Effects of amoxicillin and metronidazole as an adjunct to scaling and root planing on glycemic control in patients with periodontitis and type 2 diabetes: A short-term randomized controlled trial.

OBJECTIVE: To assess the effects of amoxicillin and metronidazole with scaling and root planing (SRP) on periodontal parameters and glycemic control in patients with severe periodontitis and diabetes mellitus. BACKGROUND: Adjunctive antibiotics use is advantageous for treating periodontitis in patients with severe periodontitis and diabetes. However, the effects of adjunctive antibiotic use on hemoglobin A1c (HbA1c) levels remain unclear. METHODS: This short-term, randomized controlled trial enrolled patients with severe periodontitis and type 2 diabetes. The patients were randomly allocated to SPR only (i.e., control) or SPR + antibiotics (500 mg of amoxicillin and 200 mg of metronidazole, three times daily for 7 days) groups. Periodontal and hematological parameters were assessed at baseline and 3 months after treatment. Inter- and intra-group analyses were performed using Student's t-tests, Mann-Whitney U tests, and the binary logistic regression models. p-values of <.05 were considered statistically significant. RESULTS: This study enrolled 49 patients, with 23 and 26 patients in the SRP-only and SRP + antibiotics groups, respectively. The periodontal parameters improved significantly and similarly in both groups after treatment (p < .05). The SRP + antibiotics group had more sites of improvement than the SRP-only group when the initial probing depth was >6 mm. (698 [78.96%] vs. 545 [73.35%], p = .008). The HbA1c levels decreased in the SRP-only and SRP + antibiotics groups after treatment (0.39% and 0.53%, respectively). The multivariable binary logistic regression model demonstrated that antibiotics administration and a high baseline HbA1c level were associated with a greater reduction in the HbA1c level (odds ratio = 4.551, 95% confidence interval: 1.012-20.463; odds ratio = 7.162, 95% confidence interval: 1.359-37.753, respectively). CONCLUSIONS: SRP and SRP plus systemic antibiotics were beneficial for glycemic control. Adjunctive antibiotic use slightly improved the outcome for patients with severe periodontitis and poorly controlled diabetes.

The long-term effect of periodontitis treatment on changes in blood inflammatory markers in patients with generalized aggressive periodontitis.

BACKGROUND: Periodontitis is characterized by local inflammatory conditions in the periodontium, its severe form has been associated with elevated systemic inflammatory markers. However, the long-term effects of periodontal inflammation control on systemic inflammatory markers are unclear. OBJECTIVE: This study aimed to investigate the long-term effects of periodontal therapy on the levels of peripheral venous blood inflammatory markers in patients with generalized aggressive periodontitis (GAgP), all of whom were now diagnosed as Stage III or IV Grade C periodontitis. METHODS: Patients with GAgP were consecutively recruited from April 2013 to August 2014 (T0). Active periodontal treatment (APT) was provided, and follow-ups were conducted over a 3- to 5-year period (T1). Clinical parameters were assessed and fasting venous blood was collected at T0 and T1. Complete blood cell counts were obtained, and biochemical analyses were performed to evaluate the levels of serum components. The correlations between probing depth (PD) and hematological parameters were analyzed. RESULTS: A total of 49 patients with GAgP completed APT and follow-ups. Probing depth (PD) reduced from 5.10 ± 1.07 mm at T0 to 3.15 ± 0.65 mm at T1. For every 1-mm reduction in PD after treatment, the neutrophil count, neutrophil-lymphocyte ratio, and total protein concentration were reduced by 0.33 × 109 /L, 0.26, and 1.18 g/L, respectively. In contrast, the albumin/globulin ratio increased by 0.10. CONCLUSION: This study indicated that periodontal therapy may have beneficial effects on peripheral venous blood inflammatory markers in patients with GAgP during long-term observation.

[Relationship between short-chain fatty acids in the gingival crevicular fluid and periodontitis of stage â ¢ or â £].

