scholarly journals Porphyromonas gingivalisandTreponema denticolaMixed Microbial Infection in a Rat Model of Periodontal Disease

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Raj K. Verma ◽  
Sunethra Rajapakse ◽  
Archana Meka ◽  
Clayton Hamrick ◽  
Sheela Pola ◽  
...  
Keyword(s):  
Periodontal Disease ◽  
Rat Model ◽  
Alveolar Bone ◽  
Treponema Denticola ◽  
Periodontal Pathogens ◽  
Microbial Infection ◽  
Morphometric Measurements ◽  
Th2 Immune Response ◽  
Microbial Infections ◽  
Antibody Levels

Porphyromonas gingivalisandTreponema denticolaare periodontal pathogens that express virulence factors associated with the pathogenesis of periodontitis. In this paper we tested the hypothesis thatP. gingivalisandT. denticolaare synergistic in terms of virulence; using a model of mixed microbial infection in rats. Groups of rats were orally infected with eitherP. gingivalisorT. denticolaor mixed microbial infections for 7 and 12 weeks.P. gingivalisgenomic DNA was detected more frequently by PCR thanT. denticola. Both bacteria induced significantly high IgG, IgG2b, IgG1, IgG2a antibody levels indicating a stimulation of Th1 and Th2 immune response. Radiographic and morphometric measurements demonstrated that rats infected with the mixed infection exhibited significantly more alveolar bone loss than shaminfected control rats. Histology revealed apical migration of junctional epithelium, rete ridge elongation, and crestal alveolar bone resorption; resembling periodontal disease lesion. These results showed thatP. gingivalisandT. denticolaexhibit no synergistic virulence in a rat model of periodontal disease.

scholarly journals TheTreponema denticolaChymotrypsin-Like Protease Dentilisin Induces Matrix Metalloproteinase-2-Dependent Fibronectin Fragmentation in Periodontal Ligament Cells

2010 ◽  
Vol 79 (2) ◽  
pp. 806-811 ◽  
Author(s):  
Di Miao ◽  
J. Christopher Fenno ◽  
John C. Timm ◽  
Nam Eok Joo ◽  
Yvonne L. Kapila
Keyword(s):  
Periodontal Disease ◽  
Periodontal Ligament ◽  
Alveolar Bone ◽  
Inflammatory Responses ◽  
Tissue Homeostasis ◽  
Matrix Metalloproteinase 2 ◽  
Periodontal Ligament Cells ◽  
Treponema Denticola ◽  
Periodontal Pathogens ◽  
Culture Supernatants

ABSTRACTPeriodontal disease is a bacterially mediated chronic inflammatory disease that results in destruction of the periodontal ligament (PDL) and alveolar bone that surround and support the dentition. While their precise roles are not well understood, periodontal pathogens, includingTreponema denticola, are believed to initiate the destructive inflammatory responses and dysregulation of tissue homeostasis that characterize the disease. These responses are believed to result from both proinflammatory effects of acylated bacterial membrane components (lipopolysaccharides and lipoproteins) and degradative effects of secreted bacterial proteases. Host-derived matrix metalloproteinases (MMPs) are key enzymes both in tissue homeostasis and tissue destruction. MMP expression is modulated in part by specific proteolytic fragments of fibronectin (FN), which are associated with periodontal disease. FN is a predominant extracellular matrix component in the periodontium. We examined the ability ofTreponema denticolaand its acylated outer membrane PrtP protease complex to induce both activation of MMP-2 and generation of FN fragments in human PDL cell culture supernatants.T. denticolaparent and isogenic mutant strains, as well as MMP-2 small interfering RNA and specific inhibitors of MMP-2 and PrtP activity, were used to examine protein expression, gelatinolytic activity, and FN fragmentation in culture supernatants.T. denticolaand its purified protease induced both MMP-2 activation and FN fragmentation. Here, we demonstrate that PrtP proteolytic activity induces the activation of MMP-2 and that active MMP-2 is required for FN fragmentation. These results suggest a specific mechanism by which theT. denticolaprotease may disrupt homeostatic processes required for the maintenance of periodontal health.

