Tumor necrosis factor‐α gene polymorphisms in relation to periodontitis

Craandijk, J; Krugten, M V van; Verweij, C. L.; Velden, U. van der; Loos, Bruno G.

doi:10.1034/j.1600-051x.2002.290105.x

Cited by 78 publications

(74 citation statements)

References 44 publications

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“…Thus, the association between TNF-␣ polymorphisms, its production, and disease has been studied by a number of investigators. While in a number of studies it was concluded that such an association exists (57)(58)(59)(60)(61), other studies did not find evidence for this (62)(63)(64). This is not surprising since factors modulating the cytokine synthesis or molecules mediating its activity such as TNF receptors are also expected to impact TNF-␣-dependent functions.…”

Section: Discussionmentioning

confidence: 89%

Toll-like Receptor 9 Regulates Tumor Necrosis Factor-α Expression by Different Mechanisms

Amcheslavsky

Zou

Bar‐Shavit

2004

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 89%

Toll-like Receptor 9 Regulates Tumor Necrosis Factor-α Expression by Different Mechanisms

Amcheslavsky

Zou

Bar‐Shavit

2004

Journal of Biological Chemistry

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“…The changes caused by SNPs in the gene expression or in its product can lead to individuals with a certain genotype having a higher susceptibility to a particular disease with a greater degree of severity (31). The AA genotype in the TNF-α -308 G>A polymorphism has been significantly associated with increased production of TNF-α and, in some cases, with increased morbidity and mortality in sepsis, malaria, chronic obstructive pulmonary disease, leishmaniasis, systemic lupus erythematosus, autoimmune type 1 hepatitis, and other diseases mediated by the immune system (32).…”

Section: Discussionmentioning

confidence: 99%

Association Between Apical Periodontitis and TNF-α -308 G>A Gene Polymorphism: A Systematic Review and Meta-Analysis

et al. 2017

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Currently, investigations have focused on the identification of Single Nucleotide Polymorphisms (SNP) involved in host response and its ability to generate an immunity deficiency. The aim of this study was to perform a systematic review (SR) and metaanalysis to evaluate the association between TNF-α -308 G>A polymorphism and apical periodontitis (AP) phenotypes. A broad search for studies was conducted. The following databases were used: PubMed, Scopus, Web of Science, and VHL (Medline, SciELO, Ibecs, and Lilacs). The MeSH terms "Periapical Periodontitis," "Periapical Abscess," "Polymorphism, Genetic," and "Polymorphism, Single Nucleotide" were used. MeSH synonyms, related terms, and free terms were included. Clinical investigations of individuals with different AP phenotypes in permanent teeth were selected. After application of the eligibility criteria, selected studies were qualified by assessing their methodological quality. A fixed effect model was used for the meta-analysis. The initial search identified 71 references. After excluding duplicate abstracts, 33 were selected. From these, two were eligible for quality assessment and were classified as being of moderate evidence. The included studies did not demonstrate association between AP and TNF-α -308 G>A SNP. However, the meta-analysis demonstrated an association between the genotype distribution and AP phenotype (OR= 0.49; confidence interval= 0.25, 0.96; p=0.04). The role of TNF-α -308 G>A SNP in AP phenotypes is debatable. Further studies are needed to confirm and understand the underlying mechanisms of the identified association.

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“…Galbraith et al (1998) determined TNF genotypes in chronic periodontitis patients and healthy controls and found no differences in the three bi-allelic polymorphisms of TNF␣ (-238, -308, +252). More recently, Craandijk et al (2002) also found no significant associations between a different series of four TNF␣ gene polymorphisms and periodontitis patients.…”

Section: (7) Tumor Necrosis Factor ␣ ␣ (Tnf␣ ␣)mentioning

confidence: 99%

Genes and Gene Polymorphisms Associated with Periodontal Disease

Kinane

Hart

2003

Critical Reviews in Oral Biology & Medicine

279

252

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ABSTRACT:The scientific literature during the last ten years has seen an exponential increase in the number of reports claiming links for genetic polymorphisms with a variety of medical diseases, particularly chronic immune and inflammatory conditions. Recently, periodontal research has contributed to this growth area. This new research has coincided with an increased understanding of the genome which, in turn, has permitted the functional interrelationships of gene products with each other and with environmental agents to be understood. As a result of this knowledge explosion, it is evident that there is a genetic basis for most diseases, including periodontitis. This realization has fostered the idea that if we can understand the genetic basis of diseases, genetic tests to assess disease risk and to develop etiology-based treatments will soon be reality. Consequently, there has been great interest in identifying allelic variants of genes that can be used to assess disease risk for periodontal diseases. Reports of genetic polymorphisms associated with periodontal disease are increasing, but the limitations of such studies are not widely appreciated. While there have been dramatic successes in the identification of mutations responsible for rare genetic conditions, few genetic polymorphisms reported for complex genetic diseases have been demonstrated to be clinically valid, and fewer have been shown to have clinical utility. Although geneticists warn clinicians on the over-enthusiastic use and interpretation of their studies, there continues to be a disparity between the geneticists and the clinicians in the emphasis placed on genes and genetic polymorphism associations. This review critically reviews genetic associations claimed for periodontal disease. It reveals that, despite major advances in the awareness of genetic risk factors for periodontal disease (with the exception of periodontitis associated with certain monogenetic conditions), we are still some way from determining the genetic basis of both aggressive and chronic periodontitis. We have, however, gained considerable insight into the hereditary pattern for aggressive periodontitis. Related to our understanding that it is autosomal-dominant with reduced penetrance comes a major clinically relevant insight into the risk assessment and screening for this disease, in that we appreciate that parents, offspring, and siblings of patients affected with aggressive periodontitis have a 50% risk of this disease also. Nevertheless, we must exercise caution and proper scientific method in the pursuit of clinically valid and useful genetic diagnostic tests for chronic and aggressive periodontitis. We must plan our research using plausible biological arguments and carefully avoid the numerous bias and misinterpretation pitfalls inherent in researching genetic associations with disease.

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Tumor necrosis factor‐α gene polymorphisms in relation to periodontitis

Abstract: Genetic polymorphisms in the TNF-alpha gene at positions -376, -308, -238 and +489 could not be identified as susceptibility or severity factors in periodontitis, irrespective of the smoking status of the patients.

Cited by 78 publications

References 44 publications

Toll-like Receptor 9 Regulates Tumor Necrosis Factor-α Expression by Different Mechanisms

Toll-like Receptor 9 Regulates Tumor Necrosis Factor-α Expression by Different Mechanisms

Association Between Apical Periodontitis and TNF-α -308 G>A Gene Polymorphism: A Systematic Review and Meta-Analysis

Genes and Gene Polymorphisms Associated with Periodontal Disease

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