Abstract
Lumbar disc herniation (LDH) is one of the most common causes of low back and leg pain. While mechanical and degenerative factors have long been considered the main contributors, persistent or recurrent symptoms in many patients suggest additional biological mechanisms. Recent research has highlighted the microbiome as a potential modulator of inflammation, immune response, and pain sensitization, introducing the "gut-spine axis" concept. This scoping review summarizes the current evidence on the role of both gut and local disc microbiota in LDH. A systematic search of PubMed/MEDLINE and Scopus was conducted up to June 2025, following PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews) guidelines. Twenty-six studies were included, encompassing preclinical and clinical investigations. Animal models showed that LDH may alter gut microbial composition and that microbiome-targeted interventions can reduce inflammation, neuroinflammatory signaling, and pain sensitivity. In human studies, low-virulence bacteria, particularly Cutibacterium acnes, were frequently detected in surgically excised intervertebral discs, although results were inconsistent due to methodological heterogeneity and potential contamination. Some studies reported associations between bacterial colonization and Modic changes, disc height loss, or chronic pain. Additionally, genetic and metabolomic data suggest that gut dysbiosis and related microbial metabolites may influence systemic immune and metabolic pathways implicated in disc degeneration and pain perception. Overall, the current evidence suggests the biological plausibility of microbiome involvement in LDH pathophysiology, acting through both systemic and local mechanisms. However, the available data remain preliminary, and no mechanistic study has confirmed the observed correlations to date. Further standardized, contamination-aware studies are required to clarify causality and explore microbiome-targeted therapeutic strategies.