Exploring the possible applications of catechin (gel) for oral care of the elderly and disabled individuals

SummaryThe oral cavity contains more than hundreds of microbial species. An increase in the number of these microorganisms like high pathogenic potential species, such as cariogenic and periodontopathic bacteria, and the change of microbial biota may result in, not only oral infection, but also systemic diseases, such as infective endocarditis and aspiration pneumonia. It is very important to control the growth of these microorganisms and its biota just after oral cleaning in order to suppress disease onset. In this regard, it is useful to use the anti-microbial component which acts against pathogenic microorganisms. Here, we highlight the importance of catechin, and feature its possible oral, especially periodontal applications. By combining catechin with gel (catechin gel), antimicrobial activity of catechin was prolonged in gel and catechin anti-oxidization property was observed. Catechin gel inhibited the growth of the Actinomyces, periodontopathic bacteria and Candida strains tested, but did not inhibit that of the oral streptococci that are important in the normal oral flora. In contrast, commercially available moisture gels containing antimicrobial components showed antimicrobial activity against all of the tested strains including the oral streptococci. This show that catechin has selective antimicrobial activity, attributable to hydrogen peroxide production. This paper reviews previous works using catechin and, likewise, catechin gel may be show its possible oral application for prevent dental caries and periodontal disease

Microbial interaction of periodontopathic bacteria and Epstein-Barr virus and their implication of periodontal diseases

AbstractEpstein-Barr virus (EBV) is a ubiquitous human gamma herpesvirus that infects more than 90% of the world's population. EBV infection causes several human diseases, including infectious mononucleosis, autoimmune disorders, and a number of malignancies. Interestingly, evidence accumulated over the past 10 years supports the role for EBV as a pathogenic agent of periodontal disease because bacterial activities alone do not explain several of its clinical characteristics. Despite this, it remains unclear how EBV is reactivated in the oral cavity and how activated EBV leads to the progression of periodontal diseases. We focused on the microbial interaction between bacteria and viruses in the etiology of infectious disease and found that the periodontal pathogen Porphyromonas gingivalis could induce EBV reactivation via chromatin modification. Our observations provide evidence for a possible microbial interaction between bacteria and EBV that may contribute to the pathogenesis of EBV-related diseases. This review describes the molecular mechanisms involved in the maintenance of EBV latency and its reactivation by periodontopathic bacteria. In addition, we discuss possible mechanisms by which EBV reactivation may facilitate progression of periodontal disease in infected individuals

Outer Membrane Vesicles of Helicobacter pylori TK1402 are Involved in Biofilm Formation

<p>Abstract</p> <p>Background</p> <p><it>Helicobacter pylori </it>forms biofilms on glass surfaces at the air-liquid interface in <it>in vitro </it>batch cultures; however, biofilms of <it>H. pylori </it>have not been well characterized. In the present study, we analyzed the ability of <it>H. pylori </it>strains to form biofilms and characterized the underlying mechanisms of <it>H. pylori </it>biofilm formation.</p> <p>Results</p> <p>Strain TK1402 showed strong biofilm forming ability relative to the other strains in Brucella broth supplemented with 7% FCS. The strong biofilm forming ability of TK1402 is reflected the relative thickness of the biofilms. In addition, outer membrane vesicles (OMV) were detected within the matrix of only the TK1402 biofilms. Biofilm formation was strongly correlated with the production of OMV in this strain. We further observed that strain TK1402 did not form thick biofilms in Brucella broth supplemented with 0.2% β-cyclodextrin. However, the addition of the OMV-fraction collected from TK1402 could enhance biofilm formation.</p> <p>Conclusion</p> <p>The results suggested that OMV produced from TK1402 play an important role in biofilm formation in strain TK1402.</p

Outer Membrane Vesicles of Porphyromonas gingivalis Elicit a Mucosal Immune Response

We previously reported that mutation of galE in Porphyromonas gingivalis has pleiotropic effects, including a truncated lipopolysaccharide (LPS) O-antigen and deglycosylation of the outer membrane protein OMP85 homolog. In the present study, further analysis of the galE mutant revealed that it produced little or no outer membrane vesicles (OMVs). Using three mouse antisera raised against whole cells of the P. gingivalis wild type strain, we performed ELISAs to examine the reactivity of these antisera with whole cells of the wild type or the galE mutant. All three antisera had significantly lower reactivity against the galE mutant compared to wild type. OMVs, but not LPS, retained the immunodominant determinant of P. gingivalis, as determined by ELISAs (with wild type LPS or OMVs as antigen) and absorption assays. In addition, we assessed the capacity of OMVs as a vaccine antigen by intranasal immunization to BALB/c mice. Synthetic double-stranded RNA polyriboinosinic polyribocytidylic acid [Poly (I∶C)], an agonist of Toll-like receptor 3 (TLR3), was used as the mucosal adjuvant. Vaccination with OMV elicited dramatically high levels of P. gingivalis-specific IgA in nasal washes and saliva, as well as serum IgG and IgA. In conclusion, the OMVs of P. gingivalis have an important role in mucosal immunogenicity as well as in antigenicity. We propose that P. gingivalis OMV is an intriguing immunogen for development of a periodontal disease vaccine

