Smoking and Polymorphisms of the Interleukin‐1 Gene Cluster (IL‐1β, IL‐1α, and IL‐1RN) in Patients with Periodontal Disease

Meisel, Peter; Siegemund, A.; Dombrowa, Sylke; Sawaf, Hazem; Fanghaenel, J.; Kocher, T.

doi:10.1902/jop.2002.73.1.27

Cited by 90 publications

(89 citation statements)

References 27 publications

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“…Similar results were reported by McDevitt et al (2000) and from smaller studies by McGuire and Nunn (1999), Laine et al (2001), and Gore et al (1998) (who showed that the two polymorphisms within the composite genotype may be in linkage disequilibrium). Other contradictory reports, such as Meisel et al (2002), stated that the composite genotype showed a strong interaction with smoking [one of the established risk factors for periodontitis (Kinane and Chestnutt, 2000)], whereas non-smokers, even genotype-positive, were not at any increased risk. A similarly contradictory study (Papapanou et al, 2001) of 132 periodontitis patients who were age-and sex-matched with controls did not show any association with the composite genotype and periodontitis.…”

Section: (6):430-449 (2003)mentioning

confidence: 99%

Genes and Gene Polymorphisms Associated with Periodontal Disease

Kinane

Hart

2003

Critical Reviews in Oral Biology & Medicine

293

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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Section: (6):430-449 (2003)mentioning

confidence: 99%

Genes and Gene Polymorphisms Associated with Periodontal Disease

Kinane

Hart

2003

Critical Reviews in Oral Biology & Medicine

293

252

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“…Kornman et al (17) found a significantly higher prevalence of positive genotypes in non-smokers with severe PD, and Shirodaria et al (35) reported a significant association between the IL-1A polymorphism (+4845) and a higher risk of severe PD in non-smokers. However, findings of studies from 3 consecutive years (20,36,37) showed that only smokers with positive IL-1 genotype were at a higher risk of PD, concluding that tobacco use is a more important risk factor than genetics. Drozdzik et al (38) found no significant association between the presence of the IL-1B polymorphism (+3953) and the periodontal status of patients, consistent with the present study, describing plaque index and age as more influential risk factors.…”

Section: Discussionmentioning

confidence: 98%

Interleukin-1 gene polymorphisms and periodontal status in a Spanish population

et al. 2012

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Abstract. The aim of this study was to investigate the possible association between interleukin (IL)-1A (+4845) and/or IL-1B (+3954) gene polymorphisms and the onset and progression of chronic periodontal disease (PD), an issue that remains controversial. The relationship between IL-1β concentration in the gingival crevicular fluid (GCF) and disease activity was also evaluated. The study was performed on 25 individuals with no gingivitis or PD and on 25 subjects with active chronic PD. Two samples of GCF were obtained from each subject and IL-1β was determined by enzyme-linked immunoabsorbent assay. Blood samples (10 ml) were drawn from each subject to detect polymorphisms in IL-1A (+4845) and IL-1B (+3954) by polymerase chain reaction. Mean GCF IL-1β concentrations were higher in patients with active chronic PD compared to the control group. No significant association was found in either group between GCF IL-1β concentration and the presence of polymorphisms in IL-1A (+4845), IL-1B (+3954) or both genotypes. No significant difference was found in either group with regard to the presence of polymorphisms in IL-1A (+4845), IL-1B (+3954) or both genotypes (p=0.556). The concentration of IL-1β in GCF was almost 2-fold higher in patients with chronic PD than in the healthy individuals. The presence of polymorphisms in IL-1A (+4845) and/or IL-1B (+3954) genotypes is not associated with IL-1β overproduction in GCF and is not a risk factor for chronic PD. IL-1β is considered a suitable marker of the severity and progression of chronic PD. The presence of IL-1A (+4845) and/or IL-1B +3954 gene polymorphisms does not appear to be a risk factor for chronic PD. Therefore, the IL-1A (+4845) and/or IL-1B +3954 gene polymorphisms cannot be considered genetic markers of chronic PD. Moreover, these polymorphisms do not indicate an overproduction of IL-1β in GCF.

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“…17,18,19,20,21 Toda la información obtenida sirvió para corroborar que según las concentraciones de las principales citocinas proinflamatorias (IL-1beta y FNT-alfa) se presenta el cuadro clínico de la enfermedad periodontal, en cuanto a la aparición y grado de progresión, más aún a partir del estudio del polimorfismo de la IL-1 22 se apreció la utilidad de una prueba para determinar el polimorfismo del mismo 23 , aunque existe todavía controversia al respecto.…”

Section: Variación En Los Niveles De Expresión Del Sap Según El unclassified

Sistema Activador del Plasminógeno en la Enfermedad Periodontal

Visag

2014

Odontol. sanmarquina

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El sistema activador del plasminógeno participa activamente en la dinámica de la enfermedad periodontal y se encuentra finamente compensado en cuanto a sus activadores e inhibidores, aunque existen periodos donde las bolsas periodontales reagudizadas pueden romper el fino equilibrio entre activadores (t-PA) e inhibidores del plasminógeno (PAI-2) desencadenando el progreso de la enfermedad periodontal; cabe destacar la participación de patógenos bacterianos como la Porphyromona gingivalis, que se caracteriza por generar el desbalance entre los principales activadores e inhibidores con el consecuente incremento de la actividad fibrinolítica. Los efectos del desbalance de los constituyentes del sistema activador del plasminógeno, en particular t-PA, toma mayor relevancia en los eventos hemorrágicos a nivel gingival de pacientes con deficiencias de los factores de la coagulación como los anticoagulados por warfarina y enfermedad hepática severa como la cirrosis. El sistema activador del plasminógeno como parte del sistema fibrinolítico es descrito según la literatura más relevante en cuanto a su participación en la patogénesis de la enfermedad periodontal y sus componentes son descritos comparativamente a nivel local o periodontal con el nivel sistémico.

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Smoking and Polymorphisms of the Interleukin‐1 Gene Cluster (IL‐1β, IL‐1α, and IL‐1RN) in Patients with Periodontal Disease

Abstract: The results provide evidence that the composite genotypes studied show interaction with smoking, the main exposition-related risk factor of periodontal disease. Non-smoking subjects are not at increased risk, even if they are genotype-positive.

Cited by 90 publications

References 27 publications

Genes and Gene Polymorphisms Associated with Periodontal Disease

Genes and Gene Polymorphisms Associated with Periodontal Disease

Interleukin-1 gene polymorphisms and periodontal status in a Spanish population

Sistema Activador del Plasminógeno en la Enfermedad Periodontal

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