ABSTRACT
It is urgently necessary to clarify the effect of extraction of impacted mandibular third molar (IMTM) on the periodontal tissue of adjacent second molars (ASMs). In this study, the ASM periodontal condition and pathogenic microbes were assessed before IMTM extraction and at 1, 4, 8 and 12 weeks postoperatively. Based on the inclusion and exclusion criteria, our study revealed that IMTM extractions adversely affected distal ï¼ periodontal probing depth (dPPD), attachment loss (dAL), plaque index (dPLI) and bleeding on probing (dBOP) within 8 weeks, but these indices gradually normalize after 12 weeks. The subgingival pathogens near the ASMs distal surface, Porphyromonas and Pseudomonas, were significantly increased postoperatively. Moreover, relevance of ASMs clinical indices and subgingival microbes after IMTM extractions was found. In contrast to the situation in chronic periodontitis, the effects of IMTM extraction on dPPD, dAL, dPLI and dBOP of ASMs were mainly correlated with Pseudomonas. Additionally, while the IMTM extractions have adverse distal periodontal indices of ASMs within 8 weeks and increase subgingival pathogens, the modified triangular flap (MTF) had fewer distal periodontal indices and less Pseudomonas. Compared to the traditional envelope flap and triangular flap, the MTF benefits the periodontal health, which could be considered as the priority option for IMTM extractions.
Subject(s)
Mandible , Microbiota , Molar, Third , Tooth Extraction , Tooth, Impacted , Humans , Molar, Third/surgery , Male , Tooth, Impacted/surgery , Adult , Female , Mandible/surgery , Mandible/microbiology , Periodontal Index , Periodontium/microbiology , Periodontium/surgery , Young Adult , Surgical FlapsABSTRACT
Periodontitis affects billions of people worldwide. To address relationships of periodontal niche cell types and microbes in periodontitis, we generated an integrated single-cell RNA sequencing (scRNAseq) atlas of human periodontium (34-sample, 105918-cell), including sulcular and junctional keratinocytes (SK/JKs). SK/JKs displayed altered differentiation states and were enriched for effector cytokines in periodontitis. Single-cell metagenomics revealed 37 bacterial species with cell-specific tropism. Fluorescence in situ hybridization detected intracellular 16 S and mRNA signals of multiple species and correlated with SK/JK proinflammatory phenotypes in situ. Cell-cell communication analysis predicted keratinocyte-specific innate and adaptive immune interactions. Highly multiplexed immunofluorescence (33-antibody) revealed peri-epithelial immune foci, with innate cells often spatially constrained around JKs. Spatial phenotyping revealed immunosuppressed JK-microniches and SK-localized tertiary lymphoid structures in periodontitis. Here, we demonstrate impacts on and predicted interactomics of SK and JK cells in health and periodontitis, which requires further investigation to support precision periodontal interventions in states of chronic inflammation.
Subject(s)
Cell Communication , Keratinocytes , Periodontitis , Single-Cell Analysis , Humans , Keratinocytes/metabolism , Keratinocytes/immunology , Periodontitis/microbiology , Periodontitis/metabolism , Periodontitis/immunology , Periodontitis/pathology , Cytokines/metabolism , Periodontium/microbiology , Periodontium/metabolism , Periodontium/pathology , Immunity, Innate , In Situ Hybridization, Fluorescence , Male , Metagenomics/methods , Bacteria/metabolism , Bacteria/genetics , Female , Adult , Adaptive ImmunityABSTRACT
OBJECTIVES: The use of probiotics could promote the balance of the subgingival microbiota to contribute to periodontal health. This study aimed to identify the potential of bacteria commonly associated with healthy periodontal tissues as probiotic candidates. MATERIAL AND METHODS: A systematic review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines using the PubMed, Scopus, Science Direct, ProQuest, and Ovid databases as well as the combination of Medical Subject Headings (MeSH) and non-MeSH terms. Based on the selection criteria, original studies published in English and identifying the microorganisms present in the periodontium of healthy individuals and patients with periodontitis using the high-throughput 16S ribosomal gene sequencing technique were included. RESULTS: Out of 659 articles, 12 met the criteria for this review. These articles were published from 2012 to 2020 and mainly originated from the United States, China, and Spain. Most of these studies reported adequate criteria for selecting participants, using standardized clinical criteria, and compliance with quality based on the tools used. In periodontal healthy tissue were identified species like Actinomyces viscosus, Actinomyces naeslundii, Haemophilus parainfluenzae, Rothia dentocariosa, Streptococcus sanguinis, Streptococcus mitis, Streptococcus oralis, Streptococcus gordonii, Streptococcus intermedius, and Prevotella nigrescens which have recognized strains with a capacity to inhibit periodontopathogens. CONCLUSIONS: S. sanguinis, S. oralis, S. mitis, and S. gordonii are among the bacterial species proposed as potential probiotics because some strains can inhibit periodontopathogens and have been reported as safe for humans.
