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

Porcine Enamel Protein Fractions Contain Transforming Growth Factor‐β1

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141064/1/jper1688.pd

Amelogenin Stimulates Bone Sialoprotein (BSP) Expression Through Fibroblast Growth Factor 2 Response Element and Transforming Growth Factorâ β1 Activation Element in the Promoter of the BSP Gene

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141420/1/jper1482.pd

IMMUNOLOGICAL DIFFERENTIATION OF HUMAN TISSUE-NONSPECIFIC TYPE ALKALINE PHOSPHATASES BY A MONOCLONAL ANTIBODY TO THE ENZYME OF HUMAN OSTEOBLAST-LIKE CELLS

Monoclonal antibodies against alkaline phosphatase [ALP; ortho-phosphoric monoester phosphohydrolase, alkaline optimum, EC 3.1.3.1.] of cultured human osteoblast-like cells (HBC) were raised in mice. Immuno-reactions of tissue-nonspecific type ALP from human bone, dental pulp, liver and kidney as well as intestinal and placental types to the monoclonal antibodies were compared by a dot immunoassay and ELISA. One clone was able to recognize antigenic differences among tissue-nonspecific type ALPs in addition to intestinal and placental ALPs; it reacted favorably with ALPs from HBC, human bone, kidney and dental pulp, but not with human liver enzyme. Similarly, the antibody immunoreacted with bone-derived ALP but not with liver-derived enzyme present in human serum.The present monoclonal antibody preparation can be utilized in basic studies as well as in clinical laboratory tests to distinguish minor heterogeneity among human Al Ps

Prevalence of Epstein-Barr virus DNA and Porphyromonas gingivalis in Japanese peri-implantitis patients

Abstract Background Peri-implantitis (PI) is an inflammatory reaction associated with functional deterioration of supporting bones around the dental implant. Recent studies suggested Epstein–Barr virus (EBV) is involved in the pathogenesis of periodontitis. We investigated the association between EBV and Porphyromonas gingivalis in Japanese PI patients. Methods Fifteen periodontally healthy individuals, 15 healthy implant patients and 15 PI patients were recruited. Forty five subgingival plaque samples were collected from the deepest probing pocket depth (PPD) site from each patient. Real-time PCR was used to detect EBV DNA and P. gingivalis. Results EBV and P. gingivalis were detected in 7 and 3 PPD sites of the healthy controls, in 9 and 4 PPD sites of the healthy implants, and in 13 and 14 PPD sites of the PI patients. P. gingivalis and coexistence of EBV and P. gingivalis were detected significantly higher in the PI patients than healthy controls and healthy implant patients. EBV was detected significantly higher in the PI patients than healthy controls. Conclusions Higher levels of EBV and P. gingivalis were detected in PPD sites of PI patients. These results suggest that coexistence of EBV and P. gingivalis may serve pathogenic factors cause for PI in Japanese dental patients

Higher prevalence of Epstein-Barr virus DNA in deeper periodontal pockets of chronic periodontitis in Japanese patients.

Periodontitis, a complex chronic inflammatory disease caused by subgingival infection, is among the most prevalent microbial diseases in humans. Although traditional microbiological research on periodontitis has focused on putative bacteria such as Porphyromonas gingivalis, the herpes virus is proposed to be involved in the pathogenesis of periodontitis because bacterial etiology alone does not adequately explain various clinical aspects. In this study, we established for the first time, more Epstein-Barr virus (EBV) DNA is found deeper in periodontal pockets of chronic periodontitis in Japanese patients. Subgingival samples were collected from 85 patients with chronic periodontitis having two periodontal sites with probing depths (PD) of ≤ 3 mm (shallow) or ≥ 5 mm (deep) and were subjected to a nested polymerase chain reaction. EBV DNA was more frequently detected in patients with deeper PD sites (66%) than in those with shallow PD sites (48%) or healthy controls (45%). Coexistence of EBV DNA and P. gingivalis was significantly higher in patients with deeper PD sites (40%) than in those with shallow PD sites (14%) or healthy controls (13%). Although no difference in clinical index for periodontitis, the odds ratio of EBV DNA in patients with deeper PD sites was 2.36, which was 2.07-fold higher than that in those with shallow PD sites. Interestingly, the odds of acquiring chronic periodontitis (PD ≥ 5 mm) were higher in the presence of both EBV DNA and P. gingivalis compared with either EBV DNA or P. gingivalis only. In addition, we also observed that EBV-encoded small RNA (EBER) in positive cells of human gingival tissues. These results would suggest that EBV DNA may serve as a pathogenic factor leading to chronic periodontitis among Japanese patients

Exposure to Porphyromonas gingivalis Induces Production of Proinflammatory Cytokine via TLR2 from Human Respiratory Epithelial Cells

Aspiration pneumonia is a major health problem owing to its high mortality rate in elderly people. The secretion of proinflammatory cytokines such as interleukin (IL)-8 and IL-6 by respiratory epithelial cells, which is induced by infection of respiratory bacteria such as Streptococcus pneumoniae, contributes to the onset of pneumonia. These cytokines thus play a key role in orchestrating inflammatory responses in the lower respiratory tract. In contrast, chronic periodontitis, a chronic inflammatory disease caused by the infection of periodontopathic bacteria, typically Porphyromonas gingivalis, is one of the most prevalent microbial diseases affecting humans globally. Although emerging evidence has revealed an association between aspiration pneumonia and chronic periodontitis, a causal relationship between periodontopathic bacteria and the onset of aspiration pneumonia has not been established. Most periodontopathic bacteria are anaerobic and are therefore unlikely to survive in the lower respiratory organs of humans. Therefore, in this study, we examined whether simple contact by heat-inactivated P. gingivalis induced proinflammatory cytokine production by several human respiratory epithelial cell lines. We found that P. gingivalis induced strong IL-8 and IL-6 secretion by BEAS-2B bronchial epithelial cells. P. gingivalis also induced strong IL-8 secretion by Detroit 562 pharyngeal epithelial cells but not by A549 alveolar epithelial cells. Additionally, Toll-like receptor (TLR) 2 but not TLR4 was involved in the P. gingivalis-induced proinflammatory cytokine production. Furthermore, P. gingivalis induced considerably higher IL-8 and IL-6 production than heat-inactivated S. pneumoniae. Our results suggest that P. gingivalis is a powerful inflammatory stimulant for human bronchial and pharyngeal epithelial cells and can stimulate TLR2-mediated cytokine production, thereby potentially contributing to the onset of aspiration pneumonia

Detection of EBER in inflamed gingival connective tissue of patients with chronic periodontitis.

<p>Serial sections of periodontitis lesion were stained with HE (a), EBER ISH (b) and (c) anti CD19 antibody, respectively. Original magnification; x200.</p