OBJECTIVE: To analyze the concentration of formic acid, propionic acid and butyric acid in gingival crevicular fluid (GCF) of patients with stages Ⅲ and Ⅳ periodontitis, and their relationship with periodontitis. METHODS: The study enrolled 37 systemically healthy patients with periodontitis and 19 healthy controls who visited Department of Periodontology, Peking University School and Hospital of Stomatology from February 2008 to May 2011. Their GCFs were collected from the mesial-buccal site of one molar or incisor in each quadrant. Periodontal clinical parameters, including plaque index(PLI), probing depth(PD), bleeding index(BI), and attachment loss(AL). Concentrations of formic acid, propionic acid and butyric acid in the supernatant of the GCFs were analyzed by high-performance capillary electrophoresis (HPCE). The prediction ability of formic acid, propionic acid and butyric acid with the risk of periodontitis and the differences between grade B and grade C periodontitis were analyzed. RESULTS: In this study, 32 patients with stage Ⅲ and 5 patients with stage Ⅳ were enrolled, including 9 patients with grade B and 28 patients with grade C. Clinical periodontal variables in the patients with periodontitis were significantly higher than those in the control group (P<0.001). Formic acid was significantly lower in periodontitis than that in the control group [5.37 (3.39, 8.49) mmol/L vs. 12.29 (8.35, 16.57) mmol/L, P<0.001]. Propionic acid and butyric acid in periodontitis were significantly higher than those in the control group: Propionic acid, 10.23 (4.28, 14.90) mmol/L vs. 2.71 (0.00, 4.25) mmol/L, P < 0.001; butyric acid, 2.63 (0.47, 3.81) mmol/L vs. 0.00 (0.00, 0.24) mmol/L, P<0.001. There was no significant difference in formic acid, propionic acid and butyric acid concentrations between grade B and grade C periodontitis (P>0.05). Propionic acid and butyric acid in the deep pocket were significantly higher than in the shallow pocket, while the concentration of formic acid decreased with the increase of PD. Propionic acid (OR=1.51, 95%CI: 1.29-1.75) and butyric acid (OR=3.72, 95%CI: 1.93-7.17) were risk factors for periodontitis, while formic acid (OR=0.87, 95%CI: 0.81-0.93) might be a protective factor for periodontitis. Propionic acid (AUC=0.852, 95%CI: 0.805－0.900), butyric acid (AUC=0.889, 95%CI: 0.841－0.937), f (formic acid, AUC=0.844, 95%CI: 0.793－0.895) demonstrated a good predictive capacity for the risk of periodontitis. CONCLUSION: The concentration of formic acid decrease in the GCF of periodontitis patients, which is a protective factor for periodontitis, its reciprocal have good predictive capacity. However, propionic acid and butyric acid increase, which are risk factors for periodontitis and have good predictive capacity. The concentration of formic acid, propionic acid, and butyric acid vary with probing depth, but there is no significant difference between grade B and grade C periodontitis.

[Histopathological characteristics of peri-implant soft tissue in reconstructed jaws with vascularized bone flaps].

OBJECTIVE: To analyze the histopathological characteristics of peri-implant soft tissue in reconstructed jaws and the changes after keratinized mucosa augmentation (KMA) with free gingival graft (FGG). METHODS: Twenty patients were enrolled in this study. Five patients of them, who were periodontal and systemic healthy and referred for crown lengthening before restoration with healthy keratinized gingiva collected were enrolled as healthy controls. 15 patients of them were with fibula or iliac bone flaps jaw reconstruction (10 with fibula flap and 5 with iliac flap), who were referred to FGG and implant exposures before restoration. Soft tissue was collected before FGG in reconstructed jaws, and in 5 patients (3 with fibula flap and 2 with iliac flap) 8 weeks after FGG if a second surgery was conducted. Histological analysis with hematoxylin-eosin stain and immunological analysis to interlukin-1 (IL-1), interlukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were performed. RESULTS: Thickness from the bottom of stratum basale to the top of stratum granulosum and thickness of keratinized layer in reconstructed jaws were significantly lower compared with that of natural healthy keratinized gingiva [0.27 (0.20, 0.30) mm vs. 0.36 (0.35, 0.47) mm, P<0.05; 16.49 (14.90, 23.37) µm vs. 26.37 (24.12, 31.53) µm, P<0.05]. In the reconstructed area, thickness from the bottom of stratum basale to the top of stratum granulosum increased after KMA with FGG [0.19 (0.16, 0.25) mm vs. 0.38 (0.25, 0.39) mm, P=0.059] and the thickness of keratinized layer significantly increased after KMA with FGG [16.42 (14.16, 22.35) µm vs. 28.57 (27.16, 29.14) µm, P<0.05], which was similar to that in the control group. Furthermore, the number of positive cells of IL-1, IL-6 and TNF-α significantly increased after KMA [0.67 (0.17, 8.93) vs. 11.00 (9.16, 18.00); 13.00 (8.50, 14.14) vs. 21.89 (15.00, 28.12); 0.22 (0.04, 0.63) vs. 2.83 (1.68, 5.00), respectively, P<0.05] as well as the average optical density value [0.15 (0.14, 0.17) vs. 0.18 (0.17, 0.21); 0.28 (0.26, 0.33) vs. 0.36 (0.33, 0.37); 0.23 (0.22, 0.29) vs. 0.30 (0.28, 0.42), respectively, P<0.05], which was similar to that in the healthy keratinized gingiva. CONCLUSION: The lack of rete pegs and inflammatory factors were common in soft tissue with jaw reconstruction. FGG can improve the quality of the epithelium and may improve the stability of the mucosa around implants.