Comparison of Sampling Techniques For qPCR Quantification of Periodontal Pathogens

2018 ◽  
Vol 68 (12) ◽  
pp. 2853-2856 ◽  
Author(s):  
Igor Jelihovschi ◽  
Cristian Drochioi ◽  
Aida Corina Badescu ◽  
Raoul Vasile Lupusoru ◽  
Alexandra Elena Munteanu ◽  
...  
Keyword(s):  
Periodontal Disease ◽  
Periodontal Diseases ◽  
Pcr Analysis ◽  
Treponema Denticola ◽  
Subgingival Plaque ◽  
Periodontal Pathogens ◽  
Radiographic Evidence ◽  
Gingival Bleeding ◽  
As Species ◽  
Qpcr Quantification

The diagnosis of periodontal disease is mainly based on use of clinical and radiographic evidence. In this study we employed a quantitative PCR analysis of Aggregatibacter actinomycetemcomitans and Treponema denticola as species strongly involved in periodontal diseases, burden in periodontal pockets to detect the main sampling factors that interfere with qPCR results. From 22 patients with advanced periodontal disease, subgingival plaque was comparatively collected by paper points and periodontal Gracey curettes. Samples were collected from the same situs in presence of gingival bleeding and absence of bleeding. The concordance and agreement of results between samples were assessed. The present study demonstrates that subgingival plaque sampling with sterile absorbable paper points is often accompanied by gingival bleeding resulting in quantification biases of periodontal pathogens.

scholarly journals Invasion of Oral and Aortic Tissues by Oral Spirochete Treponema denticola in ApoE−/−Mice Causally Links Periodontal Disease and Atherosclerosis

2014 ◽  
Vol 82 (5) ◽  
pp. 1959-1967 ◽  
Author(s):  
Sasanka S. Chukkapalli ◽  
Mercedes F. Rivera ◽  
Irina M. Velsko ◽  
Ju-Youn Lee ◽  
Hao Chen ◽  
...  
Keyword(s):  
Periodontal Disease ◽  
Alveolar Bone ◽  
Tissue Growth ◽  
Aortic Tissue ◽  
Treponema Denticola ◽  
Rapid Progression ◽  
Causative Role ◽  
Igg Antibody ◽  
Content Type ◽  
Periodontal Infection

ABSTRACTTreponema denticolais a predominantly subgingival oral spirochete closely associated with periodontal disease and has been detected in atherosclerosis. This study was designed to evaluate causative links between periodontal disease induced by chronic oralT. denticolainfection and atherosclerosis in hyperlipidemic ApoE−/−mice. ApoE−/−mice (n= 24) were orally infected withT. denticolaATCC 35404 and were euthanized after 12 and 24 weeks.T. denticolagenomic DNA was detected in oral plaque samples, indicating colonization of the oral cavity. Infection elicited significantly (P= 0.0172) higher IgG antibody levels and enhanced intrabony defects than sham infection.T. denticola-infected mice had higher levels of horizontal alveolar bone resorption than sham-infected mice and an associated significant increase in aortic plaque area (P≤ 0.05). Increased atherosclerotic plaque correlated with reduced serum nitric oxide (NO) levels and increased serum-oxidized low-density lipoprotein (LDL) levels compared to those of sham-infected mice.T. denticolainfection altered the expression of genes known to be involved in atherosclerotic development, including the leukocyte/endothelial cell adhesion gene (Thbs4), the connective tissue growth factor gene (Ctgf), and the selectin-E gene (Sele). Fluorescentin situhybridization (FISH) revealedT. denticolaclusters in both gingival and aortic tissue of infected mice. This is the first study examining the potential causative role of chronicT. denticolaperiodontal infection and vascular atherosclerosisin vivoin hyperlipidemic ApoE−/−mice.T. denticolais closely associated with periodontal disease and the rapid progression of atheroma in ApoE−/−mice. These studies confirm a causal link for active oralT. denticolainfection with both atheroma and periodontal disease.

scholarly journals Role of Porphyromonas gingivalis Phosphoserine Phosphatase Enzyme SerB in Inflammation, Immune Response, and Induction of Alveolar Bone Resorption in Rats

