• Journal of Periodontal and Implant Science
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• v.43 no.1
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• pp.3-11
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• 2013

Periodontitis is a chronic inflammation of periodontal tissue caused by subgingival plaque-associated bacteria. Periodontitis has long been understood to be the result of an excessive host response to plaque bacteria. In addition, periodontal pathogens have been regarded as the causative agents that induce a hyperinflammatory response from the host. In this brief review, host-microbe interaction of nonperiodontopathic versus periodontopathic bacteria with innate immune components encountered in the gingival sulcus will be described. In particular, we will describe the susceptibility of these microbes to antimicrobial peptides (AMPs) and phagocytosis by neutrophils, the induction of tissue-destructive mediators from neutrophils, the induction of AMPs and interleukin (IL)-8 from gingival epithelial cells, and the pattern recognition receptors that mediate the regulation of AMPs and IL-8 in gingival epithelial cells. This review indicates that true periodontal pathogens are poor activators/suppressors of a host immune response, and they evade host defense mechanisms.

• 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.

• The Journal of the Korean dental association
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• v.47 no.8
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• pp.522-533
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• 2009

Purpose: Infection with HIV-1 virus has become a critical worldwide public health problem. The oral complications of HIV infection with its progression of impairment of the host response to combat infection present unique challenges to the periodontists. Material and Methods : Medline research was carried out to find relationship of the progression of HIV infection to the occurrence of oral lesions including the HIV-related periodontal diseases. Results: The linear gingival erythema, necrotizing ulcerative periodontitis, necrotizing ulcerative gingivitis and oral candidiasis are common lesions in HIV-infected individuals. The linear gingival erythema and necrotizing ulcerative periodontitis lesions in HIV-infected subjects were found to have a similar microbiological profile. There are several general considerations in the periodontal management of the HIV-infected patient with or without periodontal disease. The altered immunity and host response in patients with HIV infection may also affect the incidence and severity of other common forms of periodontal disease not associated with HIV infection. Conclusion: Periodontal diseases in HIV-infected individuals present unique challenges in diagnosis, monitoring, treatment and maintenance. Therefore exact HIV staging, geographic location, antiviral and antimicrobial therapies and oral habits should be taken into consideration when treating HIV-infected patients.

• 대한치주과학회:학술대회논문집
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• 2005.11a
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• pp.163-164
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• 2005

• Journal of Periodontal and Implant Science
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• v.29 no.1
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• pp.103-115
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• 1999

The ultimate goal of periodontal therapy is the regeneration of periodontal tissue which has been lost due to destructive periodontal disease. Various periodontal procedures have been used throughout the years in an attempt to reestablish attachment of periodontal tissues to root surfaces affected by periodontitis. Flap debridement surgery has been demonstrated to be a successful procedure in gaining the probing attachment level and reducing probing depth. A tendency towards impaired wound healing following periodontal procedures in smokers has been clinically documented. But, previous clinical studies on healing response in smokers are based on a retrospective design. The purpose of this study was to evaluate the treatment outcome following flap debridement surgery in smokers compared to nonsmokers. 25 patients with moderate to advanced periodontitis were included for study. Among these patients, 13 patients were smokers, and 12 patients were nonsmokers. Mucoperiosteal flap was raised with the sulcular incision. No antibiotic treatment was administered postsurgery. The patients was recalled at monthly intervals during a period of 6 months following the surgery. The patients were received supragingival scaling and oral hygiene reinforcement. All the recordings, including modified O' Leary plaque control record, bleeding on probing, probing pocket depth, probing attachment level,were recorded, presurgery and 6 months postsurgery. The changes of all the recordings at 6 months after flap debridement surgery revealed the following results: 1. PI on all the dentitions and surgical sites showed no statistical significance between smokers and nonsmokers at presurgery. But, smokers demonstrated a significantly lower % of PI than nonsmokers at 6 months postsurgery. 2. Smokers demonstrated a greater % of BOP sites than nonsmokers on the surgical sites and all the dentitions, presurgery and 6 months postsurgery. But, there was no statistical significance between two groups. 3. Smokers exhibited significantly less reduction of probing depth in the 3 mm or less probing pocket depth(PPD) group, 6mm or more PPD group and total PPD group when compared to nonsmokers at 6 months postsurgery. 4. Smokers exhibited significantly less gain of probing attachment level(PAL) in the 3mm or less PPD group, 6 mm or more PPD group and total PPD group when compared to nonsmokers at 6 months postsurgery.

• Journal of dental hygiene science
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• v.19 no.4
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• pp.254-260
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• 2019

Background: The primary aims of periodontal disease treatment is to remove dental plaque and calculus, the main causes of tooth loss, and restore periodontal tissue destroyed by inflammation. Periodontal disease treatment should also help maintain the alveolar bone, alleviate inflammation, and promote periodontal ligament cell proliferation, which is essential for tissue regeneration. Conventional antibiotics and anti-inflammatories have adverse side effects, especially during long-term use, so there is a need for adjunct treatment agents derived from natural products. The purpose of this study was to investigate whether the herbal flavone baicalein has the osteogenic activity under inflammatory conditions, and assess the involvement of osteoblast immediate early response 3 (IER3) expression. Methods: Human osteoblastic MG-63 cells were cultured with the pro-inflammatory cytokines tumor necrosis factor α and interleukin 1β in the presence and absence of baicalein. Proliferation was assessed using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay, and expression of IER3 mRNA was assessed using real-time polymerase chain reaction. The expression of IER3 protein levels and activation of associated signal transduction pathways were assessed using western blotting. Results: Baicalein increased IER3 mRNA and protein expression synergistically. In addition, baicalein reversed the suppression of cell proliferation, and the downregulation of osteogenic transcription factor runt-related transcription factor 2 and osterix induced by pro-inflammatory cytokines. Baicalein also upregulated the phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK 1/2). The upregulation of IER3 by pro-inflammatory cytokines was blocked by pretreatment with inhibitors of AKT, p38, JNK, and ERK 1/2. Conclusion: Baicalein mitigates the deleterious responses of osteoblasts to pro-inflammatory cytokines. Further, IER3 enhanced the effect of baicalein via activation of AKT, p38, JNK, and ERK pathways.

