ABSTRACT
@#In recent years, the etiology of periodontitis has tended to be based on the theory of flora imbalance. That is, periodontitis is not caused by specific bacteria but by the breakdown of the oral flora balance, which leads to an immune imbalance. Imbalanced bacterial flora cooperate with each other to produce virulent factors that destroy organism tissues and induce immune cells to produce abnormal levels of cytokines, causing greater damage. This article reviews the initiation of a flora imbalance, the interaction between bacteria, the immune damage of the host and the prevention and treatment of the flora imbalance. The literature review shows that peroxidase released by inflammatory reactions, host immune responses to pathogenic microorganisms and some systemic factors, such as diabetes, can trigger flora imbalance. As a result, ion transport, substance synthesis and metabolism of bacteria change; virulence factors increase; and the oral flora balance is disrupted. Red complex bacteria enter gingival epithelial cells, produce adhesin, and selectively inhibit the expression of specific chemokines, which is beneficial for other pathogenic bacteria to enter gingival epithelial cells. Toxicity factors increase throughout the body, directly destroying body tissues and inducing innate and adaptive immune responses, thus causing related immune damage. The dysbacteriosis model of periodontitis provides a new idea for the prevention and treatment of periodontitis, such as using biological factors, bacteriophages, probiotics and other methods to reduce the number of periodontal pathogens to restore the steady state of periodontal flora.
ABSTRACT
Aim: The aim of this study was to analyze the expression level and localization of Toll-like receptor (TLR) 4 in gingival samples of healthy and chronic periodontitis subjects by indirect immunofluorescence technique (IFT). Materials and Methods: In this study, gingival tissue samples were obtained from 25 healthy and 25 periodontitis individuals. The tissues were processed and the initial characterization was done by hematoxylin and eosin staining. The expression and localization of the TLR4 receptor were determined in the epithelial and connective layer cells of the gingival tissue using the indirect IFT. Immunofluorescence images were acquired and quantitative expression of TLRs was analyzed by calculating the percentage of cells showing positive results. Results: We found that the healthy control group exhibited significantly lower values of TLR4 expression in comparison with the periodontitis patients. We also found that in patients with periodontitis the concentration of TLR4 was higher in the epithelium as compared to their expression in connective tissue cells. Conclusions: These data suggested a definite involvement of TLR4 in initiating and progression of an inflammatory response in periodontitis.
ABSTRACT
The gingival epithelium of the oral cavity is constantly exposed to exogenous stimuli such as bacterial toxins, allergens, and thermal changes. These exogenous stimuli are resisted by innate host defense in gingival epithelial cells. However, it is unclear exactly how the exogenous stimuli affect detrimentally on the human gingival epithelial cells. Here, we investigated whether the allergen, such as house dust mite (HDM) extract, is linked to Ca2+ signaling and proinflammatory cytokine expression in primary cultured human gingival epithelial cells. HDM extract induced an increase in intracellular Ca2+ concentration ([Ca2+]i) in a dose-dependent manner. Extracellular Ca2+ depletion did not affected on the HDM extract-induced increase in [Ca2+]i. The HDM extract-induced increase in [Ca2+]i was abolished by the treatment with U73122 and 2-APB, which are inhibitors of phospholipase C (PLC) and inositol 1,4,5-trisphosphate (IP3) receptor. Moreover, HDM extract induced the mRNA expression of pro-inflammatory cytokine, interleukin (IL)-8. These results suggest that HDM extract triggers PLC/IP3-dependent Ca2+ signaling and IL-8 mRNA expression in primary cultured human gingival epithelial cells.