Deep learning improves prediction of periodontal therapy effectiveness in Chinese patients.

THE OBJECTIVE: This study aims to propose a new model to predict the specific treatment effectiveness at site level by analyzing massive amounts of periodontal clinical data with deep learning methods. THE BACKGROUND DATA DISCUSSING THE PRESENT STATUS OF THE FIELD: In light of the low accuracy of current tools, the proposed models cannot fully meet the needs of clinical effectiveness prediction and cannot be applied to on site level prognosis development and formulation of specific treatment plan. MATERIALS AND METHODS: Periodontal examination data of 9273 Chinese patients were extracted and used to propose a Sequence-to-Sequence model after performing data management and reconstruction. The model was optimized by introducing the Attention mechanism. RESULTS: In the test set, the model obtained an average site-level probing depth (PD) accuracy (defined as the proportion of sites with <1 mm deviation of the predicted result from the true value) of 92.4% and high sensitivity (98.6%) for the pocket closure variable. For sites with baseline PD <5 mm, the model achieved a prediction accuracy of 94.6%, while it decreased to 79.9% at sites with PD ≥5 mm. In contrast, for teeth with initial mean PD ≥5 mm, the prediction accuracy significantly differed between molars and non-molars. CONCLUSION: Our model is the first to predict the site-level effectiveness with high accuracy and sensitivity. Future prediction models should incorporate deep learning for improved clinical prediction.

Development and international validation of logistic regression and machine-learning models for the prediction of 10-year molar loss.

AIM: To develop and validate models based on logistic regression and artificial intelligence for prognostic prediction of molar survival in periodontally affected patients. MATERIALS AND METHODS: Clinical and radiographic data from four different centres across four continents (two in Europe, one in the United States, and one in China) including 515 patients and 3157 molars were collected and used to train and test different types of machine-learning algorithms for their prognostic ability of molar loss over 10 years. The following models were trained: logistic regression, support vector machine, K-nearest neighbours, decision tree, random forest, artificial neural network, gradient boosting, and naive Bayes. In addition, different models were aggregated by means of the ensembled stacking method. The primary outcome of the study was related to the prediction of overall molar loss (MLO) in patients after active periodontal treatment. RESULTS: The general performance in the external validation settings (aggregating three cohorts) revealed that the ensembled model, which combined neural network and logistic regression, showed the best performance among the different models for the prediction of MLO with an area under the curve (AUC) = 0.726. The neural network model showed the best AUC of 0.724 for the prediction of periodontitis-related molar loss. In addition, the ensembled model showed the best calibration performance. CONCLUSIONS: Through a multi-centre collaboration, both prognostic models for the prediction of molar loss were developed and externally validated. The ensembled model showed the best performance in terms of both discrimination and validation, and it is made freely available to clinicians for widespread use in clinical practice.

A prospective, multicentre study of 6-mm short implants in posterior alveolar bone supporting splinted crowns: A 5-year follow-up study.

