Plaque Biofilm Research Articles

Heterogeneous lineage-specific arginine deiminase expression within dental microbiome species.

Tooth decay is the most common preventable chronic disease, affecting more than two billion people globally. The development of caries on teeth is primarily a consequence of acid production by cariogenic bacteria that inhabit the plaque microbiome. Other bacterial strains in the oral cavity may suppress or prevent tooth decay by producing ammonia as a byproduct of the arginine deiminase metabolic pathway, increasing the pH of the plaque biofilm. While the benefits of arginine metabolism on oral health have been extensively documented in specific bacterial groups, the prevalence and consistency of arginine deiminase system (ADS) activity among oral bacteria in a community context remain an open question. In the current study, we use a multi-omics approach to document the pervasiveness of the expression of the ADS operon in both health and disease to better understand the conditions in which ADS activity may prevent tooth decay.

Stimuli-responsive graphdiyne-silver nanozymes for catalytic ion therapy of dental caries through targeted biofilms removal and remineralization

Clinical mechanical decontamination and irrigants are not consistently effective in preventing intractable biofilm-induced dental caries, especially when biofilms have caused demineralization. Constructing stimuli-responsive nanocatalysts with improved catalytic activity for plaque biofilm removal and remineralization enhancement remains challenging. Herein, a coordination-reduction strategy driven by L-cysteine and graphdiyne (GDY) is employed to anchor low-dose Ag nanoparticles/Ag+ to GDY nanosheets to obtain GDY/L-cys/Ag (GLA) nanozymes. Subsequently, biomimetic approach is used to encapsulate GLA into a GS ointment composed of gelatin methacryloyl and sodium alginate to form biodegradable and adhesive GLA/GS. GLA demonstrates acidic plaque biofilm-activated peroxidase-like activity, surpassing affinity toward H2O2 than natural horseradish peroxidase, effectively catalyzing low-dose H2O2 into highly toxic hydroxyl radicals (•OH). This catalytic activity simultaneously enhances Ag+ release triggered by acidic plaque biofilms, generating additional reactive oxygen species that can suppress plaque biofilms on ex vivo human teeth by the synergistic effect of catalysis and released ions. Importantly, GLA/GS serves as template nucleation sites crosslinked to rich Ca2+, thereby attracting PO43- from saliva, prompting growth into hydroxyapatite on tooth enamel, facilitating rapid remineralization. Due to the safe nanocatalytic ion therapy, in an in vivo rodent model, GLA/GS + H2O2 effectively prevents dental caries without influencing surrounding oral tissues.

Oral microbiota-host interaction: the chief culprit of alveolar bone resorption.

There exists a bidirectional relationship between oral health and general well-being, with an imbalance in oral symbiotic flora posing a threat to overall human health. Disruptions in the commensal flora can lead to oral diseases, while systemic illnesses can also impact the oral cavity, resulting in the development of oral diseases and disorders. Porphyromonas gingivalis and Fusobacterium nucleatum, known as pathogenic bacteria associated with periodontitis, play a crucial role in linking periodontitis to accompanying systemic diseases. In periodontal tissues, these bacteria, along with their virulence factors, can excessively activate the host immune system through local diffusion, lymphatic circulation, and blood transmission. This immune response disruption contributes to an imbalance in osteoimmune mechanisms, alveolar bone resorption, and potential systemic inflammation. To restore local homeostasis, a deeper understanding of microbiota-host interactions and the immune network phenotype in local tissues is imperative. Defining the immune network phenotype in periodontal tissues offers a promising avenue for investigating the complex characteristics of oral plaque biofilms and exploring the potential relationship between periodontitis and associated systemic diseases. This review aims to provide an overview of the mechanisms underlying Porphyromonas gingivalis- and Fusobacterium nucleatum-induced alveolar bone resorption, as well as the immunophenotypes observed in host periodontal tissues during pathological conditions.

