New insights into leading cause of back pain

New research published in Communications Biology reveals that gene activity changes might be responsible for the breakdown of the spine's shock-absorbing capabilities, leading to back pain. Mice studies suggest a buildup of minerals in the spine, akin to bone formation in the wrong place, hardening the spine. This condition, known as intervertebral disc degeneration (IVDD), affects a significant portion of the population and currently has no available treatments.

Surgery is the only long-term solution. Genetic factors play a role in IVDD, with a gene linked to the collagen IX protein being associated with early-onset disc problems. Researchers studied zebrafish bred without a functional copy of this gene to understand how genetic faults contribute to disc disease. As the fish aged, their spines developed issues similar to human disc disease, including fused bones and mineral deposits in the tissue between vertebrae.

This hardening was preceded by a breakdown in a supportive layer in the developing spine. The researchers identified disruptions in fat metabolism, a growth-control pathway called mTOR, phosphate handling, and vitamin A signaling—all processes linked to mineral buildup. They also found that a drug used for osteoporosis, known as a bisphosphonate, could block mineral buildup, while reducing food intake or using drugs that dampen fat metabolism could lessen spinal fusions.

The study's lead author, Dr. Erika Kague, notes that decades of surgery being the only option for disc disease could soon change, with their findings pointing to several ways to slow down the hardening of the spine. Dr. Caroline Aylott of Arthritis UK expresses hope for new therapeutic approaches for the 9.5 million people in the UK suffering from back pain.

The research, funded by the Biomedical and Bioscience Research Council (BBSRC), demonstrates how publicly funded discovery bioscience can generate knowledge to address significant health challenges.