• Journal of Periodontal and Implant Science
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• 제47권5호
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• pp.328-338
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• 2017

Purpose: Chronic periodontitis is an inflammatory disease induced by pathogenic bacterial accumulation. A novel index, the periodontal inflamed surface area (PISA), represents the sum of the periodontal pocket depth of bleeding on probing (BOP)-positive sites. It is advantageous for data processing and analysis because it can be treated as a continuous variable to quantify periodontal inflammation. In the present study, we evaluated correlations between PISA and periodontal classifications, and examined PISA as an index integrating the discrete conventional periodontal indexes. Methods: This study was a cross-sectional subgroup analysis of data from a prospective cohort study investigating the association between chronic periodontitis and the clinical features of ankylosing spondylitis. Data from 84 patients without systemic diseases (the control group in the previous study) were analyzed in the present study. Results: PISA values were positively correlated with conventional periodontal classifications (Spearman correlation coefficient=0.52; P<0.01) and with periodontal indexes, such as BOP and the plaque index (PI) (r=0.94; P<0.01 and r=0.60; P<0.01, respectively; Pearson correlation test). Porphyromonas gingivalis expression and the presence of serum P. gingivalis antibodies were significant factors affecting PISA values in a simple linear regression analysis, together with periodontal classification, PI, bleeding index, and smoking, but not in the multivariate analysis. In the multivariate linear regression analysis, PISA values were positively correlated with the quantity of current smoking, PI, and severity of periodontal disease. Conclusions: PISA integrates multiple periodontal indexes, such as probing pocket depth, BOP, and PI into a numerical variable. PISA is advantageous for quantifying periodontal inflammation and plaque accumulation.

• Journal of Periodontal and Implant Science
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• 제26권1호
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• pp.117-132
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• 1996

The purpose of this study was to evaluate the bacterial adherence on e-PTFE membrane immersed in whole saliva from subjects with different periodontal status. Experiment involved 3 subject groups: 5 persons with healthy periodontium(probing depth below 3mm and no signs of gingival inflammation including bleeding on probing), 10 patients with gingivitis(probing depth below 3mm and apparent signs of gingival inflammation), and 10 patients with advanced periodontitis(probing depth over 7mm and apparent signs of gingival inflammation). Each disease group was included before and after scaling and root planing treatment. After obtaining whole saliva from each subject, e-PTFE membrane(Gore-Tex periodontal membrane : $GTPM^{(R)}$, W.L. Gore & Associates, Flagstaff, USA) specimens were immersed at room temperature in the saliva aliqouts for 1, 3, 7 days. The weight between pre - and post - immersion in saliva was measured with the analytical balance and the difference was recorded. The specimens were processed for SEM observation. The bacterial adherence on the membrane specimens was evaluated using the scanning electron microscope images. The obtained results were as follows : 1. There was no difference in the weight of bacteria adherent to e-PTFE membrane specimens according to the periodontal status and the immersion periods. 2. As the exposure time to saliva increased, the bacterial adherence to the membrane specimen significantly increased in all groups(P<0.005). 3. As the severity of periodontal disease increased, the bacterial adherence to the membrane specimens significantly increased(p<0.001). 4. After scaling and root planing, the bacterial adherence to the membrane specimens significantly decreased in gingivitis and periodontitis patient group(P<0.001). These results suggest that bacterial contamination on exposed barrier membrane surface be reduced through improvement of periodontal status and oral health environment before and after GTR procedure for the successful outcome.

• Journal of Periodontal and Implant Science
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• 제28권3호
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• pp.465-475
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• 1998

The purpose of this study was to investigate the comparative effects of subgingival irrigation using some oral mouth rinses on early healing process of periodontal inflammation. The study population consisted of 13 patients with periodontal inflammation and distributed into 4 groups. Oral hygiene instruction, delicate scaling and root planing were done and then irrigated per 3 days during 2 weeks in situ with 1 of 4 solutions ; normal saline, C31G, Benzotonium chloride and tetracycline. Examination regarding probing pocket depth, plaque index, sulcular bleeding index, gingival index, gingival recession and leukocytes differential count was performed. Evaluation was made at the baseline and 2 weeks after non-surgical periodontal therapy. The results were as follows : 1. Clinical indices including probing pocket depth, plaque index, sulcular bleeding index, gingival index and gingival recession were significantly improved from baseline to 2 weeks. But there was no significant differences among 4 groups. 2. PMNs percent on leukocytes differential count was significantly decreased from baseline to 2 weeks on all groups. Those of tetracycline and C31G were significantly decreased than those of normal saline group. These results suggest that clinical indices were not different, but the decrease of inflammation were significantly different among some mouth rinses.

