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Background/Purpose: This study was conducted to evaluate the influence of mucogingival parameters, including keratinized mucosa (KM) and attached gingiva (AG), on the outcome of non-surgical periodontal therapy (NSPT). Methods: A total of 204 non-smoking patients with generalized chronic periodontitis who received NSPT between 2012 and 2014 were included. The Mantel–Haenszel chi-square test was used to assess the associations between initial mucogingival parameters and initial clinical parameters on the buccal aspect, and the associations between initial mucogingival parameters and outcome clinical parameters on the buccal aspect of the sites with severe periodontal destruction. The generalized liner model was used to evaluate the contribution of initial clinical parameters to the outcome of NSPT. Results: KM ≥ 3 mm was associated with greater probing pocket depth (PD), less gingival recession (REC), and less clinical attachment level (CAL), and AG

Connective tissue growth factor (CCN2) has been associated with the pathogenesis of various fibrotic diseases, including oral submucous fibrosis (OSF). The chemical constituents of areca nut along with the mechanical trauma cause OSF. The coarse fibers of areca nut injure the mucosa and hence sphingosine-1-phosphate (S1P) is released at the wounded sites. Recent studies have shown that S1P is involved in wound healing and the development of fibrosis. The aims of this study were to investigate the effects of S1P on CCN2 expression in human buccal fibroblasts (HBFs) and identify the potential targets for drug intervention or chemoprevention of OSF. Methods: Western blot analyses were used to study the effects of S1P on CCN2 expression and its signaling pathways in HBFs and whether epigallocatechin-3-gallate (EGCG), the main and most significant polyphenol in green tea, could inhibit this pathway. Results: S1P significantly enhanced CCN2 synthesis in HBFs. This effect can be inhibited by c-Jun NH2-terminal kinase (JNK) inhibitor and extracellular signal-regulated kinase inhibitor but not by P38 mitogen-activated protein kinase inhibitor. Interestingly, EGCG completely blocked S1P-induced CCN2 expression via suppressing S1P-induced JNK phosphorylation. Conclusion: S1P released by repetitive mechanical trauma during AN chewing may contribute to the pathogenesis of OSF through upregulating CCN2 expression in HBFs. EGCG could be an adjuvant to the current offered therapy options or the prevention of OSF through suppression of JNK activation.

Inflammatory response is triggered after recognition of microbial ligands by innate receptors such as Toll-like receptors (TLRs) and Nucleotide oligomerization domain (NOD)-like receptors (NLRs). In this study, we examined serial frozen sections of gingival biopsies from patients with gingivitis or periodontitis by immunohistochemical analysis for the topographic expression patterns of selected innate receptors and their association with cell proliferation in clinically healthy and diseased gingival tissues. Methods: A total of 19 gingival biopsies were collected from patients at the School of Dentistry, National Taiwan University Medical Center according to approved protocol and with informed consent. The specimens were assigned to either the gingivitis group or periodontitis group after clinical evaluation using gingival index. Frozen sections of gingival biopsies were stained with hematoxylin and eosin for histological evaluation. Serial sections of the same samples were stained with a panel of antibodies for immunohistochemical analysis. Expression of each protein marker was compared in the oral versus the sulcular epithelium of the same section. Results: Expression of cytokeratin 19 (CK19) was markedly increased in the basement membranes of the oral epithelium and in all layers of the pocket epithelium where it caused evident cell proliferation and migration of sulcular epithelial cells into the lamina propria of periodontitis tissue. TLR4 and the cytoplasmic NLRP3 were expressed in all sections examined regardless of disease state. However, expression of TLR9-, CK19- and collagenolytic matrix metalloproteinase-13 and activated NF-κB subunit p65 was more commonly found in periodontitis tissues than in gingivitis tissues. Conclusion: Activation of TLR9 signaling in the pocket epithelium was highly associated with periodontal inflammation and possibly with loss of tissue integrity. Further studies of mechanisms by which TLR9 signaling is activated in the periodontal epithelium may lead to new strategies for treating periodontitis.

Connective tissue growth factor (CTGF/CCN2) is involved in the development and progression of fibrotic diseases, including gingival overgrowth (GO). Recent studies indicate that lysophosphatidic acid (LPA) is also significantly involved in wound healing and the development of fibrosis. This study investigated whether epigallocatechin-3-gallate (EGCG) can inhibit LPA-induced CCN2 expression in human gingival fibroblast (GF) and its mechanism. Methods: Western blot analyses were used to study the signaling pathways of LPA-induced CCN2 expression in human GFs and the effects of EGCG on this pathway. Results: LPA stimulated CCN2 synthesis in human GFs. This effect can be significantly inhibited bytransforming growth factor-β type I receptor/ALK5, Smad3, and JNK inhibitors but not ERK, P38, and MAPK inhibitors. EGCG completely inhibited LPA-induced CCN2 expression through attenuating the LPA-induced JNK and Smad3 phosphorylation in human GFs. Conclusion: LPA produced at the surgical wound may contribute to the recurrence of GO by upregulating CCN2 expression in human GFs. This effect was mediated by Smad3 and JNK activation and ALK5 transactivation. EGCG could be a useful agent for reducing the recurrence of GO after surgery through suppression of JNK and Smad3 activations.