Subject(s)
Periodontium , Probiotics , Humans , Probiotics/therapeutic use , Periodontium/microbiology , Periodontitis/microbiology , Bacteria/genetics , Bacteria/classification , Bacteria/isolation & purification , MicrobiotaABSTRACT
Periodontitis is a bacteria-induced inflammatory disease that damages the tissues supporting the teeth, gums, periodontal ligaments, and alveolar bone. Conventional treatments such as surgical procedures, anti-inflammatory drugs, and antibiotics, are somewhat effective; however, these may lead to discomfort and adverse events, thereby affecting patient outcomes. Therefore, this study aimed to find an effective method to prevent the onset of periodontal disease and explore the specific mechanisms of their action.The impact of thiostrepton on Porphyromonas gingivalis and periodontal ligament stem cells was evaluated in an inflammatory microenvironment. In vivo experiments were performed using a mouse periodontitis model to assess the effectiveness of locally applied thiostrepton combined with a silk fibroin hydrogel in impeding periodontitis progression. Thiostrepton exhibited significant antimicrobial effects against Porphyromonas gingivalis and anti-inflammatory properties by regulating the MAPK pathway through DUSP2. Locally applied thiostrepton effectively impeded the progression of periodontitis and reduced tissue damage. Thiostrepton treatment is a promising and tolerable preventive strategy for periodontitis, offering antimicrobial and anti-inflammatory benefits. These findings suggest the potential of thiostrepton as a valuable addition to periodontitis management, warranting further research and clinical exploration to improve patient outcomes.
Subject(s)
Anti-Bacterial Agents , Anti-Inflammatory Agents , Periodontitis , Porphyromonas gingivalis , Animals , Porphyromonas gingivalis/drug effects , Periodontitis/drug therapy , Mice , Anti-Bacterial Agents/pharmacology , Anti-Bacterial Agents/therapeutic use , Anti-Inflammatory Agents/pharmacology , Anti-Inflammatory Agents/therapeutic use , Humans , MAP Kinase Signaling System/drug effects , Periodontal Ligament/drug effects , Periodontal Ligament/pathology , Disease Models, Animal , Mice, Inbred C57BL , Stem Cells/drug effects , Male , Periodontium/drug effects , Periodontium/microbiology , Periodontium/pathologyABSTRACT
The concept of homeostatic medicine has helped the researchers to understand the periodontal tissues in a completely new dimension. Periodontal tissues are subjected to complex external environmental stimuli and the internal tissues are continuously undergoing active remodeling. Periodontal regional immunity is continuously activated by local stimuli and interacts with the epithelial barrier, stromal tissue/extracellular matrix, and bone-coupled systems in a complex manner. Together, this complex network shapes the periodontal homeostasis. Under physiological conditions, moderate regional immunity relies on barrier function, intrinsic immune cells to control periodontal microbiota and maintain homeostasis. Under pathological conditions, pathogenic microbiota drive the periodontal homeostasis imbalance through over-activated regional immunity such as neutrophils, helper T (Th) 17 cells and B cells, causing periodontitis. Using the most basic immunological classification as a framework, this paper provides a systematic overview of the above mechanisms by which regional immunity regulates periodontal homeostasis, reviews the translational studies that have been carried out on homeostatic remodeling strategies targeting regional immunity, and proposes a series of periodontal homeostasis medicine research directions worth exploring, as well as potential new targets and strategies for homeostatic remodeling.
Subject(s)
Homeostasis , Periodontitis , Periodontium , Humans , Periodontitis/immunology , Periodontitis/microbiology , Periodontium/immunology , Periodontium/microbiology , B-Lymphocytes/immunology , Neutrophils/immunology , Microbiota , Th17 Cells/immunologyABSTRACT
Background: Research has suggested 2 potential mechanisms by which the periodontal inflammatory response may communicate to distant organs: 1) direct translocation of periodontal bacteria from the oral cavity to another organ system; and 2) inflammation as a result of metastatic periodontal inflammation. The purpose of this scoping review is to explore these mechanisms as potential mediators between periodontitis and Alzheimer's disease. Methods: A reiterative literature search of peer-reviewed articles was performed in the PubMed and Scopus databases using keywords or combinations such as Alzheimer's disease AND periodontitis OR periodontal disease AND inflammation. Results: A total of 777 articles were identified. After eliminating duplicates and reviewing titles and abstracts, 84 articles were selected for full-text review. Following full-text review, 19 articles met the eligibility criteria for the study. Discussion: The review of the literature highlights how periodontitis may contribute to neuroinflammation by the introduction of periodontal bacteria and/or proinflammatory cytokines locally produced at the periodontium. Conclusion: Inflammation is an important mechanism in the onset and progression of both periodontitis and Alzheimer's disease. Nevertheless, further studies are necessary to better understand the multifactorial pathogenesis of Alzheimer's disease.
