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dc.contributor.advisorBartold, P. Mark-
dc.contributor.advisorGully, Neville-
dc.contributor.advisorGibson, Rachel-
dc.contributor.advisorZilm, Peter-
dc.contributor.authorGatej, Simona Marieta-
dc.description.abstractObjectives: This study investigated the role of Lactobacillus rhamnosus GG (LGG) on bone loss and local and systemic inflammation in an in vivo mouse model of induced periodontitis. Changes in the gastrointestinal physiology and the influence of different probiotic administration methods were also investigated. Methods: 36 mice were allocated into six groups (n = 6 per group). Experimental periodontitis was induced in three of the groups by oral inoculation with Porphyromonas gingivalis and Fusobacterium nucleatum over a period of 44 days. The probiotic LGG was administered via two different methods (oral inoculation and oral gavage) prior to, and during, disease induction. The antimicrobial activity of LGG on the pathogens used was tested. Alveolar bone levels were assessed using in vivo micro-computed tomography. Gingival and intestinal tissue changes were evaluated using histological analysis. Systemic and intestinal inflammation were assessed by measuring the level of the pro-inflammatory markers IL-6 and LIX in tissue and blood serum using multiplex assays and immunohistochemistry. The phylogenetic structure and diversity of the intestinal microbiota were analysed by sequencing the 16S rRNA genes of the caecal content. Statistical significance was accepted when for p < 0.05. Results: Pre-treatment with LGG either via oral gavage or oral inoculation significantly reduced bone loss (p < 0.0001), gingival inflammation (p < 0.0001) and TRAP positive cells (p = 0.0020 – 0.0176) for the probiotic treated groups when compared with controls. Analysis of the pro-inflammatory marker LIX expression in serum demonstrated a significant increase in systemic inflammation for the disease mice when compared with controls. LGG demonstrated no antimicrobial activity against P. gingivalis and F. nucleatum . There were significant changes in the histology of the gastrointestinal tract of disease mice when compared with controls (p < 0.05). Additionally, disease mice presented a significant increase in the expression of the inflammatory marker IL-6 in gut tissue when compared with controls. Mice pre-treated with LGG via gavage had significantly reduced tissue inflammation scores in the duodenum and significantly lower levels of IL-6 in the ileum when compared with disease. Oral inoculation with P. gingivalis and F. nucleatum led to a significant change in the bacterial composition of the caecal microbiome of the control group versus disease (p < 0.05). LGG therapy prevented gut microbiome changes induced by P. gingivalis and F. nucleatum, regardless of the probiotic mode of administration. Conclusions: Administration of P gingivalis and F nucleatum induced significant changes in intestinal and systemic inflammation and significant changes in the intestinal microbiome. Therapy with LGG effectively supressed bone loss and local inflammation for all probiotic treated groups when compared with disease irrespective of the mode of administration. Additionally, pre-treatment with LGG exerted a protective effect against intestinal and systemic inflammation and had a significant influence on the composition of the gut microbiome, promoting beneficial bacteria in the intestines of treated mice. Clinically, in the future, LGG may offer a low-risk, easy to use treatment option for the management of periodontitis.en
dc.subjectalveolar bone lossen
dc.subjectLactobacillus rhamnosus GGen
dc.titleClinical and microbiological effects of probiotics in experimental induced periodontitisen
dc.contributor.schoolAdelaide Dental Schoolen
dc.provenanceThis electronic version is made publicly available by the University of Adelaide in accordance with its open access policy for student theses. Copyright in this thesis remains with the author. This thesis may incorporate third party material which has been used by the author pursuant to Fair Dealing exceptions. If you are the owner of any included third party copyright material you wish to be removed from this electronic version, please complete the take down form located at:
dc.description.dissertationThesis (Ph.D.) -- University of Adelaide, Adelaide Dental School, 2018en
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