Capsular-defective <i>Porphyromonas gingivalis</i> mutant strains induce less alveolar bone resorption than W50 wild-type strain due to a decreased Th1/Th17 immune response and less osteoclast activity

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dc.contributor.authorMonasterio, Gustavo
dc.contributor.authorFernandez, Baltasar
dc.contributor.authorCastillo, Francisca
dc.contributor.authorRojas, Carolina
dc.contributor.authorCafferata, Emilio A.
dc.contributor.authorRojas, Leticia
dc.contributor.authorAlvarez, Carla
dc.contributor.authorFernandez, Alejandra
dc.contributor.authorHernandez, Marcela
dc.contributor.authorBravo, Denisse
dc.contributor.authorVernal, Rolando
dc.date.accessioned2025-01-23T21:15:12Z
dc.date.available2025-01-23T21:15:12Z
dc.date.issued2019
dc.description.abstractBackground Encapsulation of Porphyromonas gingivalis has been demonstrated as responsible of several host immunological changes, which have been associated with the pathogenesis of periodontitis. Using a murine model of periodontitis and two isogenic non-capsulated mutants of P. gingivalis, this study aimed to analyze whether P. gingivalis encapsulation induces more severe alveolar bone resorption, and whether this bone loss is associated with a T-helper (Th)1 and Th17-pattern of immune response. Methods Experimental periodontal infections were generated by oral inoculation with the encapsulated W50 wild-type strain or isogenic non-encapsulated Delta PG0116-PG0120 (GPA) and Delta PG0109-PG0118 (GPC) mutants of P. gingivalis. Periodontal infections induced with the encapsulated HG184 or non-encapsulated ATCC 33277 strains of P. gingivalis were used as controls. Alveolar bone resorption was analyzed using microcomputed tomography and scanning electron microscopy. The expression levels of Th1, Th2, Th17, or T regulatory-associated cytokines and RANKL, as well as the periodontal bacterial load, were quantified by quantitative polymerase chain reaction. The detection of Th1 and Th17 lymphocytes was analyzed by flow cytometry. Results In the periodontal lesions, both capsular-defective knockout mutant strains of P. gingivalis induced less alveolar bone resorption than the encapsulated W50 wild-type strain. This decreased bone loss was associated with a dismissed RANKL expression, decreased Th1- and Th17-type of cytokine expression, reduced Th1 and Th17 lymphocyte detection, and low osteoclast finding. Conclusion These data demonstrate that encapsulation of P. gingivalis plays a key role in the alveolar bone resorption induced during periodontitis, and this bone loss is associated with a Th1- and Th17-pattern of immune response triggered in the periodontal lesions.
dc.fuente.origenWOS
dc.identifier.doi10.1002/JPER.18-0079
dc.identifier.eissn1943-3670
dc.identifier.issn0022-3492
dc.identifier.urihttps://doi.org/10.1002/JPER.18-0079
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/101073
dc.identifier.wosidWOS:000467617600010
dc.issue.numero5
dc.language.isoen
dc.pagina.final534
dc.pagina.inicio522
dc.revistaJournal of periodontology
dc.rightsacceso restringido
dc.subjectbone resorption
dc.subjectcytokines
dc.subjectosteoclasts
dc.subjectPorphyromonas gingivalis
dc.subjectRANKL
dc.subjectT lymphocytes
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleCapsular-defective <i>Porphyromonas gingivalis</i> mutant strains induce less alveolar bone resorption than W50 wild-type strain due to a decreased Th1/Th17 immune response and less osteoclast activity
dc.typeartículo
dc.volumen90
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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