Contexte: La recherche a suggéré 2 possibilités de mécanismes par lesquels la réponse inflammatoire parodontale peut communiquer avec des organes distants : 1) la translocation directe des bactéries parodontales de la cavité buccale vers un autre système organique; et 2) l'inflammation découlant d'une inflammation parodontale métastatique. Le but de cet examen de la portée est d'explorer ces mécanismes en tant que médiateurs potentiels entre la parodontite et la maladie d'Alzheimer. Méthodologie: Une recherche documentaire réitérative d'articles évalués par des pairs a été effectuée dans les bases de données PubMed et Scopus en utilisant les mots-clés ou des combinaisons de mots-clés tels que maladie d'Alzheimer ET parodontite OU maladie parodontale ET inflammation (en anglais). Résultats: Un total de 777 articles a été répertorié. Après avoir éliminé les doublons et examiné les titres et les résumés, 84 articles ont été sélectionnés pour être examinés dans leur intégralité. À la suite de l'examen du texte complet, 19 articles répondaient aux critères d'admissibilité de l'étude. Discussion: L'analyse documentaire souligne comment la parodontite peut contribuer à la neuroinflammation en introduisant des bactéries parodontales ou des cytokines pro-inflammatoires produites localement au niveau du parodonte. Conclusion: L'inflammation est un mécanisme important dans l'apparition et la progression à la fois de la parodontite et de la maladie d'Alzheimer. Néanmoins, d'autres études sont nécessaires pour mieux comprendre la pathogenèse multifactorielle de la maladie d'Alzheimer.
Subject(s)
Alzheimer Disease , Periodontitis , Humans , Porphyromonas gingivalis , Alzheimer Disease/etiology , Periodontitis/complications , Periodontium/microbiology , InflammationABSTRACT
INTRODUCTION: Markers of poor oral health are associated with impaired cognition and higher risk of Alzheimer disease (AD) and thus may help predict AD. OBJECTIVES: The aim of this study was to evaluate the cross-sectional association between empirically derived groups of 19 IgG antibodies against periodontal microorganisms and cognition in middle-aged and older adults. METHODS: The study population consisted of participants of the third National Health and Nutrition Examination Survey (NHANES III) (1988 to 1994), who were 60 y and older, among whom cognition and IgG antibodies against 19 periodontal microorganisms were measured (N = 5,162). RESULTS: In multivariable quantile regression analyses, the Orange-Red (Prevotella melaninogenica, Prevotella intermedia, Prevotella nigrescens, Porphyromonas gingivalis) and Yellow-Orange (Staphylococcus intermedius, Streptococcus oralis, Streptococcus mutans, Fusobacterium nucleatum, Peptostreptococcus micros, Capnocytophaga ochracea) cluster scores were negatively associated with cognition. A 1-unit higher cluster score for the Orange-Red cluster was associated on average with a lower cognitive score (ß for 30th quantile = -0.2640; 95% confidence interval [CI], -0.3431 to -0.1848). Similarly, a 1-unit higher score for the Yellow-Orange cluster was associated with a lower cognitive score (ß for 30th quantile = -0.2445; 95% CI, -0.3517 to -0.1372). CONCLUSION: Groups of IgG antibodies against periodontal microorganisms were associated with lower cognition among free living adults 60 years and older, who were previously undiagnosed with cognitive impairment. Though poor oral health precedes the development of dementia and AD, oral health information is currently not used, to our knowledge, to predict dementia or AD risk. Combining our findings with current algorithms may improve risk prediction for dementia and AD. KNOWLEDGE TRANSLATION STATEMENT: IgG antibodies against periodontal microorganisms were associated with lower cognition among adults 60 years and older previously undiagnosed with cognitive impairment. Periodontal disease may predict cognition among older adults.
Subject(s)
Cognition , Immunoglobulin G , Periodontium , Cross-Sectional Studies , Dementia , Periodontitis , Periodontium/microbiology , Oral Health , Humans , Male , Female , Middle Aged , Aged , Aged, 80 and overABSTRACT
The skin, oral cavity, digestive and reproductive tracts of the human body harbor symbiotic and commensal microorganisms living harmoniously with the host. The oral cavity houses one of the most heterogeneous microbial communities found in the human organism, ranking second in terms of species diversity and complexity only to the gastrointestinal microbiota and including bacteria, archaea, fungi, and viruses. The accumulation of microbial plaque in the oral cavity may lead, in susceptible individuals, to a complex host-mediated inflammatory and immune response representing the primary etiological factor of periodontal damage that occurs in periodontitis. Periodontal disease is a chronic inflammatory condition affecting about 20-50% of people worldwide and manifesting clinically through the detection of gingival inflammation, clinical attachment loss (CAL), radiographic assessed resorption of alveolar bone, periodontal pockets, gingival bleeding upon probing, teeth mobility and their potential loss in advanced stages. This review will evaluate the changes characterizing the oral microbiota in healthy periodontal tissues and those affected by periodontal disease through the evidence present in the literature. An important focus will be placed on the immediate and future impact of these changes on the modulation of the dysbiotic oral microbiome and clinical management of periodontal disease.
