The Potential of Bioactive Plant Phytochemicals, Pro-Resolving Anti-Inflammatory Lipids, and Statins in the Inhibition of Intervertebral Disc Degeneration, Low Back Pain Resolution, Disc Functional Repair, and Promotion of Intervertebral Disc Regener

This comprehensive narrative review of bioactive plant compounds, pro-resolving anti-inflammatory lipids, and statins shows their potential in the inhibition of intervertebral disc degeneration (IVDD), pain resolution, tissue repair, and disc regeneration. IVDD is a multifactorial disease involving a multitude of signaling pathways, leading to the loss of normal disc function. An influx of nociceptive mechanoreceptors generate low back pain (LBP). IL6 and IL8 levels are elevated in patients undergoing spinal fusion to alleviate LBP, indicating these pro-inflammatory mediators may be major contributors to the generation of LBP. Apoptosis of disc cells leads to the depletion of key extracellular matrix components that equip the disc with its weight-bearing properties. A biomechanically incompetent degenerated IVD stimulates nociceptor mechanoreceptor activity, generating pain. Myo-tendinous, vertebral body, muscle, and facet joint tissues also contain pain receptors. Disturbance of the normal architecture of the IVD also generates pain in these tissues. Plant compounds have been used in folkloric medicine for centuries. This review attempts to provide a scientific basis for their purported health benefits; however, further studies are still required to substantiate this. Until this evidence is available, it would be prudent to be cautious in the use of such compounds. A diverse range of plant compounds (flavonoids, terpenoids, glycosides, alkaloids, and polyphenolics) inhibit inflammation and apoptosis, reduce spinal pain, and stimulate tissue repair by targeting cell signaling pathways in IVDD. Pro-resolving lipid mediators (lipoxin A4, resolvin D1, protectins, and maresins) also reduce inflammation, maintaining disc health and function. Cholesterol lowering statins disrupt phosphorylation in cell signaling pathways inhibiting IVDD, promoting tissue repair and regeneration.