AIM: To evaluate the clinical and radiographic outcomes of 6-mm short implants, placed in the posterior jaws and supporting splinted crowns, at 5 years after early loading. MATERIALS AND METHODS: Forty-five patients with 95 implants (diameter: 4 mm; length: 6 mm) were enrolled at three centres. Two to three implants were placed in either the maxillary or the mandibular posterior region in each patient and restored with screw-retained splinted crowns at 6 weeks later. Clinical and radiographic outcomes were evaluated at implant placement, at loading, and at 6, 12, 24, 36, and 60 months after loading. Biological and mechanical complications were recorded. Marginal changes in bone level in relation to clinical parameters were evaluated using a generalized linear mixed model. RESULTS: During the 5 years of follow-up, the mean change in the marginal bone level (MBL) was 0.04 ± 0.14 mm. Four implants in four patients were lost before loading, one implant in one patient was lost at the 5-year follow-up, and two patients were lost to follow-up. The survival and success rates were 88.4% (38/43) at the patient level. The incidence rates of peri-implant mucositis and peri-implantitis were 29.4% and 7.0%, respectively. The rate of technical complications was 14.0%. CONCLUSIONS: Over a 5-year period, 6-mm short implants supporting early loaded splinted crowns in maxillary or mandibular posterior regions showed stable MBLs and acceptable technical and biological complication rates.

Interactions of periodontal pathogens with platelets in the gingival crevicular fluid of patients with periodontitis.

AIM: To explore the immunological defensive effects of platelets on periodontal pathogens in the gingival crevicular fluid (GCF). MATERIALS AND METHODS: GCF samples were collected from 20 patients with periodontitis and 10 healthy controls. Platelets in the GCF were detected by immunocytochemistry and immunofluorescence. Isolated platelets from healthy volunteers were co-cultured with Porphyromonas gingivalis (Pg) and Fusobacterium nucleatum (Fn). The interactions between platelets and periodontal pathogens were observed by transmission and scanning electron microscopy. The isolated platelets plus neutrophils were co-cultured with Pg or Fn, and the formation of neutrophil extracellular traps (NETs) was evaluated by staining with Sytox Green. RESULTS: The platelet level in the GCF was higher in patients with periodontitis than in healthy controls. Platelets interacted with bacteria and neutrophils in the GCF. In vitro, platelets recruited and engulfed periodontal pathogens. In response to periodontal pathogens, neutrophils released web chromatin, and platelets promoted the formation of intensive NETs. CONCLUSIONS: Platelets, migrating to the gingival sulcus, may exert direct antibacterial effects or assist neutrophils.

Calprotectin levels in gingival crevicular fluid and serum of patients with chronic periodontitis and type 2 diabetes mellitus before and after initial periodontal therapy.

BACKGROUND: This study is aimed to compare the total amount of calprotectin in gingival crevicular fluid (GCF) and the concentration of calprotectin in serum among the patients with type 2 diabetes mellitus and chronic periodontitis (DM-P), the patients with chronic periodontitis (CP) and the healthy controls, as well as the variation of these indicators before and three months after the initial periodontal therapy for the DM-P patients. METHODS: 35 patients with DM-P patients, 32 patients with CP patients, and 43 healthy controls were recruited. Calprotectin levels in serum and GCF, periodontal parameters, fasting blood glucose (FBG), and HbA1c were measured at baseline for all the groups and three months after the initial periodontal therapy for the DM-P patients. RESULTS: At baseline, the calprotectin levels in GCF and serum were the highest in DM-P, followed by CP, and the lowest in healthy controls. GCF calprotectin was significantly and positively correlated with serum calprotectin and probing depth (PD), while serum calprotectin had a significant positive correlation with GCF calprotectin and HbA1c. Periodontal parameters, HbA1c, and serum and GCF calprotectin became significantly reduced after the initial periodontal treatment. The reduction of serum calprotectin was consistent with that of HbA1c, while the decrease of GCF calprotectin was in agreement with that of PD, attachment loss (AL), and bleeding on probing (BOP). CONCLUSIONS: The levels of calprotectin in serum and GCF in the DM-P patients are significantly higher than those in CP patients and healthy controls, which significantly reduced 3 months after the initial periodontal therapy. Furthermore, it suggests diabetic patients might exhibit more pronounced inflammation periodontally and systemically.