Subject(s)
Microbiota , Periodontal Diseases , Periodontitis , Dysbiosis/microbiology , Humans , Periodontal Diseases/complications , Periodontitis/etiology , Periodontitis/therapy , Periodontium/microbiologyABSTRACT
BACKGROUND: This paper aims to investigate the correlation between high mobility group protein-1 (HMG-b1), antioxidant enzyme-1 (paraoxon-1, PON-1), monocyte chemoattractant protein-1 (monocyte chemoattractant protein-1, MCP-1), P. gingivalis, and MSAF. MATERIALS AND METHODS: The total sample size comprised of 73 cases in both groups. These patients were further subdivided into 2 groups: the MSAF group and the control group. 38 women were in the MSAF group and 35 women with term amniotic fluid serum were in the control group. The MSAF group was selected as a full-term singleton amniotic fluid fecal infection group. Clinical data were collected, and specimens were collected. Fecal staining of amniotic fluid and full-term amniotic fluid removes the placenta and umbilical cord blood. The expression of HMGB1 in the placenta was observed by immune-histochemical staining of MSAF and control groups. The content of PON-1 in cord blood was determined by ELISA. RESULTS: Correlation between maternal and neonatal clinical data and MSAF was done; MSAF group mean gestational age was 41.38 ± 1.40 weeks; control group mean gestational age was 39.20 ± 1.24 weeks. This study found no correlation between the birth weight, maternal age, sex, first/transmaternal, hyperthyroidism, hypothyroidism, and anemia between the MSAF and control group with nonsignificant P value (P > 0.05). However, the fatal age, gestational diabetes, gestational hypertension, umbilical cord abnormalities, placental abnormalities, and neonatal asphyxia factors were statistically different with a significant P value of <0.05 between both groups. HMGB1 and Periodontal P. gingivalis are mostly expressed in placental trophoblast, vascular endothelial cells, and amniotic epithelial and interstitial cells. After HE staining of 72 placentas by HE in MSAF and control, 6 had acute chorioamnionitis (5.1 control), 32 had chronic (23.9), 35 had abnormal placentas, and three in MSAF had chorionic columnar metaplasia. In immune-histochemistry experiments, the HMGB1 expression intensity of placental tissue was higher in the MSAF group (P < 0.05); however, the level of PON-1 was lower in the MSAF group as compared to the controls (P < 0.05). CONCLUSIONS: Gestational age and placental abnormalities are clinical high-risk factors for MSAF. HMGB1, PON-1, MCP-1, and Periodontal P. gingivalis may be involved in the development of MSAF, suggesting an oxidative/antioxidant imbalance with inflammation, and may be one of the mechanisms for MSAF development.
Subject(s)
Amniotic Fluid , Aryldialkylphosphatase , Chemokine CCL2 , HMGB1 Protein , Porphyromonas gingivalis , Amniotic Fluid/chemistry , Antioxidants , Aryldialkylphosphatase/chemistry , Bacteroidaceae Infections , Chemokine CCL2/chemistry , Endothelial Cells , Female , HMGB1 Protein/chemistry , Humans , Infant , Infant, Newborn , Male , Meconium , Periodontium/microbiology , Placenta , PregnancyABSTRACT
Electronic cigarettes (e-cigs) have become prevalent as an alternative to conventional cigarette smoking, particularly in youth. E-cig aerosols contain unique chemicals which alter the oral microbiome and promote dysbiosis in ways we are just beginning to investigate. We conducted a 6-month longitudinal study involving 84 subjects who were either e-cig users, conventional smokers, or nonsmokers. Periodontal condition, cytokine levels, and subgingival microbial community composition were assessed, with periodontal, clinical, and cytokine measures reflecting cohort habit and positively correlating with pathogenic taxa (e.g., Treponema, Saccharibacteria, and Porphyromonas). α-Diversity increased similarly across cohorts longitudinally, yet each cohort maintained a unique microbiome. The e-cig microbiome shared many characteristics with the microbiome of conventional smokers and some with nonsmokers, yet it maintained a unique subgingival microbial community enriched in Fusobacterium and Bacteroidales (G-2). Our data suggest that e-cig use promotes a unique periodontal microbiome, existing as a stable heterogeneous state between those of conventional smokers and nonsmokers and presenting unique oral health challenges. IMPORTANCE Electronic cigarette (e-cig) use is gaining in popularity and is often perceived as a healthier alternative to conventional smoking. Yet there is little evidence of the effects of long-term use of e-cigs on oral health. Conventional cigarette smoking is a prominent risk factor for the development of periodontitis, an oral disease affecting nearly half of adults over 30 years of age in the United States. Periodontitis is initiated through a disturbance in the microbial biofilm communities inhabiting the unique space between teeth and gingival tissues. This disturbance instigates host inflammatory and immune responses and, if left untreated, leads to tooth and bone loss and systemic diseases. We found that the e-cig user's periodontal microbiome is unique, eliciting unique host responses. Yet some similarities to the microbiomes of both conventional smokers and nonsmokers exist, with strikingly more in common with that of cigarette smokers, suggesting that there is a unique periodontal risk associated with e-cig use.
