Oral Biofilms and Human Health

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Biofilm".

Deadline for manuscript submissions: 30 May 2024 | Viewed by 7542

Special Issue Editors


E-Mail Website
Guest Editor
Colgate Palmolive Co., New York, NY, USA
Interests: clinical methods & diagnostics
Colgate Palmolive Co., New York, NY, USA
Interests: oral microbiome and immunology

E-Mail Website
Guest Editor
School of Dentistry, University of Washington, Seattle, WA, USA
Interests: bacteria/host interactions; lps biochemistry; host inflammatory response

E-Mail Website
Guest Editor
Department of Periodontics and Oral Health Sciences, University of Washington, Seattle, WA 98195 USA
Interests: bacteria-host interactions

Special Issue Information

Dear Colleagues,

With the advent of multi-omics assays and analysis techniques, more detailed information is becoming more available regarding the composition and function of biofilms. Using oligonucleotide probes, the spatial organization and metabolic activity of biofilms during assembly can now be more closely studied to link their functional role in maintaining health as well as the causes of disease. These complex assemblies of microorganisms are embedded in an exopolymeric substance matrix rich in nucleic acids, proteins, lipids, liposaccharides, and electrolytes, allowing the biofilm to adhere to surfaces more efficiently and protect it from environmental insults. When these biofilms are not regularly removed via mechanical action or host cell turnover, it becomes very difficult for antibacterials to penetrate and disrupt, allowing biofilms to persist and elicit an inflammatory response in the oral cavity. While the mouth’s innate immune defense can protect the host against many pathogens, sustained inflammation leads to oral tissue damage and contributes to systemic issues. Chronic oral inflammation can negatively impact systemic health, pregnancy outcomes, cognitive health, and respiratory illnesses. This association was best exemplified during the course of the recent SARS-CoV-2 pandemic, with published reports showing worse outcomes in terms of deaths and hospitalizations for those people with severe gum disease. There is also increasing evidence that host genetics can also increase some individuals’ susceptibility to infections, making them more predisposed to periodontal disease. Therefore, it is critical to identify precise therapies to help people reduce their oral inflammatory burden and support a healthier mouth. Research needs to continue to use precision health approaches to address differences in the host response to bacteria and oral biofilms. In order to explore opportunities to better manage oral diseases and their impact on the host response, researchers and experts in oral biofilms and host–microbial interactions are invited to contribute to this Special Issue. Original research articles and reviews are welcome. Research areas may also include how precision diagnostics and therapeutics can be applied to prevent and personalize the treatment of oral diseases.

Dr. LaTonya Kilpatrick-Liverman
Dr. Carlo Daep
Prof. Dr. Richard Darveau
Dr. Jeffrey S. McLean
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Microorganisms is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • dental plaque
  • oral biofilm
  • precision health
  • therapeutics
  • inflammation
  • immunity
  • microbiome
  • imaging
  • diagnostics
  • single-cell sequencing

