• Journal of Periodontal and Implant Science
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• 제43권3호
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• pp.111-120
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• 2013

Periodontitis is a common oral disease that is characterized by infection and inflammation of the tooth supporting tissues. While its incidence is highly associated with outgrowth of the pathogenic microbiome, some patients show signs of predisposition and quickly fall into recurrence after treatment. Recent research using genetic associations of candidates as well as genome-wide analysis highlights that variations in genes related to the inflammatory response are associated with an increased risk of periodontitis. Intriguingly, some of the genes are regulated by epigenetic modifications, supposedly established and reprogrammed in response to environmental stimuli. In addition, the treatment with epigenetic drugs improves treatment of periodontitis in a mouse model. In this review, we highlight some of the recent progress identifying genetic factors associated with periodontitis and point to promising approaches in epigenetic research that may contribute to the understanding of molecular mechanisms involving different responses in individuals and the early detection of predispositions that may guide in future oral treatment and disease prevention.

• 치위생과학회지
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• 제17권1호
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• pp.81-86
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• 2017

Bacterial infection and smoking are an important risk factors involved in the development and progression of periodontitis. However, the signaling mechanism underlying the host immune response is not fully understood in periodontal lesions. In this study, we determined the expression of janus kinase (JAK)/signal transducer and activator of transcription (STAT) on Porphyromonas gingivalis lipopolysaccharide (LPS)- and nicotine-induced cytotoxicity and the production of inflammatory mediators, using osteoblasts. The cells were cultured with 5 mM nicotine in the presence of $1{\mu}g/ml$ LPS. Cell viability was determined using MTT assay. The role of JAK on inflammatory mediator expression and production, and the regulatory mechanisms involved were assessed via enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction, and Western blot analysis. LPS- and nicotine synergistically induced the production of cyclooxgenase-2 (COX-2) and prostaglandin $E_2$ ($PGE_2$) and increased the protein expression of JAK/STAT. Treatment with an JAK inhibitor blocked the production of COX-2 and $PGE_2$ as well as the expression of pro-inflammatory cytokines, such as tumor necrosis factor-${\alpha}$, interleukin-$1{\beta}$ ($IL-1{\beta}$), and IL-6 in LPS- and nicotine-stimulated osteoblasts. These results suggest that JAK/STAT is closely related to the LPS- and nicotine-induced inflammatory effects and is likely to regulate the immune response in periodontal disease associated with dental plaque and smoking.

• Journal of Periodontal and Implant Science
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• 제45권6호
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• pp.252-256
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• 2015

Purpose: The purpose of this report was to describe the clinical and microbiological characteristics of two rare cases of necrotizing stomatitis, and the outcomes of a non-invasive treatment protocol applied in both cases. Methods: We report two cases of necrotizing stomatitis in a rare location in the hard palate of a 40-year-old woman and a 28-year-old man. Neither had a relevant medical history and both presented with highly painful ulceration in the palate and gingival margin that was accompanied by suppuration and necrosis. 3% hydrogen peroxide was applied to the lesions using sterile swabs, and antibiotic and anti-inflammatory treatment was prescribed to both patients in addition to two daily oral rinses of 0.2% chlorhexidine. Results: In both cases, radiological examination ruled out bone involvement, and exfoliative cytology revealed a large inflammatory component and the presence of forms compatible with fusobacteria and spirochetes. There was a rapid response to treatment and a major improvement was observed after 48 hours, with almost complete resolution of the ulcerated lesions and detachment of necrotic areas with partial decapitation of gingival papillae. Conclusions: Necrotizing periodontal lesions can hinder periodontal probing and the mechanical removal of plaque in some cases due to the extreme pain suffered by the patients. We present a non-invasive treatment approach that can manage these situations effectively.

• Journal of Periodontal and Implant Science
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• 제28권4호
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• pp.611-632
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• 1998

Chitosan has been known as a wound healing agent. The purpose of this study was to evaluate the biocompatibility and guided bone regenerative effect of chitosan and chitosan-cellulose membranes. The effects of chitosan and chitosan-cellulose membranes on the growth and survival of human periodontal ligament cells were examined by rapid colorimetric MTT(tetrazolium) assay, and the tissue response and resorption pattern were observed by implanting the membranes into the subcutaneous tissue of the back of rats for 6 weeks. To evaluate the guided bone regenerative potential of membranes, the amount of newly formed bone in the rat calvarial defects(8mm in diameter) was measured by histomorphometry and radiomorphometry 1,2 and 4 weeks after implantation of membranes. Chitosan and chitosan-cellulose membranes showed no adverse effect on the growth and survival of human periodontal ligament cells. When membranes were subcutaneously implanted, inflammatory reaction was observed at 1 week and which gradually subsided 2weeks after implantation. Membranes remained intact throughout the experimental period of 6 weeks. Radiomorphometric analysis of the craniotomy sites revealed that chitosan and chitosan-cellulose membrane implanted sites showed increased radiopacity over control. Statistically significant differences with control were found in chitosan-cellulose membrane implanted group at 2 and 4 weeks, and chitosan membrane implanted group at 4 weeks(P<0.05). Histomorphometric data indicated a pattern of osseous healing similar to radiomorphometric analysis. There was a statistically significant difference between control and chitosan-cellulose membrane implanted group at 4 weeks(P<0.05). These results implicate that chitosan and chitosan-cellulose membrane might be useful for guided bone regeneration.