• 생명과학회지
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• 제23권4호
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• pp.602-608
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• 2013

만성적인 염증이 다단계 발암과정에서 다면적인 역할을 하고 있음은 이미 잘 알려진 사실이다. 치주 질환의 원인은 구강 박테리아에서 분비되는 내독소들과 염증 유발인자들의 생성 등이 관여하는 다양한 요인들을 포함하며, 이는 잘못된 구강 위생 관리가 신체의 여러 가지 전신병적 원인과 연관되어 있음을 의미한다. 비위생적인 구강 상태와 연관된 만성 염증, 흡연, 알콜 섭취의 증가 등은 암의 발병 위험 요소로 작용함은 명확한 사실이다. 최근에는 구강 위생과 치아 손실이 위장관암, 폐암 및 췌장암 뿐만 아니라 혈구암 발병 증가와 직접적인 연관성이 있음이 밝혀졌다. 또한 흡연은 악성 질환 발병의 위험 요소로서 구강 위생의 강력한 위해요인임은 명백하며, 역학적 조사결과들에 의하면 구강 박테리아에 의한 치주 질환은 만성 염증을 통하여 흡연과 알콜 연관 발암원을 활성시킴으로서 다양한 암의 발병 위험 요소를 증가시킬 수 있는 것으로 나타났다. 따라서 암 뿐만 아니라 다른 다양한 질환의 예방을 위한 적절한 구강 관리는 필수적이다. 본 논문에서는 암예방을 위한 악성질환의 위해 요소로서 염증과 치주질환 및 구강 위생과의 연관성을 논하였다.

• International Journal of Oral Biology
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• 제38권3호
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• pp.87-92
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• 2013

Periodontal inflammation increases the risk of tooth loss, particularly in cases where there is an associated loss of alveolar bone and periodontal ligament (PDL). Histological and morphometric evaluation of periodontal inflammation is difficult. Especially, the lengths of the periodontal ligament and interdental alveolar bone space have not been quantified. A quantitative imaging procedure applicable to an animal model would be an important clinical study. The purpose of this study was to quantify the loss of alveolar bone and periodontal ligament by evaluation with micro-computed tomography (micro-CT). Another purpose was to investigate differences in infections with systemic E. coli LPS and TNF-${\alpha}$ on E. coli lipopolysaccharide (LPS) in loss of alveolar bone and periodontal ligament model on mice. This study showed that linear measurements of alveolar bone loss were represented with an increasing trend of the periodontal ligament length and interdental alveolar process space. The effects of systemic E. coli LPS and TNF-${\alpha}$ on an E. coli LPS-induced periodontitis mice model were investigated in this research. Loss of periodontal ligament and alveolar bone were evaluated by micro-computed tomography (micro-CT) and calculated by the two- and three dimensional microstructure morphometric parameters. Also, there was a significantly increasing trend of the interdental alveolar process space in E. coli LPS and TNF-${\alpha}$ on E. coli LPS compared to PBS. And E. coli LPS and TNF-${\alpha}$ on E. coli LPS had a slightly increasing trend of the periodontal ligament length. The increasing trend of TNF-${\alpha}$ on the LPS-induced mice model in this experiment supports the previous studies on the contribution of periodontal diseases in the pathogenesis of systemic diseases. Also, our findings offer a unique model for the study of the role of LPS-induced TNF-${\alpha}$ in systemic and chronic local inflammatory processes and inflammatory diseases. In this study, we performed rapidly quantification of the periodontal inflammatory processes and periodontal bone loss using micro-computed tomography (micro-CT) in mice.

• Journal of Microbiology and Biotechnology
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• 제28권8호
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• pp.1270-1281
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• 2018