A Long-Term Split-Mouth Randomized Controlled Trial to Assess Implant Treatment Outcome Using Implants with a Different Surface Roughness

The influence of implant surface roughness on implant treatment outcome is still under debate. A rougher implant surface improves osseointegration but yields greater plaque accumulation and biofilm formation. Hybrid implants have a minimally rough component coronally and a moderately rough implant body. The aim of this split-mouth study is to evaluate the long-term outcome of treatment with hybrid and moderately rough implants after 6 years. As a secondary aim, Oral Health Quality of Life (OHQoL) was assessed after one and six years. Fully edentulous patients received an overdenture supported by two implants. One implant had a hybrid surface (MSC) and one implant had a moderately rough surface (DCC). Radiographic crestal bone loss (CBL), plaque score, bleeding on probing (BoP) and periodontal probing depth (PPD) were determined at one and six years. OHQoL was evaluated using the Oral Health Impact Profile-14 (OHIP-14) questionnaire and a Visual Analogue Scale (VAS). Twenty-one patients with 42 implants were evaluated after 6 years. No implants failed and a mean CBL of 0.26 mm (SD: 0.42) for the MSC group and 0.17 mm (SD: 0.29) for the DCC group was observed, which was not statistically significant. Periodontal parameters were comparable after 6 years and a significant improvement in OHQoL was observed. This randomized controlled trial concludes that hybrid implants are a predictable treatment alternative for moderately rough implants in patients with an overdenture supported by two implants.

SMU_1361c regulates the oxidative stress response of Streptococcus mutans.

Dental caries is the most common chronic infectious disease around the world and disproportionately affects the marginalized socioeconomic group. Streptococcus mutans, considered a primary etiological agent of caries, depends on the coordinated physiological response to tolerate the oxidative stress generated by commensal species within dental plaque, which is a critical aspect of its pathogenicity. Here, we identified and characterized a novel tetracycline repressor family regulator, SMU_1361c, which appears to be acquired by the bacteria via horizontal gene transfer. Surprisingly, smu_1361c functions as a negative transcriptional regulator to regulate gene expression outside its operon and is involved in the oxidative stress response of S. mutans. The smu_1361c overexpression strain UA159/pDL278-1361c was more susceptible to oxidative stress and less competitive against hydrogen peroxide generated by commensal species Streptococcus gordonii and Streptococcus sanguinis. Transcriptomics analysis revealed that smu_1361c overexpression resulted in the significant downregulation of 22 genes, mainly belonging to three gene clusters responsible for the oxidative stress response. The conversed DNA binding motif of SMU_1361c was determined by electrophoretic mobility shift and DNase I footprinting assay with purified SMU_1361c protein; therefore, smu_1361c is directly involved in gene transcription related to the oxidative stress response. Crucially, our finding provides a new understanding of how S. mutans deals with the oxidative stress that is required for pathogenesis and will facilitate the development of new and improved therapeutic approaches for dental caries.IMPORTANCEStreptococcus mutans is the major organism associated with the development of dental caries, which globally is the most common chronic disease. To persist and survive in biofilms, S. mutans must compete with commensal species that occupy the same ecological niche. Here, we uncover a novel molecular mechanism of how tetracycline repressor family regulator smu_1361c is involved in the oxidative stress response through transcriptomics analysis, electrophoretic mobility shift assay, and DNase I footprinting assay. Furthermore, we demonstrated that smu_1361c mediates S. mutans sensitivity to oxidative stress and competitiveness with commensal streptococci. Therefore, this study has revealed a previously unknown regulation between smu_1361c and genes outside its operon and demonstrated the importance of smu_1361c in the oxidative stress response and the fitness of S. mutans within the plaque biofilms, which can be exploited as a new therapy to modulate ecological homeostasis and prevent dental caries.

Bioceramic micro-fillers reinforce antibiofilm and remineralization properties of clear aligner attachment materials.

