Modified approach of regenerative treatment for distal intrabony defect beneath non-keratinized mucosa at terminal molar: A case report.

BACKGROUND: Intrabony defects beneath non-keratinized mucosa are frequently observed at the distal site of terminal molars. Consequently, the application of regenerative treatment using the modified wedge-flap technique is considered impractical for these specific dental conditions. CASE SUMMARY: This article proposes a modified surgical procedure aimed at exposing the distal intrabony defect by making a vertical incision in the keratinized buccal gingiva. The primary objective is to maintain gingival flap stability, thereby facilitating periodontal regeneration. The described technique was successfully employed in a case involving the left mandibular second molar, which presented with an intrabony defect without keratinized gingiva at the distal site. In this case, an incision was made on the disto-buccal gingival tissue, creating a tunnel-like separation of the distal non-keratinized soft tissue to expose the intrabony defect. Subsequently, bone grafting and guided tissue regeneration surgeries were performed, resulting in satisfactory bone fill at 9 mo postoperatively. CONCLUSION: This technique offers a regenerative opportunity for the intrabony defects beneath non-keratinized mucosa and is recommended for further research.

Long-term success and influencing factors of regenerative surgery for intra-bony defects: A retrospective cohort study.

BACKGROUND: The composite outcome measure (COM) more comprehensively assesses the clinical efficacy of regenerative surgery than a single probing measurement. We aimed to assess long-term success defined by the COM (clinical attachment level [CAL] gain of ≥3 mm and postsurgery probing pocket depth [PPD] ≤ 4 mm) and influencing factors of regenerative surgery using bone substitutes and resorbable collagen membrane (RM) for intra-bony defects (IBDs). METHODS: We retrospectively collected data from patients who underwent regenerative surgery using deproteinized bovine bone mineral (DBBM) and RM for IBDs. CAL and PPD values were compared at baseline (preoperative), 1 year (short-term), and at the last follow-up (5-10 years). Multivariate logistic regressions were performed to identify factors influencing COM-based long-term success. RESULTS: Eighty-one defects in 75 teeth of 33 patients who completed follow-up (6.5 ± 1.4 years) were included. One tooth was lost. All defects with complete follow-up exhibited long-term average CAL gain (3.00 ± 2.00 mm, 95% confidence interval [CI]: 2.56-3.44 mm, p < 0.001) and PPD reduction (2.06 ± 1.91 mm, 95% CI: 1.64-2.49 mm, p < 0.001). Long-term success was achieved in 38.8% of IBDs. CAL and PPD values were comparable between 1 year and the last follow-up. Logistic regression analyses revealed that male sex (odds ratio [OR] = 0.23, 95% CI: 0.07-0.75) and bleeding on probing (BOP) during supportive periodontal therapy (OR = 0.96, 95% CI: 0.94-0.99) were risk factors for long-term success. CONCLUSIONS: Regenerative surgery with DBBM and RM for IBDs can achieve some degree of long-term success defined by COM. However, within this study's limitations, male sex and higher BOP incidence postoperatively are negatively associated with optimal long-term success. CLINICAL TRIAL NUMBER: ChiCTR2300069016.

Investigation of peri-implant diseases prevalence and related risk indicators in patients with treated severe periodontitis over 4 years after restoration.

Background/purpose: History of periodontitis is a well-documented risk indicator of peri-implantitis. However, the influence of severity of periodontitis is still unclear, especially for severe periodontitis. This study was aimed to investigate the prevalence of peri-implant disease and analyze the risk indicators in patients with treated severe periodontitis. Materials and methods: A total of 182 implants from 88 patients (44 males and 44 females) with severe periodontitis with a mean fellow-up period of 76.5 months were enrolled in this study. Patient and implant information, and periodontal and peri-implant conditions were collected to evaluate the prevalence of peri-implant disease and risk indicators. Results: The prevalence of peri-implantitis was 9.1% and 6.6% at the patient-level and implant-level. The prevalence of peri-implant mucositis was 76.1% and 51.1% at the patient-level and implant-level. Risk indicators of peri-implantitis included older age (OR: 1.132), poor proximal cleaning habits (OR: 14.218), implants in anterior area (OR: 10.36), poor periodontal disease control (OR: 12.76), high peri-implant plaque index (OR: 4.27), and keratinized tissue width (KTW)＜2 mm (OR: 19.203). Conclusion: Implants in patients with severe periodontitis after periodontal treatment and maintenance show a low prevalence (9.1%) of peri-implantitis and a relatively high prevalence (76.2%) of peri-implant mucositis. Patient age, peri-implant proximal cleaning habits, implant position, periodontal disease control, peri-implant plaque index, and KTW are associated with prevalence of peri-implantitis.

