Evaluating the causal effect of atherosclerosis on the risk of intervertebral disc degeneration

Abstract

BackgroundIntervertebral disc degeneration (IDD) and atherosclerosis are two common age‐related conditions that can cause significant morbidity. While previous studies have suggested an association between the two conditions, the nature of this association remains unclear.MethodsWe used Mendelian randomization (MR) to investigate the causal relationship between IDD and atherosclerosis. We identified genetic variants associated with IDD using summary statistics from a large genome‐wide association study (GWAS). These variants were then used as instrumental variables to infer causal relationships with atherosclerosis in summary statistics from a separate GWAS.ResultsOur MR analysis provided evidence for a causal relationship between IDD and atherosclerosis. We found that the genetic predisposition to atherosclerosis was associated with a higher risk of IDD (odds ratio [OR] = 3.55, 95% confidence interval [CI]: 1.07–11.74, p = 0.04). The IVW estimates were consistent with the observational findings and other robust MR methods. Sensitivity analyses suggested that our findings were robust to potential sources of bias.ConclusionsOur study provides evidence for a causal link between IDD and atherosclerosis, suggesting that interventions targeting atherosclerosis could have potential benefits for reducing the risk of IDD. Further research is needed to explore the underlying mechanisms that link these two conditions and to investigate potential therapeutic interventions.

A comprehensive review of cell transplantation and platelet‐rich plasma therapy for the treatment of disc degeneration‐related back and neck pain: A systematic evidence‐based analysis

“… 15 In part, the avascular nature results in limited gas, nutrient, and cell replenishment, and the overall cell density in the IVD is low compared to other tissue structures. 16 , 17 , 18 Moreover, the quality of cells shows a rapid decline, with a loss of progenitor cell types and a switch from active proteoglycan‐producing cells to fibrotic and senescent cell types. 19 , 20 , 21 This complex and progressive pathway of structural destruction is complemented by the secretion of inflammatory factors that may promote the influx of immunogenic cells, worsening the pathology.…”