Low back pain is a significant global health issue, contributing to high disability rates and economic costs, particularly due to intervertebral disc degeneration linked to senescent cells.

In a recent study, researchers utilized a mouse model lacking the sparc gene, which effectively simulates human low back pain and disc degeneration, to investigate molecular changes related to senescence.

After eight weeks of treatment with a combination of synthetic and natural senolytics, RG-7112 and o-vanillin, the mice exhibited significant pain reduction, particularly with full-dose therapies, which also improved discomfort and cold sensitivity.

The treatment not only reduced pain but also led to a notable increase in intervertebral disc volume and improved histological scores of disc degeneration in the treated mice.

Additionally, the study found a significant reduction in senescence markers in the spinal cord dorsal horn, a critical area for pain sensation, suggesting that the treatments may decrease pain-related neuroplasticity.

All ten senescence-associated secretory phenotype (SASP) factors that increased in sparc-deficient mice were decreased with treatment, demonstrating the efficacy of senolytic therapy in reducing senescence markers in intervertebral discs.

Bone health was also positively impacted, with treatments improving bone density and thickness in the vertebrae of treated mice compared to their untreated counterparts.

Both senolytics showed promise as safe and effective treatments for low back pain, indicating potential for future human trials, especially given the favorable safety profile of o-vanillin compared to RG-7112.

However, further research is needed to optimize dosing and delivery methods to enhance therapeutic effects while minimizing side effects.