Subject(s)
Electronic Nicotine Delivery Systems , Microbiota , Periodontium , Vaping , Adult , Cytokines , Humans , Longitudinal Studies , Periodontitis , Periodontium/microbiologyABSTRACT
In periodontal health, oral streptococci constitute up to 80% of the plaque biofilm. Yet, destructive inflammatory events of the periodontium are rare. This observation suggests that oral streptococci may possess mechanisms to co-exist with the host. However, the mechanisms employed by oral streptococci to modulate the innate immune response have not been well studied. One of the key virulence factors produced by oral streptococci is hydrogen peroxide (H2O2). In mammalian cells, H2O2 triggers the activation of nuclear factor erythroid 2-related factor 2 (Nrf2), a key pathway mediating antioxidant defence. This study aimed to determine (1) if H2O2 producing oral streptococci activated the Nrf2 pathway in macrophages, and (2) if the activation of Nrf2 influenced the innate immune response. We found that oral streptococci downregulated the innate immune response in a H2O2 dependent manner through the activation of the Nrf2. The activation of the Nrf2 signalling pathway led to the inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NFĸB), the key transcription factor regulating pro-inflammatory response. This study showed for the first time that oral streptococci are unlikely passive bystanders but could play an active role in the maintenance of periodontal health by preventing overt inflammation.
Subject(s)
Hydrogen Peroxide/metabolism , Immunity, Innate , Mouth Mucosa/microbiology , Periodontium/microbiology , Streptococcus/metabolism , Streptococcus/physiology , Animals , Humans , Inflammation/prevention & control , Macrophages/immunology , Macrophages/metabolism , Mice , NF-E2-Related Factor 2/metabolism , NF-kappa B/metabolism , RAW 264.7 Cells , Signal TransductionABSTRACT
Periodontitis is a chronic inflammatory immune disease associated with a dysbiotic state, influenced by keystone bacterial species responsible for disrupting the periodontal tissue homeostasis. Furthermore, the severity of periodontitis is determined by the interaction between the immune cell response in front of periodontitis-associated species, which leads to the destruction of supporting periodontal tissues and tooth loss in a susceptible host. The persistent bacterial challenge induces modifications in the permeability and ulceration of the sulcular epithelium, which facilitates the systemic translocation of periodontitis-associated bacteria into distant tissues and organs. This stimulates the secretion of pro-inflammatory molecules and a chronic activation of immune cells, contributing to a systemic pro-inflammatory status that has been linked with a higher risk of several systemic diseases, such as type 2 diabetes mellitus (T2DM) and gestational diabetes mellitus (GDM). Although periodontitis and GDM share the common feature of systemic inflammation, the molecular mechanistic link of this association has not been completely clarified. This review aims to examine the potential biological mechanisms involved in the association between periodontitis and GDM, highlighting the contribution of both diseases to systemic inflammation and the role of new molecular participants, such as extracellular vesicles and non-coding RNAs, which could act as novel molecular intercellular linkers between periodontal and placental tissues.
Subject(s)
Diabetes, Gestational , Periodontitis , Periodontium , Diabetes Mellitus, Type 2/metabolism , Diabetes Mellitus, Type 2/microbiology , Diabetes, Gestational/metabolism , Diabetes, Gestational/microbiology , Female , Humans , Periodontitis/etiology , Periodontitis/metabolism , Periodontitis/microbiology , Periodontium/metabolism , Periodontium/microbiology , PregnancyABSTRACT
Dental biofilm is a complex microbial community influenced by many exogenous and endogenous factors. Despite long-term studies, its bacterial composition is still not clearly understood. While most of the research on dental biofilms was conducted in humans, much less information is available from companion animals. In this study, we analyzed the composition of canine dental biofilms using both standard cultivation on solid media and amplicon sequencing, and compared the two approaches. The 16S rRNA gene sequences were used to define the bacterial community of canine dental biofilm with both, culture-dependent and culture-independent methods. After DNA extraction from each sample, the V3-V4 region of the 16S rRNA gene was amplified and sequenced via Illumina MiSeq platform. Isolated bacteria were identified using universal primers and Sanger sequencing. Representatives of 18 bacterial genera belonging to 5 phyla were isolated from solid media. Amplicon sequencing largely expanded this information identifying in total 284 operational taxonomic units belonging to 10 bacterial phyla. Amplicon sequencing revealed much higher diversity of bacteria in the canine dental biofilms, when compared to standard cultivation approach. In contrast, cultured representatives of several bacterial families were not identified by amplicon sequencing.
