• Journal of Periodontal and Implant Science
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• v.38 no.1
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• pp.31-40
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• 2008

Purpose: The probiotic effects of lactic acid bacteria have widely been researched in diverse human pathogens, but only a few effects are reported against oral pathogens. The antimicrobial effects of the Enterococcus faecium 7413 isolated from Korean infants on the 9 pathogen including 6 oral streptococci were investigated the clinical use of the antimicrobial peptide for oral microflora control. Materials and Methods: E. faecium 7413 was identified by morphological, biochemical tests and 16S rDNA sequence analysis. Inhibitory effects of culture supernatants were determined for their ability to grow on agar plate containing pathogenic bacteria. Result: The culture supernatant of Enterococcus faecium 7413 showed inhibitory effects on oral pathogens, namely Streptococcus pyogenes KCTC 3556, S. pneumoniae KCTC 5080, S. mutans ATCC 25175, S. anginosus ATCC 33397, S. constellatus KCTC 3268, S. intermedius ATCC 27823 and Shigella flexneri KCTC 2008. Whereas it did not affect the multiplication of E. coli strains, KCTC 1041 and ATCC 43894. Conclusion: The data obtained in this study could be useful for future development of effective probiotics allowing prevention for oral pathogens.

• Journal of Periodontal and Implant Science
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• v.36 no.3
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• pp.653-659
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• 2006

Oral malodor may cause a significant social or psychological handicap to those suffering from it. Oral malodor has been correlated with the concentration of volatile sulfur compounds (VSC) produced in the oral cavity. Specific bacteria identified in the production of VSC have been reported and many of these bacteria are commonly suspected periodontal pathogens. The aim of this study was to estimate the change of the VSC concentration after periodontal treatment, Twenty subjects with probing depth $(PD)\;{\geq}5mm$ (experimental group) and 20 subjects with PD<5mm (control group) participated. VSC concentration measurement was made with gas chromatography. VSC concentration was measured at pre-treatment, 2 weeks after scaling and 1 month after periodontal treatment(root planning and flap operation). Maximum probing depth and bleeding on probing(BOP) were also examed at pretreatment and 1 month after periodontal treatment, The conclusions were as follow: 1. In the experimental group VSC concentration and CH3SH/H2S ratio were higher than control group. (p<0.05) 2. Both VSC concentration and CH3SH/H2S ratio showed decrease after periodontal treatment, But only CH3SH/H2S ratio after 1 month periodontal treatment was statistically significantly different from pre-treatment. (p<0.05) 3. CH3SH/H2S ratio tended to be on increase according to maximum probing depth and bleeding on probing. Periodontal disease could be a factor that caused oral malodor and oral malodor could be decreased after periodontal treatment.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.291-297
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• 2015

An oral environment is constantly exposed to environmental factors and microorganisms. The periodontal ligament (PDL) fibroblasts within this environment are subject to bacterial infection and allergic reaction. However, how these condition affect PDL fibroblasts has yet to be elucidated. PDL fibroblasts were isolated from healthy donors. We examined using reverse transcription-polymerase chain reaction and measuring the intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$). This study investigated the receptors activated by exogenous bacterial pathogens (Lipopolysaccharide and peptidoglycan) and allergens (German cockroach extract and house dust mite) as well as these pathogenic mediators-induced effects on the intracellular $Ca^{2+}$ signaling in human PDL fibroblasts. Moreover, we evaluated the expression of pro-inflammatory cytokines (interleukin (IL)-$1{\beta}$, IL-6, and IL-8) and bone remodeling mediators (receptor activator of NF-${\kappa}B$ ligand and osteoprotegerin) and intracellular $Ca^{2+}$-involved effect. Bacterial pathogens and allergic mediators induced increased expression of pro-inflammatory cytokines, and these results are dependent on intracellular $Ca^{2+}$. However, bacterial pathogens and allergic mediators did not lead to increased expression of bone remodeling mediators, except lipopolysaccharide-induced effect on receptor activator of NF-${\kappa}B$ ligand expression. These experiments provide evidence that a pathogens and allergens-induced increase in $[Ca^{2+}]_i$ affects the inflammatory response in human PDL fibroblasts.