Subject(s)
Humans , Allergens , Bacterial Toxins , Epithelial Cells , Epithelium , Inositol 1,4,5-Trisphosphate , Interleukin-8 , Interleukins , Mouth , Pyroglyphidae , RNA, Messenger , Type C PhospholipasesABSTRACT
PURPOSE: Periodontal pathogens can invade the host tissue. Morphologic studies have revealed bacteria within the pocket epithelium, gingival connective tissues, alveolar bone, and oral epithelium. The objective of this study was to visualize and evaluate presence of Porphyromonas gingivalis and Tannerella forsythia in crevicular epithelial cells of periodontally healthy subjects and chronic periodontitis patients. MATERIALS AND METHODS: A total of 666 crevicular epithelial cells in the samples obtained from 27 chronic periodontitis patients and 9 healthy volunteers were examined. Specific probes for P. gingivalis and T. forsythia and a universal probe for detection of all eubacteria targeting 16S rRNA for fluorescence in situ hybridization was used in conjunction with confocal laser scanning microscopy. RESULTS: 98.99% of sulcular epithelial cells from healthy volunteers and 84.40% of pocket epithelial cells from periodontitis patients were found to harbor bacteria. P. gingivalis and T. forsythia were discovered more often in crevicular epithelial cells from periodontitis patients. CONCLUSION: P. gingivalis and T. forsythia can invade crevicular epithelial cells and intracellular bacteria may act as a source of bacteria for persistent infection.
Subject(s)
Humans , Bacteria , Chronic Periodontitis , Collodion , Connective Tissue , Epithelial Cells , Epithelium , Fluorescence , Forsythia , In Situ Hybridization , Periodontitis , Porphyromonas gingivalisABSTRACT
objective: To investigate the effect of human serum albumin(HSA)on the attachment of human gingival epithelial cells(HGEs)to commercial pure titanium(cpTi).Methods: HGEs were cultured, the cells of passage 2～5 were seeded on to cpTi samples which were preincubated in keratinocyte serum free medium with 50 mg/ml HSA or without HSA. Cell attachment was studied by immunofluorescence analysis.Results: HGEs were cultured and identified by positive expression of cytokeratin. 4,12 and 24 h after seeding attached cells on HSA preincubated cpTi were 218,730 and 849, those on the control 417,745 and 864, respectively.Conclusion: The early stage of cell attachment of HGEs on to cpTi may be inhibited by HSA.
ABSTRACT
Objective: To determine if the hemagglutinin A (HagA) of Porphyromonas gingivalis could be involved in the adhesion and invasion in human gingival epithelial cells (HGEC). Methods:P. gingivalis 381 hagA mutant was constructed by conjugation method. The whole length of hagA gene was cloned into pYA292 in Salmonella typhimurium x4072 (S. typhimurium-hagA). The strains were used to test their ability of adhesion and invasion into HGEC using a standard antibiotic protection assay. S. typhimurium x4072 strains containing empty vectors were used as negative control. HagA expression in S. typhimurium-hagA was confirmed by Western blot. Results:Although there were no significant differences between P. gingivalis 381 hagA mutant and wild type in adhesion and invasion into HGEC, the adhesion values of S. typhimurium-hagA to HGEC were increased by 3 times compared to their respective controls, while the invasion ability of S. typhimurium-hagA was 4 times greater than that of the negative controls. Conclusion: These results suggest that HagA may participate in P. gingivalis adhesion and invasion into HGEC.
ABSTRACT
Objective:To study the effects of green-tea polyphenol, (epigallocatechin gallate,EGCg) on the cellular inflammatory responses of gingival epithelial cells. In order to find out a safe and efficient inflammation-inhibitor for periodontitis prevention and treatment. Methods:A model of cellular inflammatory responses of gingival epithelial cells stimulated by Porphyromonas gingivalis vesicles in vitro was established. The effects of EGCg on PGE2 production of gingival epithelial cells was detected by ELISA. Further more, the effects of EGCg on COX (cyclooxygenase)-2 and MMP (matrix metalloproteinase)-3 mRNA expression were determined by Real-time RT-PCR. Results:EGCg dose-dependently inhibited PGE2 production and COX-2, MMP-3 mRNA expressions. Conclusion:EGCg has inhibitory effects on cellular inflammatory responses of gingival epithelial cells and possesses the potentiality to be a periodontal inflammation-inhibitor.