The expression levels of chemotaxis-related molecules CXC chemokine receptor 1, interleukin-8, and pro-platelet basic protein in gingival tissues.

Background/purpose: Excessive host immune response is thought to be an important cause of periodontal tissue damage during periodontitis. The potent chemotaxis produced by locally released chemokines is the key signal to trigger this response. Here, we aimed to investigate the expression of CXC chemokine receptor 1 (CXCR1), and chemokines interleukin-8 (IL-8) and pro-platelet basic protein (PPBP) in human inflammatory gingival tissues compared with healthy tissues. Materials and methods: A total of 54 human gingival tissues, 27 healthy and 27 inflammatory samples, were collected. Fifteen specimens of each group were employed for quantitative reverse transcription polymerase chain reaction to determine the mRNA levels of CXCR1, IL-8, and PPBP. Six samples of each group were used for Western blotting to investigate the protein expression of CXCR1 and for enzyme-linked immunosorbent assay to evaluate the protein levels of IL-8 and PPBP, respectively. Results: The mRNA levels of chemokine receptor CXCR1, chemokine IL-8, and PPBP in inflammatory gingival tissues were significantly higher than those in healthy controls (P < 0.05). The protein levels of CXCR1, IL-8, and PPBP in inflammatory gingival tissues were also significantly higher than those in healthy gingival tissues (P < 0.05). Conclusion: When compared to healthy gingival tissues, the expression of CXCR1, IL-8, and PPBP in inflammatory gingival tissues is higher.

Activation of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 6 by Porphyromonas gingivalis regulates programmed cell death in epithelium.

Background/purpose: Gingival epithelial cells form a physiological barrier against bacterial invasion. Programmed cell death (PCD) regulated by pathogen precognition receptors (PRRs) lead to tissue destruction and is closely related to inflammatory diseases. The purpose of this study was to investigate whether nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 6 (NLRP6) expresses in periodontal epithelium and induces PCD of epithelial cells infected by Porphyromonas gingivalis (P. gingivalis), therefore involves in periodontitis. Material and methods: The expression of NLRP6 was detected in periodontal epithelium from human gingival sections and HaCaT cells stimulated by P. gingivalis. NLRP6 was over-expressed by adenovirus infection in HaCaT or knocked down by siRNA in P. gingivalis infected HaCaT, and the cell death was observed by transmission electron microscopy and flow cytometry analysis. In addition, qPCR and Western blot were performed to determine the expression of NLRP6 and the pyroptosis excutors, caspase-1 and gasdermin D. Enzyme-linked immunosorbent assay were performed to detect the secretion of IL-1ß and IL-18. Results: NLRP6 was up-regulated in both gingival epithelium of patients with periodontitis and P. gingivalis infected HaCaT. Over-expression of NLRP6 in HaCaT led to caspase-1 dependent pyroptosis. Interestingly, knockdown of NLRP6 with siRNA followed by P. gingivalis stimulation inhibited pyroptosis and induced apoptosis. Conclusion: Up-regulation of NLRP6 by P. gingivalis in HaCaT led to pyroptosis, while knocking down NLRP6 inhibited pyroptosis and induced apoptosis, which indicated this PRR may play a crucial role in periodontitis by regulating PCD in periodontal epithelium.

Does vestibular incision improve the outcomes of vestibular incision subperiosteal tunnel technique: A randomized clinical trial for treatment of multiple adjacent type 1 gingival recession.

