Association of Interleukin-6 in Degenerative Lumbar Disorder: A Systematic Review

Introduction: Degenerative disorder of lumbar spine, lumbar spondylosis is characterised by disc degeneration and osteophyte formation. Low Back Pain (LBP) is exacerbated by chronic degeneration, which leads to inflammation, elevated cytokine production and activation of inflammatory pathways. Interleukin-6 (IL-6) and other cytokines worsen disc degeneration and discomfort and increased levels of IL-6 is associated with the severity of this condition. Aim: To find out the association between IL-6 levels and degenerative lumbar disorders and its related conditions. Materials and Methods: The present systematic review was conducted following PRISMA guidelines and the protocol was registered in PROSPERO (Registration No.: CRD42024479518). An extensive search of four databases i.e., PubMed, Scopus, Web of Science and Embase from October 2023 to May 2024 was carried out. Studies with cohort, case-control, cross-sectional, human research designed were considered for this review. Two independent reviewers extracted the data and evaluated the methodological quality and risk of bias using National Heart Lung and Blood Institute (NHLBI) scale. Disagreement between the two primary investigators during the evaluation process was resolved by a second pair of reviewers through discussion. Results: Out of total 106 articles, six studies met the inclusion criteria and were included in the qualitative synthesis. No studies were eligible for quantitative meta-analysis due to heterogeneity in study design and outcome reporting. The outcome of included studies consistently showed elevated IL-6 levels in patients with lumbar spondylosis or disc degeneration and related disorders. Increase IL-6 expression was associated with enhanced inflammatory activity and greater severity of clinical symptoms. Conclusion: The present review suggests a significant strong association between IL-6 and degenerative lumbar disorders, indicating that IL-6 plays a vital role in the pathophysiology of this condition.