Subject(s)
Biofilms , Microbiota , Tooth/microbiology , Animals , Bacteria/classification , Bacteria/genetics , Dogs , Metagenome , Metagenomics/methods , Periodontium/microbiology , Phylogeny , RNA, Ribosomal, 16S/geneticsABSTRACT
Systemic inflammation induced by periodontitis is suggested to be the link between periodontitis and cardiovascular disease. The aim of this work was to explore the oral microbiome in periodontitis in relation to disease severity and systemic inflammation. The saliva and subgingival microbiome from periodontal pocket samples of patients with severe (n = 12) and mild periodontitis (n = 13) were analyzed using metagenomic shotgun sequencing. The taxa and pathways abundances were quantified. The diversity was assessed and the abundances to phenotype associations were performed using ANCOM and linear regression. A panel of inflammatory markers was measured in blood and was associated with taxa abundance. The microbial diversity and species richness did not differ between severe and mild periodontitis in either saliva or periodontal pockets. However, there were significant differences in the microbial composition between severe and mild periodontitis in the subgingival microbiome (i.e., pocket samples) and, in a lower grade, in saliva, and this is positively associated with systemic inflammatory markers. The "red complex" and "cluster B" abundances in periodontal pockets were strongly associated with inflammatory markers interleukin-6 and the white blood cell count. Our data suggest that systemic inflammation in severe periodontitis may be driven by the oral microbiome and may support the indirect (inflammatory) mechanism for the association between periodontitis and cardiovascular disease.
Subject(s)
Metagenome , Microbiota/genetics , Periodontitis/microbiology , Periodontium/microbiology , Aged , Biomarkers/metabolism , Cardiovascular Diseases/etiology , Cardiovascular Diseases/immunology , Cardiovascular Diseases/microbiology , Cardiovascular Diseases/pathology , Female , Gene Expression , Genetic Variation , Humans , Inflammation , Interleukin 1 Receptor Antagonist Protein/genetics , Interleukin 1 Receptor Antagonist Protein/immunology , Interleukin-6/genetics , Interleukin-6/immunology , Leukocytes/immunology , Leukocytes/microbiology , Male , Middle Aged , Periodontitis/complications , Periodontitis/immunology , Periodontitis/pathology , Periodontium/immunology , Periodontium/pathology , Phenotype , Phylogeny , Severity of Illness IndexABSTRACT
The present in vivo study determined the microbiological counts of the gingival crevicular fluid (GCF) among patients with fixed dental prostheses fabricated using three different techniques. A total of 129 subjects were divided into three study groups: first, cobalt-chrome-based, metal-ceramic prostheses fabricated by the conventional method (MC, n = 35); the second group consisted of cobalt-chrome-based, metal-ceramic prostheses fabricated by the computer-aided design and computer-aided manufacturing (CAD/CAM) technique (CC-MC, n = 35); the third group comprised zirconia-based ceramic prostheses fabricated using the CAD/CAM technique (CC-Zr, n = 35). The control consisted of 24 patients using prostheses fabricated with either MC, CC-MC, or CC-Zr. The GCF was obtained from the subjects before treatment, and 6 and 12 months after the prosthetic treatment. Bacteriological and bacterioscopic analysis of the GCF was performed to analyze the patients' GCF. The data were analyzed using SPSS V20 (IBM Company, Chicago, IL, USA). The number of microorganisms of the gingival crevicular fluid in all groups at 12 months of prosthetic treatment reduced dramatically compared with the data obtained before prosthetic treatment. Inflammatory processes in the periodontium occurred slowly in the case of zirconium oxide-based ceramic constructions due to their biocompatibility with the mucous membranes and tissues of the oral cavity as well as a reduced risk of dental biofilm formation. This should be considered by dentists and prosthodontists when choosing restoration materials for subjects with periodontal pathology.