Introduction: Clear aligners, while offering a more hygienic alternative to fixed appliances, are still associated with challenges including plaque accumulation and enamel demineralization. The aim of the present study was to investigate the antibiofilm and remineralization effectiveness of innovative flowable composite attachments containing bioceramic micro-fillers. Methods: Four experimental attachments were formulated and bonded to human enamel specimens: 3M Filtek Supreme flowable composite (Filtek SF) + 10% bioactive glass 45S5 (BAG), Filtek SF + 30% BAG, Filtek SF + 10% Bredigite (BRT), Filtek SF + 30% BRT. Plaque biofilms were grown on the bonded enamel using a standardized protocol and the biofilm-killing effect was assessed by confocal laser scanning microscopy and scanning electron microscopy. Vickers microhardness was measured to evaluate the remineralization effect of the attachments containing bioceramic fillers after acid challenge. Shear bond test was performed to assess the bonding strength. Results: Attachments with bioceramic fillers significantly inhibited plaque biofilm growth in 3 weeks on enamel, contributing over 20% bacterial cell killing in 10% filler groups and over 30% killing in 30% filler groups. All four experimental groups demonstrated significantly higher microhardness values than the control group without fillers on the attachment side. The shear bonding strength was not compromised in the attachments with micro-fillers. Discussion: Proper incorporation of bioceramic micro-fillers in attachments provides an innovative approach for clear aligner therapy with reinforced antibiofilm and remineralization effects without weakening shear bonding strength.

Injectable thermosensitive hydrogel loading erythropoietin and FK506 alleviates gingival inflammation and promotes periodontal tissue regeneration.

Background: Periodontitis is a chronic multifactorial inflammatory disease associated with dysbiotic plaque biofilms and characterized by progressive destruction of the tooth-supporting apparatus. Therefore, there is significant potential in the discovery of drugs that inhibit periodontal inflammatory responses and promote periodontal regeneration. Methods: In this study, we generated a periodontitis rat model to detect the effects of chitosan/β-sodium glycerophosphate (β-GP)/glycolic acid (GA) hydrogel carried Erythropoietin and FK506 (EPO-FK506-CS/β-GP/GA). A total of forty-eight male Wistar rats were used to establish the periodontitis model. Drug injection was administered every 3days for a total of five times over a 2-week period. After a period of 2weeks following implantation, the rats underwent anesthesia, and a section of their maxillae encompassing the maxillary first and secondmolars, along with the alveolar bone, was obtained. micro-CT scanning, histopathology, immunohistochemistry and reverse transcription-quantitative PCR (RT-qPCR) assays were performed. Meanwhile, ELISA assay was performed to detect the levels of inflammatory mediators (TNF-α, IL-6 and IL-1β). Results: The synthesis and characterization of EPO-FK506-CS/β-GP/GA revealed that the hydrogel has stability and sustained release of drugs. The application of FK506+EPO was found to significantly enhance new bone formation in the defect area, as evidenced by the results of HE staining. Additionally, the use of FK506+EPO in the treated groups led to a notable increase in the density of alveolar bone, as observed through micro-CT analysis, when compared to the Model group. EPO-FK506-CS/β-GP/GA hydrogel exhibited notable efficacy in modulating inflammatory mediators (TNF-α, IL-6 and IL-1β). Furthermore, the osteoinductive properties of the EPO-FK506-CS/β-GP/GA hydrogel were extensive, as evidenced by a significant upregulation in the expression of key markers (Collagen I, Runx2, OPN, and OCN) associated with osteoblastic differentiation. Conclusion: Taken together, EPO-FK506-CS/β-GP/GA hydrogel alleviates gingival inflammation and promotes periodontal tissue regeneration in the periodontitis.

In Vitro Antibacterial Activity of a Novel Acid-Activated Antimicrobial Peptide against Streptococcus mutans.

