Comparison of Inflammatory Cytokines Expression in Intervertebral Disk Protrusion with or without Low Back Pain

Abstract

Introduction It is recognized that inflammation is tightly associated with intervertebral disk (IVD) degeneration and low back pain (LBP), but the association between IVD degeneration and LBP is still controversial. The aim of this study was to demonstrate the difference of inflammation cytokines expression in the IVD herniation patients nucleus pulposus with or without the presence of LBP, elucidate the role of inflammation cytokines for pain generation. Materials and Methods Surgical IVD tissues were harvested from IVD protrusion patients with LBP ( n = 20) or without LBP ( n = 20). Immunohistochemistrical analysis was performed to examine the expression of interleukin-1β (IL-1β), tumor necrosis factor (TNFα), inducible nitric oxide synthetase (iNOS), and substance P in these IVD samples. Nine evenly spaced separate 10× magnification fields for each tissue sample and antibody target were evaluated for the immune-reactivity positive cell percentage to compare the inflammation cytokines expression between the two groups. Results Immunohistochemistrical analysis showed that IL-1β, TNFα, iNOS, and substance P were expressed in both groups. The immune-reactivity positive cell percentage of IL-1β, TNFα, iNOS, and substance P are 18.44 ± 12.17, 23.9 ± 9.32, 21.86 ± 11.57, and 37.44 ± 14.40, respectively, in group of intervertebral disk (IVD) protrusion patients with LBP, whereas 17.82 ± 4.90, 17.56 ± 9.54, 29.74 ± 5.62, and 24.98 ± 10.36 in group of IVD protrusion patients without LBP. There were no significant statistical differences for the immunoreactivity positive cell percentage of IL-1β, TNFα, iNOS, and substance P between the two groups, but the expression of substance P was stronger in group of IVD protrusion patients with LBP. Conclusion Similar expression pattern of IL-1β, TNFα, and iNOS between both groups might indicate that they are not associated with LBP generation. However, substance P overexpression in IVD may be responsible for LBP pathomechanism. I confirm having declared any potential conflict of interest for all authors listed in this abstract Yes Disclosure of Interest None declared