Differential Expression of RANKL and Osteoprotegerin in Gingival                Crevicular Fluid of Patients with Periodontitis

Mogi, Makio; Otogoto, Jun-ichi; Ota, Norio; Togari, Akifumi

doi:10.1177/154405910408300216

Cited by 220 publications

(290 citation statements)

References 20 publications

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“…The relative RANKL/OPG expression ratio is a measure of clinical relevance, its local increase in the tissues is associated with the occurrence of periodontitis [10,11,25]. In the present experimental system, the RANKL/OPG ratio was also calculated, as an indicator of the cells' capacity to enhance osteoclastogenesis and bone resorption.…”

Section: Discussionmentioning

confidence: 99%

The RANKL–OPG system is differentially regulated by supragingival and subgingival biofilm supernatants

et al. 2011

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Periodontitis is an inflammatory condition that destroys the tooth supporting tissues, including the alveolar bone. It is triggered by polymicrobial biofilms attaching on tooth surfaces, which can be supragingival or subgingival. Bone resorption is triggered by receptor activator of NF-B ligand (RANKL) and blocked by its soluble decoy receptor osteoprotegerin (OPG), which are cytokines of the tumor necrosis factor ligand and receptor families, respectively. The present study aimed to comparatively investigate the effects of the Zürich in vitro supragingival and subgingival biofilm models, on RANKL and OPG gene expression in primary human gingival fibroblasts (GF) cultures. The cells were challenged with biofilm culture supernatants for up-to 24h. RANKL and OPG gene expression in the cells was analyzed by quantitative real-time polymerase chain reaction (qPCR) and their relative RANKL/OPG ratio was calculated. Both biofilm supernatants induced RANKL expression, but the subgingival caused a more pronounced up-regulation compared to the supragingival (10-fold at 6h and 100-fold at 24h). Changes in OPG expression in response to either biofilm were more limited. Accordingly, the subgingival biofilm caused a greater enhancement of the relative RANKL/OPG ratio (4-fold at 6h and 110-fold 24h). In conclusion, subgingival biofilms exhibit a stronger potency for inducing molecular mechanisms of bone resorption than supragingival biofilms, in line with their higher virulence nature for the development of periodontitis. AbstractPeriodontitis is an inflammatory condition that destroys the tooth supporting tissues, including the alveolar bone. It is triggered by polymicrobial biofilms attaching on tooth surfaces, which can be supragingival or subgingival. Bone resorption is triggered by RANKL and blocked by its soluble decoy receptor OPG, which are cytokines of the tumor necrosis factor ligand and receptor families, respectively. The present study aimed to comparatively investigate the effects of the Zürich in vitro supragingival and subgingival biofilm models, on RANKL and OPG gene expression in primary human GF cultures. The cells were challenged with the biofilms for up-to 24 hours. RANKL and OPG gene expression in the cells was analysed by qPCR and their relative RANKL/OPG ratio was calculated. Both biofilms induced RANKL expression, but the subgingival caused a more pronounced up-regulation compared to the supragingival (10-fold at 6 h and 100-fold at 24 h). Changes in OPG expression in response to either biofilm were more limited. Accordingly, the subgingival biofilm caused a greater enhancement of the relative RANKL/OPG ratio (4-fold at 6 h and 110-fold 24 h). In conclusion, subgingival biofilms exhibit a stronger potency for inducing molecular mechanisms of bone resorption than supragingival biofilms, in line with their higher virulence nature for the development of periodontitis.

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Section: Discussionmentioning

confidence: 99%

The RANKL–OPG system is differentially regulated by supragingival and subgingival biofilm supernatants

et al. 2011

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“…It has been reported that CDT of A. actinomycetemcomitans regulates the expression of receptor activator of NF-kB ligand (RANKL) and osteoprotegerin by periodontal ligament cells (Belibasakis et al, 2005). Since expression of these molecules is involved in osteoclast differentiation, they have a central role in the regulation of bone resorption, a key component of periodontitis (Liu et al, 2003;Mogi et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Differential effect of the cytolethal distending toxin of Actinobacillus actinomycetemcomitans on co-cultures of human oral cells