Dental caries is an oral disease associated with infection by microbial biofilm. The metabolic activity of cariogenic bacteria results in a pH decrease in the plaque biofilm, causing tooth demineralization. This acidic environment favors the growth of cariogenic bacteria that are highly resistant to strong acids, which, in turn, produce more acid resulting in a further decrease in the pH of the plaque biofilm. Therefore, the strategy of utilizing the acidic dental plaque microenvironment to prevent and treat dental caries has become a hot research topic in recent years, such as the development of pH-sensitive drug delivery systems. Design of a new acid-activated antibacterial peptide. To design and synthesis an acid targeted antimicrobial peptide with the GWHHFFHFFHFF sequence. Minimum inhibitory concentration (MIC) and minimum bacterial concentration (MBC) testing confirmed its antibacterial activity. Propidium iodide (PI) staining was used to detect nucleic acid leakage. Determination of anti-biofilm activity by biofilm inhibition assay. A phototoxicity study confirmed the phototoxicity of PPIX-P12. MIC and MBC testing confirmed that P12 possessed acid-activated anti-Streptococcus mutans activity. Bactericidal kinetic experiments and propidium iodide (PI) staining experiments showed that P12 killed planktonic S. mutans UA159 cells leading to the leakage of nucleic acids in the acidic medium. Moreover, P12 showed acid-activated anti-biofilms at the early and mature biofilm stages. P12 was conjugated with the phototherapeutic agent protoporphyrin IX (PpIX) to construct the protoporphyrin derivative PpIX-P12. In vitro experiments revealed that PpIX-P12 displayed better antibacterial activity in pH 5.5 medium than in pH 7.2 medium. In conclusion, we designed an acid-activated AMP, which had no antimicrobial activity at neutral pH, but had antimicrobial activity at an acidic pH.

Periodontitis: etiology, conventional treatments, and emerging bacteriophage and predatory bacteria therapies.

Inflammatory periodontal diseases associated with the accumulation of dental biofilm, such as gingivitis and periodontitis, are very common and pose clinical problems for clinicians and patients. Gingivitis is a mild form of gum disease and when treated quickly and properly is completely reversible. Periodontitis is an advanced and irreversible disease of the periodontium with periods of exacerbations, progressions and remission. Periodontitis is a chronic inflammatory condition that damages the tissues supporting the tooth in its socket, i.e., the gums, periodontal ligaments, root cementum and bone. Periodontal inflammation is most commonly triggered by bacteria present in excessive accumulations of dental plaque (biofilm) on tooth surfaces. This disease is driven by disproportionate host inflammatory immune responses induced by imbalance in the composition of oral bacteria and changes in their metabolic activities. This microbial dysbiosis favors the establishment of inflammatory conditions and ultimately results in the destruction of tooth-supporting tissues. Apart microbial shift and host inflammatory response, environmental factors and genetics are also important in etiology In addition to oral tissues destruction, periodontal diseases can also result in significant systemic complications. Conventional methods of periodontal disease treatment (improving oral hygiene, dental biofilm control, mechanical plaque removal, using local or systemic antimicrobial agents) are not fully effective. All this prompts the search for new methods of therapy. Advanced periodontitis with multiple abscesses is often treated with antibiotics, such as amoxicillin, tetracycline, doxycycline, minocycline, clindamycin, or combined therapy of amoxicillin with metronidazole. However, due to the growing problem of antibiotic resistance, treatment does not always achieve the desired therapeutic effect. This review summarizes pathogenesis, current approaches in treatment, limitations of therapy and the current state of research on the possibility of application of bacteriophages and predatory bacteria to combat bacteria responsible for periodontitis. We present the current landscape of potential applications for alternative therapies for periodontitis based on phages and bacteria, and highlight the gaps in existing knowledge that need to be addressed before clinical trials utilizing these therapeutic strategies can be seriously considered.

Breaking Down the Barrier: Understanding How Magnesium Deficiency Contributes to Periodontitis

A common disturbing dental malaise which ultimately results in low quality of life is periodontitis, a chronic bacterial infections disease that is caused by the dental plaque biofilm. Both tissues and blood need enough magnesium, this is a natural and one of essential minerals that is highly abundant in the human body. Different diseases due to a magnesium deficiency can be formed. Results from clinical and nutritional data supported this hypothesis. However, The relationship between magnesium deficiency and periodontitis requires further research. This paper examines some possible ways in which these two are connected. This article focuses on presenting a valuable and resourceful material for those who are eager to acknowledge the role that magnesium level plays in periodontal disease as well as providing potential means to the creation of advanced and effective periodontitis prevention and treatment approaches.

