Increased Interleukin-18 in the Gingival Tissues Evokes Chronic Periodontitis after Bacterial Infection

Yoshinaka, Kotaro; Shoji, Nobuyuki; Nishioka, Takashi; Sugawara, Yumiko; Hoshino, Tomoaki; Sugawara, Shunji; Sasano, Takashi

doi:10.1620/tjem.232.215

Cited by 17 publications

(11 citation statements)

References 28 publications

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“…In vivo , when using IL-18 transgenic (Tg) mice, IL-18 overexpression was related to periodontal disease [35]. When IL-18Tg and wild-type mice were inoculated intraorally with Porphyromonas gingivalis , after seventy days of infection, there was periodontal bone loss in IL-18Tg mice but not in wild-type.…”

Section: Discussionmentioning

confidence: 99%

IL18 Polymorphism and Periodontitis Susceptibility, Regardless of IL12B, MMP9, and Smoking Habits

Tsuneto

Souza

Alencar

et al. 2019

Mediators of Inflammation

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Genetic variations contribute to the susceptibility in the development of periodontitis. The aim of this study was to investigate the influence of IL18, IL12, and MMP9 polymorphisms in the chronic periodontitis. This case-control study involved 381 individuals matched by gender and age. Genotyping of IL18 (rs187238 and rs1946518) and IL12B (rs3212227) was performed by PCR-SSP and PCR-RFLP was used for MMP9 (rs3918242). IL-18 and MMP-9 were quantified in the serum by ELISA. SNPStats and OpenEpi software were used for statistical analysis and, in order to eliminate smoking as a confounding factor, the analyses were also performed in nonsmoking subjects. The IL18-137G/C genotype was associated with the risk of chronic periodontitis in nonsmokers (Pc=0.03; OR=1.99; overdominant inherence model). In the multivariate analyses, homozygous IL18-137G/G and IL18-607C/C were more frequent in males compared to women with these same genotypes (OR=2.51 and OR=3.30, respectively). The serum levels of the IL-18 in patients were higher than those in healthy controls (P=0.005). IL12B and MMP9 polymorphisms and MMP-9 serum concentration were similar in patients and controls. In this study, IL18 was associated with chronic periodontitis susceptibility. Men had greater risk than women for developing the disease when IL18 polymorphism was considered and the susceptibility was independent of the smoking status.

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Section: Discussionmentioning

confidence: 99%

IL18 Polymorphism and Periodontitis Susceptibility, Regardless of IL12B, MMP9, and Smoking Habits

Tsuneto

Souza

Alencar

et al. 2019

Mediators of Inflammation

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“…IL-18 is a member of the IL-1 family and can induce production of both Th1 and Th2 cytokines. Mice overexpressing IL-18 in the gingival tissues, develop periodontal destruction after being infected with P. gingivalis ( 57 ). The mechanisms of action of excess IL-18 in the gingiva appear to be T-cell mediated, as the NF-κB and RANKL levels were increased in the transgenic mice after P. gingivalis infection, whereas the interferon-γ was decreased.…”

Section: Mouse Models Of Genes Associated With the Inflammatory Respomentioning

confidence: 99%

Genes Critical for Developing Periodontitis: Lessons from Mouse Models

et al. 2017

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Since the etiology of periodontitis in humans is not fully understood, genetic mouse models may pinpoint indispensable genes for optimal immunological protection of the periodontium against tissue destruction. This review describes the current knowledge of genes that are involved for a proper maintenance of a healthy periodontium in mice. Null mutations of genes required for leukocyte cell–cell recognition and extravasation (e.g., Icam-1, P-selectin, Beta2-integrin/Cd18), for pathogen recognition and killing (e.g., Tlr2, Tlr4, Lamp-2), immune modulatory molecules (e.g., Cxcr2, Ccr4, IL-10, Opg, IL1RA, Tnf-α receptor, IL-17 receptor, Socs3, Foxo1), and proteolytic enzymes (e.g., Mmp8, Plasmin) cause periodontitis, most likely due to an inefficient clearance of bacteria and bacterial products. Several mechanisms resulting in periodontitis can be recognized: (1) inefficient bacterial control by the polymorphonuclear neutrophils (defective migration, killing), (2) inadequate antigen presentation by dendritic cells, or (3) exaggerated production of pro-inflammatory cytokines. In all these cases, the local immune reaction is skewed toward a Th1/Th17 (and insufficient activation of the Th2/Treg) with subsequent osteoclast activation. Finally, genotypes are described that protect the mice from periodontitis: the SCID mouse, and mice lacking Tlr2/Tlr4, the Ccr1/Ccr5, the Tnf-α receptor p55, and Cathepsin K by attenuating the inflammatory reaction and the osteoclastogenic response.

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“…Periodontal disease is a common and complex inflammatory disease that results in progressive destruction of the tooth-supporting soft and hard tissues of the periodontium [ 1 ]. The resulting damage affects the alveolar bone as well as the periodontal ligament (PDL).…”

Section: Introductionmentioning

confidence: 99%

Anti-inflammatory effects of low-level laser therapy on human periodontal ligament cells: in vitro study

et al. 2017

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Periodontal disease is a chronic inflammatory disease that is commonly treated with surgical and nonsurgical techniques. However, both approaches have limitations. Low-level laser therapy (LLLT) has been widely applied in reducing inflammatory reactions, and research indicates that LLLT induces an anti-inflammatory effect that may enhance periodontal disease therapy. The purpose of this study was to investigate the anti-inflammatory effect of LLLT on human periodontal ligament cells (hPDLCs) in an inflammatory environment and aimed to determine the possible mechanism of action. Cells were cultured and treated with or without lipopolysaccharide (LPS) from Porphryromonas gingivalis or Escherichia coli, followed by irradiation with a gallium-aluminum-arsenide (GaAlAs) laser (660 nm) at an energy density of 8 J/cm2. Quantitative real-time polymerase chain reactions were used to assess the expression of pro-inflammatory genes, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, and IL-8. The dual-luciferase reporter assay was used to examine nuclear factor-κB (NF-κB) transcriptional activity. An enzyme-linked immunosorbent assay was used to monitor the concentration of intracellular cyclic adenosine monophosphate (cAMP). Both LPS treatments significantly induced the mRNA expression of pro-inflammatory cytokines. However, LLLT inhibited the LPS-induced pro-inflammatory cytokine expression and elevated intracellular levels of cAMP. The LLLT inhibitory effect may function by downregulating NF-κB transcriptional activity and by increasing the intracellular levels of cAMP. LLLT might inhibit LPS-induced inflammation in hPDLCs through cAMP/NF-κB regulation. These results should be further studied to improve periodontal therapy.

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Increased Interleukin-18 in the Gingival Tissues Evokes Chronic Periodontitis after Bacterial Infection

Cited by 17 publications

References 28 publications

IL18 Polymorphism and Periodontitis Susceptibility, Regardless of IL12B, MMP9, and Smoking Habits

IL18 Polymorphism and Periodontitis Susceptibility, Regardless of IL12B, MMP9, and Smoking Habits

Genes Critical for Developing Periodontitis: Lessons from Mouse Models

Anti-inflammatory effects of low-level laser therapy on human periodontal ligament cells: in vitro study

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