Study Ties Common Back Ailment to Faulty Gene

FRIDAY, Sept. 28 (HealthDay News) -- Lower back pain that occurs when discs in the spine deteriorate over time may be linked to a specific gene, according to a new study.

Researchers at King's College London said their findings could lead to the development of new treatments for this common type of back pain, known as lumbar disc degeneration.

Vertebrates develop bony growths called osteophytes when the discs next to them become dehydrated and lose height. These growths can lead to lower back pain. More than one-third of middle-aged women have at least one degenerate disc, the researchers said, and between 65 and 80 percent of the people with this condition inherited it.

By comparing the spines of 4,600 people using MRI images and mapping their genes, the study found the PARK2 gene, in particular, was linked to those with degenerating discs. This gene, they explained, may be turned off in people with lumbar disc degeneration. The researchers also said this gene could affect how quickly discs in the spine deteriorate.

It's still unclear how the PARK2 gene may get turned off in people with lumbar disc degeneration. The researchers suggested environmental factors, such as lifestyle or diet, could play a role.

"Further work by disc researchers to define the role of this gene will, we hope, shed light on one of the most important causes of lower back pain," said Dr. Frances Williams, senior lecturer from the department of twin research and genetic epidemiology at King's College London, in a college news release.

The study authors added that more research is needed to fully explain how this condition is triggered. Their research uncovered an association between the gene and disc problems, not a cause and effect.

"It is feasible that if we can build on this finding and improve our knowledge of the condition, we may one day be able to develop new, more effective treatments for back pain caused by this common condition," Williams added.

The study was published online Sept. 19 in the Annals of Rheumatic Diseases.

-- Mary Elizabeth Dallas

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SOURCE: King's College London, news release, Sept. 21, 2012