Subject(s)
Dental Prosthesis/microbiology , Gingival Crevicular Fluid/microbiology , Tooth/microbiology , Adolescent , Adult , Biofilms/drug effects , Ceramics/therapeutic use , Computer-Aided Design , Female , Humans , Male , Middle Aged , Periodontium/microbiology , Young Adult , Zirconium/therapeutic useABSTRACT
Periodontitis is a chronic infectious disease characterized by loss of periodontal attachment and resorption of alveolar bone. Dysregulated oral microbial community is the initial factor of periodontitis and causes excessive infiltration of immune cells in periodontal tissues. Macrophage, as an important part of the innate immune system, interacts continually with oral pathogens. Macrophages can recognize and phagocytize pathogens and apoptotic neutrophils and produce the specialized pro-resolving mediators (SPMs) playing an important role in maintaining the homeostasis of tissue microenvironment. However, macrophages may also induce abnormal immune responses with the overstimulation from pathogens, leading to the destruction of periodontal tissues and alveolar bone. Looking for targeted drugs that can regulate the activities of oral pathogens and the functions of macrophages provides a new idea for periodontitis treatment. This review summarizes the interaction between macrophages and periodontal pathogens in periodontitis, focusing on the pro-inflammation and anti-inflammation phenotypes of macrophages, and briefly concludes potential new methods of periodontitis therapy targeted at oral pathogens and macrophages.
Subject(s)
Macrophages/pathology , Periodontitis/microbiology , Periodontitis/pathology , Periodontium/microbiology , Periodontium/pathology , Animals , Humans , Inflammation/pathology , Models, Biological , Periodontitis/therapy , Toll-Like Receptors/metabolismABSTRACT
Two mixed-ligand complexes on the basis of L ligand [L = 3,6-bis(imidazol-1-yl)pyridazine] have been prepared under the solvothermal reaction conditions via the Zn(II) salts reacting with the ligands of L in the existence of two positional isomerous carboxylic acid ligands and their chemical formula respectively are [Zn5(L)(1,2-BDC)4(µ3-OH)2] n (1, 1,2-H2BDC = 1,2-benzenedicarboxylic acid ) and {[Zn4(L)2(1,3-HBDC) (1,3-BDC)(µ3-OH)4]·ClO4·3H2O} n (2, 1,3-H2BDC = 1,3-benzenedicarboxylic acid). The inhibitory influence of the two compounds against the inflammatory response in periodontium was evaluated by measuring the inflammatory cytokines releasing with ELISA detection kit. The results of ELISA assay indicated that compound 1 showed much stronger inhibitory influences than compound 2 against the inflammatory cytokines releasing. In addition to this, the suppression activity of the compounds against the survival gene of Porphyria gingivalis was detected via the real time Reverse Transcription-Polymerase Chain Reaction, and the results suggested that compound 1 could evidently suppresses the survival gene expression of Porphyria gingivalis, which is much better than the biological activity of compound 2. Above all, compound 1 was more outstanding than compound 2 on chronic periodontitis treatment by inhibiting the Porphyria gingivalis survival.
Subject(s)
Bacterial Physiological Phenomena/genetics , Chronic Periodontitis/drug therapy , Chronic Periodontitis/microbiology , Coordination Complexes/pharmacology , Coordination Complexes/therapeutic use , DNA-Directed RNA Polymerases/genetics , DNA-Directed RNA Polymerases/metabolism , Gene Expression/drug effects , Genes, Bacterial/genetics , Periodontium/metabolism , Periodontium/microbiology , Porphyrias/genetics , Zinc Compounds/pharmacology , Zinc Compounds/therapeutic use , Animals , Coordination Complexes/chemistry , Crystallization , Cytokines/metabolism , Disease Models, Animal , Dogs , Enzyme-Linked Immunosorbent Assay , Inflammation Mediators/metabolism , Molecular Conformation , Polymers , Zinc Compounds/chemistryABSTRACT
OBJECTIVES: The effect of antiretroviral therapy (ART) on the oral pathogenic microbes in human immunodeficiency virus-1 seropositive patients remains relatively unexplored. Thus, the present study assessed the effect of ART on the sub-gingival levels of 3 pathogenic microbes. MATERIALS AND METHODS: The study groups consisted of 60 human immunodeficiency virus-1 seropositive patients divided into 3 groups of 20 each. Group 1 had periodontitis and did not start with the ART. Group 2 had periodontitis and started with ART (Tenofovir Disoproxil Fumarate 300 mg + Lamivudine 300 mg + Efavirenz 600 mg) at least 6 months before the study. Group 3 with normal periodontium, and have not started ART. The sub-gingival loads of Cytomegalovirus, Epstein-Barr virus, and the Porphyromonas gingivalis levels were assessed, along with the CD4 counts. RESULTS: The cytomegalovirus load was highest in group 1, followed by groups 2, and 3 (p-value of 0.271). The Epstein-Barr load was highest for group 2, followed by group 3, and 1 (p-value of 0.022). The P.gingivalis load was highest in group 2, followed by groups 1 and 3, (p-value of 0.028). The Epstein-Barr and Cytomegalovirus counts were significantly higher (p-value < 0.02) when the CD4 counts were less than 500 cells/cu3. CONCLUSION: ART did not cause any significant reduction in the sub-gingival levels of any of the 3 examined microbes. Given the lack of any significant effect on the sub-gingival microbial loads by the ART, human immunodeficiency virus patients may require additional anti-microbial agents and regular mechanical plaque removal to maintain their periodontal status.