OBJECTIVE: The purpose of this study was to compare the clinical outcomes of vestibular incision subperiosteal tunnel technique (VISTA) and tunnel approach combined with connective tissue graft (CTG) for treatment of type 1 (RT1) multiple gingival recession. MATERIALS AND METHODS: Twenty-four patients with a total of 59 nonmolar recession teeth were randomly allocated to VISTA + CTG or Tunnel + CTG group. Recession depth and width, probing depth, clinical attachment level, width of keratinized tissue, gingival thickness, flap tension, mean root coverage (MRC), complete root coverage (CRC), patient-centered, and esthetic outcomes (root coverage esthetic scores, RES) were assessed at baseline and 12 months after surgery. RESULTS: At 12 months, MRC of 91.13 ± 16.96% and 91.40 ± 13.53%, CRC of 70.97% and 67.86% were observed for VISTA + CTG and Tunnel + CTG group respectively, with no significant difference between the two groups (p > 0.05). High RES of 8.52 ± 1.46 and 8.82 ± 1.44 was obtained in VISTA + CTG and Tunnel + CTG group respectively, without showing a significant difference (p = 0.245), while less scar formation was observed in Tunnel + CTG group (p < 0.01). CONCLUSIONS: Both procedures were effective for root coverage in RT1 multiple gingival recession at 12 months. Better esthetic result with less scar formation was obtained in tunnel approach combined with CTG without vestibular incision. (Registration number: ChiCTR-INR-16007845, registered on 19/12/2015, http://www.chictr.org.cn). CLINICAL SIGNIFICANCE: VISTA + CTG and Tunnel + CTG were both effective for root coverage in RT1 multiple gingival recession, with satisfying esthetic outcomes. However, it is suggested in critical esthetic areas, treatment options of making vertical incisions should be carefully considered.

Role of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 6 in activation of inflammation in human umbilical vein endothelial cells stimulated by Porphyromonas gingivalis-an in vitro study.

Background/purpose: Porphyromonas gingivalis (P. gingivalis) could induce the activation of vascular endothelial cells and promote the formation of atherosclerosis. Nucleotide-binding oligomerization domain-like receptor family pyrin domain containing (NLRP) 6 could recognize P. gingivalis, but its role in atherosclerosis was unknown. The purpose of this study is to investigate the role of NLRP6 in the activation of inflammation in human umbilical vein endothelial cells (HUVECs) stimulated by P. gingivalis. Materials and methods: The expression level of NLRP6 in HUVECs with or without P. gingivalis-challenge was observed. Down-regulating the expression of NLRP6 in HUVECs, the expression levels of interleukin (IL)-1ß, IL-6, IL-8, tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein (MCP)-1 were detected. Then, the HUVECs with NLRP6-overexpressed were stimulated by P. gingivalis, the levels of inflammatory cytokines above were examined and compared with those in HUVECs triggered by P. gingivalis only. To evaluate the effect of NLRP6 on bacterial immune escape, the NLRP6 was overexpressed, and the colonies of P. gingivalis that survived in HUVECs were calculated. Results: NLRP6 was expressed in HUVECs and decreased after P. gingivalis stimulation. Downregulation of NLRP6 decreased the expression levels of IL-1ß, IL-6, IL-8, TNF-α and MCP-1 in HUVECs. Those cytokines above in NLRP6-overexpressed HUVECs with P. gingivalis-stimulation significantly increased than in the cells with P. gingivalis-stimulation only. Furthermore, over-expression of NLRP6 decreased the colonies of P. gingivalis survival in HUVECs. Conclusion: NLRP6 regulated the activation of inflammation in HUVECs triggered by P. gingivalis and played an important role in P. gingivalis survival in endothelial cells.

Role of immune-related lncRNAs--PRKCQ-AS1 and EGOT in the regulation of IL-1ß, IL-6 and IL-8 expression in human gingival fibroblasts with TNF-α stimulation.