Effects of butyric acid on the periodontal tissue

Butyric acid, an extracellular metabolite from periodontopathic bacteria, induces apoptosis in murine thymocytes, splenic T-cells, as well as human Jurkat T-cells and peripheral blood mononuclear cells. Butyric acid-induced apoptosis is mediated by ceramide production, as well as reactive oxygen species (ROS) synthesis in mitochondria and subsequently JNK activation in MAP kinase cascades. Although the production of ROS and ceramide by themselves do not completely influence butyric acid-induced apoptosis, it can be concluded that ROS and ceramide production are the major contributors to butyric acid-induced apoptosis. Human gingival fibroblasts rescue butyric acid-induced T-cell apoptosis via proinflammatory cytokines, which are produced by fibroblasts stimulated with butyric acid. Moreover, T-cell adherence to fibroblasts is enhanced by butyric acids and butyric acid-induced T-cell apoptosis is down-regulated by T-cell adhesion to gingival fibroblasts. Butyric acid significantly suppresses the viability of inflamed gingival fibroblasts and induces apoptosis in a dose-dependent manner, whereas intact gingival fibroblasts isolated from healthy humans are resistant to butyric acid. This review focuses on the effects of butyric acid and its possible contribution to destruction of gingival tissues and modulation of local immunity at gingival sites (175/max. 200)

Role of Cell-Cell Communication in Inhibiting Butyric Acid-Induced T-Cell Apoptosis

We have previously demonstrated that human gingival fibroblasts rescue butyric acid-induced T-cell apoptosis via proinflammatory cytokines such as interleukin 6 (IL-6) and IL-11, which are produced by fibroblasts stimulated with butyric acid. In this study, we determined if T-cell adhesion to human gingival fibroblasts influenced the susceptibility of T cells to butyric acid-induced apoptosis. We have shown that the number of Jurkat T cells adherent to gingival fibroblasts (Gin-1 cells) was significantly increased by the addition of butyric acid. All Jurkat cells that adhered to Gin-1 cells remained viable, while the nonadherent Jurkat cells dropped into apoptosis. The increase in T-cell adhesion to fibroblasts was also observed when Jurkat cells, but not Gin-1 cells, were pretreated with butyric acid. The expression levels of CD44, very late antigen 2 (VLA-2) and VLA-5 but not of leukocyte function-associated antigen 1 (LFA-1) and VLA-4 on Jurkat cells were increased following treatment with butyric acid. Furthermore, pretreatment of butyric acid-sensitized Jurkat cells with monoclonal antibodies against CD44, VLA-2, and VLA-5, but not LFA-1 and VLA-4, followed by coculture with Gin-1 cells inhibited T-cell adhesion to fibroblasts and increased apoptosis of nonadherent T cells after coculture of gingival fibroblasts and Jurkat cells. These results indicate that T-cell adherence to fibroblasts is enhanced by butyric acid and that butyric acid-induced T-cell apoptosis is down-regulated by T-cell adhesion to gingival fibroblasts through an interaction with the adhesion molecules CD44, VLA-2, and VLA-5 expressed on T cells stimulated with butyric acid

Gingival Periodontal Disease (PD) Level-Butyric Acid Affects the Systemic Blood and Brain Organ: Insights Into the Systemic Inflammation of Periodontal Disease

Butyric acid (BA) is produced by periodontopathic bacterial pathogens and contributes to periodontal disease (PD) induction. Moreover, PD has been associated with detrimental effects which subsequently may lead to systemic disease (SD) development affecting certain organs. Surprisingly, the potential systemic manifestations and organ-localized effects of BA have never been elucidated. Here, we simulated BA-based oral infection among young (20-week-old) rats and isolated blood cytosol to determine BA effects on stress network-related signals [total heme, hydrogen peroxide (H2O2), catalase (CAT), glutathione reductase (GR), free fatty acid (FFA), NADP/NADPH], inflammation-associated signals [caspases (CASP12 and CASP1), IL-1β, TNF-α, metallomatrix proteinase-9 (MMP-9), and toll-like receptor-2 (TLR2)], and neurological blood biomarkers [presenilin (PS1 and PS2) and amyloid precursor protein (APP)]. Similarly, we extracted the brain from both control and BA-treated rats, isolated the major regions (hippocampus, pineal gland, hypothalamus, cerebrum, and cerebellum), and, subsequently, measured stress network-related signals [oxidative stress: total heme, NADPH, H2O2, GR, and FFA; ER stress: GADD153, calcium, CASP1, and CASP3] and a brain neurodegenerative biomarker (Tau). In the blood, we found that BA was no longer detectable. Nevertheless, oxidative stress and inflammation were induced. Interestingly, amounts of representative inflammatory signals (CASP12, CASP1, IL-1β, and TNF-α) decreased while MMP-9 levels increased which we believe would suggest that inflammation was MMP-9-modulated and would serve as an alternative inflammatory mechanism. Similarly, TLR2 activity was increased which would insinuate that neurological blood biomarkers (APP, PS1, and PS2) were likewise affected. In the brain, BA was not detected, however, we found that both oxidative and ER stresses were likewise altered in all brain regions. Interestingly, tau protein amounts were significantly affected in the cerebellar and hippocampal regions which coincidentally are the major brain regions affected in several neurological disorders. Taken together, we propose that gingival BA can potentially cause systemic inflammation ascribable to prolonged systemic manifestations in the blood and localized detrimental effects within the brain organ