• 한국치위생학회지
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• 제12권2호
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• pp.275-284
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• 2012

Objectives : The purpose of this study was to examine the oral health behavior of shipbuilding company workers in some regions in a bid to provide information on the oral health plans for industrial fields. Methods : The subjects in this study were 310 workers in 10 shipbuilding companies and suppliers in Jeolla Namdo Province, on whom a self-administered survey was conducted. Results : 1. Concerning general information about the subjects who participated in the research, gender was possessed 94.8% by men and 5.2% by women. Age was the largest in 31~40 years old with 44.2%. Marital status was the largest in the married with 64.5%. It was the largest in under high school graduate with 71.9% for academic background, in 2,000,000 won~3,000,000 won with 49.0% for monthly family income, and in cooking with 33.9% for work field. 2. Research subjects' toothbrushing time was indicated to be the largest in after having breakfast. It was indicated to be twice a day with 41.3% for toothbrushing frequency. 90.3% of the respondents are not using auxiliary oral hygiene devices. 3. Recognition on periodontal health status was found larger in workers whose response was that their own periodontal health status is 'healthy' than workers who responded that their status is 'not healthy.' Workers, who don't have subjective symptom on periodontal status, were indicated to be larger. 4. Ratio of subjects with tooth scaling experience accounted for 59.7%. The ratio of tooth scaling experience was indicated to be different depending on academic background and monthly family income. Conclusions : Academic credential, monthly family income and the line of work were identified as the main factors to affect oral health care of the shipbuilding workers. Oral health education and dynamic implementation of corporate oral health promotion which are designed to meet the needs of workers are required.

• Journal of Periodontal and Implant Science
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• 제44권1호
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• pp.39-47
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• 2014

Purpose: Peri-implantitis, a clinical term describing the inflammatory process that affects the soft and hard tissues around an osseointegrated implant, may lead to peri-implant pocket formation and loss of supporting bone. However, this imprecise definition has resulted in a wide variation of the reported prevalence; ${\geq}10%$ of implants and 20% of patients over a 5- to 10-year period after implantation has been reported. The individual reporting of bone loss, bleeding on probing, pocket probing depth and inconsistent recording of results has led to this variation in the prevalence. Thus, a specific definition of peri-implantitis is needed. This paper describes the vast variation existing in the definition of peri-implantitis and suggests a logical way to record the degree and prevalence of the condition. The evaluation of bone loss must be made within the concept of natural physiological bony remodelling according to the initial peri-implant hard and soft tissue damage and actual definitive load of the implant. Therefore, the reason for bone loss must be determined as either a result of the individual osseous remodelling process or a response to infection. Methods: The most current Papers and Consensus of Opinion describing peri-implantitis are presented to illustrate the dilemma that periodontologists and implant surgeons are faced with when diagnosing the degree of the disease process and the necessary treatment regime that will be required. Results: The treatment of peri-implantitis should be determined by its severity. A case of advanced peri-implantitis is at risk of extreme implant exposure that results in a loss of soft tissue morphology and keratinized gingival tissue. Conclusions: Loss of bone at the implant surface may lead to loss of bone at any adjacent natural teeth or implants. Thus, if early detection of peri-implantitis has not occurred and the disease process progresses to advanced peri-implantitis, the compromised hard and soft tissues will require extensive, skill-sensitive regenerative procedures, including implantotomy, established periodontal regenerative techniques and alternative osteotomy sites.

• Journal of Periodontal and Implant Science
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• 제50권5호
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• pp.291-302
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• 2020

Purpose: The objective of this study was to investigate whether phelligridin D could reduce glucose-induced oxidative stress, attenuate the resulting inflammatory response, and restore the function of human periodontal ligament cells (HPDLCs). Methods: Primary HPDLCs were isolated from healthy human teeth and cultured. To investigate the effect of phelligridin D on glucose-induced oxidative stress, HPDLCs were treated with phelligridin D, various concentrations of glucose, and glucose oxidase. Glucose-induced oxidative stress, inflammatory molecules, osteoblast differentiation, and mineralization of the HPDLCs were measured by hydrogen peroxide (H₂O₂) generation, cellular viability, alkaline phosphatase (ALP) activity, alizarin red staining, and western blot analyses. Results: Glucose-induced oxidative stress led to increased production of H₂O₂, with negative impacts on cellular viability, ALP activity, and calcium deposition in HPDLCs. Furthermore, HPDLCs under glucose-induced oxidative stress showed induction of inflammatory molecules (intercellular adhesion molecule-1, vascular cell adhesion protein-1, tumor necrosis factor-alpha, interleukin-1-beta) and disturbances of osteogenic differentiation (bone morphogenetic protein-2, and -7, runt-related transcription factor-2), cementogenesis (cementum protein-1), and autophagy-related molecules (autophagy related 5, light chain 3 I/II, beclin-1). Phelligridin D restored all these molecules and maintained the function of HPDLCs even under glucose-induced oxidative stress. Conclusions: This study suggests that phelligridin D reduces the inflammation that results from glucose-induced oxidative stress and restores the function of HPDLCs (e.g., osteoblast differentiation) by upregulating autophagy.

