IADR Abstract Archives
Local and Systemic Effects of Probiotics in Induced Periodontitis
Objectives: The 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.
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 IL-8 and IL-6 expression 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. A linear mixed-effects model was performed and statistical significance was accepted when the p value was less than 0.05.
Results: Pre-treatment with probiotics 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. All groups showed less systemic inflammation when compared with the disease group. LGG demonstrated no antimicrobial activity against the pathogens used. The gut microbiome was significantly altered at the genus level following periodontitis induction and probiotic gavage (p<0.05). Additionally, these modifications were associated with significant changes in intestinal inflammation (p<0.05).
Conclusions: LGG effectively supressed bone loss irrespective of the mode of administration. Induced periodontitis in a mouse model lead to changes in the gut microbiome. Different probiotic treatment modalities had an effect on the gut microbiota.
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 IL-8 and IL-6 expression 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. A linear mixed-effects model was performed and statistical significance was accepted when the p value was less than 0.05.
Results: Pre-treatment with probiotics 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. All groups showed less systemic inflammation when compared with the disease group. LGG demonstrated no antimicrobial activity against the pathogens used. The gut microbiome was significantly altered at the genus level following periodontitis induction and probiotic gavage (p<0.05). Additionally, these modifications were associated with significant changes in intestinal inflammation (p<0.05).
Conclusions: LGG effectively supressed bone loss irrespective of the mode of administration. Induced periodontitis in a mouse model lead to changes in the gut microbiome. Different probiotic treatment modalities had an effect on the gut microbiota.