Pro-inflammatory cytokine interleukin-6-induced hepcidin, a key mediator of periodontitis-related anemia of inflammation.

OBJECTIVES: To investigate whether anemia of inflammation (AI) occurs in periodontitis patients and to further explore underlying pathogenesis of periodontitis-related AI by an experimental periodontitis model. BACKGROUND: Previous studies have reported periodontitis patients could show a tendency toward AI. However, the relationship between periodontitis and AI remains unclear, and the related pathological mechanisms have not been identified. MATERIALS AND METHODS: Periodontal clinical parameters, inflammatory markers, and anemia-related indicators were compared between 98 aggressive periodontitis (AgP) patients and 103 healthy subjects. An experimental periodontitis model was induced by ligature placement in mice. The changes in mice inflammatory markers, anemia indicators, hepcidin mRNA expression, and serum hepcidin concentrations were measured. Human and mouse liver cells were treated with interleukin-6 (IL-6) for analyzing the changes in hepcidin expression based on mRNA and protein levels. RESULTS: AgP patients exhibited higher white blood cell counts, IL-6, and C-reactive protein. Adjusted linear regression analyses showed correlations between AgP and decreased hemoglobin (HGB) and hematocrit (HCT). The ligature-induced periodontitis caused systemic inflammation and elevated IL-6 levels. Lower red blood cell counts, HGB, and HCT were detected, whereas the levels of hepcidin mRNA expression and serum hepcidin concentrations increased. The treatment of hepatocytes with IL-6 induced both hepcidin mRNA expression and hepcidin secretion. CONCLUSIONS: Systemic inflammation induced by periodontitis leads to an increased risk for AI. IL-6-induced hepcidin could play a central mediator role and act as a key pathologic mechanism. Our results demonstrate periodontitis may be considered as an additional inflammatory disease contributing to the development of AI.

The occurrence of peri-implant mucositis associated with the shift of submucosal microbiome in patients with a history of periodontitis during the first two years.

AIM: To investigate the dynamic changes of peri-implant microbiome in patients with a history of periodontitis and to construct a microbial prediction model. MATERIALS AND METHODS: The prospective study was performed at one month (T1), one year (T2) and two years (T3) after restoration. Clinical examinations [probing depth (PD), bleeding on probing (BOP), suppuration (SUP)], radiographic examinations and sample collection were conducted at three timepoints. Peri-implant sulcular fluid (PISF) was collected and analysed by 16S rRNA gene sequencing. Generalized linear mixed model (GLMM) was used to identify differences. RESULTS: Totally, 168 subjects were assessed for eligibility. Twenty-two patients were recruited in the longitudinal study. Eventually, 67 PISF samples from 24 implants of 12 patients were collected and analysed. Peri-implant microbiome showed increasing diversity and complexity over time. Disease-associated genera Porphyromonas, Tannerella, Treponema and Prevotella dramatically increased from T1 to T3. The prediction model for clinical suppuration at T1 showed a high accuracy of 90%. CONCLUSION: The dysbiosis of peri-implant microbiome increased with time during the two-year observation in patients with a history of periodontitis. Genera of Porphyromonas, Tannerella, Treponema and Prevotella were biomarkers of peri-implant mucositis. Microbiota at the early stage could predict subsequent microbial dysbiosis and clinical suppuration.

The prevalence and severity of periodontal disease in Mainland China: Data from the Fourth National Oral Health Survey (2015-2016).

