Inflammatory Biomarkers in Smokers: Implications for Ligamentum Flavum Hypertrophy

BACKGROUND Ligamentum flavum (LF) hypertrophy is a key contributor to spinal pathologies such as lumbar and cervical disc herniations and spinal stenosis. Smoking, as a modifiable lifestyle factor, is implicated in systemic inflammation and oxidative stress, potentially exacerbating LF hypertrophy. This study aimed to compare the expression of alpha-1 antitrypsin (AAT), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in the lumbar ligamentum flavum from 27 smokers and 31 non-smokers. MATERIAL AND METHODS LF tissue samples were collected during spinal surgeries. Demographic, anthropometric, and clinical data were recorded. ELISA was used to quantify levels of AAT, IL-1ß, IL-6, and TNF-alpha. Statistical analyses included t-tests, Mann-Whitney U tests, and receiver operating characteristic (ROC) curve analyses. Statistical significance was set at p<0.05. RESULTS Smokers exhibited significantly higher levels of IL-1ß (p<0.001), IL-6 (p=0.004), and TNF-alpha (p<0.001), while AAT levels were significantly lower (p<0.001) compared to non-smokers. ROC analysis identified IL-1ß (AUC=0.828; p<0.001) and TNF-alpha (AUC=0.801; p<0.001) as highly effective markers for distinguishing smokers from non-smokers, while IL-6 (AUC=0.730; p=0.003) showed moderate diagnostic accuracy. AAT (AUC=0.867; p<0.001) demonstrated excellent sensitivity (96.3%) for detecting smoking-related effects. CONCLUSIONS Smoking contributes significantly to systemic inflammation and oxidative stress, leading to biochemical changes that may drive LF hypertrophy. These findings underscore the importance of smoking cessation as a modifiable risk factor in the management of spinal pathologies.