Kang

Korostoff

Volgina

et al. 2005

Journal of Medical Microbiology

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The periodontal pathogen Actinobacillus actinomycetemcomitans expresses a cytolethal distending toxin (CDT) that typically arrests the growth of eukaryotic cells at either the G 0 /G 1 or G 2 /M phase of the cell cycle. It was previously found that CDT failed to arrest the growth of human periodontal ligament fibroblasts (HPLFs) when grown in pure culture. In contrast, proliferation of an oral epithelial cell line was rapidly inhibited by the toxin. In this study, the feasibility of using mixed-cell cultures and cell-specific markers to evaluate the response of oral cells, when in heterogeneous populations, to CDT was established. Proliferation of epithelial cells was rapidly inhibited and the cells were selectively eliminated in co-culture with HPLFs or cementoblasts by 24-48 h postintoxication. Epithelial cells and HPLFs were detected and counted in co-cultures following cellspecific immunolabelling with antibodies against simian virus 40 large T antigen and the Ab-1 surface antigen, respectively. These results demonstrated that the activities of potential virulence factors, such as CDT, from periodontal pathogens can be successfully examined in mixed-cell cultures. This approach is especially relevant to infectious diseases that affect tissues with a diverse cellular composition, such as the periodontium.

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“…Nuestros actuales resultados son concordantes con hallazgos previos de nuestro grupo de investigación y con resultados descritos por Mogi y colaboradores, que establecen mayores niveles de RANKL en el fluido gingival crevicular (FGC) de individuos con periodontitis, con niveles de severidad de enfermedad leve, moderada y avanzada, en comparación con sujetos sin enfermedad periodontal 34,35 . En nuestros datos, no encontramos asociación significativa entre los niveles de pacientes con periodontitis mostraron niveles detectables de mARN de RANKL y estos fueron significativamente mayores que los encontrados en sujetos controles sanos.…”

Section: Papel De Los Linfocitos T Cd4unclassified

Papel de los linfocitos T CD4+ en la destrucción ósea observada durante la periodontitis crónica

Vernal

Dutzan

León

et al. 2006

Avances en Periodoncia

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RESUMENPropósito: La periodontitis crónica es una enfermedad de naturaleza inflamatoria y etiología infecciosa, caracterizada por la destrucción del aparato de inserción del diente, cemento radicular, ligamento periodontal y hueso alveolar, y que causa la pérdida de los dientes. Durante su desarrollo se establece un denso infiltrado inflamatorio celular, constituido principalmente por linfocitos T, con la capacidad de secretar una serie de citoquinas que participan en los eventos patogénicos de la enfermedad, regulando la inflamación de los tejidos periodontales y la destrucción del hueso alveolar. En la artritis reumatoide, la citoquina recientemente identificada RANKL (Ligando del receptor activador del factor nuclear κB) es expresada por los linfocitos T CD4 + , participando directamente en los procesos de estimulación de la diferenciación osteoclástica y en la activación de osteoclastos maduros, y por lo tanto, en la destrucción ósea articular. El objetivo del presente estudio es determinar si mayores niveles de RANKL se encuentran asociados a la periodontitis crónica y si estos son sintetizados por los linfocitos T CD4 + reclutados en los sitios con periodontitis crónica. Material y métodos:En 33 pacientes mayores de 35 años de edad afectados de periodontitis crónica y 20 individuos controles sanos, se determinaron los niveles de mensajero de ácido desoxiribonucleico (mARN) de RANKL en biopsias de encía mediante transcriptasa reversareacción en cadena de la polimerasa (RT-PCR) en tiempo real. A partir de las mismas biopsias, células gingivales totales fueron aisladas para inmunotipificar y cuantificar los leucocitos infiltrantes gingivales e identificar las células responsables de la expresión de RANKL mediante doble tinción por citometría de flujo.Resultados: Los pacientes con periodontitis mostraron mayores niveles de mARN de RANKL en comparación a individuos sanos, observándose que la expresión de RANKL se incrementó en 238,3 veces con relación a los sujetos controles. Los individuos con periodontitis mostraron mayores porcentajes de linfocitos T CD4 Conclusión: Estos datos demuestran que mayores niveles de RANKL se encuentran asociados a la periodontitis y que estos mayores niveles se pueden explicar en parte a la actividad de los Vernal R, Dutzan N, León R, Gamonal J. Papel de los linfocitos T CD4 + en la destrucción ósea observada durante la periodontitis crónica.

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Differential Expression of RANKL and Osteoprotegerin in Gingival Crevicular Fluid of Patients with Periodontitis

Abstract: GCF, gingival crevicular fluid; IL, interleukin; OPG, osteoprotegerin; RANKL, receptor activator for NF-kappaB ligand.

Cited by 220 publications

References 20 publications

The RANKL–OPG system is differentially regulated by supragingival and subgingival biofilm supernatants

The RANKL–OPG system is differentially regulated by supragingival and subgingival biofilm supernatants

Differential effect of the cytolethal distending toxin of Actinobacillus actinomycetemcomitans on co-cultures of human oral cells

Papel de los linfocitos T CD4+ en la destrucción ósea observada durante la periodontitis crónica

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