Scientists Discover a New Way To Stop Pain Nerves From Invading the Spine
Summary
Researchers have uncovered a bone-driven signaling pathway that links spinal degeneration to chronic low back pain (LBP), a prevalent health issue affecting individuals worldwide and placing considerable pressure on healthcare systems.
Key Insights
What is a bone-driven signaling pathway and how does it relate to spinal degeneration?
A bone-driven signaling pathway is a molecular mechanism initiated by bone cells that influences nerve growth and pain sensation. In spinal degeneration, increased osteoclast activity (bone-resorbing cells) leads to acidosis in the bone microenvironment, which activates sensory nerves and triggers pain signals. Additionally, osteoclasts secrete NETRIN1, a nerve attractant factor that promotes sensory nerve innervation into degenerating bone tissue. This bone-initiated process explains how structural degeneration of the spine translates into chronic pain by essentially inviting pain nerves to grow into affected areas.
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How do inflammatory mediators and nerve growth factors contribute to chronic low back pain in spinal degeneration?
When intervertebral discs degenerate, inflammatory mediators accumulate in the disc tissue and stimulate sinuvertebral nerves, causing chronic pain. Nerve growth factor (NGF) signaling increases pain sensitivity through multiple mechanisms and promotes the growth of pain-transmitting nerve fibers into degenerating disc tissue. Additionally, the p38 MAPK signaling pathway becomes activated in degenerative discs, triggering inflammation and the release of matrix metalloproteinases that further degrade the disc structure. This creates a vicious cycle where inflammation promotes nerve growth, which in turn amplifies pain signals and accelerates further degeneration.