Published Papers (4 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

29 pages, 13049 KiB  
Article
Specific Oral Microbial Differences in Proteobacteria and Bacteroidetes Are Associated with Distinct Sites When Moving from Healthy Mucosa to Oral Dysplasia—A Microbiome and Gene Profiling Study and Focused Review
by Allan Radaic, Eliah R. Shamir, Kyle Jones, Alessandro Villa, Nandita R. Garud, Aaron D. Tward, Pachiyappan Kamarajan and Yvonne L. Kapila
Microorganisms 2023, 11(9), 2250; https://doi.org/10.3390/microorganisms11092250 - 07 Sep 2023
Viewed by 1383
Abstract
Oral potentially malignant disorders (OPMDs) are a group of conditions that carry a risk of oral squamous cell carcinoma (OSCC) development. Recent studies indicate that periodontal disease-associated pathogenic bacteria may play a role in the transition from healthy mucosa to dysplasia and to [...] Read more.
Oral potentially malignant disorders (OPMDs) are a group of conditions that carry a risk of oral squamous cell carcinoma (OSCC) development. Recent studies indicate that periodontal disease-associated pathogenic bacteria may play a role in the transition from healthy mucosa to dysplasia and to OSCC. Yet, the microbial signatures associated with the transition from healthy mucosa to dysplasia have not been established. To characterize oral microbial signatures at these different sites, we performed a 16S sequencing analysis of both oral swab and formalin-fixed, paraffin-embedded tissue (FFPE) samples. We collected oral swabs from healthy mucosa (from healthy patients), histologically normal mucosa adjacent to dysplasia, and low-grade oral dysplasia. Additionally, FFPE samples from histologically normal mucosa adjacent to OSCC, plus low grade and high-grade oral dysplasia samples were also collected. The collected data demonstrate significant differences in the alpha and beta microbial diversities of different sites in oral mucosa, dysplasia, and OSCC, as well as increased dissimilarities within these sites. We found that the Proteobacteria phyla abundance increased, concurrent with a progressive decrease in the Firmicutes phyla abundance, as well as altered levels of Enterococcus cecorum, Fusobacterium periodonticum, Prevotella melaninogenica, and Fusobacterium canifelinum when moving from healthy to diseased sites. Moreover, the swab sample analysis indicates that the oral microbiome may be altered in areas that are histologically normal, including in mucosa adjacent to dysplasia. Furthermore, trends in specific microbiome changes in oral swab samples preceded those in the tissues, signifying early detection opportunities for clinical diagnosis. In addition, we evaluated the gene expression profile of OSCC cells (HSC-3) infected with either P. gingivalis, T. denticola, F. nucelatum, or S. sanguinis and found that the three periodontopathogens enrich genetic processes related to cancer progression, including skin keratinization/cornification, while the commensal enriched processes related to RNA processing and adhesion. Finally, we reviewed the dysplasia microbiome literature and found a significant decrease in commensal bacteria, such as the Streptococci genus, and a simultaneous increase in pathogenic bacteria, mainly Bacteroidetes phyla and Fusobacterium genus. These findings suggest that features of the oral microbiome can serve as novel biomarkers for dysplasia and OSCC disease progression. Full article
(This article belongs to the Special Issue Oral Biofilms and Human Health)
Show Figures

Figure 1

12 pages, 2210 KiB  
Article
Saliva Decreases Sucrose-Induced Cariogenicity in an Experimental Biological Caries Model
by Rodrigo A. Giacaman, Rodrigo Umaña, María José Nuñez, Natalia Díaz-Garrido, Constanza Echeverría, Natalia García-Manríquez, Alex Mira, Constanza E. Fernández, Karla Gambetta-Tessini and Carla P. Lozano
Microorganisms 2023, 11(6), 1426; https://doi.org/10.3390/microorganisms11061426 - 29 May 2023
Cited by 1 | Viewed by 1751
Abstract
Objective. Whether a minimum quantity of saliva inhibit the caries process remains uncertain. This study aimed to investigate the impact of saliva dilutions on an in vitro caries model using Streptococcus mutans (S. mutans) biofilms. Methods. S. mutans biofilms were cultivated [...] Read more.
Objective. Whether a minimum quantity of saliva inhibit the caries process remains uncertain. This study aimed to investigate the impact of saliva dilutions on an in vitro caries model using Streptococcus mutans (S. mutans) biofilms. Methods. S. mutans biofilms were cultivated on enamel and root dentin slabs, in culture media containing different proportions of saliva (v/v): 0%, 5%, 10%, 25%, 50%, 75%, and 100% saliva, and exposed to a 10% sucrose solution (5 min, 3x/day), with appropriate controls. After 5 (enamel) and 4 (dentin) days, demineralization, biomass, viable bacteria, and polysaccharide formation were analyzed. The acidogenicity of the spent media was monitored overtime. Each assay was performed in triplicate across two independent experiments (n = 6). Results. In both enamel and dentin, an inverse relationship was observed between acidogenicity, demineralization, and the proportion of saliva. Even small quantities of saliva incorporated into the media led to a noticeable reduction in enamel and dentin demineralization. Saliva presence resulted in significant reductions in biomass, viable S. mutans cells, and polysaccharides, with the effects being concentration-dependent for both tissues. Conclusions. High quantities of saliva can almost completely inhibit sucrose-induced cariogenicity, while even small amounts exhibit a dose-dependent caries-protective effect. Full article
(This article belongs to the Special Issue Oral Biofilms and Human Health)
Show Figures

