RANKL in human periapical granuloma: Possible involvement in periapical bone destruction

R. Vernal*, A. Dezerega, N. Dutzan, A. Chaparro, R. León, S. Chandía, A. Silva, J. Gamonal

*Autor correspondiente de este trabajo

Resultado de la investigación: Contribución a una revistaArtículorevisión exhaustiva

58 Citas (Scopus)

Resumen

OBJECTIVES: The cytokine receptor activator of nuclear factor κB-ligand (RANKL) has been involved in both the physiological and pathological regulation of osteoclast life span and bone metabolism. Periapical granuloma is a periradicular lesion characterized by periapical bone destruction. The aims of this study were to associate the RANKL mRNA levels to periapical granulomas using the real-time reverse transcriptase-polymerase chain reaction (RT-PCR) technique and to determine the specific cell involved in RANKL synthesis. METHODS: In eight periapical granuloma and eight periodontal ligament samples from periodontally healthy volunteers, RANKL mRNA was detected by real-time RT-PCR. Expression of RANKL on infiltrate leukocytes was further investigated by flow cytometry in six periapical granulomas. RESULTS: Receptor activator of nuclear factor κB-ligand mRNA levels were higher in periapical granulomas than in healthy periodontal ligament as its RANKL mRNA cycle threshold (Ct) and ΔCt were significantly lower than that of controls (33.07 ± 1.24 vs 36.96 ± 1.69 and 11.58 ± 3.02 vs 15.60 ± 3.31, respectively). A 16.2-fold (2.0-131.6) higher RANKL gene expression was detected in the granulomas compared with the control tissues. We determined by flow cytometry that lymphocytes were the predominant leukocyte cells (53.31%), and monocytes and dendritic cells were the main RANKL synthesizers in granuloma lesions. CONCLUSIONS: These data indicate that monocytes synthesized RANKL in periapical granulomas and suggest that RANKL is involved in bone loss associated with periapical lesions.

Idioma originalInglés
Páginas (desde-hasta)283-289
Número de páginas7
PublicaciónOral Diseases
Volumen12
N.º3
DOI
EstadoPublicada - may 2006
Publicado de forma externa

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