• Journal of Periodontal and Implant Science
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• v.30 no.1
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• pp.111-120
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• 2000

Purpose We designed this study for the purpose of determining the relationship between periodontal disease activity and PLBW, using the evaluation of probing pocket depth, loss of attachment, gingival index, gingival crevicular fluid amount and subgingival microflora. Methods A total of 100 volunteer mothers(mean age 30.44) at the Department of Obstetrics and Gynecology Seoul National University Hospital were selected for this study.Pregnancy outcomes were categorized into cases and controls in two ways. our definition was based on the following; Group 1 : Any PLBW cases Vs. All NBW controls Group 2 : PLBW cases Vs. NBW controls A periodontal exam was performed on the Ramfjord( #16, 21, 24, 36, 41, 44) teeth and Clinical evaluation consisted of probing pocket depth, loss of attachment, gingival index and gingival crevicular fluid amount. Subgingival plaque samples were collected by three sterile #35 paper points. The total number of anaerobic colonies and aerobic bacteria were enumerated after incubation. Antisera to P. gingivalis, P. intermedia, A. actinomycetemcomitans were produced in white rabbits with live whole cells suspensions. The specific fluorescent bacteria obtained by immunofluorescence and total cell counts obtained by dark-field microscopy were counted on four fields. The percent of each specific microorganism in the total cell count was determined. Results Any PLBW and PLBW cases showed significantly greater probing depth and attachment loss than all NBW and NBW controls. Cases group had significantly increased anaerobic bacterial counts compared with control group and no differences in the other microbes. This study confirmed that periodontal disease is a statistically significant risk factor for PLBW by investigating clinical parameters and subgingival plaque analysis.

• International Journal of Oral Biology
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• v.48 no.2
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• pp.9-18
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• 2023

The rapid detection of bacteria in the oral cavity, its species identification, and bacterial count determination are important to diagnose oral diseases caused by pathogenic bacteria. The existing clinical microbial diagnosis methods are time-consuming as they involve observing patients' samples under a microscope or culturing and confirming bacteria using polymerase chain reaction (PCR) kits, making the process complex. Therefore, it is required to analyze the development status of substances and systems that can rapidly detect and analyze pathogenic microorganisms in the oral cavity. With research advancements, a close relationship between oral and systemic diseases has been identified, making it crucial to identify the changes in the oral cavity bacterial composition. Additionally, an early and accurate diagnosis is essential for better prognosis in periodontal disease. However, most periodontal disease-causing pathogens are anaerobic bacteria, which are difficult to identify using conventional bacterial culture methods. Further, the existing PCR method takes a long time to detect and involves complicated stages. Therefore, to address these challenges, the concept of point-of-care (PoC) has emerged, leading to the study and implementation of various chair-side test methods. This study aims to investigate the different PoC diagnostic methods introduced thus far for identifying pathogenic microorganisms in the oral cavity. These are classified into three categories: 1) microbiological tests, 2) microchemical tests, and 3) genetic tests. The microbiological tests are used to determine the presence or absence of representative causative bacteria of periodontal diseases, such as A. actinomycetemcomitans, P. gingivalis, P. intermedia, and T. denticola. However, the quantitative analysis remains impossible, and detecting pathogens other than the specific ones is challenging. The microchemical tests determine the activity of inflammation or disease by measuring the levels of biomarkers present in the oral cavity. Although this diagnostic method is based on increase in the specific biomarkers proportional to inflammation or disease progression in the oral cavity, its commercialization is limited due to low sensitivity and specificity. The genetic tests are based on the concept that differences in disease vulnerability and treatment response are caused by the patient's DNA predisposition. Specifically, the IL-1 gene is used in such tests. PoC diagnostic methods developed to date serve as supplementary diagnostic methods and tools for patient education, in addition to existing diagnostic methods, although they have limitations in diagnosing oral diseases alone. Research on various PoC test methods that can analyze and manage the oral cavity bacterial composition is expected to become more active, aligning with the shift from treatment-oriented to prevention-oriented approaches in healthcare.

• Journal of Periodontal and Implant Science
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• v.31 no.4
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• pp.661-668
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• 2001