Background/purpose: It was reported that lncRNAs have an effect on immune-related diseases, however, their roles in periodontitis remain to be investigated. The aim of this study was to look for immune-related lncRNAs in periodontitis, and to preliminarily explore their function in vitro. Materials and methods: CIBERSORT was used to analyze abundance of immune cell in the periodontal tissue. Correlation between the expression profile of lncRNAs and abundance of immune cell was calculated and immune-related lncRNAs were identified. The expressions of immune-related lncRNAs identified were validated by RT-qPCR with 15 periodontitis and 15 healthy gingival tissues. The expressions of PRKCQ-AS1 and EGOT in HGFs were detected under the stimulation of different concentrations of TNF-α (0, 10, 15, 20, 30 ng/mL) and different duration (0, 12, 24 and 48 h). Then, siRNA was used to silence PRKCQ-AS1 and EGOT in HGFs. The expression level of IL-1ß, IL-6, IL-8 of the HGFs after stimulated by 15 ng/mL TNF-α, and the activation of NF-κB pathway was observed. Results: PRKCQ-AS1 and EGOT were identified as top 2 immune-related lncRNAs in periodontal tissues. The expressions of PRKCQ-AS1 and EGOT were significantly up-regulated in inflamed periodontal tissue and in HGFs under TNF-α stimulation. After knock-down of PRKCQ-AS1 and EGOT, expression level of IL-1ß, IL-6, and IL-8 in HGFs with TNF-α stimulation were decreased, and activation of NF-κB pathway was inhibited. Conclusion: PRKCQ-AS1 and EGOT were firstly identified as immune-related lncRNAs in periodontal tissue, and they regulate the expression of IL-1ß, IL-6, and IL-8 of HGFs through the NF-κB pathway.

The impact of periodontitis on vascular endothelial dysfunction.

Periodontitis, an oral inflammatory disease, originates from periodontal microbiota dysbiosis which is associated with the dysregulation of host immunoinflammatory response. This chronic infection is not only harmful to oral health but is also a risk factor for the onset and progress of various vascular diseases, such as hypertension, atherosclerosis, and coronary arterial disease. Vascular endothelial dysfunction is the initial key pathological feature of vascular diseases. Clarifying the association between periodontitis and vascular endothelial dysfunction is undoubtedly a key breakthrough for understanding the potential relationship between periodontitis and vascular diseases. However, there is currently a lack of an updated review of their relationship. Therefore, we aim to focus on the implications of periodontitis in vascular endothelial dysfunction in this review.

Whole-transcriptome analysis of periodontal tissue and construction of immune-related competitive endogenous RNA network.

BACKGROUND: In periodontitis, noncoding RNAs may play a regulatory role in the immune microenvironment through competitive endogenous RNA. We aimed to profile noncoding RNA expression and construct immune-related ceRNA network in periodontitis. METHODS: Five inflamed periodontal tissue and five healthy gingivae were collected for whole-transcriptome sequencing. Differential gene, functional enrichment, and protein-protein interaction network analysis were performed to explore the function of differentially expressed genes. CIBERSORTx was used to analyze level of immune cell infiltration in the periodontal tissue. An immune-related competitive endogenous RNA network was constructed and expression of key regulators in the network was validated. RESULTS: Compared with healthy gingiva, 200 mRNAs, 90 long noncoding RNAs, 65 microRNAs, and 518 circular RNAs were differentially expressed, and cell chemotaxis was significantly enhanced in inflamed periodontal tissue. Immune cell infiltration analysis showed that neutrophils, macrophages M1, T follicular helper cells, and naive B cells were significantly increased in periodontitis. Key regulators including JUN, FOS, THBS1, KLF2, WIF1, were identified and their expression was then validated. CONCLUSION: We constructed an immune-related competitive endogenous RNA network in periodontal tissue, which provided new insights into immune homeostasis in periodontitis and laid a foundation for further study of noncoding RNAs. Key regulators in this network may be promising targets for future periodontitis treatment.

NLRC5 modulates bone metabolism and plays a role in periodontitis.

