Abstract
Intervertebral disc degeneration (IDD) is a major pathological process implicated in low back pain and is a prerequisite to disk herniation. Interleukin-1 α (IL-1α) was thought to be involved in the pathogenesis of disc degeneration by increasing the production of extracellular matrix degradation enzymes and by inhibiting extracellular matrix synthesis. IL-1α may provide insight about the etiology of IDD. We performed a hospital-based case–control study involving 200 IDD patients and 200 controls in the Chinese Han population. Genotyping was performed using a custom-by-design 48-Plex single nucleotide polymorphism Scan™ Kit. Our study indicated that IL-1α -899C/T polymorphism could increase the risk of IDD under the homozygous, recessive, and allelic models. Subsequently, we validated this significant association by a meta-analysis. Stratification analysis of ethnicity in this meta-analysis also obtained a significant association among Asians and Caucasians. In conclusion, the present study finds that IL-1α -899C/T polymorphism is associated with the risk of IDD. Larger studies with more diverse ethnic populations are needed to confirm these results.
Highlights
Low back pain (LBP) is a chronic and common medical problem with enormous socioeconomic implications [1]
Among the 200 Intervertebral disc degeneration (IDD) patients, 11 patients were classified as Type I, 38 as Type II, and 151 as Type III according to the signal intensity changes in vertebral body
We found that the TT genotype of this polymorphism was associated with an elevated risk of IDD (TT vs CC, Odds ratios (ORs) 2.35, 95% confidence interval (CI), 1.16–4.73, P=0.017)
Summary
Low back pain (LBP) is a chronic and common medical problem with enormous socioeconomic implications [1]. Eighty-four percent of the population was expected to suffer from LBP at some point in their lifetime [2]. Intervertebral disc degeneration (IDD) was considered as the major cause of clinical LBP, with an obscure molecular mechanism [3]. Robert et al [5] found that as IDD proceeds, there are elevated levels of inflammatory cytokines (interleukin 1 (IL-1) and tumor necrosis factor α), enhanced aggrecan and collagen degradation, and changes in disc cell phenotype. IL-1 may contribute to IDD by decreasing the synthesis and increasing the catabolism of proteoglycans [6]. Maeda et al [8] indicated that the decline in proteoglycan synthesis and increased cell sensitivity to IL-1α with age could contribute to the degeneration of discs
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