Anti-P. gingivalis immune sera were obtained from mice immunized with either P. gingivalis alone, or F. nucleaturm followed by P. gingivalis. Two groups of immune sera were examined for binding capacity to P. gingivalis biofilm by confocal laser scanning microscope, Antibody avidity index was also determined for each immune sera. The results indicated that prior immunization of mice with F. nucleaturm impaired P. gingivalis-specific immune sera in binding capacity to biofilm and antibody avidity to P. gingivalis. Elevated antibody responses in patients with destructive periodontal disease has often been related to suboptimal level of protective antibody $(opsonophagocytosis)^{1-3)}$ while post-immune sera obtained with experimental animals using a single periodontal pathogen demonstrated satisfactory levels of protective function against the homologous bacterial $challenge^{4,5)}$.The reason is unclear why elevated IgG responses in periodontal patients to periodontal pathogens do not necessarily reflect their protective function. Such an immune deviation might be derived from the fact that destructive periodontal disease is cumulative result of immunopathologic processes responding to an array of different colonizing microorganisms sequentially infecting in the subgingival environmental niche. Fusobacterium nucleaturm is one of the key pathogens in gingivitis, in the transitional phase of conversion of gingivitis into destructive periodontitk, and in adult $periodontitis^{6-8)}$. It also plays a central role in coaggregation with other important microbial species in subgingival $area^{6,9,10)}$ as well as in $biofilm^{11)}$, especially with Porphyromonas gingjvalis in synergism of virulence in human periodontal disease or in animal $models^{12-14)}$. This organism has also been reported to have immune modulating activity for secondary immune response to Actinobacillus $actinomycetemcomitans^{15)}$. It is presumed that sequential colonization and intermicrobial coaggregation between intermediate and late colonizers could potentially modulate the immune responses and development of specific T cell phenotypes in periodontal lesions. We have recently demonstrated the skewed polarization of P. gingivalis-specific helper T cell clones in mice immunized with F. nucleaturm followed by P. $gingivalis.^{16)}$. Consequently F. nucleaturm may initially prime the immune cells and modify their responses to the successive organism, P. gingivalis. This could explain why one frequently observes non-protective serum antibodies to P. gingivalis in periodontal patients in contrast with those obtained from animals that were immunized with $P.gingivalis\;alone^{17)}$. The present study was performed to investigate the immune modulating effect of F. nucleatum on serum binding to experimental biofilms and the avidity of anti-P. gingivalis antibody.

• International Journal of Oral Biology
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• v.36 no.3
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• pp.109-116
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• 2011

Periodontitis results from the activation of host immune and inflammatory defense responses to subgingival plaque bacteria, most of which are gram-negative rods with lipopoly-saccharides (LPSs) in their cell walls. LPSs have been known to induce proinflammatory responses and recently it was reported also that they induce the expression of microRNAs (miRNAs) in host cells. In our current study therefore, we aimed to examine and compare the miRNA expression patterns induced by the LPSs of major periodontopathogens in the human gingival epithelial cell line, Ca9-22. The cells were treated with 1 ${\mu}g$/ml of E. coli (Ec) LPS or 5 ${\mu}g$/ml of an LPS preparations from four periodontopathogens Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi), Aggregatibacter actinomycetemcomitans (Aa), and Fusobacterium nucleatum (Fn) for 24 h. After small RNA extraction from the treated cells, miRNA microarray analysis was carried out and characteristic expression profiles were observed. Fn LPS most actively induced miRNAs related to inflammation, followed by Aa LPS, Pi LPS, and Ec LPS. In contrast, Pg LPS only weakly activated miRNAs related to inflammation. Among the miRNAs induced by each LPS, miR-875-3p, miR-449b, and miR-520d-3p were found to be commonly up-regulated by all five LPS preparations, although at different levels. When we further compared the miRNA expression patterns induced by each LPS, Ec LPS and Pi LPS were the most similar although Fn LPS and Aa LPS also induced a similar miRNA expression pattern. In contrast, the miRNA profile induced by Pg LPS was quite distinctive compared with the other bacteria. In conclusion, miR-875-3p, miR-449b, and miR-520d-3p miRNAs are potential targets for the diagnosis and treatment of periodontal inflammation induced by subgingival plaque biofilms. Furthermore, the observations in our current study provide new insights into the inflammatory miRNA response to periodontitis.

• The Journal of Korean Academy of Prosthodontics
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• v.46 no.2
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• pp.116-124
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• 2008

Statement of the problem: Implant systems result in gaps and cavities between implant and abutment that can act as a trap for bacteria and thus possibly cause inflammatory reactions in the peri-implant soft tissues. Purpose: Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Treponema denticola, and Aggregatibacter actinomycetemcomitans, related to implant-abutment interface microleakage. Material and methods: Samples were taken from 27 subjects with sterilized paper points and were transported in $1{\times}PBS$. The detection of periodontopathogens were performed by polymerase chain reaction with species-specific primers based on 16S rDNA. Results: Our data showed that the detection rate of P. gingivalis and P. intermedia in implant fixture was 59% and 82% in patients respectively. Detection rate of P. gingivalis and P. intermedia in implant crevice was 44% and 82% in patients. Detection rate of P. gingivalis and P. intermedias in tongue was 82% and 82% in patients. Conclusion: Current implant systems cannot safely prevent microbial leakage and bacterial colonization of the inner part of the implant.