INTRODUCTION: NOD-like receptor C5 (NLRC5) plays a significant role in the immune system, and is one of the largest members of the pattern recognition receptor family. Previous studies have found that NLRC5 might be involved in the regulation of various diseases, such as fibrotic diseases and cancers; however, its effect on bone metabolism-related diseases has not been reported. METHODS: Skeletons of Nlrc5-/- mice generated by CRISPR/Cas9 and wild-type (WT) mice were compared using X-ray, micro-computed tomography, double labeling, and histological examination. Tartrate-resistant acid phosphatase and pit-absorption assays were performed to evaluate the effect of NLRC5 on osteoclasts differentiation and osteoclastic capacity. The influence of NLRC5 on osteoblasts differentiation and bone formation were studied using alkaline phosphatase and alizarin red staining, respectively. Experimental periodontitis was induced by Porphyromonas gingivalis infection and ligature to investigate the role of NLRC5 in inflammatory periodontal bone loss. RESULTS: Adenovirus-mediated NLRC5 overexpression in human bone marrow mesenchymal stem cells regulated osteogenesis positively. The femoral osteogenesis ability was significantly weakened in Nlrc5-/- mice. Histology showed that the area of the femoral trabeculae in the Nlrc5-/- mice was less than that in the WT mice, and radiology suggested that the Nlrc5-/- mice had fewer trabeculae and a thinner bone cortex than those of the WT mice. Nlrc5 knockout decreased osteoblast mineralization and increased osteoclastogenesis in vitro. NLRC5 was downregulated in periodontitis and P. gingivalis infection. In the experimental periodontitis model, the alveolar bone loss, inflammatory cell infiltration, and inflammatory cytokines secretion (interleukin [IL]-1ß, IL-6, and tumor necrosis factor alpha [TNF-α]) in the Nlrc5-/- mice were significantly enhanced compared to WT mice. CONCLUSION: We verified a novel role of NLRC5 in bone metabolism by regulating both osteoclasts activity and osteoblasts activity. Our results revealed a protective effect of NLRC5 against periodontal inflammation and alveolar bone destruction. NLRC5 could be a novel treatment target to prevent periodontal bone destruction.

Efficacy of periodontal minimally invasive surgery with and without regenerative materials for treatment of intrabony defect: a randomized clinical trial.

OBJECTIVES: The minimally invasive surgical technique was modified in suture (MISTms) in this study. The trial was to determine the efficacy of MISTms with and without regenerative materials for the treatment of intrabony defect and to identify factors influencing 1-year clinical attachment level (CAL) gain. METHODS: Thirty-six patients with interdental intrabony defects were randomly assigned to MISTms (MISTms alone, 18) or MISTms plus deproteinized bovine bone mineral and collagen membrane (MISTms combined, 18). Wound healing was evaluated by early healing index (EHI) at 1, 2, 3, and 6 weeks. Probing depth (PD), CAL, gingival recession, radiographic defect depth, and distance from the base of defect to the cementoenamel junction were recorded at baseline and 1 year postoperatively. A one-year composite outcome measure based on the combination of CAL gain and post-surgery PD was evaluated. Factors influencing 1-year CAL gain were analyzed. RESULTS: Fifteen patients in MISTms-alone and 16 in the MISTms-combined group finished the study. The MISTms-alone group showed significantly better wound healing at 1 week. CAL significantly gained in the MISTms-alone and MISTms-combined group, with 2.53 ± 1.80 mm and 2.00 ± 1.38 mm respectively. The radiographic bone gain was 3.00 ± 1.56 mm and 3.85 ± 1.69 mm respectively. However, there were no significant differences between the two groups about 1-year outcomes. Lower EHI (optimal wound healing) and more baseline CAL positively influenced 1-year CAL gain. CONCLUSIONS: MISTms is an effective treatment for intrabony defects. The regenerative materials do not show an additional effect on 1-year outcomes. Early wound healing and baseline CAL are factors influencing 1-year CAL gain. CLINICAL RELEVANCE: MISTms with and without regenerative materials are both effective treatments for intrabony defect. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: ChiCTR2100043272.

STAT1/SOCS1/3 Are Involved in the Inflammation-Regulating Effect of GAS6/AXL in Periodontal Ligament Cells Induced by Porphyromonas gingivalis Lipopolysaccharide In Vitro.