AIM: To evaluate periodontal conditions in adults in mainland China based on data from the 4th National Oral Health Survey. MATERIALS AND METHODS: Data of adult subjects (35- to 44-year-old group [N = 4409], 55- to 64-year-old group [N = 4622], and 65- to 74-year-old group [N = 4428]) were analysed. Demographic, socio-economic, personal habit, dental history, and health attitude data were obtained using a questionnaire. Periodontal condition was assessed using the standardized case definitions of the 2018 classification scheme. A multivariate analysis was performed to investigate the relationship between periodontitis severity and age, smoking status, gender, and region using generalized additive models after adjusting for confounders. RESULTS: The frequency of subjects with periodontitis was 52.8%, 69.3%, and 64.6% in the three age groups, respectively. The frequency of subjects with severe periodontitis (stage III or IV) was 10.6%, 37.3%, and 43.5% in the three age groups, respectively. The severity of periodontal disease was positively associated with age. Current and former smokers exhibited significantly greater disease severity than non-smokers after adjustment for confounders. No significant difference of severity was found between males and females. CONCLUSION: Within the limitations of the study, the prevalence of periodontitis is very high among adults in mainland China. Periodontal status is associated with age and smoking status.

A nomogram prediction for mandibular molar survival in Chinese patients with periodontitis: A 10-year retrospective cohort study.

AIMS: To develop a nomogram prediction model of mandibular molar survival by comprehensively analysing clinical and radiographic risk factors of mandibular molar loss. MATERIALS AND METHODS: Four hundred and seventy-eight mandibular molars of 139 subjects who underwent non-surgical periodontal treatment were examined retrospectively within a mean follow-up period of 11.1 years. The association of risk factors including clinical and radiographic parameters with mandibular molar loss was assessed using univariate and multivariate Cox regression analyses. A nomogram prediction model was developed, and the validation and discriminatory ability of it were analysed. RESULTS: Hundred and four molars were lost in this study. Probing depth (PD), attachment loss (AL), furcation involvement (FI), bleeding on probing (BOP), tooth mobility and radiographic bone loss were significantly associated with tooth loss (p < .01). A gradient effect of degree of FI on mandibular molar loss existed increasing from degree Ⅱ (HR = 2.37, 95% CI: 1.48, 3.79) to Ⅲ (HR = 5.61, 95% CI: 3.01, 10.45) versus none & degree Ⅰ. The area under the curve (AUC) of the model was 0.891. The calibration curve and decision curve analysis demonstrated good performance and high net benefit of nomogram, respectively. CONCLUSIONS: A specific nomogram could be adopted to predict the mandibular molar survival and formulate tailored treatment plans in Chinese.

Integration of genome-wide association study and expression quantitative trait loci data identifies AIM2 as a risk gene of periodontitis.

AIM: To identify risk variants associated with gene expression in peripheral blood and to identify genes whose expression change may contribute to the susceptibility to periodontitis. MATERIAL AND METHODS: We systematically integrated the genetic associations from a recent large-scale periodontitis GWAS and blood expression quantitative trait loci (eQTL) data using Sherlock, a Bayesian statistical framework. We then validated the potential causal genes in independent gene expression data sets. Gene co-expression analysis was used to explore the functional relationship for the identified causal genes. RESULTS: Sherlock analysis identified 10 genes (rs7403881 for MT1L, rs12459542 for SIGLEC5, rs12459542 for SIGLEC14, rs6680386 for S100A12, rs10489524 for TRIM33, rs11962642 for HIST1H3E, rs2814770 for AIM2, rs7593959 for FASTKD2, rs10416904 for PKN1, and rs10508204 for WDR37) whose expression may influence periodontitis. Among these genes, AIM2 was consistent significantly upregulated in periodontium of periodontitis patients across four data sets. The cis-eQTL (rs2814770, ~16 kb upstream of AIM2) showed significant association with AIM2 (p = 6.63 × 10-6 ) and suggestive association with periodontitis (p = 7.52 × 10-4 ). We also validated the significant association between rs2814770 and AIM2 expression in independent expression data set. Pathway analysis revealed that genes co-expressed with AIM2 were significantly enriched in immune- and inflammation-related pathways. CONCLUSION: Our findings implicate that AIM2 is a susceptibility gene, expression of which in gingiva may influence periodontitis risk. Further functional investigation of AIM2 may provide new insight for periodontitis pathogenesis.

Platelets as inflammatory mediators in a murine model of periodontitis.

