Project description:Periodontal disease (PD) is characterized by inflammation affecting the tissue surrounding the teeth, primarily affecting the soft tissues, like the gingiva. However, without proper treatment, the condition exacerbates and progresses to impact the deeper structures, as the alveolar bone. The periodontal inflammation leads to the alveolar bone resorption, that eventually results in the complete loss of tooth support. Given its potential consequences, periodontal disease is a significant public health concern, as one of the primary causes of tooth loss, contributing to issues such as impaired mastication, speech difficulties, low self-esteem, and quality of life. Notably, comorbidities, like hypertension, can exacerbate the progression and severity of periodontal disease. In addition, the coexistence of periodontal disease and hypertension is highly likely to occur due to sharing of several risk factors. A better understanding of the underling molecular mechanisms associated to the severity of periodontal disease in the context of hypertension would greatly contribute to the advancement of translational research in the field of periodontics. MicroRNAs, a class of small non-coding RNA molecules, have an important role in regulating gene expression at the post-transcriptional level. These molecules can regulate multiple mRNA targets through complementary base pairing between the miRNA 5' seed sequence and the mRNA 3' untranslated region (UTR). Therefore, microRNAs can potentially modulate a wide variety of cellular processes, in both normal and pathological contexts. Presently, most of the studies in the field concentrate on the periodontium soft tissues, while our understanding of microRNA modulation in the alveolar bone remains comparatively limited. We used microarray analysis to evaluate the expression profiles of microRNAs in the mandibles of Wistar and SHR rats with periodontal disease, compared to their respective control groups. Our aim was to identify microRNAs of interest that could possibly be associated to the periodontal disease-induced alveolar bone loss.

Project description:<h4><strong>BACKGROUND AND HYPOTHESIS: </strong>It is presently unclear why there is a high prevalence of periodontal disease in individuals living with chronic kidney disease. Whilst some have argued that periodontal disease causes chronic kidney disease, we hypothesized that alterations in saliva and the oral microenvironment in organisms with kidney disease may initiate periodontal disease by causing dysbiosis of the oral microbiota.</h4><h4><strong>METHODS: </strong>Experimental kidney disease was created using adenine feeding and subtotal nephrectomy in rats, and by adenine feeding in mice. Loss of periodontal bone height was assessed using a dissecting microscope supported by micro-CT, light, confocal and electron microscopy, and immunohistochemistry. Salivary biochemistry was assessed using NMR spectroscopy. The oral microbiome was evaluated using culture-based and molecular methods, and the transmissibility of dysbiosis was assessed using co-caging and microbial transfer experiments into previously germ-free recipient mice.</h4><h4><strong>RESULTS: </strong>We demonstrate that experimental kidney disease causes a reproducible reduction of alveolar bone height, without gingival inflammation or overt hyperparathyroidism but with evidence of failure of bone formation at the periodontal crest. We show that kidney disease alters the biochemical composition of saliva and induces progressive dysbiosis of the oral microbiota, with microbial samples from animals with kidney disease displaying reduced overall bacterial growth, increased alpha diversity, reduced abundance of key components of the healthy oral microbiota such as Streptococcus and Rothia, and an increase in minor taxa including those from gram-negative phyla Proteobacteria and Bacteroidetes. Co-housing diseased rats with healthy ones ameliorates the periodontal disease phenotype, whilst transfer of oral microbiota from mice with kidney disease causes periodontal disease in germ-free animals with normal kidney function.</h4><h4><strong>CONCLUSIONS: </strong>We advocate that periodontal disease should be regarded as a complication of kidney disease, initiated by oral dysbiosis through mechanisms independent of overt inflammation or hyperparathyroidism.</h4>

Project description:Analysis of gingival crevicular fluid (GCF) samples may give information of the identity of unattached (planktonic) subgingival bacteria, the 35 forefront candidates for systemic dispersal via ulcerated periodontal pocket epithelium. Our study represents the first one targeting the identity of bacteria in gingival crevicular fluid. Methodology/Principal findings: We determined bacterial species diversity in GCF samples of a group of periodontitis patients and delineated contributing bacterial and host-associated factors. Subgingival paper point (PP) samples from the same sites were taken for comparison. After DNA extraction, 16S rRNA genes were PCR amplified and DNA-DNA hybridization was performed using a microarray for over 300 bacterial species or groups. Altogether 133 species from 41 genera and 8 phyla 45 were detected with 9 to 62 and 18 to 64 species in GCF and PP samples, respectively, 46 per patient. Projection to latent structures by means of partial least squares (PLS) was applied to the multivariate data analysis. PLS regression analysis showed that species of genera including Campylobacter, Selenomonas, Porphyromonas, Catonella, Tannerella, Dialister, Peptostreptococcus, Streptococcus and Eubacterium had significant positive correlations and the number of teeth with low-grade attachment loss a significant negative correlation to species diversity in GCF samples. OPLS/O2PLS discriminant analysis revealed significant positive correlations to GCF sample group membership for species of genera Campylobacter, Leptotrichia, Prevotella, Dialister, Tannerella, Haemophilus, Fusobacterium, Eubacterium, and Actinomyces. Conclusions/Significance: Among a variety of detected species those traditionally classified as Gram-negative anaerobes growing in mature subgingival biofilms were the main predictors for species diversity in GCF samples as well as responsible for distinguishing GCF samples from PP samples. GCF bacteria may provide new prospects for studying dynamic properties of subgingival biofilms. The microbial profiles of GCF and subgingival plaque were analyzed from 17 subjects with periodontal disease.

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