Probiotic Effect on Periodontal Disease: A Meta-Analysis Study

Periodontal disease remains a major worldwide oral health problem, affecting about 538 million people all around the globe. It is caused by changes in local microflora inhabiting the plaque biofilm from Gram-positive to Gram-negative facultatively anaerobic bacteria, destroying the periodontal membrane and surrounding alveolar bone. Mechanical debridement of biofilm and antibiotics has been used as conventional therapy for gingivitis and periodontitis. However, the uncertain efficacy of the current treatment leads to using probiotics as a promising strategy to combat the periodontal pathogen. An antibiotic application might contribute to antimicrobial resistance and environmental pollution due to non-degradable residue. Probiotics could be an alternative treatment for periodontal disease. This meta-analysis study aims to assess the potential of probiotic bacteria to reduce the magnitude of the inflammatory response, especially in the pro-inflammatory cytokines. Electronic databases such as Google Scholar, Science Direct, and PubMed were used to search for related articles up to May 2021. Randomized Controlled Clinical Trials (RCTs) or controlled clinical trials were included in the study, whereby the concentration of IL-1β and TNF-α were chosen as the main outcome variables. Independent screening resulted in four eligible publications being included in the meta-analysis. However, the overall mean difference for the concentration of IL-1β (MD: -0.32; 95% CI: -1.88, 1.25; P = 0.69) and TNF-α (MD: 0; 95% CI: -0.20, 0.20; P= 0.98) did not show any statistical significance difference between probiotic and placebo groups. Therefore, the study results demonstrated weak evidence to support the usage of probiotics in reducing the magnitude of inflammatory response in patients with periodontal disease. Smaller sample sizes and limited available data may contribute to this conclusion. Hence, future randomized controlled clinical trials with larger sample sizes and a longer intervention period must be considered to evaluate the efficacy of probiotics in periodontal disease.

Efficacy of Probiotics Versus Tetracycline Fibers as Adjuvants to Scaling and Root Planing on Interleukin 1β Levels in Type 2 Diabetic Patients With Periodontitis: A Clinical and Biochemical Study.

Background Periodontitis, a chronic inflammatory disease, is triggered by the plaque biofilm culminating in periodontal attachment loss, bone loss, and tooth loss. Diabetes, a globally prevalent disease, causes an increased inflammatory response to the microflora associated with periodontitis. It has been observed that the link between these two diseases is bidirectional. Tissue repair is impaired in diabetic patients with periodontitis. Local drug delivery systems selectively target the inflamed sites contrary to systemic antibiotics which lead to resistance and many other adverse effects.Probiotics aid in the growth of beneficial microorganisms and have immunomodulatory effects on the host. Tetracyclines have anti-collagenase properties and reduce the bacterial load, curbing the progression of periodontitis. Interleukin (IL) 1β, a strong marker of periodontal tissue destruction, plays a pivotal role in inflammation, immune regulation, and bone resorption in periodontitis. This study evaluated and compared the benefits of probiotics and tetracycline fibers when used as adjunctive tools after scaling and root planing (SRP) on IL1β levels in type 2 diabetic patients with periodontitis. Methodology A total of 36 patients participated in this study. Group I included 12 patients with periodontitis and uncontrolled diabetes (HbA1c levels >7). After SRP, six patients received tetracycline fibers (IA), and six patients received probiotics (1B) as locally delivered agents. Group II included 12 patients with periodontitis and diabetes under control (HbA1c levels 6-7%). After SRP, six patients received tetracycline fibers (IIA), and six patients received probiotics (IIB) as locally delivered drugs (test groups). Group III, the control group, included 12 patients with periodontitis only, wherein a placebo was used as a local drug delivery (LDD) after SRP. The clinical parameters, such as plaque index, gingival index, and probing pocket depth, were recorded preoperatively and at eight and 12 weeks after non-surgical periodontal therapy. IL1β levels were assessed by enzyme-linked immunosorbent assay at baseline and six weeks after SRP. Results On intra and intergroup comparison, all groups showed improvement in both the clinical and biochemical parameters but significant results were seen in Group IIA (p < 0.01) when compared to the other groups. Conclusions Group II (well-controlled diabetics) performed significantly better than the other groups, which was followed by Group III. The use of LDDs as adjunctive tools after SRP was not beneficial in Group I (uncontrolled diabetics).

