Association between TNF‐α G‐308A (rs1800629) polymorphism and susceptibility to chronic periodontitis and type 2 diabetes mellitus: A meta‐analysis

Shi, Liu-xia; Zhang, Liu; Zhang, Donglin; Zhou, Jianhua; Xuejuan, Jiang; Jin, Yuelong; Chang, Weiwei

doi:10.1111/jre.12820

Cited by 24 publications

(28 citation statements)

References 49 publications

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“…Single‐nucleotide polymorphisms of the human tumor necrosis factor‐alpha gene TNF‐α , such as rs1800629 (−308 promoter polymorphism; A/G), leads to increased expression of the inflammatory cytokine tumor necrosis factor‐alpha, and it has also been connected to autoimmune diseases, including rheumatoid arthritis. Recently, the TNF‐α rs1800629 polymorphism was also found to be significantly associated with periodontal diseases 15 …”

Section: Rheumatoid Arthritis In the Reflection Of Periodontitis?mentioning

confidence: 99%

Pros and cons of causative association between periodontitis and rheumatoid arthritis

Kozieł

Potempa

2022

Periodontology 2000

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In the context of a possible causative link between periodontal diseases and rheumatoid arthritis, it is worth noting that though periodontal diseases with associated dysbiotic microflora were prevalent in ancient populations as diverse as the Egyptians, prehistoric Scots, early pre-Columbian Americans, the Roman British, and medieval European populations, [1][2][3][4][5][6] bioarchaeological/paleontological studies have failed to reveal convincing evidence of rheumatoid arthritis. The first recognized description of rheumatoid arthritis dates to the beginning of the 19th century. 7 Owing to a lack of conclusive evidence, there are three hypotheses concerning the origin of rheumatoid arthritis: (a) it has an ancient origin; (b) it has a modern origin; and (c) it originated in the New World and was transmitted to the Old World after Columbus discovered the Americas. Therefore, if periodontal diseases (with pathogens dating back to the Neolithic period) underline development of rheumatoid arthritis, the first hypothesis would gain support in and lend credibility to an anecdotal report attributed to Hippocrates of the successful treatment of joint pain by extraction of bad teeth. Here, we present and critically discuss current research data, either supporting or negating the causative link between periodontal diseases and rheumatoid arthritis, in the context of the underlying inflammatory pathobiology of both diseases and possible involvement of periodontal pathogens. | RHEUMATOID ARTHRITIS IN THE REFLEC TION OF PERIODONTITIS?Rheumatoid arthritis is a common, systemic autoimmune disease having a reported prevalence ranging from 0.5% to 1% in the adult population worldwide, with a female-to-male ratio of 3:1. This chronic disease is characterized by inflammation of the synovial lining of joints leading to the destruction of cartilage, erosion of bone, pain, and chronic disability. Rheumatoid arthritis usually affects joints in the hands, feet, and wrists, but progression of the disease may also affect the kidneys, skin, lungs, and liver. The disease is strongly associated with cardiovascular damage and other systemic complications, increasing mortality. The etiology of rheumatoid arthritis is complex, and its underlying pathogenic mechanisms are not fully elucidated.However, this disease shares striking similarities with periodontal diseases in its immunological, biological, and genetic background, suggesting a strong association between these two disorders. 8 | Genetic and environmental risk factorsNumerous studies have identified genes implicated in the genetic predisposition to rheumatoid arthritis, the strongest of which is the shared epitope motif, a specific five amino acid sequence in the type II human leukocyte antigen (HLA) of the major histocompatibility complex class II protein. Several alleles are considered to contain the shared epitope motif, many of which are located in the HLA-DRβ1 region. Expression of specific HLA-DRβ1 polymorphisms is associated with increased risk of developing rheumatoid arthriti...

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Section: Rheumatoid Arthritis In the Reflection Of Periodontitis?mentioning

confidence: 99%

Pros and cons of causative association between periodontitis and rheumatoid arthritis

Kozieł

Potempa

2022

Periodontology 2000

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“…In total, these polymorphisms may modify the expression and production of IL-1 and TNFα, affect host immune response and susceptibility to inflammatory diseases. Previous studies demonstrated that TNFα G-308A [ 18 , 19 ], IL-1α C-889T [ 20 ] and IL-1β C+3954T [ 21 ] polymorphisms were associated with risk of chronic periodontitis. The association between these polymorphisms with susceptibility to implant failure, marginal bone loss and peri-implantitis have also been widely explored, which, however, yielded inconsistent results [ 22 – 24 ].…”