Subject(s)
Antiretroviral Therapy, Highly Active , Cytomegalovirus/growth & development , HIV Infections , HIV-1/growth & development , Herpesvirus 4, Human/growth & development , Periodontitis , Porphyromonas gingivalis/growth & development , Adult , Anti-HIV Agents/pharmacology , Anti-HIV Agents/therapeutic use , Bacteroidaceae Infections/complications , Bacteroidaceae Infections/microbiology , CD4 Lymphocyte Count , Cytomegalovirus Infections/complications , Cytomegalovirus Infections/virology , Epstein-Barr Virus Infections/complications , Epstein-Barr Virus Infections/virology , Female , HIV Infections/complications , HIV Infections/drug therapy , HIV Infections/virology , Humans , Male , Periodontitis/complications , Periodontitis/microbiology , Periodontitis/virology , Periodontium/drug effects , Periodontium/microbiology , Periodontium/pathology , Periodontium/virologyABSTRACT
The aim of the study was to clarify whether orthodontic forces and periodontitis interact with respect to the anti-apoptotic molecules superoxide dismutase 2 (SOD2) and baculoviral IAP repeat-containing protein 3 (BIRC3). SOD2, BIRC3, and the apoptotic markers caspases 3 (CASP3) and 9 (CASP9) were analyzed in gingiva from periodontally healthy and periodontitis subjects by real-time PCR and immunohistochemistry. SOD2 and BIRC3 were also studied in gingiva from rats with experimental periodontitis and/or orthodontic tooth movement. Additionally, SOD2 and BIRC3 levels were examined in human periodontal fibroblasts incubated with Fusobacterium nucleatum and/or subjected to mechanical forces. Gingiva from periodontitis patients showed significantly higher SOD2, BIRC3, CASP3, and CASP9 levels than periodontally healthy gingiva. SOD2 and BIRC3 expressions were also significantly increased in the gingiva from rats with experimental periodontitis, but the upregulation of both molecules was significantly diminished in the concomitant presence of orthodontic tooth movement. In vitro, SOD2 and BIRC3 levels were significantly increased by F. nucleatum, but this stimulatory effect was also significantly inhibited by mechanical forces. Our study suggests that SOD2 and BIRC3 are produced in periodontal infection as a protective mechanism against exaggerated apoptosis. In the concomitant presence of orthodontic forces, this protective anti-apoptotic mechanism may get lost.
Subject(s)
Baculoviral IAP Repeat-Containing 3 Protein/genetics , Gene Expression Regulation , Periodontal Ligament/metabolism , Periodontium/metabolism , Superoxide Dismutase/genetics , Animals , Apoptosis/genetics , Baculoviral IAP Repeat-Containing 3 Protein/metabolism , Caspase 3/genetics , Caspase 3/metabolism , Caspase 9/genetics , Caspase 9/metabolism , Cells, Cultured , Fibroblasts/cytology , Fibroblasts/metabolism , Fusobacterium nucleatum/physiology , Gingiva/cytology , Gingiva/metabolism , Host-Pathogen Interactions , Humans , Periodontal Ligament/cytology , Periodontal Ligament/microbiology , Periodontium/cytology , Periodontium/microbiology , Rats , Superoxide Dismutase/metabolismABSTRACT
Smoking is a risk factor for periodontal disease, and a cause of oral microbiome dysbiosis. While this has been evaluated for traditional cigarette smoking, there is limited research on the effect of other tobacco types on the oral microbiome. This study investigates subgingival microbiome composition in smokers of different tobacco types and their effect on periodontal health. Subgingival plaques were collected from 40 individuals, including smokers of either cigarettes, medwakh, or shisha, and non-smokers seeking dental treatment at the University Dental Hospital in Sharjah, United Arab Emirates. The entire (~ 1500 bp) 16S rRNA bacterial gene was fully amplified and sequenced using Oxford Nanopore technology. Subjects were compared for the relative abundance and diversity of subgingival microbiota, considering smoking and periodontal condition. The relative abundances of several pathogens were significantly higher among smokers, such as Prevotella denticola and Treponema sp. OMZ 838 in medwakh smokers, Streptococcus mutans and Veillonella dispar in cigarette smokers, Streptococcus sanguinis and Tannerella forsythia in shisha smokers. Subgingival microbiome of smokers was altered even in subjects with no or mild periodontitis, probably making them more prone to severe periodontal diseases. Microbiome profiling can be a useful tool for periodontal risk assessment. Further studies are recommended to investigate the impact of tobacco cessation on periodontal disease progression and oral microbiome.