Association Between FokI Polymorphism of Vitamin D Receptor Gene and Lumbar Spine Disc Degeneration

Abstract

Objective The aim of the present meta-analysis was to explore the association between FokI polymorphism of the vitamin D receptor gene and lumbar spine disc degeneration. Design The search was performed in PubMed, Scopus, and Web of Science databases up to January 2020. The authors selected nine studies comprising a total of 1549 cases and 1672 controls. The association analysis included the allelic, dominant, recessive, homozygous, and heterozygous genetic models. Odds ratios with 95% confidence intervals were used to evaluate the association. The Newcastle-Ottawa Scale was used to measure the quality of the studies included in the analyses; a cut-off of 6 stars was applied. Results This meta-analysis indicated that FokI polymorphism is significantly associated with lumbar degenerative disc disorder and disc herniation in the homozygous (odds ratio, 1.77; 95% confidence interval, 1.23–2.54; Z test P = 0.002, Q test P = 0.416) and recessive (odds ratio, 1.53; 95% confidence interval, 1.23–1.90; Z test P < 0.000, Q test P = 0.224) models. Conclusions This study indicates that the vitamin D receptor gene FokI polymorphism may be correlated with the risk of developing a lumbar degenerative disc disorder and disc herniation. However, the small sample population studied and the lack of an evaluation of environmental factors must be taken as limitations in the present meta-analysis.

A Case-Control Study of the Fokl Polymorphism of the Vitamin D Receptor Gene in Bulgarians With Lumbar Disc Herniation

“…They concluded that FokI polymorphisms are linked with the elevated risk of IDD, including LDH, among Caucasians but not among the Asian population[9]. Another meta-analysis of Castillo-Avila et al, including 1,549 patients and 1,672 controls, indicated a statistically significant correlation between FokI polymorphisms and IDD[26]. Lan et al suggested that VDR mutations might hinder vitamin D metabolism, leading to the modulation of autophagy and the progression of IDD.…”