2010 ◽  
Vol 78 (11) ◽  
pp. 4560-4569 ◽  
Author(s):  
Brian Bainbridge ◽  
Raj K. Verma ◽  
Christie Eastman ◽  
Bilal Yehia ◽  
Mercedes Rivera ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Epithelial Cells ◽  
Periodontal Disease ◽  
Porphyromonas Gingivalis ◽  
Rat Model ◽  
Alveolar Bone ◽  
Critical Role ◽  
Polymorphonuclear Neutrophil ◽  
Gingival Epithelial Cells ◽  
Phosphatase Enzyme

ABSTRACT Porphyromonas gingivalis secretes a serine phosphatase enzyme, SerB, upon contact with gingival epithelial cells in vitro. The SerB protein plays a critical role in internalization and survival of the organism in epithelial cells. SerB is also responsible for the inhibition of interleukin-8 (IL-8) secretion from gingival epithelial cells infected with P. gingivalis. This study examined the ability of a P. gingivalis SerB mutant to colonize the oral cavity and induce gingival inflammation, immune responses, and alveolar bone resorption in a rat model of periodontal disease. Both P. gingivalis ATCC 33277 and an isogenic ΔSerB mutant colonized the oral cavities of rats during the 12-week experimental period. Both of the strains induced significant (P < 0.05) systemic levels of immunoglobulin G (IgG) and isotypes IgG1, IgG2a, and IgG2b, indicating the involvement of both T helper type 1 (Th1) and Th2 responses to infection. Both strains induced significantly (P < 0.05) higher levels of alveolar bone resorption in infected rats than in sham-infected control rats. However, horizontal and interproximal alveolar bone resorption induced by the SerB mutant was significantly (P < 0.05) lower than that induced by the parental strain. Rats infected with the ΔSerB mutant exhibited significantly higher levels of apical migration of the junctional epithelium (P < 0.01) and polymorphonuclear neutrophil (PMN) recruitment (P < 0.001) into the gingival tissues than rats infected with the wild type. In conclusion, in a rat model of periodontal disease, the SerB phosphatase of P. gingivalis is required for maximal alveolar bone resorption, and in the absence of SerB, more PMNs are recruited into the gingival tissues.

scholarly journals Systemic Antibiotics Influence Periodontal Parameters and Oral Microbiota, But Not Serological Markers

2021 ◽  
Vol 11 ◽  
Author(s):  
Elisa Kopra ◽  
Laura Lahdentausta ◽  
Milla Pietiäinen ◽  
Kåre Buhlin ◽  
Päivi Mäntylä ◽  
...  
Keyword(s):  
Alveolar Bone ◽  
Serum Antibody ◽  
Oral Microbiota ◽  
Microbiota Composition ◽  
Periodontal Pathogens ◽  
Linear Regression Models ◽  
Periodontal Inflammation ◽  
The Mean ◽  
Antibody Levels ◽  
Systemic Antibiotics

The use of systemic antibiotics may influence the oral microbiota composition. Our aim was to investigate in this retrospective study whether the use of prescribed antibiotics associate with periodontal status, oral microbiota, and antibodies against the periodontal pathogens. The Social Insurance Institution of Finland Data provided the data on the use of systemic antibiotics by record linkage to purchased medications and entitled reimbursements up to 1 year before the oral examination and sampling. Six different classes of antibiotics were considered. The Parogene cohort included 505 subjects undergoing coronary angiography with the mean (SD) age of 63.4 (9.2) years and 65% of males. Subgingival plaque samples were analysed using the checkerboard DNA-DNA hybridisation. Serum and saliva antibody levels to periodontal pathogens were analysed with immunoassays and lipopolysaccharide (LPS) activity with the LAL assay. Systemic antibiotics were prescribed for 261 (51.7%) patients during the preceding year. The mean number of prescriptions among them was 2.13 (range 1–12), and 29.4% of the prescriptions were cephalosporins, 25.7% penicillins, 14.3% quinolones, 12.7% macrolides or lincomycin, 12.0% tetracycline, and 5.8% trimethoprim or sulphonamides. In linear regression models adjusted for age, sex, current smoking, and diabetes, number of antibiotic courses associated significantly with low periodontal inflammation burden index (PIBI, p &lt; 0.001), bleeding on probing (BOP, p = 0.006), and alveolar bone loss (ABL, p = 0.042). Cephalosporins associated with all the parameters. The phyla mainly affected by the antibiotics were Bacteroidetes and Spirochaetes. Their levels were inversely associated with the number of prescriptions (p = 0.010 and p &lt; 0.001) and directly associated with the time since the last prescription (p = 0.019 and p &lt; 0.001). Significant inverse associations were observed between the number of prescriptions and saliva concentrations of Prevotella intermedia, Tannerella forsythia, and Treponema denticola and subgingival bacterial amounts of Porphyromonas gingivalis, P. intermedia, T. forsythia, and T. denticola. Saliva or serum antibody levels did not present an association with the use of antibiotics. Both serum (p = 0.031) and saliva (p = 0.032) LPS activity was lower in patients having any antibiotic course less than 1 month before sampling. Systemic antibiotics have effects on periodontal inflammation and oral microbiota composition, whereas the effects on host immune responses against the periodontal biomarker species seem unchanged.

