Increased Expression of Inflammatory Cytokines and Discogenic Neck Pain.

OBJECTIVE: Although neck pain has become a serious economic and social problem worldwide, the etiology remains poorly understood. The aim of current study is to explore the possible pathogenesis of discogenic neck pain by analyzing the relationship between inflammatory cytokines and discogenic neck pain and provide a valuable reference for the prevention and treatment of discogenic neck pain. METHODS: A total of 111 cervical disc samples were collected between October 1, 2021, and October 1, 2022: 38 samples from the discogenic neck pain group, 41 samples from the symptomatic control group, and 32 samples from the normal control group. The concentration of nitric oxide (NO), interleukin (IL)-1, interleukin (IL)-6, and tumor necrosis factor alpha (TNF-α) was determined using the enzyme-linked immunosorbent assay in each sample, and the degeneration degree of the target discs were evaluated using T2-weighted sagittal magnetic resonance imaging (MRI) according to the Miyazaki disc degeneration grading system. Whether the differences among the three groups were statistically significant was tested using one-way analysis of variance and an unpaired t-test, respectively. RESULTS: The differences of the baseline characteristics were not statistically significant between the discogenic neck pain group and the symptomatic control group (p > 0.05). The expression of inflammatory cytokines in disc samples from the discogenic neck pain group (NO: 9.89 ± 1.75, IL-1ß: 10.74 ± 1.92, IL-6:31.65 ± 2.46, and TNF-α: 5.96 ± 1.91) was increased in comparison with the disc samples from both the symptomatic control group (NO: 7.15 ± 2.78, IL-1ß: 8.03 ± 1.87, IL-6: 25.79 ± 2.12, and TNF-α: 4.18 ± 2.87) and the normal control group (NO: 6.11 ± 1.37, IL-1ß: 5.84 ± 2.25, IL-6: 20.65 ± 1.26, and TNF-α: 2.05 ± 0.58). The differences were statistically significant (p < 0.001). Further, there were no statistical differences in the degree of degeneration between discogenic neck pain group and symptomatic control group. CONCLUSIONS: The increased expression of inflammatory cytokines in diseased cervical intervertebral discs might play a key role in the pathogenesis of discogenic neck pain. Although inflammation is involved in intervertebral disc degeneration, there is no linear positive correlation between the concentration of inflammatory cytokines and the degree of disc degeneration.

Predictive Factors Associated with Chronic Neck Pain in Patients with Cervical Degenerative Disease: A Retrospective Cohort Study.

Purpose: To explore the predictive factors of neck pain (NP) in patients with cervical degenerative disease by retrospectively analyzing their occupational and demographic characteristics and to provide a valuable reference for preventing and treating chronic NP. Patients and Methods: We retrospectively reviewed the occupational and demographic data of patients with cervical degenerative disease who had undergone anterior cervical surgery between June 2021 and December 2022 at our center. The patients were divided into NP and no-NP groups based on whether they had chronic NP before surgery. Relevant occupational and demographic data from all patients were statistically analyzed, and all variables were made categorical. Forward stepwise logistic regression models were constructed for preoperative chronic neck pain to explore the possible risk factors associated with chronic neck pain. Results: The differences in smoking, being an office worker, BMI, and disease types between NP and no-NP groups were statistically significant. In contrast, there were no statistically significant in age, sex, academic level, duration, and degeneration grade between the two groups. Moreover, further logistic regression analysis indicated that smoking, being an office worker, having an abnormal BMI, and cervical spondylotic radiculopathy (CSR) were related to chronic neck pain. Conclusion: The present study indicated that smoking, being an office worker, having an abnormal BMI, and CSR were predisposing risk factors for NP associated with cervical degenerative disease. Although intervertebral disc degeneration is the pathology basis of NP, the degeneration grade was not related to the occurrence of NP in our current study. Therefore, quitting smoking, avoiding sedentariness, and maintaining a normal BMI may prevent NP to some extent.

Bioinformatics Research and qRT-PCR Verify Hub Genes and a Transcription Factor-MicroRNA Feedback Network in Intervertebral Disc Degeneration.

The present study explores the potentials of bioinformatics analysis to identify hub genes linked to intervertebral disc degeneration (IDD) and explored the potential molecular mechanism of transcription factor-microRNA regulatory network. Furthermore, the hub genes were identified through quantitative reverse transcriptase PCR (qRT-PCR). GEO database expression profile datasets for candidate genes (GSE124272) were downloaded. Genes that were differentially expressed (DEGs) were detected utilizing limma technique in the R programming language. Search Tool for the Retrieval of Interacting Genes/Proteins and NetworkAnalyst software identified hub genes. The Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis as well as Gene Ontology annotation of the DEGs were performed using Metascape. Using Bioinformatics data from the TRRUST, StarBase, and TransmiR databases, a TF-miRNA-hub genes network was constructed. qRT-PCR was utilized to confirm the result. As compared to healthy persons, 521 DEGs, comprising 203 down-regulated and 318 up-regulated genes, as well as 7 core genes, were found in people with IDD. Analysis revealed that all seven essential genes were under-expressed. qRT-PCR further confirmed the low expression of these seven important genes. Based on the TRRUST database, 16 TFs that could target five junction genes were then predicted. According to the StarBase database, four miRNAs were linked to crucial genes, while the TransmiR database predicted regulatory connections between four miRNAs and five TFs. The expression of the TP53-(hsa-miR-183-5p)-CCNB1 TF-miRNA-mRNA interaction network was discovered to be correlated with IDD. Throughout this investigation, a network of TF-miRNA-mRNA connections was built for investigation of the probable molecular mechanisms responsible for IDD. The identification of hub genes associated with IDD may reveal promising IDD treatment strategies.