Section: Introductionmentioning

confidence: 99%

Association between common polymorphisms in IL-1 and TNFα and risk of peri-implant disease: A meta-analysis

2021

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Background Pro-inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor α (TNFα) play important roles in host immune response and bone metabolism during dental implant osseointegration. Whether the functional polymorphisms in IL-1α, IL-1β and TNFα were associated with peri-implant disease was unclear, and we performed the present meta-analysis for this purpose. Methods Eligible studies investigating IL-1α C-889T, IL-1β C+3954T and C-511T, TNFα G-308A, composite genotype of IL-1α C-889T and IL-1β C+3954T for association with peri-implant disease, including peri-implantitis (PI), marginal bone loss (MBL) and implant failure/loss (IF/IL), were searched on several literature databases prior to April 30, 2021. Odds ratio (OR) and corresponding 95% confidence interval (CI) were calculated for each polymorphism in different genetic models and for composite genotype comparing carriers to non-carriers. Results Twenty-seven studies (1324 cases with peri-implant disease and 1808 controls with healthy implants) were included. There was significant correlation between IL-1α C-889T and peri-implant disease in all genetic models. IL-1β C+3954T was associated with peri-implant disease risk in allelic (OR = 1.66, 95%CI 1.17–2.35, p = 0.004) and dominant model (OR = 1.74, 95%CI 1.19–2.53, p = 0.004), and in subgroups of Asians, Caucasians, non-smokers, IF/IL and PI. TT genotype of IL-1β C-511T increased the risk of peri-implant disease (OR = 1.68, 95%CI 1.15–2.43, p = 0.007) and MBL (OR = 4.33, 95%CI 1.72–10.9, p = 0.002) compared to CC+CT genotypes. We did not observed a significant association between TNFα G-308A and peri-implant diseases in overall or subgroups analysis. Carriers of positive composite genotype of IL-1α C-889T and IL-1β C+3954T had 1.95-fold (95%CI 1.35–2.80, p<0.001) risk of peri-implant disease and 1.76-fold (95%CI 1.05–2.95, p = 0.032) risk of IF/IL than non-carriers. Conclusion Functional polymorphisms of IL-1α (C-889T), IL-1β (C+3954T, C-511T) and composite genotype of IL-1 can be used as predictive markers for peri-implant disease, whereas TNFα G-308A polymorphism was not associated with peri-implant disease.

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“…Genetic polymorphisms may increase the risk of inflammatory disease varied by region and race/ethnicity ( 47 ). A recent study reported that in the Asian population, tumor necrosis factor (TNF)-α G-308A (rs1800629) polymorphism is linked with increased susceptibility to chronic periodontitis ( 48 ). Also, smokers are at least 50% more likely to develop periodontitis than non-smokers, with faster progression, severer deterioration, and poorer treating efficacy ( 49 , 50 ).…”

Section: Dysbiosis and Dysregulated Inflammation Drive Periodontitismentioning

confidence: 99%

Th17 Cells in Periodontitis and Its Regulation by A20

et al. 2021

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Periodontitis is a prevalent chronic disease that results in loss of periodontal ligament and bone resorption. Triggered by pathogens and prolonged inflammation, periodontitis is modulated by the immune system, especially pro-inflammatory cells, such as T helper (Th) 17 cells. Originated from CD4+ Th cells, Th17 cells play a central role for they drive and regulate periodontal inflammation. Cytokines secreted by Th17 cells are also major players in the pathogenesis of periodontitis. Given the importance of Th17 cells, modulators of Th17 cells are of great clinical potential and worth of discussion. This review aims to provide an overview of the current understanding of the effect of Th17 cells on periodontitis, as well as a brief discussion of current and potential therapies targeting Th17 cells. Lastly, we highlight this article by summarizing the causal relationship between A20 (encoded by TNFAIP3), an anti-inflammatory molecule, and Th17 cell differentiation.

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Association between TNF‐α G‐308A (rs1800629) polymorphism and susceptibility to chronic periodontitis and type 2 diabetes mellitus: A meta‐analysis

Cited by 24 publications

References 49 publications

Pros and cons of causative association between periodontitis and rheumatoid arthritis

Pros and cons of causative association between periodontitis and rheumatoid arthritis

Association between common polymorphisms in IL-1 and TNFα and risk of peri-implant disease: A meta-analysis

Th17 Cells in Periodontitis and Its Regulation by A20

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