The Involvement of IL-23 and the Th17 Pathway in Periodontitis

Ohyama, Hideki; Kato-Kogoe, Nahoko; Kuhara, Ayako; Nishimura, Fusanori; Nakasho, Keiji; Yamanegi, Koji; Yamada, Naoko; Hara, Masaki; Yamane, Junko; Terada, Nobuyuki

doi:10.1177/0022034509339889

Cited by 161 publications

(165 citation statements)

References 34 publications

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“…Th17 lymphocytes, like Th1 cells, are also noted for their stimulatory role in osteoclastogenesis (Yago et al 2009). Th17 cells are observed in chronic periodontitis sites, and Th17 related cytokines are produced in periodontal lesions (Takahashi et al 2005, Vernal et al 2005, Ohyama et al 2009). …”

Section: Adaptive Immunitymentioning

confidence: 99%

Infection and inflammatory mechanisms

Dyke

Winkelhoff

2013

Journal of Periodontology

146

123

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This introductory article examines the potential mechanisms that may play a role in the associations between periodontitis and the systemic conditions being considered in the EFP/AAP Workshop in Segovia, Spain. Three basic mechanisms have been postulated to play a role in these interactions; metastatic infections, inflammation and inflammatory injury, and adaptive immunity. The potential role of each alone and together is considered in in vitro and animal studies and in human studies when available. This is not a systematic or critical review, but rather an overview of the field to set the stage for the critical reviews in each of the working groups.

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Section: Adaptive Immunitymentioning

confidence: 99%

Infection and inflammatory mechanisms

Dyke

Winkelhoff

2013

Journal of Periodontology

146

123

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“…For example, it was reported that IL-17 is protective against Porphyromonas gingivalis-induced bone loss via mobilization of neutrophils in a murine model (Yu et al, 2007). However, clinical studies reported increased IL-17 levels associated with chronic periodontitis (Takahashi et al, 2005;Vernal et al, 2005;Ohyama et al, 2009). In addition, peripheral blood mononuclear cells from patients with gingivitis and periodontitis stimulated with outer membrane protein of P. gingivalis express IL-17 (Oda et al, 2003).…”

Section: Introduction Imentioning

confidence: 99%

IL-17 in Sera from Patients with Aggressive Periodontitis

Schenkein¹,

Koertge²,

Brooks

et al. 2010

J Dent Res

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Interleukin-17 (IL-17), the prototype cytokine produced by the Th17 subset of T-helper cells, plays a role in inflammatory responses, autoimmunity, and antimicrobial responses in a variety of infectious and inflammatory diseases. In view of the inflammatory nature and severity of aggressive periodontitis, we hypothesized that IL-17 might be detected in sera from patients with aggressive periodontitis. We used ELISA to measure IL-17 serum concentrations from 67 periodontally healthy (NP) individuals and from 53 patients with localized (LAgP) and 49 patients with generalized (GAgP) aggressive periodontitis. IL-17 was barely detectable in sera from periodontally healthy individuals (1.9 ± 2.0 pg/mL), but was present at significantly higher concentrations in sera from those with LAgP (7.6 ± 2.2 pg/mL) and GAgP (17.1 ± 2.3 pg/mL). Multivariate analyses demonstrated associations of IL-17 concentrations with periodontal attachment loss, but not with current smoking. Therefore, Th17 responses may be characteristic of AgP, and IL-17 may play a role in the pathogenesis of aggressive periodontitis.

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“…En efecto, diversos estudios han asociado tanto una respuesta linfocitaria efectora tipo Th1 como una tipo Th2 a la progresión de la enfermedad periodontal (42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53)(54)(55) . Además, durante los últimos años, tanto el fenotipo Th17 como el Treg han sido implicados en la patogenia de la periodontitis (56)(57)(58)(59)(60)(61)(62)(63) . Trabajos previos de nuestro grupo de investigación han evidenciado una respuesta asociada tanto a un fenotipo Th1 como a un fenotipo Th17 durante la progresión de la periodontitis (35,44,57,64) .…”

Section: Discussionunclassified

Variabilidad de la síntesis de RANKL por linfocitos T frente a distintos serotipos capsulares de Porphyromonas gingivalis

Navarrete

Silva

Sanz

et al. 2010

Rev. Clin. Periodoncia Implantol. Rehabil. Oral

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RESUMENPropósito: Las periodontitis representan un grupo heterogéneo de infecciones periodontales cuya etiología son las bacterias residentes en el biofilm subgingival. Aunque este biofilm está constituido por una amplia variedad de especies bacterianas, sólo un número limitado de especies, como Porphyromonas gingivalis, se ha asociado a la etiología de la enfermedad. P. gingivalis expresa diversos factores de virulencia que pueden causar daño directo a los tejidos del hospedero; sin embargo, su mayor patogenicidad involucra la inducción de una respuesta inmuno-inflamatoria, durante la cual se secretan una amplia variedad de citoquinas, quimioquinas y mediadores inflamatorios que pueden inducir la destrucción de los tejidos de soporte de los dientes y la pérdida de ellos. Método: En esta investigación, se evaluó si los distintos serotipos capsulares (K) de P. gingivalis pueden determinar los niveles de síntesis de RANKL, citoquina clave en la destrucción del hueso alveolar durante la periodontitis. Para ello, se cuantificaron los niveles de expresión de RANKL mediante PCR cuantitativa y los niveles de secreción mediante ELISA en linfocitos T activados en presencia de los serotipos capsulares K1-K6 de P. gingivalis, y estos se correlacionaron a los niveles de expresión de los factores de transcripción asociados a cada uno de los fenotipos de linfocitos efectores: Th1 (T-bet), Th2 (GATA-3), Th17 (RORC2) y Treg (Foxp3). Resultados: Mayores niveles de expresión y secreción de RANKL fueron detectados en linfocitos T activados en presencia de los serotipos K1 y K2 de P. gingivalis, en comparación a los detectados ante los otros serotipos. Además, estos mayores niveles de RANKL se correlacionaron positivamente con los niveles de expresión de RORC2. Conclusión: Estos datos demuestran que la síntesis de RANKL por linfocitos T se restringe a ciertos serotipos capsulares de P. gingivalis (K1 y K2) y permiten sugerir que los serotipos K1 y K2 de P. gingivalis podrían asociarse a la destrucción del hueso alveolar y a la pérdida de los dientes durante la periodontitis. ABSTRACTAim: Periodontitis represents a heterogenic group of periodontal infections elicited by bacteria residing at the subgingival biofilm. Although this biofilm is constituted by a broad variety of bacterial species, only a limited number has been associated with the periodontitis aetiology, among them Porphyromonas gingivalis. P. gingivalis express a number of virulence factors that contribute to direct tissue damage; however, their pathogenicity relies mainly on the induction of a host immuno-inflammatory response. This leads to the release of a broad array of cytokines, chemokines and inflammatory mediators, which cause destruction of the tooth-supporting alveolar bone and ultimately tooth loss. Method: In the present investigation, in order to determine whether different P. gingivalis serotypes might lead to a differential RANKL synthesis, a key cytokine involved in alveolar bone resorption, the mRNA expression and secretion of RANKL and the expression ...

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The Involvement of IL-23 and the Th17 Pathway in Periodontitis

Cited by 161 publications

References 34 publications

Infection and inflammatory mechanisms

Infection and inflammatory mechanisms

IL-17 in Sera from Patients with Aggressive Periodontitis

Variabilidad de la síntesis de RANKL por linfocitos T frente a distintos serotipos capsulares de Porphyromonas gingivalis

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