Researchers at the Universities of Edinburgh and Bristol studied zebrafish bred without a functioning copy of the col9a1b gene, which is associated with collagen IX, a protein that helps bind structural fibers inside spinal discs. As the fish aged, they developed vertebral fusion and mineral deposits that hardened the tissue between bones, closely resembling human intervertebral disc degeneration.
The mineralization did not begin immediately. First, a supportive scaffold layer within the developing spine deteriorated, and mineral deposits appeared only after this early structural damage. Gene-activity analysis revealed disruptions in fat processing, the mTOR growth pathway, phosphate control, and vitamin A signaling, each previously linked to abnormal mineral accumulation.
The team tested several interventions. A bisphosphonate, a class of bone-protecting medication already used to treat osteoporosis, prevented minerals from accumulating. Reducing food intake and using drugs that suppress fat metabolism also lessened spinal fusion.
The findings highlight phosphate regulation and fat metabolism as promising areas for future medicines. No medications currently halt or reverse disc degeneration in humans, and surgery remains the only long-term treatment.
The study was funded by Arthritis UK and the Biotechnology and Biological Sciences Research Council and published in Communications Biology. Researchers caution that more work is needed before any clinical application.
A drug already used for osteoporosis blocked spinal damage in a new study
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