Periodontitis involves chronic inflammation of the tissues around the teeth caused by plaque and the corresponding immune response. Growth arrest-specific protein 6 (GAS6) and AXL receptor tyrosine kinase (AXL) are known to be involved in inflammatory diseases, while signal transducer and activator of transcription-1 (STAT1) and suppressor of cytokine signaling (SOCS) are related to inflammatory processes. Moreover, miRNA34a directly targets AXL to regulate the AXL expression. However, the specific roles of GAS6 and AXL in periodontitis remain unclear. This study was designed to explore the effect and mechanism of AXL on the expression of inflammatory cytokines induced by Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS) in human periodontal ligament cells (hPDLCs). The effects of different concentrations of P. gingivalis LPS on the expression of GAS6/AXL in hPDLCs were observed. Additionally, the effect of LPS on AXL was investigated by transfection of the miRNA34a inhibitor. AXL was knocked down or overexpressed to observe the release of inflammatory cytokines interleukin- (IL-) 8 and IL-6. The results showed that the expression levels of GAS6 and AXL decreased after P. gingivalis LPS infection. Transfection of a miR-34a inhibitor to hPDLCs demonstrated a role of miR-34a in the downregulation of AXL expression induced by LPS. Moreover, AXL knockdown or overexpression influencing the expression of IL-8 and IL-6 was investigated under LPS stimulation. AXL knockdown decreased the expression of STAT1 and SOCS1/3. Overall, these results demonstrate that AXL inhibits the expression of LPS-induced inflammatory cytokines in hPDLCs and that STAT1 and SOCS1/3 are involved in the regulation of inflammation by GAS6/AXL.

Effect of Pudilan Keyanning antibacterial mouthwash on dental plaque and gingival inflammation in patients during periodontal maintenance phase: study protocol for double-blind, randomised clinical trial.

INTRODUCTION: Plaque control plays a critical role in the prevention and treatment of periodontitis. Antibacterial mouthwash is one of the most important tools for plaque control. Pudilan, including extracts of Scutellaria baicalensis root, Taraxacum mongolicum, Bunge corydalis herb and Isatis indigotica, was reported playing the role of anti-inflammatory and anti-bacterial. However, its effect on dental plaque and periodontal inflammation remains unknown. We aimed to assess the efficacy of Pudilan Keyanning antibacterial mouthwash which contains the active essence of Pudilan and 0.03%-0.06% cetylpyridinium chloride, as well as Pudilan active essence for plaque control and gingival anti-inflammation in patients during periodontal maintenance phase. METHODS AND ANALYSIS: In this double-blind, randomised, placebo-controlled clinical trial, a total of 120 participants during periodontal maintenance phase will be enrolled. After supragingival scaling, they will be randomly assigned into three groups in a 1:1:1 ratio: the Pudilan Keyanning antibacterial mouthwash group, a chlorhexidine acetate mouthwash (0.12%) group or a placebo group with mouthwash containing the same components as the Pudilan Keyanning mouthwash except for Pudilan active ingredients. They will rinse with mouthwash, respectively, two times per day for 6 weeks. Clinical parameters (such as plaque index, bleeding index) and the level of volatile sulfide in the breath will be measured and analysed. The subgingival plaque will be collected and analysed microbiologically. Questionnaire feedback will be analysed. ETHICS AND DISSEMINATION: The study protocol (V.4) was reviewed and approved by the Medical Ethical Committee of Peking University School and Hospital of Stomatology (Ethics Approval No. PKUSSIRB-201950153b). All participants signed a written consent form. TRIAL REGISTRATION NUMBER: ChiCTR2000041253.

Treatment of periodontal intrabony defects using bovine porous bone mineral and guided tissue regeneration with/without platelet-rich fibrin: A randomized controlled clinical trial.