Periodontal disease is triggered by the host immune response to pathogens in the microbial biofilm. Worsening of periodontal disease destroys the tooth-supporting tissues and alveolar bone. As oral inflammation can induce systemic diseases in humans, it is important to prevent periodontal disease. In this study, we demonstrated that Curcuma xanthorrhiza supercritical extract (CXS) and its active compound, xanthorrhizol (XAN), exhibit anti-inflammatory effects on lipopolysaccharide (LPS)-treated human gingival fibroblast-1 cells and anti-osteoclastic effects on receptor activator of nuclear factor kappa B ligand (RANKL)-treated RAW264.7 cells. LPS-upregulated inflammatory factors, such as nuclear factor kappa B p65 and $interleukin-1{\beta}$, were prominently reduced by CXS and XAN. In addition, RANKL-induced osteoclastic factors, such as nuclear factor of activated T-cells c1, tartrate-resistant acid phosphatase, and cathepsin K, were decreased in the presence of CXS and XAN. CXS and XAN inhibited the mitogen-activated protein kinase (MAPK)/activator protein-1 (AP-1) signaling pathway. Collectively, these results provide evidence that CXS and XAN suppress LPS-induced inflammation and RANKL-induced osteoclastogenesis by suppressing the MAPK/AP-1 pathway.

• 대한치과의사협회지
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• 제51권9호
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• pp.501-510
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• 2013

This paper reviews a current view regarding the association between periodontitis and atherosclerotic cardiovascular diseases (ACVD). Many evidences have suggested that there exist biological mechanisms by which periodontitis can lead to ACVD. Periodontal infection can lead to direct bacterial invasion into endothelial tissues through the blood stream, then the bacteria can activate the host inflammatory response followed by atheroma formation, maturation and exacerbation. Also, chronic periodontal infections may indirectly induce endothelial activation or dysfunction through a state of systemic inflammation as evidenced by elevated plasma acute proteins, IL-6 and fibrinogen as well. There is moderate evidence that periodontal treatment can reduce systemic inflammation and improvement of both clinical surrogate markers. But there is no periodontal intervention study available on primary ACVD prevention. There is consistent and strong epidemiologic evidence, including in vitro, animal and clinical studies, that periodontitis imparts increased risk for future ACVD. However, evidences from intervention trials to date are not sufficient to confirm the multi directional causality of periodontitis in ACVD etiology. Well-designed intervention trials on the impact of periodontal treatment on the prevention of ACVD outcomes are needed.

• Journal of Periodontal and Implant Science
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• 제44권4호
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• pp.207-213
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• 2014

Purpose: The study was aimed at investigating changes in periodontal parameters and superoxide dismutase activity triggered by root surface debridement with and without micronutrient supplementation in postmenopausal women. Methods: Forty-three postmenopausal chronic periodontitis patients were divided into two groups: group 1 (n=22) were provided periodontal treatment in the form of scaling and root planing (SRP) and group 2 (n=21) patients received SRP along with systemic administration of micronutrient antioxidants. Patients in both groups were subjected to root surface debridement. Group 2 patients also received adjunctive micronutrient antioxidant supplementation. Serum and salivary superoxide dismutase (SOD) activity along with periodontal parameters were recorded at baseline and 3 months after therapy. Results: Salivary and serum SOD values significantly (P<0.05) improved with periodontal treatment. Improvement in systemic enzymatic antioxidant status along with reduction in gingival inflammation and bleeding on probing (%) sites was significantly greater in group 2 as compared to group 1. Conclusions: Adjunctive micronutrient supplements reduce periodontal inflammation and improve the status of systemic enzymatic antioxidants in postmenopausal women.

• International Journal of Oral Biology
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• 제35권1호
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• pp.27-33
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• 2010

Periodontal disease is a major oral disorder and comprises a group of infections that lead to inflammation of the gingiva and the destruction of periodontal tissues. $PPAR{\gamma}$ plays an important role in the regulation of several metabolic pathways and has recently been implicated in inflammatory response pathways. However, its effects on periodontal inflammation have yet to be clarified. In our current study, we evaluated the anti-inflammatory effects of $PPAR{\gamma}$ on periodontal disease. Human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS) showed high levels of intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), matrix metalloproteinase-2 (MMP-2), and -9 (MMP-9). Moreover, these cells also showed upregulated activities for extracellular signal regulated kinase (ERK1/2), inducible nitric oxide synthase (iNOS) and cyclooxygnase-2. However, cells treated with Ad/$PPAR{\gamma}$ and rosiglitazone in same culture system showed reduced ICAM-1, VCAM-1, MMP-2, -9 and COX-2. Finally, the anti-inflammatory effects of $PPAR{\gamma}$ appear to be mediated via the suppression of the ERK1/2 pathway and consequent inhibition of NF-kB translocation. Our present findings thus suggest that $PPAR{\gamma}$ indeed has a pivotal role in gingival inflammation and may be a putative molecular target for future therapeutic strategies to control chronic periodontal disease.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제42권6호
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• pp.393-393
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• 2016