This study examined the association of IL1 genetic polymorphisms (IL-1A +4845, IL-1B +3954 & IL-1RN +2018) with periodontal disease status of Down syndrome (DS) individuals.
These results suggest that the NLRP3 inflammasome, followed by a response from the IL-1 family, is critical in periodontal disease induced by wild-type P. gingivalis challenge via sustained inflammation.
These results demonstrate that IL-1 is produced and released locally in periodontal disease at concentrations sufficient to mediate tissue inflammation and bone resorption.
There is a gene-environmental interaction because diabetic subjects bearing a variant IL-1 genotype C/T or T/T had an enhanced risk for periodontal disease in comparison with their IL-1 wild-type counterparts.
The results of this study showed that the heterozygous variant genotype of the IL1rs16944 was significantly associated with a reduced risk of periodontal disease in young Japanese women.
The results of this study have shown an interaction of the IL-1 positive genotype with age, smoking and P. gingivalis which suggests that IL-1 genotype is a contributory but non-essential risk factor for periodontal disease progression in this population.
The results indicated that the IL-1 haplotype may be of limited value for the prognosis of periodontal disease progression following non-surgical periodontal therapy.
The low prevalence of some of the IL-1 gene polymorphisms in the ethnic groups included in this study limits the validity of conclusions on genotype associations with clinical findings, but there was a trend suggesting that allele 1 at IL-1B (-511) and IL-1B (+3954) was overrepresented among diabetics with periodontal disease.
The interleukin-1 (IL-1) gene family has been associated with susceptibility to periodontal diseases, including aggressive periodontitis (AgP); however, the results are still conflicting.
The aims of this retrospective study were to describe (1) the absolute failure rate of Brånemark System implants (Nobel Biocare AB, Göteborg, Sweden) consecutively installed over a 10-year period in partially edentulous patients treated for periodontal disease prior to implant treatment and under regular professional maintenance, (2) the rate of interleukin-1 (IL-1) polymorphism in those patients who experienced at least one implant failure during the first year of function, and (3) the prevalence of periodontal pathogens in dental and periimplant sites with and without signs of inflammation.
The aims of the present study were to determine the distribution of IL-1 gene polymorphism (IL-1A+4845 and IL-1B+3954) and their association with periodontal disease severity and to determine the significance of detecting the composite genotype (IL-1A allele2+IL-1B allele2) versus detecting either of them alone.
The aim of this study is to determine the prevalence of IL-1β+3954 and IL-1α-889 polymorphism in a group of Lebanese individuals of homogeneous ethnicity and the possible association between genotype positive individuals and the severity of periodontal disease.
Since IL-1 has been implicated in the pathogenesis of both BD and periodontal disease, we aimed to investigate the possible relation of the periodontal scores and SNPs of IL-1alpha-889C/T, IL-1beta-511C/T, and IL-1beta+3962T/C with BD compared to healthy controls (HC) and recurrent aphtous stomatitis (RAS).
Porphyromonas gingivalis is now recognized as a major pathogen in the chronic inflammatory periodontal diseases and it has previously been reported that a crude LAP fraction from this organism could induce IL-1 and interleukin 6 (IL-6) synthesis.
Knowledge of IL-1 genotype status would be important in developing a treatment plan and predicting tooth survival for a new patient who smokes and presents with periodontal disease, especially if restorative care is needed.
It also confirmed that both IL-1 genotyping and smoking history provide objective risk factors for periodontal disease in a private practice environment.
Interleukin-1 (IL-1) is a proinflammatory cytokine that is highly elevated in response to bacterial biofilms and is a potential risk factor for periodontal diseases.
In this study, we tested the hypothesis that allele 2 of the IL-1A gene at position -889 might act to elevate levels of IL-1alpha protein in patients with periodontal disease.