Mineral trioxide aggregate (MTA) was one of most popular biomaterials for endodontic treatment in the past decade. Its superb biocompatibility, sealing ability and surface for tissue adhesion all make MTA a potential candidate for many dental applications, such as apexification, perforation repair, repair of root resorption, and as a root-end filling material. There are many review articles regarding the physical, chemical and biological properties of MTA. However, there are few reviews discussing the relationship between the composition and hydration behavior of MTA. The aim of this article was to provide a systematic review regarding the compositional characteristics and hydration behavior of MTA.

Background. Cysteine-rich 61 (Cyr61 [CCN1]) has disparate functions in tumorigenesis that are dependent on the cell types. The aim of the study was to investigate its role in the growth of oral squamous cell carcinoma (SCC). Methods. The study used immunohistochemistry to examine Cyr61 expression in 93 oral SCC specimens and assessed the effect of Cyr61 overexpression on proliferation and migration of oral SCC cells in vitro and xenograft growth in severe combined immunodeficient (SCID) mice. Results. High expression of Cyr61 significantly correlated with large tumor size (p = .009) and advanced tumor stage (p = .036). Multivariate analysis revealed that high Cyr61 (relative risk [RR] 2.44, 95% confidence interval [CI] 1.209-4.95, p = .010) significantly correlated with mortality. Forced expression of Cyr61 stimulated the motility and growth of Ca9-22 cells in vitro and enhanced xenograft growth in SCID mice. Conclusions. Cyr61 is a positive growth modulator of oral SCC and Cyr61 overexpression is an independent prognostic indicator for patients with oral SCC. [ABSTRACT FROM AUTHOR]

Background; In a previous study, we evaluated the in vivo effects of an Nd:YAG laser on periodontal disease by measuring crevicular interleukin (IL)-1β levels before and after laser application. It was found that laser therapy was less effective than traditional scaling and root planing. These results might be due to incomplete removal of microbial residues and cementum-bound endotoxin on root surfaces by the laser. In this study, we explored the in vitro effectiveness of an Nd:YAG laser for the elimination of cementum-bound endotoxin by measuring IL-1β changes in stimulated monocytes. Methods: Fresh human monocytes were harvested from adults without periodontitis and grown in RPMI 1640 medium. Diseased cementum particles were collected and prepared from teeth with untreated periodontitis and were irradiated with 5 levels of laser energy. Cementum particles were subjected to endotoxin testing by a limulus amebocyte lysate (LAL) assay and then were incubated with cultured monocytes. Production of IL-1β in stimulated monocytes was measured by enzyme-linked immunosorbent assay and quantified by spectrophotometry. Results: The endotoxin unit (EU) of diseased cementum was 18.4 EU/mg, which seemed to be remarkably lower than that of common periodontal pathogens including Porphyromanas gingivalis (381) at 15,300 EU/mg/ml, Prevotella intermedia (ATCC 25611) at 227 EU/mg/ml, and Fusobacterium nucleatum (ATCC 25586) at 1,967 EU/mg/ml. Monocytes subjected to stimulation by diseased cementum particles without laser irradiation produced 124 to 145 pg/ml IL-1β 9- to 18-fold higher than that of unstimulated monocytes (7.07 to 15.95 pg/ml). Diseased cementum particles after irradiation with various energy levels of the Nd:YAG laser could still stimulate monocytes to secrete 89 to 129 pg/ml IL-1β. No statistically significant difference was found in the production of IL-1β induced by diseased-bound cementum with or without laser irradiation. Conclusions: The Nd:YAG laser varying from 50 mJ, 10 pps to 150 mJ, 20 pps, for 2 minutes, did not seem to be effective in destroying diseased cementum endotoxin. [ABSTRACT FROM AUTHOR]

