The Red and Orange Complex Subgingival Microbiome of Cognitive Impairment and Cognitively Normal Elderly with Periodontitis

Increasing evidence has shown an association between periodontitis and cognitive impairment. Subgingival microbiota play a great role in periodontitis pathogenesis. However, the correlation between the subgingival microbiome and cognitive impairment remains unclear. This study aimed to evaluate the red and orange complex subgingival microbiome of cognitively impaired and cognitively normal elderly Indonesian subjects with periodontitis. Twenty-eight elderly subjects diagnosed with periodontitis underwent two cognitive examinations using the Hopkins Verbal Learning Test and the Mini-Mental State Examination. Gingival crevicular fluid taken from the periodontal pocket, at a depth between 5 and 7 mm, using a paper point was used as the subgingival samples. The subgingival microbiome in the cognitive impairment group (n = 14) and cognitively normal group (n = 14) was compared using the 16S rRNA Metagenomic iSeq™ 100 Sequencing System. There was β-diversity in the subgingival microbiota between the cognitively impaired and cognitively normal subjects. The metagenomic analysis showed a higher abundance of Porphyromonas and Treponema bacteria in the cognitive impairment group than in the normal cognitive group (p < 0.05). The abundance of Porphyromonas gingivalis and Treponema denticola was higher in the cognitively impaired elderly subjects. The role of P. gingivalis and T. denticola in the pathogenesis of cognitive impairment needs further investigation.

Subgingival Microbiota Profile in Association with Cigarette Smoking in Young Adults: A Cross-Sectional Study

While smoking is recognized as one of the factors for the development and progression of periodontal diseases, a relation between the composition of the subgingival microbiota and smoking is yet to be elucidated. The aim of this study was to investigate the prevalence of subgingival bacteria in young smokers and non-smokers without clinical signs of periodontal disease. In this cross-sectional study, performed at the Department of Pharmacology, School of Dental Medicine, University of Zagreb, we enrolled 32 periodontally healthy smokers and 32 non-smokers, aged 25–35 years old. The number of oral bacteria and the prevalence of particular bacteria were assessed for each subject. Subgingival plaque samples were collected with sterile paper points from two first molars for microbiological analyses with MALDI-TOF mass spectrometry. In smokers, a significantly higher prevalence of Actinomyces odontolyticus was observed compared to non-smokers, and a significantly lower prevalence of Streptococcus sanguinis was observed compared to non-smokers. Smoking affects the composition of subgingival microbiota, either via depletion of beneficial bacteria or the increase in pathogenic bacteria.

Subgingival Microbiota and Cytokines Profile Changes in Patients with Periodontitis: A Pilot Study Comparing Healthy and Diseased Sites in the Same Oral Cavities

Periodontitis is a common condition characterized by an exacerbated pro-inflammatory response, which leads to tissue destruction and, ultimately, alveolar bone loss. In this pilot study, we assess the microbiota composition and cytokine profile changes in patients with stage III/IV, grade B/C periodontitis, specifically by comparing healthy and diseased sites in the same oral cavity. Overall, we found that microbiota architecture was significantly disrupted between diseased and healthy sites, and that the clustering was driven, in part, by the increased relative abundances of Synergistetes in diseased sites, as well as the increased abundances of Firmicutes in healthy sites. We also observed that diseased sites were enriched in Synergistetes, TM7, SR1, Spirochaetes, Bacteroidetes and Fusobacteria, and depleted in Firmicutes, Proteobacteria, Tenericutes and Actinobacteria compared to healthy sites. We found that Interleukin-1b, Interleukin-4, Interleukin-10, and Interleukin-17A were significantly overexpressed in diseased sites, whereas Interleukin-6 and TNF-alpha do not differ significantly between healthy and diseased sites. Here, we observed concomitant changes in the subgingival plaque microbiota and cytokines profile, suggesting that this combined alteration could contribute to the pathobiology of periodontitis.