Comparison of red blood cell parameters in patients with and without periodontitis – A hospital based observational study

Dental plaque bio film aggregate around dentition is the primary etiology of periodontitis. The host inflammation mounted in response to bacterial biofilm determines the extent and severity of periodontitis. The low grade inflammation results increase in pro inflammatory cytokine levels, and this links periodontitis with other systemic diseases. Epidemiologic studies have revealed a possible association of periodontitis with some systemic diseases. There are conflicting results regarding the association of periodontitis and anemia. The aim of the study was to compare the red blood cell parameters in subjects with and without periodontitis in our population.A single calibrated examiner was entrusted to do the periodontal examination, and 48 subjects with periodontitis (Group I) and 50 age matched subjects without periodontitis (Group II) with a mean age of 33.45 yrs. +/- 7.86 were recruited for the study. Gingival index and full mouth periodontal charting were done and 2ml blood samples were collected for estimation of blood parameters.Group I showed a statistically insignificant difference in hemoglobin levels compared to group II (P value-0.065) where as MCH and MCHC showed a statistically significant difference between the groups (P value-0.012, 0.002 respectively).The inflammatory burden increases with the severity of Periodontitis and this may lead to the development of anemia.

Identifying genes for regulating osteogenic differentiation of human periodontal ligament stem cells in inflammatory environments by bioinformatics analysis.

Periodontitis is an immuno-inflammatory disease caused by dental plaque biofilms and inflammations. The regeneration of bone tissue in inflammatory environment is of great significance for the treatment of periodontal disease, but the specific molecular mechanism of bone formation in periodontitis still needs further exploration. The objective of this study was to identify key osteogenesis-related genes (ORGs) in periodontitis. We used two datasets from the Gene Expression Omnibus (GEO) database to find differentially expressed mRNAs and miRNAs, further performed Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Then we predicted the downstream genes of the differentially expressed miRNAs (DEMs) by the TargetScan database and established a miRNA-mRNA regulatory network. Finally, the osteogenic mechanism of periodontitis was explored through quantitative real-time PCR (qRT-PCR) by inducing inflammatory environment and osteogenic differentiation of hPDLSCs. Through differential expression analysis and prediction of downstream target genes of DEMs, we created a miRNA-mRNA regulatory network consisting of 29 DEMs and 11 differentially expressed osteogenesis-related genes (DEORGs). In addition, the qRT-PCR results demonstrated that BTBD3, PLAT, AKAP12, SGK1, and GLCE expression levels were significantly upregulated, while those of TIMP3, ZCCHC14, LIN7A, DNAH6, NNT, and ITGA6 were downregulated under the dual effects of inflammatory stimulation and osteogenic induction. DEORGs might be important factors in the osteogenic phase of periodontitis, and the miRNA-mRNA network may shed light on the clarification of the role and mechanism of osteogenesis in periodontitis and contribute to the development of novel therapeutic strategies.

Role of periodontal pathogens in atherosclerotic plaque development and progression: An overview.

Atherosclerosis is a progressive disease marked by the accumulation of lipids and fibrous components in the large arteries. It is one of the primary causes of heart disease and stroke. Periodontal diseases encompass conditions like gingivitis and periodontitis, which are multifactorial diseases associated with dysbiotic plaque biofilms that trigger an immune-inflammatory host response, eventually resulting in the destruction of periodontal tissues. Links between periodontal disease and atherosclerosis may be based on direct invasion of periodontal pathogens or inflammatory mechanisms triggered by bacteria related to periodontal lesions, locally or systemically, that may impact the initiation of the atherosclerotic lesion. The presence of periodontal pathogens within an atheromatous lesion implies hematogenous dissemination. The invasion of atheroma by periodontal pathogens results in changes in the proatherogenic and proinflammatory properties of endothelial cells, leading to endothelial dysfunction, which is a hallmark of atherosclerosis. Clinical and epidemiological studies have offered sufficient evidence of periodontitis having an adverse effect on systemic health, including atherosclerosis; however, a direct causal effect has not yet been proved. This review aims to analyse scientific results regarding the mechanism by which periodontal pathogens may cause atherosclerosis as well as to describe the role of Porphyromonas gingivalis in atherosclerotic plaque development and progression.

