TNF-α and IL-4 levels in generalized aggressive periodontitis subjects

Oral Diseases ◽  
2009 ◽  
Vol 15 (1) ◽  
pp. 82-87 ◽  
Author(s):  
MF Bastos ◽  
JA Lima ◽  
PM Vieira ◽  
MJ Mestnik ◽  
M Faveri ◽  
...  
2009 ◽  
Vol 3 (1) ◽  
pp. 184-190 ◽  
Author(s):  
P. R Moreira ◽  
J. E Costa ◽  
R. S Gomez ◽  
K. J Gollob ◽  
W. O Dutra

IL-10 and TNF-α are cytokines that have complex and opposing roles in the inflammatory responses. G/A polymorphisms at position –1082 ofIL10and –308 ofTNFAgenes have been reported to influence the expression of IL-10 and TNF-α, respectively. The aim of this study was to investigate the association between theIL10(-1082) andTNFA(- 308) gene polymorphisms with different clinical forms or severity of periodontitis in a sample of Brazilian individuals. DNA was obtained from oral swabs of 165 Brazilian individuals, which were divided into three groups: individuals with chronic periodontitis, aggressive periodontitis and individuals without clinical evidence of periodontitis. Evaluation ofIL10andTNFApolymorphisms was performed by RFLP analysis. Statistical analysis of data was performed using the χ2likelihood ratio and Fisher`s exact test. No significant differences in the genotype and allele distribution of eitherIL10orTNFAwere observed among individuals with different clinical forms or with different degrees of severity of periodontitis. Moreover, combined analysis ofIL10andTNFApolymorphisms did not show any association with periodontal status. As conclusion, theIL10andTNFAgene promoter polymorphisms investigated are not associated with different clinical forms of periodontitis or with severity of the disease in the Brazilian population polymorphisms.


2020 ◽  
Vol 21 (7) ◽  
Author(s):  
SYAMSULINA REVIANTI ◽  
DWI ANDRIANI ◽  
KRISTANTI PARISIHNI ◽  
ENDAH WAHJUNINGSIH ◽  
WIDYASTUTI

Abstract. Revianti S, Andriani D, Parisihni K, Wahjuningsih E, Widyastuti. 2020. Effectiveness of oral irrigation with an extract of green microalga Nannochloropsis oculata as an anti-inflammatory in rats infected with Aggregatibacter actinomycetemcomitans. Biodiversitas 21: 2977-2981. Aggressive periodontitis is strongly correlated with Aggregatibacter actinomycetemcomitans, a periodontopathic bacterium, which releases endotoxins and lipopolysaccharides (LPS). LPS acts as a stimulus to a variety of host cells that can promote the expression of pro-inflammatory cytokines, such as the tumor necrosis factor-α (TNF-α), in periodontal disease. The marine green microalga Nannochloropsis oculata has anti-inflammatory properties. This study aimed to examine the anti-inflammatory efficacy of oral irrigation with N. oculata extract against periodontitis induced by A. actinomycetemcomitans in a rat model. Twenty-four male Wistar rats were divided randomly into four groups (n = 6). First control group was without any treatment, the second to fourth groups were infected with A. actinomycetemcomitans and then orally irrigated with N. oculata extract at concentrations of 2.375%, 2.5%, and 2.625%. The mandibles of the euthanized rats were hemisected to measure the expression of TNF-α, interleukin-10 (IL-10, an anti-inflammatory cytokine), and osteoprotegerin (OPG) by immunohistochemistry. The first group (control) showed significantly higher expression of TNF-α and significantly lower expression of IL-10 and OPG compared to the other groups. Oral irrigation with N. oculata extracts reduced the expression of TNF-α and enhanced the expression of IL-10 and OPG in rats infected with A. actinomycetemcomitans. The effective concentration of N. oculata extract as an anti-inflammatory for oral irrigation was 2.375%.


2013 ◽  
Vol 28 (1) ◽  
pp. 108-112 ◽  
Author(s):  
Yuan Yue ◽  
Qing Liu ◽  
Chunjiao Xu ◽  
Wings TY Loo ◽  
Min Wang ◽  
...  