AIM: To investigate the role of platelets during the development of ligature-induced experimental periodontitis in mice. MATERIALS AND METHODS: Experimental periodontitis was induced by placement of sterilized 5-0 cotton ligatures around the maxillary and mandibular second molars of C57BL/6 wild-type mice. Flow cytometry was used to analyse platelet activation and platelet-leucocyte aggregate formation, and histologic analysis was used to evaluate inflammation and localization of platelets and leucocytes in periodontal tissues during the development of experimental periodontitis and in experimental periodontitis with and without antiplatelet drug treatment. RESULTS: Experimental periodontitis induced platelet activation and platelet-leucocyte interaction. Platelets and leucocytes gradually infiltrated in inflammatory gingival tissues during the development of experimental periodontitis. The inhibition of platelet activation via drug therapy led to significant inhibition of leucocyte migration and marked reduction in periodontal inflammation. CONCLUSION: This study revealed that platelets are critical for inflammation and tissue injury in periodontitis and serve as mediators of inflammation in periodontal tissue.

Association of CYP1A1 rs1048943 variant with aggressive periodontitis and its interaction with hyperlipidemia on the periodontal status.

BACKGROUND AND OBJECTIVE: CYP1A1 rs1048943 polymorphism was reported to be correlated with periodontitis; however, its association with aggressive periodontitis (AgP) has not yet been investigated. The aim of the study was to investigate the association between the CYP1A1 gene rs1048943 variant with generalized aggressive periodontitis (GAgP) and platelet activation and analyse whether its interaction with hyperlipidemia affects periodontal status in a Chinese population. METHODS: A case-control study of 224 GAgP patients and 139 healthy controls was conducted. The clinical parameters of probing depth (PD), attachment loss (AL) and bleeding index (BI) were recorded. Platelet count (PLT), platelet distribution width (PDW), platelet large cell ratio (PLCR), mean platelet volume (MPV), serum total cholesterol (TC), triacylglycerol (TG), high and low-density lipoprotein (HDL and LDL) were also measured. The CYP1A1 rs1048943 SNP was genotyped by time-of-flight mass spectrometry. Logistic and linear regression models were used to measure correlation. RESULTS: The CYP1A1 rs1048943 AG/GG genotype was associated with GAgP (OR = 1.56, 95%CI: 1.01, 2.42), PD, AL and decreased PDW, PLCR and MPV after adjustment for covariates. Gene-lipid interactions were found between CYP1A1 rs1048943 and HDL for PD (Pinteraction  = 0.0033), BI (Pinteraction  = 0.0311) and AL (Pinteraction  = 0.0141) and between CYP1A1 rs1048943 and LDL for PD (Pinteraction  = 0.013) among patients with GAgP. CONCLUSION: The G allele of the CYP1A1 rs1048943 gene was associated with GAgP, periodontal status and platelet-related inflammation status in a Chinese population. Hyperlipidemia could modulate the effect of CYP1A1 rs1048943 on the periodontal status of GAgP.

Microbiome in maintained periodontitis and its shift over a single maintenance interval of 3 months.

AIM: To assess the subgingival microbial shift of maintained periodontitis treated by ultrasonic scaling (US) or air polishing (AP) during a 3-month maintenance interval. MATERIALS AND METHODS: We conducted a 12-week randomized split-mouth controlled trial with US and AP in 17 maintained subjects (bleeding on probing [BOP%] ≤25%, probing depth [PD] ≤5 mm). They were monitored at baseline, week 2, week 8 and week 12. The V3-V4 region of the 16S rDNA from 136 subgingival plaque samples was sequenced and analysed. RESULTS: Treatment by US or AP could effectively reduce the PD, microbial richness, diversity, periodontitis-associated microbiota and pathogenic metabolism in maintained periodontitis. Bacteria recolonized after treatment and returned to the pre-treatment level 12 weeks after treatment. Ultrasonic scaling group demonstrated slight advantage in reducing BOP (%), pathogenic bacteria and metabolism than AP group. Pathogenic microbiota and commensal microbiota kept a balance in subgingival community of maintained patients during the 3-month interval. CONCLUSIONS: Treatment by US or AP effectively reduced the pathogenicity of subgingival microbiome by reducing microbial diversity, proportion of periodontitis-associated microbiota and pathogenic metabolism. It helped to keep a balanced subgingival community and stable periodontal condition over a single maintenance interval of 3 months.

