore Oegema, PhD, a professor of biochemistry and orthopaedic surgery at Rush University Medical Center in Chicago, who wrote an editorial to accompany the study.

He calls it "a new twist to an old story."

It's already known that IL-17 contributes to the chronic inflammation seen in psoriasis vulgaris, the bone resorption problem in rheumatoid arthritis and gum disease, and in the intestinal disorder Crohn's disease, Oegema writes in the editorial.

The new research, he tells WebMD, supplies evidence of IL-17 cell involvement in early disc degeneration, not simply in herniation. In time, he says, researchers may develop methods, possibly with targeted drugs, to stall the degeneration of discs that can occur with age by blocking IL-17 in that area.


Nearly everyone has low back pain at some time during their life. See Answer

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SOURCES: William J. Richardson, MD, professor of orthopaedic surgery, Duke University Medical Center, Durham, N.C.

Theodore Oegema, PhD, professor of biochemistry and orthopaedic surgery, Rush University Medical Center, Chicago.

Shamji, M. Arthritis & Rheumatism, July 2010, vol 62: pp 1974-1982.

Oegema, T. Arthritis & Rheumatism, July 2010, vol 62: pp 1840-1841.

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