Objectives This study aims to evaluate and compare cytokines in gingival crevicular fluid (GCF) and saliva of patients with aggressive periodontitis (AP) before and after treatment. Methods Forty AP patients and 40 healthy volunteers were enrolled in this study. Clinical parameters included probing depth and sulcus bleeding index. GCF and saliva were collected from both groups. The levels of IL-1β, IL-2, IL-4, IL-6, IFN-γ and TNF-α were measured using ELISA. Results The probing depth in AP patients was significantly deeper before treatment than after treatment. The concentrations of cytokines in GCF and saliva were significantly higher in AP patients than in the control group and decreased after periodontal treatment. Positive relationships were found between cytokine levels in GCF and clinical parameters. The reliability of cytokines in GCF and saliva was assessed by Cronbach's alpha analysis, which could be considered satisfactory. Conclusion Cytokine levels in GCF and saliva correlated well with clinical parameters and AP. Measurements of cytokines in saliva may be regarded as a noninvasive and quick method for monitoring periodontal disease activity.


2018 ◽  
Vol 38 (4) ◽  
Author(s):  
Poulami Majumder ◽  
Keheibamding Thou ◽  
Mandar Bhattacharya ◽  
Vineet Nair ◽  
Sujay Ghosh ◽  
...  

Background: Periodontitis is a very common inflammatory oral disease. Tumor necrosis factor-α (TNF-α) is a cytokine that has been involved with the gingival tissue destruction and remodeling occurrence. We investigated the association of single nucleotide polymorphisms (SNPs) in TNF-α gene promoter region with the susceptibility of aggressive and chronic periodontitis in the eastern Indian population. Methods: A total of 397 DNA samples from venous blood were isolated. 40 individuals were aggressive periodontitis patients, 157 were identified chronic periodontitis patients, and the remaining 200 were healthy individuals. Five SNPs of TNF-α at promoter region (rs361525, rs1800629, rs1799724, rs1800630, and rs1799964) were genotyped by PCR-sequencing in periodontitis patients and control subjects. Results: rs1800629 (-308G/A) polymorphism was more frequent in both aggressive and chronic periodontitis patients compared with the control population, though the allele frequency was different only in aggressive periodontitis patients. On the other hand, both the genotypic and allelic variation of rs361525 (-238G/A) polymorphism were found significantly less frequently in aggressive and chronic periodontitis than in controls. The other polymorphisms like rs1799724 (-857C/T) and rs1799964 (-1031T/C) were significantly different between chronic periodontitis patients and control subjects. Conclusion: The findings suggest that the rs1800629 (-308G/A) polymorphism of TNF-α gene is associated with both aggressive and chronic periodontitis while rs1799724 (-857C/T) and rs1799964 (-1031T/C) polymorphisms of TNF-α gene is associated only with the increased susceptibility to chronic periodontitis.


2010 ◽  
Vol 33 (2) ◽  
pp. 85 ◽  
Author(s):  
Kamile Erciyas ◽  
Sacide Pehlivan ◽  
Tugce Sever ◽  
Mehri Igci ◽  
Ahmet Arslan ◽  
...  

Objective: The aim of this study was to investigate links among cytokine genetic variants and generalized aggressive periodontitis (GAgP). Methods: Thirty-five patients with generalized aggressive periodontitis and 85 healthy controls without periodontitis were included in the study. Probing depth (PD), clinical attachment loss (CAL), plaque index (PI), and gingival index (GI) were recorded as clinical parameters. Polymorphisms of IL-6, IL-10, IFN-γ, TGF-ß1 and TNF-α gene were analysed using the polymerase chain reaction sequence-specific primer method (PCR-SSP). Results: No significant differences were observed for IL-6, IL-10, IFN-γ, and TGF-ß1 cytokine polymorphisms, from the genotype distribution and allele frequency, between GAgP and healthy control groups. In contrast, significant differences were observed in the TNF-α gene polymorphism between GAgP and healthy control groups (P = 0.002). Conclusion: Our data suggest that TNF-α (-308) may be associated with the development of generalized aggressive periodontitis. These results should be replicated in a larger and more diverse population of patients diagnosed with generalized aggressive periodontitis to determine of these findings are generalizable.


2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.


2001 ◽  
Vol 120 (5) ◽  
pp. A674-A674 ◽  
Author(s):  
A FUNAKOSHI ◽  
M ICHIKAWA ◽  
Y SATO ◽  
S KANAI ◽  
M OHTA ◽  
...  

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