Butyrate rather than LPS subverts gingival epithelial homeostasis by downregulation of intercellular junctions and triggering pyroptosis.

AIM: To investigate the effects of sodium butyrate (NaB) and lipopolysaccharide (LPS) on gingival epithelial barrier. MATERIAL AND METHODS: We cultured human primary gingival epithelial cells and investigated the effects of NaB and LPS on gingival epithelial barrier and involved mechanisms at in vitro and in vivo levels by immunostaining, confocal microscopy, field emission scanning electron microscopy (FE-SEM), transmission electronic microscopy (TEM), transepithelial electrical resistance (TEER), FTIC-dextran flux, flow cytometry, real-time PCR and Western blot assays. RESULTS: Our results showed that NaB, rather than LPS, destroyed the epithelial barrier by breaking down cell-cell junctions and triggering gingival epithelial cell pyroptosis with characteristic morphological changes, including swollen cells, large bubbles, pore formation in the plasma membrane and subcellular organelles changes. The upregulated expression of pyroptosis-related markers, caspase-3 and gasdermin-E (GSDME) contributed to this effect. Pyroptosis aroused by NaB is a pro-inflammatory cell death. Pyroptotic cell death provoked inflammatory responses by upregulation of IL-8 and MCP-1, and releasing intracellular contents into the extracellular microenvironment after pyroptotic rupture of the plasma membrane. CONCLUSIONS: Our new findings indicate that butyrate is a potent destructive factor of gingival epithelial barrier and pro-inflammatory mediator, which shed a new light on our understanding of periodontitis initiation.

Clinical performance of non-surgical periodontal therapy in a large Chinese population with generalized aggressive periodontitis.

AIM: This study aimed to evaluate clinical performance of non-surgical periodontal treatment (NSPT) and its influential factors in a large Chinese population with generalized aggressive periodontitis (GAgP). MATERIAL AND METHODS: Longitudinal periodontal examination data of 1,004 GAgP patients (numbers of patients with observation periods 6 weeks~, 3 months~, 6 months~, 1 year~, 3 years~ and >5 years were 203, 310, 193, 205, 70 and 23, respectively) were extracted from a hospital-based electronic periodontal charting record system and analysed by multilevel analysis. RESULTS: Mean probing depth (PD) and attachment loss (AL) reductions at patient level were 1.17 mm and 1.07 mm, respectively. Multilevel analysis demonstrated PD reductions after maintenance were mainly influenced by frequency of supportive periodontal treatment (FSPT), gender, adjunctive systemic use of antibiotics, baseline mobility, tooth type and baseline PD and bleeding index reductions were mainly influenced by FSPT, adjunctive systemic use of antibiotics, baseline AL, baseline mobility, tooth type and baseline PD. CONCLUSION: The clinical performance of NSPT on patients with GAgP was proved in the large Chinese population. Outcomes of NSPT were mainly influenced by FSPT, adjunctive systemic use of antibiotics, baseline mobility, tooth type and baseline PD.

Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions.

A new periodontitis classification scheme has been adopted, in which forms of the disease previously recognized as "chronic" or "aggressive" are now grouped under a single category ("periodontitis") and are further characterized based on a multi-dimensional staging and grading system. Staging is largely dependent upon the severity of disease at presentation as well as on the complexity of disease management, while grading provides supplemental information about biological features of the disease including a history-based analysis of the rate of periodontitis progression; assessment of the risk for further progression; analysis of possible poor outcomes of treatment; and assessment of the risk that the disease or its treatment may negatively affect the general health of the patient. Necrotizing periodontal diseases, whose characteristic clinical phenotype includes typical features (papilla necrosis, bleeding, and pain) and are associated with host immune response impairments, remain a distinct periodontitis category. Endodontic-periodontal lesions, defined by a pathological communication between the pulpal and periodontal tissues at a given tooth, occur in either an acute or a chronic form, and are classified according to signs and symptoms that have direct impact on their prognosis and treatment. Periodontal abscesses are defined as acute lesions characterized by localized accumulation of pus within the gingival wall of the periodontal pocket/sulcus, rapid tissue destruction and are associated with risk for systemic dissemination.