• International Journal of Oral Biology
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• 제45권2호
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• pp.42-50
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• 2020

Lysophosphatidic acid (LPA) is a lipid messenger mediated by G protein-coupled receptors (LPAR1-6). It is involved in the pathogenesis of certain chronic inflammatory and autoimmune diseases. In addition, it controls the self-renewal and differentiation of stem cells. Recent research has demonstrated the close relationship between periodontitis and various diseases in the human body. However, the precise role of LPA in the development of periodontitis has not been studied. We identified that LPAR1 was highly expressed in human periodontal ligament stem cells (PDLSCs). In periodontitis-mimicking conditions with Porphyromonas gingivalis-derived lipopolysaccharide (Pg-LPS) treatment, PDLSCs exhibited a considerable reduction in the cellular viability and osteogenic differentiation potential, in addition to an increase in the inflammatory responses including tumor necrosis factor-α and interleukin-1β expression and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation. Of the various LPAR antagonists, pre-treatment with AM095, an LPAR1 inhibitor, showed a positive effect on the restoration of cellular viability and osteogenic differentiation, accompanied by a decrease in NF-κB signaling, and action against Pg-LPS. These findings suggest that the modulation of LPAR1 activity will assist in checking the progression of periodontitis and in its treatment.

• International Journal of Oral Biology
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• 제34권2호
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• pp.53-59
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• 2009

Periodontal ligament (PDL) tissue is a connective tissue that is interposed between the roots of the teeth and the inner wall of the alveolar bone socket. PDL is always exposed to physiologic mechanical force such as masticatory force and PDL cells play important roles during orthodontic tooth movement by synthesizing and secreting different mediators involved in bone remodeling. The Wnt/${\beta}$-catenin signaling pathway was recently shown to play a significant role in the control of bone formation. In the present study, we applied cyclic tensile stress of 20% elongation to cultured human PDL cells and assessed its impact after six days upon components of the Wnt/${\beta}$-catenin signaling pathway. RTPCR analysis showed that Wnt1a, Wnt3a, Wnt10b and the Wnt receptor LRP5 were down-regulated, whereas the Wnt inhibitor DKK1 was up-regulated in response to these stress conditions. In contrast, little change was detected in the mRNA expression of Wnt5a, Wnt7b, Fz1, and LRP6. By western blotting we found decreased expression of the ${\beta}$-catenin and p-GSK-3${\beta}$ proteins. Our results thus show that mechanical stress suppresses the canonical Wnt/${\beta}$-catenin signaling pathway in PDL cells.

• 대한통합의학회지
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• 제7권4호
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• pp.61-69
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• 2019

Purpose : Human gingival fibroblast cell is one of the the main cell types in periodontal tissue, which they can show anti-inflammatory activity through the production of numerous lines of inflammatory mediators such as inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2 and interleukins. Porphyromonas gingivalis, one of the oral pathogens, has reported to play a critical role in the development of periodontal diseases. This study aimed to investigate anti-inflammatory and antioxidative activities of Gracilaria textorii ethanol extract (GTEE) in P. gingivalis derived lipopolysaccharide (LPS-PG) stimulated human gingival fibroblast (HGF)-1 cell line. Methods : In order to analyze anti-inflammatory and antioxidative activities of GTEE in HGF-1 cell line, NOS enzyme activity, expression levels of iNOS, COX-2, NAD(P)H quinone dehydrogenase (NQO)1 and their transcription factors were estimated by Griess reaction and western hybridization. Results : LPS-PG induced overexpression of iNOS and COX-2, which was significantly attenuated by GTEE treatment in a dose-dependent manner without any cytotoxicity. In addition, intracellular NOS activity was in accordance with the result of iNOS expression. Due to important role in the regulation of inflammatory responses, phosphorylated status of p65 and c-jun, each subunit of nuclear factor (NF)-κB and activator protein (AP)-1, was also dose-dependently ameliorated by GTEE treatment. One of phase II enzymes, NQO1, and its transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2), were analyzed since elevated phase II enzyme expression inhibited inflammatory response, which was significantly elevated by GTEE treatment in HGF-1 cell line. Conclusion : In conclusion, GTEE mitigated LPS-PG-stimulated inflammatory responses by attenuating NF-κB and AP-1 activation as well as accelerating NQO1 and Nrf2 expression in HGF-1 cell line. These results indicate that GTEE might be utilized a promising strategy for potential anti-inflammatory agent in periodontal diseases.