• IMMUNE NETWORK
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• v.3 no.4
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• pp.261-267
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• 2003

The periodontal diseases are infections caused by bacteria in oral biofilm, a gelatinous mat commonly called dental plaque, which is a complex microbial community that forms and adhere to tooth surfaces. Host immune-pathogen interaction in periodontal disease appears to be a complex process, which is regulated not only by the acquired immunity to deal with ever-growing and -invading microorganisms in periodontal pockets, but also by genetic and/or environmental factors. However, our understanding of the pathogenesis in human periodontal diseases is limited by the lack of specific and sensitive tools or models to study the complex microbial challenges and their interactions with the host's immune system. Recent advances in cellular and molecular biology research have demonstrated the importance of the acquired immune system in fighting the virulent periodontal pathogens and in protecting the host from developing further devastating conditions in periodontal infections. The use of genetic knockout and immunodeficient mouse strains has shown that the acquired immune response, in particular, $CD4^+$ T-cells plays a pivotal role in controlling the ongoing infection, the immune/inflammatory responses, and the subsequent host's tissue destruction.

• Journal of the Health Care and Life Science
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• v.11 no.2
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• pp.393-405
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• 2023

Oral diseases have been reported to affect approximately 3.5 billion people worldwide, and in Korea, gingivitis and periodontal disease ranked first in the most frequent diseases from 2019 to 2021. Microorganisms that cause oral diseases include not only some bacteria such as Streptococcus mutans, Porphyromonas gingivalis, Fusobacterium nucleatum, Streptococcus gordonii, Leptotrichia buccalis, Prevotella, and Treponema, but also fungi Candida albicans and archaea Methanobrevibacter oralis. In the process by which oral microorganisms cause periodontal disease, bacteria such as Streptococcus mutans first proliferate to form a biofilm, and then obligate anaerobes, opportunistic bacteria, and pathogens attach, proliferate and settles down, forming plaque in the subgingival area of the host with weakened immunity. In this way, various interactions within the community are important in causing oral disease. Furthermore, substances and inflammation resulting from oral microorganisms and oral diseases are closely related to the occurrence of digestive diseases, diabetes, cardiovascular diseases, cognitive function, rheumatoid arthritis, premature birth, and cancer, and vice versa.

• 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.52 no.1
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• pp.28-38
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• 2022

Purpose: Macrophages play crucial roles as early responders to bacterial pathogens and promote/ or impede chronic inflammation in various tissues. Periodontal macrophage-induced pyroptosis results in physiological and pathological inflammatory responses. The transcription factor Dec2 is involved in regulating immune function and inflammatory processes. To characterize the potential unknown role of Dec2 in the innate immune system, we sought to elucidate the mechanism that may alleviate macrophage pyroptosis in periodontal inflammation. Methods: Porphyromonas gingivalis lipopolysaccharide (LPS) was used to induce pyroptosis in RAW 264.7 macrophages. Subsequently, we established an LPS-stimulated Dec2 overexpression cellular model in macrophages. Human chronic periodontitis tissues were employed to evaluate potential changes in inflammatory marker expression and pyroptosis. Finally, the effects of Dec2 deficiency on inflammation and pyroptosis were characterized in a P. gingivalis-treated experimental periodontitis Dec2-knockout mouse model. Results: Macrophages treated with LPS revealed significantly increased messenger RNA expression levels of Dec2 and interleukin (IL)-1β. Dec2 overexpression reduced IL-1β expression in macrophages treated with LPS. Overexpression of Dec2 also repressed the cleavage of gasdermin D (GSDMD), and the expression of caspase-11 was concurrently reduced in macrophages treated with LPS. Human chronic periodontitis tissues showed significantly higher gingival inflammation and pyroptosis-related protein expression than non-periodontitis tissues. In vivo, P. gingivalis-challenged mice exhibited a significant augmentation of F4/80, tumor necrosis factor-α, and IL-1β. Dec2 deficiency markedly induced GSDMD expression in the periodontal ligament of P. gingivalis-challenged mice. Conclusions: Our findings indicate that Dec2 deficiency exacerbated P. gingivalis LPS-induced periodontal inflammation and GSDMD-mediated pyroptosis. Collectively, our results present novel insights into the molecular functions of macrophage pyroptosis and document an unforeseen role of Dec2 in pyroptosis.