The Impact of Smoking on Subgingival Plaque and the Development of Periodontitis: A Literature Review

Smoking seriously affects oral health and causes a variety of oral diseases. Numerous clinical data show that smoking significantly increases the risk of periodontitis, and the duration and amount of smoking are positively correlated with the severity of periodontitis. In fact, smoking creates an environment conducive to the colonization of periodontopathogens, which affects the process of periodontitis. Since subgingival plaque which harbors periodontopathogens is the initiation factor of periodontitis, it is critical to study the impact of smoking on subgingival microbiota for understanding the relationship between smoking and periodontitis. Continuous advances have been made on the understanding of effects of smoking on subgingival plaque and the development of periodontitis. Smoking is observed to enhance the pathogenicity of periodontopathogens, especially the red complex microorganisms, via promoting their colonization and infection, and regulating the expression and function of multiple virulence factors. Furthermore, smoking has a negative impact on periodontal microecological homeostasis, which is reflected in the decrease of commensal bacteria and the increase of periodontopathogens, as well as the changes in the interaction between periodontopathogens and their commensal microbes in subgingival biofilm, thus influencing the pathogenicity of the subgingival plaque. In summary, the mechanism of smoking on subgingival plaque microorganisms represented by the red complex and its effect on the periodontal microecology still need to be further explored. The relevant research results are of great significance for guiding the periodontal clinical treatment of smoking population. This review summarizes the effects and relevant mechanisms of smoking on subgingival plaque and the development of periodontitis.

Interdental and subgingival microbiota may affect the tongue microbial ecology and oral malodour in health, gingivitis and periodontitis

Background and Objective: Oral malodour is often observed in gingivitis and chronic periodontitis patients, and the tongue microbiota is thought to play a major role in malodorous gas production, including Volatile Sulfur Compounds (VSCs) such as hydrogen sulfide (H2S) and methanethiol (CH3SH). This study aimed to examine the link between the presence of VSCs in mouth air (as a marker of oral malodour) and the oral bacterial ecology in the tongue and periodontal niches of healthy, gingivitis and periodontitis patients. Methods: Participants were clinically assessed using plaque index, bleeding on probing (BOP) and periodontal probing depths, and VSC concentrations in their oral cavity measured using a portable gas chromatograph. Tongue scrapings, subgingival and interdental plaque were collected from healthy individuals (n=22), and those with gingivitis (n=14) or chronic periodontitis (n=15). The bacterial 16S rRNA gene region V3-V4 in these samples was sequenced and the sequences analysed using the Minimum Entropy Decomposition pipeline. Results: Elevated VSC concentrations and CH3SH:H2S were observed in periodontitis compared to health. Significant ecological shifts were observed in the tongue microbiota of healthy subjects who had higher plaque scores, suggesting a possible connection between the microbiota of the tongue and the periodontium and that key dysbiotic changes may be initiated in the clinically healthy who have higher dental plaque accumulation. Greater subgingival bacterial diversity was positively associated with H2S in mouth air. Periodontopathic bacteria known to be prolific VSC producers increased in abundance on the tongue and this was associated with increased bleeding on probing (BOP) and a greater % of periodontal pockets >6mm, supporting the suggestion that the tongue may become a reservoir for periodontopathogens. Conclusion: This study highlights the importance of the periodontal microbiota in malodour and has detected dysbiotic changes in the tongue microbiota in periodontitis.

Preliminary functional analysis of the subgingival microbiota of cats with periodontitis and feline chronic gingivostomatitis

The subgingival microbial communities of domestic cats remain incompletely characterized and it is unknown whether their functional profiles are associated with disease. In this study, we used a shotgun metagenomic approach to explore the functional potential of subgingival microbial communities in client-owned cats, comparing findings between periodontally healthy cats and cats with naturally occurring chronic periodontitis, aggressive periodontitis, and feline chronic gingivostomatitis. Subgingival samples were subjected to shotgun sequencing and the metagenomic datasets were analyzed using the MG-RAST metagenomic analysis server and STAMP v2.1.3 (Statistical Analysis of Metagenomic Profiles) software. The microbial composition was also described to better understand the predicted features of the communities. The Respiration category in the level 1 Subsystems database varied significantly among groups. In this category, the abundance of V-Type ATP-synthase and Biogenesis of cytochrome c oxidases were significantly enriched in the diseased and in the healthy groups, respectively. Both features have been previously described in periodontal studies in people and are in consonance with the microbial composition of feline subgingival sites. In addition, the narH (nitrate reductase) gene frequency, identified using the KEGG Orthology database, was significantly increased in the healthy group. The results of this study provide preliminary functional insights of the microbial communities associated with periodontitis in domestic cats and suggest that the ATP-synthase and nitrate-nitrite-NO pathways may represent appropriate targets for the treatment of this common disease.