• The korean journal of orthodontics
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• v.11 no.2
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• pp.65-70
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• 1981

In the present study orthodontic force was applied to the molars of control group and experimental group treated with the lathyrogen beta-aminopropionitrile (BAPN). Observation resulted in the following conclusions : 1) New alveolar bone formation in response to orthodontic force in BAPN-treated rats exceeded corresponding bone formation in control of cup when measured at two tension sites in the periodontal ligament. 2) BAPN administration produced disorganization of the collagenous fibers of the periodontium of experimental group. Multiple eosinophilic cell-free areas were found distributed throughout the radicular portions of affected periodontal ligaments. 3) The areas of periodontium surrounding orthodontically treated teeth exhibited relatively normal organization under these conditions, while the periodontium of adjacent nonorthodontically treated teeth was disorganized. 4) The present results suggest that the typical histologic response to orthodontic force application can occur in the presence of a chemically and physically altered periodontium.

• The Journal of the Korean dental association
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• v.50 no.8
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• pp.465-473
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• 2012

Prognosis is an anticipation of the probable response to periodontal therapy and a long-term prospect for maintaining a functional dentition. Hopeless cases or cases of simple gingivitis without systemic diseases generally have little problem to establish definite prognoses. However, it might become somewhat challenging to determine their prognoses in borderline cases. A risk factor for periodontal disease may be environmental, behavioral, or biologic factors that can be defined as an occurrence has been associated with destructive periodontitis. Some risk factors are modifiable, while others cannot be modified. Modifiable risk factors are environmental or behavioral in nature in contrast non-modifiable risk factors are usually intrinsic to the individual and therefore not easily changed. In this review, we will assess the various modifiable or non-modifiable risk factors for susceptibility 10 periodontal diseases.

• Journal of dental hygiene science
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• v.17 no.1
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• pp.73-80
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• 2017

Periodontal diseases occur from the interplay between increased bacterial response and the response of the host immune system over time. Anxiety and depression can impair immunological defense mechanisms, causing accumulation of periodontopathogens and thus exacerbating periodontal disease. We investigated the relationship of anxiety and depression to periodontal diseases in Korean women. In this study, 3,551 women aged ${\geq}19$ years were evaluated based on data from the first year (2010) of the Fifth Korea National Health and Nutrition Examination Survey. The analysis of the factors that caused periodontal diseases revealed that dental floss or interdental toothbrush nonuse behaviors have been shown to increase the risk of periodontal disease (odds ratio [OR], 1.49; 95% confidence interval [CI], 1.14~1.95). After adjusting for conditions such as age, marital status, income, educational level, economic activity, diabetes mellitus, smoking, drinking, and frequencies of toothbrushing and interdental cleaning, we found that anxiety and depression increased the risk of developing periodontal diseases (OR, 1.47; 95% CI, 1.04~2.09). People with anxiety and depression have a higher prevalence of periodontal diseases than people without anxiety and depression. Thus, periodic periodontal care and effective self-care education are needed to manage periodontal diseases.

• Journal of Periodontal and Implant Science
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• v.25 no.1
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• pp.133-145
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• 1995

The migration and proliferation of periodontal ligament cells are desired goal of periodontal regeneration therapy. PDGF and $TGF-{\beta}1$ are well known to regulate the cell activity of mesenchymal origin cell. The purpose of this study was to determine the effects of these growth factors on human gingival fibroblast and periodontal ligament cell actvity, and to identify the regulatory effect of $TGF-{\beta}1$ on the response to PDGF by MIT assay. Human gingival fibroblast and periodontal ligament cells were cultured from extracted teeth for non-periodontal reason. Cultured human gingival fibroblast and periodontal ligament cells in vitro were treated with polyperpetide growth factor PDGF and $TGF-{\beta}1$ in both a dose and time - dependent manner. Cell morphology were determined by inverted microscope and cell acitivity were determined by MIT assay. The result of this study demonstrated that PDGF and $TGF-{\beta}1$ were not changed the morphology of these cell compared with control group. PDGF or $TGF-{\beta}1$ increased cell activity of periodontal ligament cell in dose and time dependent manner but gingival fibroblast were decreased to the level of control group at third day. Additionally, incubation with $TGF-{\beta}1$ addition to PDGF resulted in a enhanced cell activity of PDGF. Therefore, cell acitivty of gingival fibroblast were not changed compared with control group. This stiudy demonstrates that PDGF and $TGF-{\beta}1$ are major mitogens for human periodontal ligament cell in vitro, and $TGF-{\beta}1$ is a regulator of cell activity to PDGF in human gingival fibroblast and periodontal ligament cell.