Italian researchers at the Catholic University of Sacred Heart in Rome found an important molecular mechanism responsible for low back pain and other acute vertebral problems like cervical axial pain, all due to aging and degeneration of the vertebral column.
The team led by Dr. Luigi Aurelio Nasto and Enrico Pola also developed an experimental drug to inhibit this degenerative mechanism, by blocking its principal culprit, the molecule, “NF-kB” and tested it successfully in mice. The study was carried out in collaboration with the University of Pittsburgh research team led by Paul Robbins, James Kang and Nam Vo (e-mail: von@upmc.edu). Researchers reported their findings in the journal Spine. Nasto and Pola found that high concentration of NF-kB causes the degeneration of intervertebral discs (the structures that separate and damp the vertebrae), a degenerative process that could affect also young adults (30 year old), especially if they adopt a sedentary lifestyle. In other words when NF-kB becomes overactive, it triggers a series of deleterious reactions that ultimately affect the physiological structure of the vertebral column.
Due to aging, obesity and sedentary lifestyle, intervertebral discs degenerate, leading to the progressive stiffening of the column. The intervertebral disc degeneration is responsible for syndromes such as chronic low back pain or neck pain that affects a large proportion of the adult population.
Back pain and neck pain are ranked among the leading causes of lost working hours and disability in adults Italian scientists found the mechanism behind the degenerative processes of the column. They studied mice that are genetically programmed to age rapidly (progeroid mice). The average lifespan of normal mice is two years. The progeroid mice age more quickly and have a lifespan of eight months. The progeroid mice perfectly mimic the process of spine degeneration that occur in old people and young adults who suffer from low back pain.
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The researchers found that NF-kB plays a role in the degeneration of the spine. NF-kB is a transcription factor, it modulates the activation of specific target genes. Researchers found that NF-kB activates many genes related to inflammation and turn off anti-inflammatory protective genes. Moreover in many studies NF-kB was found hyperactive in both the spines of old mice and old people.
The results of the Italian research suggest that NF-kB induces the onset of deleterious inflammatory processes and inhibit anti-inflammatory mechanisms. Moreover “our study shows that by inhibiting NF-kB, we can stop spine degeneration”, Dr. Nasto says. “Drugs that turn off or even only partially inactivate NF-kB could be used to prevent the degeneration of intervertebral discs in patients.”