Near infrared responsive nitric oxide and carbon monoxide nanoplatform for synergistic photodynamic therapy against periodontitis

Periodontitis is a persistent inflammatory condition caused by plaque biofilm. To achieve successful periodontal tissue repair and halt disease progression, it is imperative to concurrently address the demands for precise antibacterial, anti-inflammatory, and osteogenic interventions within the profound lesions. Herein, we synthesized an intelligent and efficient nanoplatform for the treatment of periodontitis, combining the synergistic therapeutic effects of carbon monoxide (CO) and nitric oxide (NO) gas therapy with the application of photodynamic therapy (PDT). Benefiting from the rapid adhesion to bacteria, responsive CO/NO releasing and ROS generation, the nanoplatform achieved a powerful bactericidal capacity and conspicuous biofilm elimination efficiency under 808 nm near-infrared (NIR) light irradiation. In addition, the combination of CO and NO holds paramount significance, and they serve as crucial endogenous signaling molecules capable of regulating the TLR4/NF-κB/NLRP3 pathway. This combination not only achieved critical protective effects but also fostered the promotion of osteoblast differentiation.

In Vitro Eradication of Planktonic, Saliva and Biofilm Bacteria Using Lingonberry Extract as a Photosensitizer for Visible Light Plus Water-Filtered Infrared-A Irradiation

Antimicrobial photodynamic treatment (aPDT) with visible light plus water-filtered infrared-A irradiation (VIS-wIRA) and natural single- or multi-component photosensitizers (PSs) was shown to have potent antimicrobial activity. The aim of this study was to obtain information on the antimicrobial effects of aPDT-VIS-wIRA with lingonberry extract (LE) against bacteria that play a role in oral health. Planktonic bacterial cultures of the Gram-positive E. faecalis T9, S. mutans DSM20523, S. oralis ATCC 35037 and S. sobrinus PSM 203513, the Gram-negative N. oralis 14F2 FG-15-7B, F. nucleatum ATCC 25586, and V. parvula DSM, the anaerobic F. nucleatum ATCC 25586 and V. parvula DSM 2008, and the total mixed bacteria from pooled saliva and supra- and subgingival plaques of volunteers were all treated and compared. aPDT-VIS-wIRA with LE as PS significantly (p &lt; 0.008) reduced the growth of all tested Gram-positive, Gram-negative, as well as aerobic and anaerobic bacterial strains, whereas without irradiation no reductions were seen (p &lt; 0.0001). NaCl, with or without irradiation, was ineffective. After treatment with CHX 0.2%, the highest killing rate (100%) was observed, and no bacteria (0 log10 CFU) were cultivable. The method also significantly reduced all of the bacteria present in saliva and in the gingival biofilms. Three-dimensional visualization of viable and non-viable microorganisms revealed that LE penetrated deeper into the cell wall layers than CHX 0.2%. LE was an appropriate PS for eradicating microorganisms with VIS-wIRA, either in their planktonic form or in saliva and gingival plaque biofilms. These results encourage further investigation in order to determine which LE compounds contribute to the photosensitizing effect and to evaluate the size of the effect on maintaining oral health.

Subgingival Plaque as a Potential Reservoir for SARS-CoV-2 Virus in Patients Recovered from COVID-19 Infection: A Cross-sectional Study