Figure 1

18 pages, 2304 KiB  
Article
In Vitro Preventive Effect and Mechanism of Action of Weissella cibaria CMU against Streptococcus mutans Biofilm Formation and Periodontal Pathogens
by Mi-Sun Kang, Geun-Yeong Park and A-Reum Lee
Microorganisms 2023, 11(4), 962; https://doi.org/10.3390/microorganisms11040962 - 07 Apr 2023
Cited by 4 | Viewed by 1523
Abstract
In this study, we evaluated the in vitro anti-biofilm, antibacterial, and anti-inflammatory activity of Weissella cibaria CMU (CMU), an oral probiotic, against periodontopathogens. Compared to other oral probiotics, CMU showed a superior inhibitory effect on the biofilm formation and growth of Streptococcus mutans [...] Read more.
In this study, we evaluated the in vitro anti-biofilm, antibacterial, and anti-inflammatory activity of Weissella cibaria CMU (CMU), an oral probiotic, against periodontopathogens. Compared to other oral probiotics, CMU showed a superior inhibitory effect on the biofilm formation and growth of Streptococcus mutans on orthodontic wires and artificial teeth (p < 0.05). CMU exerted potent antibacterial effects against S. mutans and Porphyromonas gingivalis according to a line test. In human gingival fibroblasts (HGFs) stimulated by P. gingivalis, Fusobacterium nucleatum, or Prevotella intermedia, CMU suppressed the gene expression of pro-inflammatory cytokines [interleukin (IL)-6, IL-1β, IL-8, and tumor necrosis factor-α] in a dose-dependent manner (p < 0.05). CMU restored the production of the tissue inhibitor of metalloproteinase-1 following its inhibition by P. gingivalis, and it suppressed the expression of matrix metalloproteinase (MMP)-1 and -3 induced by periodontopathogens (p < 0.05). Moreover, CMU needed direct contact with HGFs to exert their anti-inflammatory function, indicating that they act directly on gingival cells to modulate local inflammation. Our preclinical study provides evidence for the potential benefits of topical CMU treatments in preventing the development of caries and periodontitis caused by the dysbiosis of the dental plaque microbiome. Full article
(This article belongs to the Special Issue Oral Biofilms and Human Health)
Show Figures

Figure 1

Review

Jump to: Research

17 pages, 962 KiB  
Review
Risk Factors and Immunoinflammatory Mechanisms Leading to Atherosclerosis: Focus on the Role of Oral Microbiota Dysbiosis
by Riccardo Mattia Ricciardi, Alessia Cipollone, Damiano D’Ardes, Davide Di Giacomo, Pamela Pignatelli, Francesco Cipollone, Maria Cristina Curia, Paolo Magni and Marco Bucci
Microorganisms 2023, 11(6), 1479; https://doi.org/10.3390/microorganisms11061479 - 01 Jun 2023
Cited by 1 | Viewed by 1639
Abstract
Cardiovascular diseases (CVD), including myocardial infarction and stroke, are currently the leading cause of morbidity, disability and mortality worldwide. Recently, researchers have focused their attention on the alterations of the gut and oral microbiota, investigating the possible role of their dysbiosis in the [...] Read more.
Cardiovascular diseases (CVD), including myocardial infarction and stroke, are currently the leading cause of morbidity, disability and mortality worldwide. Recently, researchers have focused their attention on the alterations of the gut and oral microbiota, investigating the possible role of their dysbiosis in the pathogenesis and/or progression of CVD. In this regard, it has been shown that endothelial dysfunction, a major feature of CVD, can also be induced by chronic periodontal infection, due to a systemic pro-inflammatory condition, as suggested by increased plasma levels of acute phase proteins, IL-6 and fibrinogen. Moreover, proatherogenic dysfunctions can also be promoted by direct bacterial invasion of the endothelium. This review reports the current evidence about the possible role of oral microbiota dysbiosis and the related immunoinflammatory components in the pathophysiology of atherosclerosis and associated CVD. It is concluded that integration of oral microbiota sampling into clinical practice may result in a more accurate assessment of CV risk in patients and even modify their prognosis. Full article
(This article belongs to the Special Issue Oral Biofilms and Human Health)
Show Figures

Figure 1

Back to TopTop