scholarly journals Distinct Microbial Signatures between Periodontal Profile Classes

2021 ◽  
pp. 002203452110097
Author(s):  
J.T. Marchesan ◽  
K. Moss ◽  
T. Morelli ◽  
F.R. Teles ◽  
K. Divaris ◽  
...  
Keyword(s):  
African Americans ◽  
Periodontal Disease ◽  
Latent Class ◽  
Linear Models ◽  
Severe Disease ◽  
Periodontal Pathogens ◽  
Healthy Individuals ◽  
Igg Antibody ◽  
Serum Igg ◽  
Antibody Levels

Precise classification of periodontal disease has been the objective of concerted efforts and has led to the introduction of new consensus-based and data-driven classifications. The purpose of this study was to characterize the microbiological signatures of a latent class analysis (LCA)–derived periodontal stratification system, the Periodontal Profile Class (PPC) taxonomy. We used demographic, microbial (subgingival biofilm composition), and immunological data (serum IgG antibody levels, obtained with checkerboard immunoblotting technique) for 1,450 adult participants of the Dental Atherosclerosis Risk in Communities (ARIC) study, with already generated PPC classifications. Analyses relied on t tests and generalized linear models with Bonferroni correction. Men and African Americans had higher systemic antibody levels against most microorganisms compared to women and Caucasians ( P < 0.05). Healthy individuals (PPC-I) had low levels of biofilm bacteria and serum IgG levels against most periodontal pathogens ( P < 0.05). Subjects with mild to moderate disease (PPC-II to PPC-III) showed mild/moderate colonization of multiple biofilm pathogens. Individuals with severe disease (PPC-IV) had moderate/high levels of biofilm pathogens and antibody levels for orange/red complexes. High gingival index individuals (PPC-V) showed moderate/high levels of biofilm Campylobacter rectus and Aggregatibacter actinomycetemcomitans. Biofilm composition in individuals with reduced periodontium (PPC-VI) was similar to health but showed moderate to high antibody responses. Those with severe tooth loss (PPC-VII) had significantly high levels of multiple biofilm pathogens, while the systemic antibody response to these microorganisms was comparable to health. The results support a biologic basis for elevated risk for periodontal disease in men and African Americans. Periodontally healthy individuals showed a low biofilm pathogen and low systemic antibody burden. In the presence of PPC disease, a microbial-host imbalance characterized by higher microbial biofilm colonization and/or systemic IgG responses was identified. These results support the notion that subgroups identified by the PPC system present distinct microbial profiles and may be useful in designing future precise biological treatment interventions.

scholarly journals Relationship between periodontal disease (PD) and Cardiovascular Disease (CVD): a review of topic

2017 ◽  
Vol 20 (2) ◽  
pp. 45-52
Author(s):  
Cristian Herrera ◽  
Jonathan Arcos
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Periodontal Disease ◽  
Cerebrovascular Diseases ◽  
Periodontal Treatment ◽  
Periodontal Pathogens ◽  
Microbial Infection ◽  
Missing Teeth ◽  
Clinical Attachment Level ◽  
Attachment Level