BACKGROUND: To investigate the regenerative effect of adjunctive use of guided tissue regeneration (GTR), bovine porous bone mineral (BPBM), and platelet-rich fibrin (PRF) in intrabony defects. METHODS: Fourteen participants were enrolled, and for each patient their left and right two sides were randomized to the test group or control group. Only the worst intrabony defect on each side was analyzed. The test group received GTR, BPBM, and PRF, whereas the control group received only GTR and BPBM. The PRF used in the trial was fluid PRF, which combined with the BPBM to form a BPBM-PRF complex. The patients were followed up by clinical and radiographic evaluation for 24 months after surgery. RESULTS: Probing depth (PD) in the test group was significantly less than that in the control group at 12 and 24 months after surgery, and the mean difference was ≈ 0.5 to 0.7 mm. Clinical attachment level (CAL) gain in the test group was ≈ 0.9 mm higher than that in the control group at 6 months after surgery, and the difference reached 1.0 to 1.1 mm 12 and 24 months after surgery. None of the other clinical or radiographic parameters differed significantly between the two groups at any time-point after the surgery. CONCLUSION: Compared with GTR and BPBM, the combination of GTR and BPBM-PRF complex is more effective clinically, and results in better clinical outcomes.

Natural progression of periodontal diseases in Chinese villagers based on the 2018 classification.

BACKGROUND: Based on the 2018 classification, we aimed to determine the prevalence, distribution, and progression of periodontitis in the rural Chinese population without access to dental care. METHODS: In all, 404 subjects (28.7 ± 8.9 years, M:F = 182:222) were randomly enrolled in 1992 and re-called in 1996. With the new classification, the prevalence and distribution of stage, grade, and extent were characterized. Stage progression was compared with the progression of clinical attachment loss (CAL) and radiographic bone loss (RBL). RESULTS: At baseline, 94.1% villagers suffered from periodontitis, of whom 53.7% were in Stage III/IV. The prevalence of Stage III/IV increased from 18.2% in the age group of 15 to 24 years to 60.9% in 25 to 34-year-old group and 88.7% in the 35 to 44-year-old group. Significantly more Stage III/IV, generalized, and Grade C periodontitis were found in male villagers than female villagers. In 1996, the prevalence rate of periodontitis increased to 98.5%, with 80.0% in Stage III/IV. Further, 84.2% villagers presented with Grade C periodontitis based on longitudinal ΔCAL. The rate of progression (≥1 site with ΔCAL ≥3 mm) was 63.7%. Stage progression correlated significantly with CAL and RBL progression in Stage I/II, but this association was not found in Stage III/IV. Among subjects with disease progression in Stage III/IV, 90.4% shifted from localized to generalized cases. Furthermore, ceiling effects were observed in Stage III/IV. CONCLUSIONS: In villagers without access to dental care, 94.1% suffered from periodontitis, with more than half having Stage III/IV disease based on the 2018 classification. The majority cases presented with rapid periodontal progression. Although stage progression correlated significantly with CAL and RBL progression in Stage I/II, ceiling effects existed in Stage III/IV.

LOX-1 Regulates P. gingivalis-Induced Monocyte Migration and Adhesion to Human Umbilical Vein Endothelial Cells.

Porphyromonas gingivalis (P. gingivalis) is one of the main periodontal bacteria. This pathogen was reported to enhance monocyte migration and adhesion to endothelial cells in atherosclerosis. The scavenger receptor lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) plays a pivotal role in atherogenesis. The aim of this study was to investigate whether LOX-1 modulates P. gingivalis-mediated monocyte migration and adhesion to endothelial cells and how it works. The results showed that the migration and adhesion of monocytic THP-1 cells to human umbilical vein endothelial cells (HUVECs) were significantly enhanced when HUVECs or THP-1 cells were challenged with P. gingivalis. Meanwhile, the expression level of LOX-1 in both HUVECs and THP-1 cells were also significantly increased by P. gingivalis stimulation. It is well known that ligand/receptor pairs monocyte chemoattractant protein-1 (MCP-1)/CC chemokine receptor 2 (CCR2), selectins/Integrins, and cell adhesion molecules (CAMs)/Integrins mediate monocyte migration and adhesion to endothelial cells. In this study, LOX-1 was demonstrated to be crucially involved in P. gingivalis-induced THP-1 cell migration and adhesion to HUVECs, by regulating expression of ligands MCP-1, intercellular adhesion molecule-1 (ICAM-1) and E-selectin in HUVECs and that of their receptors CCR2 and Integrin αMß2 in THP-1 cells. The nuclear factor-kappa B (NF-κB) signaling pathway was proved to be involved in this process. In conclusion, LOX-1 plays a crucial role in P. gingivalis-induced monocyte migration and adhesion to endothelial cells. This result implies LOX-1 may act as a bridge in linking periodontitis to atherosclerosis.

