The Impact of Smoking on Inflammatory Biomarkers in Intervertebral Disc Degeneration: A Biochemical and Diagnostic Evaluation.
prospective_cohort · Level II
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- Also identified by DOI 10.1097/BSD.0000000000001942.
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Abstract
Prospective cohort study. To evaluate the impact of smoking on intervertebral disc degeneration (IDD) by analyzing inflammatory and anti-inflammatory biomarkers-interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and alpha-1 proteinase inhibitor (A1PI, also known as AAT)-in disc tissue samples from smokers and nonsmokers undergoing microdiscectomy. IDD is a leading cause of chronic lower back pain and disability, often requiring surgical intervention. Smoking is a well-established risk factor, promoting oxidative stress, inflammation, and impaired tissue repair. However, few studies have directly compared biochemical changes in surgically removed disc tissue from smokers and nonsmokers. Sixty-seven patients undergoing microdiscectomy for lumbar disc herniation were enrolled, with 34 classified as smokers and 33 as nonsmokers. Intervertebral disc tissue was collected intraoperatively and analyzed through enzyme-linked immunosorbent assay (ELISA) to quantify IL-1β, IL-6, TNF-α, and AAT levels. Independent t tests and Mann-Whitney U tests were applied for group comparisons. Receiver Operating Characteristic (ROC) curves assessed biomarker diagnostic accuracy. Smokers were significantly younger ( P <0.001) and had lower BMI ( P =0.031) than nonsmokers. Levels of IL-1β ( P <0.001), IL-6 ( P <0.001), and TNF-α ( P <0.001) were significantly higher in smokers, while AAT levels were lower ( P <0.001). ROC analysis showed high discriminatory power for IL-1β (AUC=0.912), IL-6 (AUC=0.899), TNF-α (AUC=0.895), and AAT (AUC=0.881) in identifying smoking-related disc degeneration. Smoking increases inflammatory activity and reduces anti-inflammatory protection in intervertebral discs, accelerating degeneration. Elevated IL-1β and TNF-α are reliable biomarkers of smoking-related inflammation, while reduced AAT indicates compromised protective mechanisms. These results support smoking cessation as a preventive strategy and highlight biomarker-based approaches for early detection and targeted therapy in IDD.