Several clinical studies had investigated the possible relationship between periodontal disease (PD) and cardiovascular disease (CVD). Some studies prove an epidemiological association between PD and CVD, that from the biological viewpoint may be linked to both chronic inflammation triggered by microbes and persistent microbial infection by periodontal pathogens. In that sense, individuals presenting deep periodontal pockets without periodontal treatment, increased number of missing teeth and other periodontal markers like clinical attachment level and bleeding on probing, seem to be important risk factors markers for cardiovascular disease. Both, EP and cerebrovascular diseases are frequent, and those association is important in Public Health setting. EP and CVD share risk factors such as age, tobacco, stress, socioeconomic status and fat metabolism, so that the chances of introducing confusion into the studies is high. Few population studies have examined the effect of periodontal treatment on the risk of developing cardiovascular events (either primary or secondary prevention), however, it must be noted that the evidence in human studies suggest a possible beneficial effect of periodontal treatment of cardiovascular function index. In this paper, we review the literature that enables the general dentist and specialist an approach to this problem and better understanding of this phenomenon to patient benefit.

scholarly journals Detection of oral spirochete (Treponema denticola) by modified Fontana staining technique from sub-gingival plaques of patients suffering from periodontal disease and to analyse the morphology of spirochetes with respect to the disease’s status

2020 ◽  
Vol 6 (8) ◽  
pp. 286
Author(s):  
Sunil Paudel ◽  
Jyoti M. Nagamoti ◽  
Ved Prakash Mishra ◽  
Suraj Twanabasu ◽  
Susan Kusma
Keyword(s):  
Periodontal Disease ◽  
Screening Method ◽  
Staining Technique ◽  
Laboratory Diagnosis ◽  
Global Scale ◽  
Personal Hygiene ◽  
Treponema Denticola ◽  
Periodontal Pathogens ◽  
Periodontal Tissues ◽  
Periodontal Infection

<p class="abstract"><strong>Background:</strong> Infections pertaining to mankind particularly those affecting the periodontal tissues are of serious concerns worldwide and are increasing on a global scale particularly in the tropical and subtropical countries like India. The clinical presentation, though very typical of periodontal infection, is often confused with other oral infection, making laboratory diagnosis and confirmation necessary. The management of periodontal infections needs personal hygiene, awareness of infection, proper diagnosis and medication. The present study was undertaken to demonstrate the oral spirochete (<em>Treponema denticola</em>) from periodontal pathogens suffering from periodontal disease.</p><p class="abstract"><strong>Methods:</strong> A total of 55 clinically diagnosed selected patients of periodontal infection attending the outpatient Department of Periodontics, V. K. Institute of Dental Science, KLE University, Belgaum were studied. Dental plaque was taken as specimens from the patients were processed by modified Fontana staining and observed in microscope.  </p><p class="abstract"><strong>Results:</strong> A total number of 55 plaque samples were stained by modified Fontana staining technique. 30 cases were positive and 25 cases were negative. Males were affected more as compared to the females and the age group ranging from 15 to 65. Farmers were more affected compared to other occupation.</p><p class="abstract"><strong>Conclusions:</strong> Microscopic method by modified silver nitrate staining can be a very useful screening method for evaluation of oral spirochetes in a clinical setting if used judiciously keeping in mind the variables that can affect the results.</p>

scholarly journals Treponema denticola dentilisin triggered TLR2/MyD88 activation upregulates a tissue destructive program involving MMPs via Sp1 in human oral cells

2021 ◽  
Vol 17 (7) ◽  
pp. e1009311
Author(s):  
Sean Ganther ◽  
Allan Radaic ◽  
Erin Malone ◽  
Pachiyappan Kamarajan ◽  
Nai-Yuan Nicholas Chang ◽  
...  
Keyword(s):  
Periodontal Disease ◽  
Alveolar Bone ◽  
Nuclear Translocation ◽  
Inflammatory Responses ◽  
Oral Microbiome ◽  
Oral Disease ◽  
Periodontal Ligament Cells ◽  
Treponema Denticola ◽  
Host Immune Responses

