Association between TNFα - 308 G/A polymorphism and oral lichen planus (OLP): a meta-analysis

Abstract

ObjectivesTo determine whether Tumor Necrosis Factor alpha (TNFα) –308 G/A polymorphism is associated with oral lichen planus (OLP).Material and MethodsA systematic electronic search of the literature was conducted to identify all published studies on the association between TNFα –308 G/A polymorphism and OLP. All case-control studies evaluating the TNFα –308 G/A polymorphisms in OLP were selected. A meta-analysis of the studies that fulfilled the inclusion criteria was performed. Odds ratios (OR) with 95% confidence intervals (CI) were also calculated.ResultsSeven studies comprising 450 OLP cases and 867 controls were included in the meta-analysis. In the pooled analysis, TNFα –308 G/A polymorphism was associated with OLP with random effects and OR of 2.33 (95%CI=1.07-5.11; p=0.03), assuming a dominant mode of inheritance (AA+GA vs. GG). In the subgroup analysis by ethnicity, TNFα –308 G/A was associated with a significantly increased odds ratio of OLP in mixed ethnicity (OR=5.22; 95%CI=1.93-14.15; p=0.001), but not in Asians (OR=1.57; 95%CI=0.54-4.54; p=0.41) or Caucasians (OR=1.45; 95%CI=0.19-11.22; p=0.72). For subgroup analysis based on HCV (hepatitis C virus) infection status, significant increased risk of OLP was found among patients with mixed HCV infection status (OR=3.77; 95%CI=1.07-13.2; p=0.038), but not in patients without HCV infection (OR=2.09; 95%CI=0.63-6.91; p=0.22) and patients with HCV infection (OR=0.48; 95%CI=0.13-1.69; p=0.25).ConclusionOur results suggest that –308 G/A polymorphism in TNFα is a potential genetic marker for OLP.

The measurement of serum tumor necrosis factor-alpha levels in patients with lichen planus

“…Lichen planus is a dermatosis that involves the local release of cytokines, the retention of lymphocytes, and the death of basal keratinocytes through lymphocyte-mediated immunological mechanisms. [ 3 ] A late hypersensitive immune reaction in the etiology has been shown to result in a type 1 T helper immune response [ Figure 1 ]. It has been reported that there is IL-2, IFN-γ, and TNF-α release around the dermal vessels, which allow adhesion molecules and T cells to accumulate.…”

“…TNF-α has a key regulatory effect in the onset and progression of lichen planus. [ 3 ] Langerhans cell activation has increased, especially in those with oral involvement. [ 9 ]…”

“…The characteristic of the lichen planus is the epidermotropism of the lymphocytic infiltration; so keratinocytes are the target cells. [ 3 4 5 ]…”

Oral lichen planus: a microbiologist point of view

“…In 2018 , Tabatabaei et al studied a single nucleotide polymorphism in codon 72 of the tumor suppressor protein P53, encoding either arginine (Arg; CGC) or proline (Pro; CCC), and concluded that the proline allele constituted a risk factor for the progression of OLP to oral squamous cell carcinoma. In the same year, Zhou and Vieira ( 2018 ) carried out a meta-analysis of the disease and reported a positive association between a tumor necrosis factor-alpha polymorphism, a G to A transitional mutation at nucleotide -308, and the development of OLP. The following year, Polesello et al ( 2019 ) reported that functional polymorphisms of the MBL2 gene, affecting either the promoter or the first exon (codons 52, 54 and 57), reduced expression of the protein and correlated with an increased risk of developing OLP; MBL2, mannose-binding lectin, is a trimeric protein with the ability to activate the complement pathway.…”

Rise and exacerbation of oral lichen planus in the background of SARS-CoV-2 infection

“…Raised cytokines: Several interleukins (IL) such as IL1, 2, 4, 5, 6, 8, 10, 12, 17, and 18 have been implicated in the causation and progression of oral lichen planus. [7] Genetic polymorphisms of IL-18 [31] , TNFα [32] , [33] , [34] , [35] , IFNγ [36] , [37] , [38] , IL-10 [33] , [35] , IL-17 [39] , IL-1ß [34] , IL-12 [40] , IL-8 [41] , IL-4 [37] have also been associated with OLP. Histopathologically, they damage the basement membrane and cause widespread tissue destruction leading to the formation of clinically observable lesions.…”