Background The Nd:YAG laser has recently been used in the treatment of periodontal disease. However, although a clinical reduction of probing depth and gingival inflammation to this new approach has been reported, it has not been fully evaluated. Interleukin-1 beta (IL-1β), a potent stimulator of bone resorption, has been identified in gingival crevicular fluid (GCF), which is closely associated with periodontal destruction. The aim of this study was to compare the effects of Nd:YAQ laser treatment versus scaling/root planing (SRP) treatment on crevicular IL-1β levels in 52 sampled sites obtained from 8 periodontitis patients. Methods: One or 2 periodontitis-affected sites with a 4 to 6 mm probing depth and horizontal bone loss from 3 adjacent single-root teeth in each of 4 separate quadrants were selected from patients for clinical documentation and IL-1β assay. Sampling site(s) from each diseased quadrant was randomly assigned to one of the following groups: 1) subgingival laser treatment (20 pps, 150 mJ) only; 2) SRP only; 3) laser treatment first, followed by SRP 6 weeks later; or 4) SRP first, followed by laser therapy 6 weeks later. The GCF was collected and the amount of IL-1β was assayed by enzyme-linked immunosorbent assay (ELISA). Clinical parameters and GCF were measured at baseline and biweekly after therapy for 12 weeks. Results: An obvious clinical improvement (marked decrease in the number of diseased sites with gingival index ≥2) and reduction of crevicular 1L-1β were found in all groups. The level of IL-1β was significantly lower in the SRP group (P = 0.035) than in the laser therapy group for the duration of the 12 weeks. The laser combined SRP therapy group showed a further reduction of IL-1β (6 to 12 weeks after treatment) than either laser therapy alone or SRP combined laser therapy. Conclusions: Our data suggest that laser therapy appeared to be less effective than traditional SRP treatment. Of the 4 treatment modalities, inclusion of SRP was found to have a superior IL-1β response, when compared to other therapies without it. In addition, no additional benefit was found when laser treatment was used secondary to traditional SRP therapy. [ABSTRACT FROM AUTHOR]

Background: Whether adjunctive tetracycline fibers can provide an additive effect to scaling and root planing in treating non-responsive sites in maintenance subjects is still controversial. Recolonization of the bacteria from untreated sites or from the extracrevicular region may explain the insignificant response to local therapy. The purpose of the present study was to evaluate the microbiological response of sites treated with tetracycline fibers combined with scaling and root planing. Methods: The study was conducted in a split-mouth design. Thirty patients on maintenance therapy having at least 2 non-adjacent sites in separate quadrants with probing depths between 4 to 8 mm with bleeding on probing, or aspartate aminotransferase enzyme levels > 300 µIU in the gingival crevicular fluid, were treated with scaling and root planing plus tetracycline fibers or with scaling and root planing only. Subgingival plaque samples were collected at baseline, end 1, 3, and 6 months following treatment. A. actino-mycetemcomitans, C. rectus, B. forsythus, E. corrodens, F. nucleatum, P gingivalis, and P. intermedia were detected by culture, immunofluorescence, or PCR technique. Results: There was a reduction of total bacterial cell count, as well as of certain periodontal pathogens, following treatment. The prevalence of A. actinomycetemcomitans, B. forsythus, and P. gingivalis and the mean proportions of C. rectus, P. intermedia, F. nucleatum, and P. gingivalis decreased after therapy, but there was no statistically significant difference between the 2 treatment groups with respect to bacterial proportions or the number of positive sites. Besides, the pathogens could not be eliminated from the periodontal pocket, and recolonization of the pocket was noted at 3 months post-treatment. Conclusions: Bacteria located within the cheek, tongue mucosa, saliva, or untreated sites may contribute to reinfection of the pockets and explain the insignificant response to local tetracycline therapy. [ABSTRACT FROM AUTHOR]

Background: The aim of the present study was to evaluate the association between the occurrence of certain specific periodontal pathogens and aspartate aminotransferase (AST) levels in gingival crevicular fluid (GCF). Methods: Thirty systemically healthy subjects with moderate to advanced periodontitis were selected. Within each subject, the AST contents of GCF from sites with probing depth between 5 mm and 7 mm were measured using a chairside colorimetric test. AST-positive site refers to one that had an AST level ≥800 µIU. Subgingival plaque samples from one AST-positive and one negative site were collected for microbiological examination. One site with probing depth ≥3 mm and no gingival inflammation was selected as a healthy control. Clinical parameters of the chosen sites, including the plaque index and gingival index scores, probing depth, and clinical attachment level were measured. Culture and immunofluorescence (IF) were used for detecting common periodontal pathogens, including Actinobacillus actinomycetemcomitans, Peptostreptococcus micros, Campylobacter rectus, Eikenella corrodens, Fusobacterium nucleatum, Capnocytophaga species, Prevotella intermedia, Prevotella melaninogenica, and Porphyromonas gingivalis. Logistic regression was used to analyze the correlation between the AST test and certain specific pathogens. Results: The GCF scores and total cultivable bacterial counts were higher in AST-positive sites than either AST-negative or healthy sites The prevalence and proportions of specific periodontal pathogens such as C. rectus. E. corrodens, F. nucleatum. Capnocytophaga species, P. intermedia, and P. gingivalis were significantly higher in positive than in negative sites. In analyzing the correlation of the proportion of 6 pathogens with the AST test by logistic regression, only P. gingivalis showed a significant positive correlation. The odds ratio of having a high proportion of P. gingivalis in the presence of a positive AST test was 1.21. Conclusions: The present study showed that at AST-positive sites, there is a higher prevalence and higher proportion of certain periodontal pathogens. Although only the correlation of P. gingivalis and AST values was statistically significant, the results imply that certain periodontal pathogens may be associated with elevation of AST levels in GCF. [ABSTRACT FROM AUTHOR]