Background Subgingival plaque biofilm is a potential harboring site for bacteria and viruses, serving as a source of entry into the bloodstream. The presence of Severe Acute Respiratory Syndrome Coronavirus 2 RNA (SARS-CoV-2 RNA) in subgingival plaque could be a possible source for cross infection due to aerosol contamination during dental procedures. Objectives The objective of this study was to investigate the presence of SARS-CoV-2 RNA in the subgingival plaque biofilm of patients who recovered from COVID-19 infection. Materials and Methods Ten subjects visiting the Outpatient clinic with a previous history of COVID-19 infection were recruited for this cross-sectional study. Subgingival plaque sample was collected from all four quadrants using a sterile curette. Nasopharyngeal and oropharyngeal swabs were taken from all the subjects. Reverse transcriptase real-time qualitative polymerase chain reaction (RT-PCR) was used to determine the presence of SARS-CoV-2 RNA using BAG SARS-CoV-2 RT-PCR kit targeting E gene, RdRp gene, and internal control. Results Ten participants (seven females and three males) with a previous history of COVID-19 infection were included in the study. Six participants previously presented with mild COVID-19 infection (uncomplicated upper respiratory tract infection, mild fever, cough, sore throat, nasal congestion, malaise, headache, without evidence of breathlessness or hypoxia), and four participants previously presented with moderate COVID-19 infection (dyspnea and or hypoxia, fever, cough, SpO2 90%–94% on room air, respiratory rate more or equal to 24 per minute) according to clinical management protocol for COVID-19, Government of India. The nasopharyngeal, oropharyngeal, and subgingival plaque samples tested negative for SARS-CoV-2 RNA. Conclusion The absence of the SARS-CoV-2 virus in the subgingival plaque sample of patients recovered from COVID-19 infection suggests that dental plaque could not be a potential reservoir of the virus. However, clinicians should take at most precautions while treating the patients recovered from COVID-19 infection and should anticipate a change in subgingival environment leading to alteration in periodontal disease progression.

Role of Glutathione in Neutrophil Chemotaxis in Periodontitis

Periodontitis is a common non-communicable inflammatory disease that leads to the destruction of periodontal tissues and tooth loss. Initiated by the plaque biofilm, there is a strong innate immune response with an abundance of neutrophils in the periodontium of affected individuals. Previous reports have shown that the intracellular concentration of glutathione in peripheral blood neutrophils from periodontitis patients and the chemotactic ability of these cells are compromised. Furthermore, other studies have described that in oxidative stress conditions neutrophil chemotaxis is aberrant and causes the glutathionylation of F-actin, a key player in chemotaxis. In this study, the effects of glutathione-modulating compounds were assessed in neutrophils isolated from healthy donors, showing that the perturbation of glutathione homeostasis decreases the chemotaxis of neutrophils. Following this, the intracellular glutathione status and chemotactic ability of neutrophils isolated from periodontitis patients was compared to that of age- and sex-matched controls. A decrease in glutathione and chemotactic ability were confirmed. Finally, the proteome of these neutrophils was explored, demonstrating a change in the abundance of proteins involved in glutathione homeostasis. Together these data suggest that peripheral blood neutrophils from periodontitis patients are compromised in their ability to cope with oxidative stress and move.

The Oral Microbiome across Oral Sites in Cats with Chronic Gingivostomatitis, Periodontal Disease, and Tooth Resorption Compared with Healthy Cats.

Feline chronic gingivostomatitis (FCGS) is a chronic mucosal and gingival inflammatory disease in which pathogenesis remains unclear. Interactions between the host inflammatory process, the host immune response, and the oral microbiome are implicated in this pathogenesis. To begin to understand this disease and the impact of the microbiome to host inflammatory disease states, we collected sterile noninvasive plaque biofilm samples from ten distinct sites within the oral cavity in cats with stomatitis (n = 12), healthy cats (n = 9), and cats with tooth resorption or periodontitis (n = 11). Analysis of full-length 16S rRNA gene sequences indicated that the microbiomes of cats with FCGS presented marked dysbiosis at multiple oral sites. Additionally, microbiome beta diversity varied with oral condition, indicating that stomatitis, periodontitis, and/or tooth resorption influence the microbiome differently. Lastly, we found that the microbiomes of swabs taken from the oral cavity were comparable to those taken from plaque using endodontic paper points, validating this as another sampling method. Collectively, our work furthers our understanding of the dysbiosis and composition of bacteria in the oral microbiome in FCGS, with hopes of contributing to the prevention, diagnosis, and treatment of this challenging condition in felines.