Oral Presentation Sydney Spinal Symposium 2025

Role of Gut Microbiome Dysbiosis in Patients with Chronic Low Back Pain: Results from an Age, Sex and BMI Matched Study. (124550)

Stone Sima 1 , Thomas Jeffries 2 , Alisha Sial 1 3 , Suhani Sharma 1 , Neha Chopra 1 4 , Fan Zhang 5 , Georgina Hold 5 , Ashish Diwan 1 3 4
  1. Spine Labs, St George and Sutherland Clinical School, Sydney, NSW, Australia
  2. School of Science, Western Sydney University, Sydney, NSW, Australia
  3. Spinal Unit, Discipline of Orthopaedic Surgery, School of Medicine, University of Adelaide, Adelaide, Australia
  4. Spine Service at St George and Sutherland Clinical School, Sydney, NSW, Australia
  5. Microbiome Research Centre, St George and Sutherland Clinical Campuses, University of New South Wales, Sydney, NSW, Australia

Introduction
Chronic low back pain (LBP) is the leading cause of disability worldwide, yet its underlying pathophysiology remains poorly understood. Current diagnostic techniques rely heavily on imaging, which is insufficient for identifying inflammatory or systemic contributors to LBP. Emerging evidence suggests a role for gut microbiome dysbiosis in inflammatory pain pathways, yet its specific contribution to chronic LBP remains unclear.

 

Methods
We conducted an age-, sex-, and BMI-matched case-control study including 28 patients with chronic LBP (>3 months, Pfirmann grade <4, no endplate changes, spondylolisthesis, or scoliosis) and 28 healthy controls. Stool samples underwent 16S rRNA V4 sequencing, and data were processed using QIIME2. Alpha and beta diversity, and taxonomic composition at phylum and genus levels, were compared using Mann-Whitney U tests.

Results
There were no significant differences in age, sex, BMI, or race between groups. LBP patients showed reduced alpha diversity (U=517, p=0.003, r=0.395) and distinct beta diversity clustering (PERMANOVA, p<0.05). At the phylum level, Proteobacteria (U=91, p<0.001) and Desulfobacterota (U=73, p<0.001) were elevated, while Bacteroidota (U=524, p=0.031) was reduced in LBP patients. At the genus level, Prevotella (U=272, p=0.045) and Faecalibacterium (U=254, p=0.024) were increased, and Parabacteroides (U=621, p<0.001) was depleted.

Conclusions
These findings indicate that gut microbiome dysbiosis may play a key role in chronic LBP among patients without identifiable surgical pathologies, likely through systemic inflammation, reinforcing the "gut-disc axis" hypothesis. Given the limitations of conventional diagnostic tools and management strategies, microbiome profiling may provide novel biomarkers for LBP and inform microbiome-targeted therapies such as probiotics, dietary modifications, and fecal microbiota transplantation. Future research should explore causal relationships and strain-specific microbial effects to refine microbiome-based interventions for chronic LBP.