Crosstalk between Akt and NF-κB pathway mediates inhibitory effect of gas6 on monocytes-endothelial cells interactions stimulated by P. gingivalis-LPS.

Correlation between periodontitis and atherosclerosis is well established, and the inherent mechanisms responsible for this relationship remain unclear. The biological function of growth arrest-specific 6 (gas6) has been discovered in both atherosclerosis and inflammation. Inhibitory effects of gas6 on the expression of inflammatory factors in human umbilical vein endothelial cells (HUVECs) stimulated by Porphyromonas gingivalis lipopolysaccharide (P. gingivalis-LPS) were reported in our previous research. Herein, the effects of gas6 on monocytes-endothelial cells interactions in vitro and their probable mechanisms were further investigated. Gas6 protein in HUVECs was knocked down with siRNA or overexpressed with plasmids. Transwell inserts and co-culturing system were introduced to observe chemotaxis and adhering affinity between monocytes and endothelial cells in vitro. Expression of gas6 was decreased in inflammatory periodontal tissues and HUVECs challenged with P. gingivalis-LPS. The inhibitory effect of gas6 on chemotaxis and adhesion affinity between monocytes and endothelial cells was observed, and gas6 promoted Akt phosphorylation and inhibited NF-κB phosphorylation. To our best knowledge, we are first to report that gas6 inhibit monocytes-endothelial cells interactions in vitro induced by P. gingivalis-LPS via Akt/NF-κB pathway. Additionally, inflammation-mediated inhibition of gas6 expression is through LncRNA GAS6-AS2, rather than GAS6-AS1, which is also newly reported.

The Effect of Streptococcus salivarius K12 on Halitosis: a Double-Blind, Randomized, Placebo-Controlled Trial.

This study was to evaluate the effect of Streptococcus salivarius K12 on tongue coating-associated halitosis. Twenty-eight subjects having tongue coating-associated halitosis were randomly divided into either a test or control group. For each of the 30 days, the test subjects sucked S. salivarius K12 tablet while the control subjects sucked placebo tablets. All the subjects did not take physical (tongue scraping) and chemical (antiseptic mouth-rinse) oral cavity pretreatment prior to use of the tablets. At baseline, and on the 1st, 7th, and 14th day after completing the course of tablets, the subjects were assessed for their organoleptic test (OLT) scores, volatile sulfur compound (VSC) levels, and tongue coating scores (TCS). During the course, all subjects kept their routine oral care habits without scraping their tongue coating. Plaque index, probing depth, and bleeding index were recorded at baseline and at the completion of the trial. On the 1st day following the end of tablet use, the OLT scores and VSC levels had significantly decreased in the test group when compared with the baseline values (P = 0.001 and P = 0.012). The TCS in the test group were also significantly decreased (P = 0.05). At days 7 and 14, the OLT scores in the test group were still significantly lower than the baseline levels (P = 0.006 and P = 0.039 respectively). However, there were no statistical differences with OLT, VSC, and TCS between the test group and the placebo group by analysis of multi-level regression model. The use of S. salivarius K12 did not have significant effect on halitosis with tongue coating cause when the tongue coating was not physically or chemically pre-treated, which implies removing tongue coating is required before Streptococcus salivarius K12 use.

A Review on Salivary Proteomics for Oral Cancer Screening.

Oral cancer has emerged as a global health problem due to its relatively high incidence and mortality. Human saliva as a diagnostic fluid can offer an easy, inexpensive, safe and non-invasive approach for disease detection. Direct contact between saliva and oral cancer lesions make detection of salivary biomarkers for oral cancer especially attractive. Proteins are important molecules involved in pathological processes of oral cancer growth, apoptosis and metastasis. Proteins such as hormones, antibodies, enzymes and cytokines in saliva secreted by oral cancer cells or by host cells not only provide comprehensive pathological information of oral cancer but also are considered potential targets for non-invasive screening of oral cancer. This article provides a review of potential salivary proteomic biomarkers in oral cancer screening.