• Journal of Periodontal and Implant Science
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• v.45 no.5
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• pp.178-183
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• 2015

Purpose: Elderly people are thought to be more susceptible to periodontal disease due to reduced immune function associated with aging. However, little information is available on the nature of immune responses against putative periodontal pathogens in geriatric patients. The purpose of this study was to evaluate the serum IgG antibody responses to six periodontal pathogens in geriatric subjects. Methods: The study population consisted of 85 geriatric patients and was divided into three groups: 29 mild (MCP), 27 moderate (MoCP), and 29 severe (SCP) chronic periodontitis patients. Serum levels of IgG antibody to Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum, and Prevotella intermedia were measured by enzyme-linked immunosorbent assay (ELISA) and compared among the groups. Results: All three groups showed levels of serum IgG in response to P. gingivalis, A. actinomycetemcomitans, and P. intermedia that were three to four times higher than levels of IgG to T. forsythia, T. denticola, and F. nucleatum. There were no significant differences among all three groups in IgG response to P. gingivalis (P=0.065), T. forsythia (P=0.057), T. denticola (P=0.1), and P. intermedia (P=0.167), although the IgG levels tended to be higher in patients with SCP than in those with MCP or MoCP (with the exception of those for P. intermedia). In contrast, there were significant differences among the groups in IgG levels in response to F. nucleatum (P=0.001) and A. actinomycetemcomitans (P=0.003). IgG levels to A. actinomycetemcomitans were higher in patients with MCP than in those with MoCP or SCP. Conclusions: When IgG levels were compared among three periodontal disease groups, only IgG levels to F. nucleatum significantly increased with the severity of disease. On the contrary, IgG levels to A. actinomycetemcomitans decreased significantly in patients with SCP compared to those with MCP. There were no significant differences in the IgG levels for P. gingivalis, T. forsythia, T. denticola, and P. intermedia among geriatric patients with chronic periodontitis.

• International Journal of Oral Biology
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• v.36 no.1
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• pp.23-29
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• 2011

Porphyromonas gingivalis, one of the major periodontal pathogens, is implicated in the initiation and progression of periodontal disease. The initial stages of periodontal inflammation are accompanied by vascular hyperpermeability. In our present study, we report that the P. gingivalis lipopolysaccharide (LPS) increases the mRNA expression of interleukin-8 (IL-8), a major inducer of vascular permeability, in vascular endothelial cells. P. gingivalis LPS also stimulated the induction of IL-8 secretion in endothelial cells. The P. gingivalis LPS-induced expression of IL-8 was primarily modulated by nuclear factor-${\kappa}$B(NF-${\kappa}$B). P. gingivalis LPS significantly enhanced the vascular permeability both in vitro and in vivo, and a blockade of the IL-8 receptor decreased the P. gingivalis LPS-induced vascular permeability. Taken together, these results suggest that P. gingivalis LPS increases vascular permeability through the NF-${\kappa}$B-dependent production of IL-8 in vascular endothelial cells.

• The Journal of Advanced Prosthodontics
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• v.2 no.4
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• pp.154-159
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• 2010

BACKGROUND. Generalized aggressive periodontitis (GAP) is a destructive periodontal disease that can develop in young age. Only a few cases of full mouth rehabilitation, using dental implants, have been reported in a patient with aggressive periodontitis. CASE DESCRIPTION. This clinical report describes the treatment procedures and results of full mouth rehabilitation in a patient with aggressive periodontitis. After all teeth were extracted, 6 implants were placed in the maxilla and mandible, respectively. Fixed detachable implant prostheses were made. The patient was satisfied with the final results. She was followed for 10 months postloading. CLINICAL IMPLICATION. For a long-term success, continuous maintenance care is critical, as the contributing factors of the disease (such as immune factors or periodontal pathogens) may not be controlled adequately.