Researchers from the Universities of Edinburgh and Bristol have identified several biological processes involved in intervertebral disc degeneration (IVDD), a progressive condition that damages the discs cushioning the spine’s bones. The study focused on how genetic defects, particularly in a gene associated with collagen IX, contribute to disc disease development.
Zebrafish bred without a functioning copy of the collagen IX gene developed spinal abnormalities closely resembling disc disease in humans. As the fish aged, their vertebrae fused and mineral deposits caused tissue between the bones to become abnormally hard. The research revealed that this mineralization process begins only after initial structural damage to a supportive scaffold layer within the spine.
Gene activity analysis identified problems in several biological pathways, including fat processing, mTOR (which regulates growth), phosphate control, and vitamin A signaling. Each of these processes has previously been linked to abnormal mineral accumulation in bone tissue.
The researchers tested multiple approaches to reduce spinal damage. A bisphosphonate, a type of bone-protecting medication already used to treat osteoporosis in patients, successfully prevented minerals from accumulating in the fish spines. Spinal fusion was also reduced when fish received restricted food or were treated with drugs that suppressed fat metabolism. According to the team, phosphate regulation and fat metabolism represent especially promising targets for future medication development.
The study, funded by Arthritis UK and BBSRC and published in Communications Biology, suggests that surgery may no longer be the only long-term treatment option for disc disease. Researchers indicated that while additional work remains necessary, the findings offer potential therapeutic approaches for a condition that has affected millions without effective treatment alternatives.
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