Periodontal disease is driven by dysbiosis in the oral microbiome, resulting in over-representation of species that induce the release of pro-inflammatory cytokines, chemokines, and tissue-remodeling matrix metalloproteinases (MMPs) in the periodontium. These chronic tissue-destructive inflammatory responses result in gradual loss of tooth-supporting alveolar bone. The oral spirochete Treponema denticola (T. denticola), is consistently found at significantly elevated levels in periodontal lesions. Host-expressed Toll-Like Receptor 2 (TLR2) senses a variety of bacterial ligands, including acylated lipopolysaccharides and lipoproteins. T. denticola dentilisin, a surface-expressed protease complex comprised of three lipoproteins has been implicated as a virulence factor in periodontal disease, primarily due to its proteolytic activity. While the role of acylated bacterial components in induction of inflammation is well-studied, little attention has been given to the potential role of the acylated nature of dentilisin. The purpose of this study was to test the hypothesis that T. denticola dentilisin activates a TLR2-dependent mechanism, leading to upregulation of tissue-destructive genes in periodontal tissue. RNA-sequencing of periodontal ligament cells challenged with T. denticola bacteria revealed significant upregulation of genes associated with extracellular matrix organization and degradation including potentially tissue-specific inducible MMPs that may play novel roles in modulating host immune responses that have yet to be characterized within the context of oral disease. The Gram-negative oral commensal, Veillonella parvula, failed to upregulate these same MMPs. Dentilisin-induced upregulation of MMPs was mediated via TLR2 and MyD88 activation, since knockdown of expression of either abrogated these effects. Challenge with purified dentilisin upregulated the same MMPs while a dentilisin-deficient T. denticola mutant had no effect. Finally, T. denticola-mediated activation of TLR2/MyD88 lead to the nuclear translocation of the transcription factor Sp1, which was shown to be a critical regulator of all T. denticola-dependent MMP expression. Taken together, these data suggest that T. denticola dentilisin stimulates tissue-destructive cellular processes in a TLR2/MyD88/Sp1-dependent fashion.

scholarly journals Approaches to Understanding Mechanisms of Dentilisin Protease Complex Expression in Treponema denticola

2021 ◽  
Vol 11 ◽  
Author(s):  
M. Paula Goetting-Minesky ◽  
Valentina Godovikova ◽  
J. Christopher Fenno
Keyword(s):  
Gene Expression ◽  
Periodontal Disease ◽  
Host Cell ◽  
Protease Activity ◽  
Alveolar Bone ◽  
Three Dimensional ◽  
Periodontal Pathogen ◽  
Dimensional Structure ◽  
Treponema Denticola ◽  
Protease Gene

The oral spirochete Treponema denticola is a keystone periodontal pathogen that, in association with members of a complex polymicrobial oral biofilm, contributes to tissue damage and alveolar bone loss in periodontal disease. Virulence-associated behaviors attributed to T. denticola include disruption of the host cell extracellular matrix, tissue penetration and disruption of host cell membranes accompanied by dysregulation of host immunoregulatory factors. T. denticola dentilisin is associated with several of these behaviors. Dentilisin is an outer membrane-associated complex of acylated subtilisin-family PrtP protease and two other lipoproteins, PrcB and PrcA, that are unique to oral spirochetes. Dentilisin is encoded in a single operon consisting of prcB-prcA-prtP. We employ multiple approaches to study mechanisms of dentilisin assembly and PrtP protease activity. To determine the role of each protein in the protease complex, we have made targeted mutations throughout the protease locus, including polar and nonpolar mutations in each gene (prcB, prcA, prtP) and deletions of specific PrtP domains, including single base mutagenesis of key PrtP residues. These will facilitate distinguishing between host cell responses to dentilisin protease activity and its acyl groups. The boundaries of the divergent promoter region and the relationship between dentilisin and the adjacent iron transport operon are being resolved by incremental deletions in the sequence immediately 5’ to the protease locus. Comparison of the predicted three-dimensional structure of PrtP to that of other subtilisin-like proteases shows a unique PrtP C-terminal domain of approximately 250 residues. A survey of global gene expression in the presence or absence of protease gene expression reveals potential links between dentilisin and iron uptake and homeostasis in T. denticola. Understanding the mechanisms of dentilisin transport, assembly and activity of this unique protease complex may lead to more effective prophylactic or therapeutic treatments for periodontal disease.

Sign in / Sign up

Export Citation Format

Share Document