Objective To evaluate two methods measuring alveolar bone loss by micro computed tomography (micro-CT)based on periodontitis model in mice.Methods The silk ligatures were tied around the right maxillary second molars of mice to induce periodontitis model.The right half maxillaries of mice model were harvested for micro-CT analysis.Three dentists were recruited for the measurement with two different methods:Modified tomography (T) method and reconstruction (R) method.Accuracy and consistency of each method were estimated by standard deviation (SD).Results The SDs of R method managed by the same operator (measurement for 3 times) or different operators (3 operators) were 34.87μm and 35.67 μm respectively,while that of T method was 7.82 μm and 14.24 μm respectively.The SDs of T method were significantly lower than those of R method (both P＜0.05).Conclusion T method is more accurate and consistent than R method for evaluating alveolar bone loss in mice periodontitis model.

Metabolic syndrome is a cluster of metabolic abnormalities including abdominal obesity, insulin resistance, hypertension and atherogenic dyslipidemia and is associated with increased risk of cardiovascular disease and diabetes. Periodontitis is a chronic inflammatory disease caused by plaque biofilm, which shares risk factors with the major noncommunicable diseases such as heart disease, diabetes and chronic respiratory disease. Many cross-sectional studies have investigated the link between periodontal disease and metabolic syndrome showing that the odds of periodontitis increase with the number of metabolic syndrome components present in an individual although the causal relationship between them has not been determined yet. In this paper, the research progress on the relationship and mechanism of periodontitis with the main characteristics of metabolic syndrome are presented in order to provide new evidences for the prevention and intervention of metabolic syndrome and periodontitis.

Objective : To evaluate the effects of root calculus residue and root cement preservation by ultrasonic subgingival scaling and root planing (SRP) with or without perioscopy. Methods : Twelve teeth extracted due to severe periodontitis were randomly divided into three groups with four teeth in each group: ① Endoscope-assisted SRP group. The root surfaces of the affected teeth were cleaned with an EMS ultrasonic treatment instrument. ② Traditional SRP group. The affected teeth were treated by ultrasonic subgingival scaling and hand root planing with a Gracey curette. ③ Untreat group. The above operations were performed by the same senior physician. Under local anesthesia, each tooth was scraped for 10 minutes and then extracted. The residual amount of calculus on the root surface after plaque staining was observed and recorded. The thickness of the retained cementum at 1/3 of the root neck was measured. Results: The residual rate of calculus on the root surface was the lowest in the endoscope-assisted SRP group, which was significantly different from the traditional SRP group and the untreated group (P < 0.001). Histological observation showed that the mean residual cementum thickness at 1/3 of the root neck increased gradually from the cemento-enamel junction (CEJ), 2.5 mm below the CEJ and 5 mm below the CEJ. Ultrasound SRP assisted by endoscopy caused less damage to the cementum and preserved the cementum better than traditional subgingival scaling (P < 0.001). Conclusion Compared with traditional SRP therapy, endoscope-assisted SRP treatment can remove subgingival plaque and calculus more effectively and can better preserve the cementum of the root surface.

Objective:To study the effects of salivary microbiota in patients with periodontitis on the tryptophan-aryl hydrocarbon receptor (AhR) signaling axis in mice with periodontitis and to provide theoretical basis as well as new ideas for the influences of periodontitis on systemic metabolism.Methods:Salivary microbiota of 12 healthy individuals and 14 patients with periodontitis were collected in Nanjing Stomatological Hospital, Medical School of Nanjing University from June to December of 2020. According to the random number table method, twenty-four mice were randomly divided into three groups: Sham group (control group), P group (periodontitis patients′ salivary microbiota group) and H group (periodontal healthy individuals′ salivary microbiota group). The maxillary second molars of all mice were treated with silk thread ligation to induce periodontitis. Phosphate buffer as well as salivary microbiota of periodontal healthy individuals and periodontitis patients were gavaged into periodontitis mice for 2 weeks. The expression of inflammatory factors in mice serum were detected by enzyme linked immunosorbent assay, and the expression of tryptophan and indole metabolites in intestinal tract and serum were detected by liquid chromatography-mass spectrometry. The expression of AhR in intestinal tract of mice was detected by immunohistochemistry and quantitative real time-PCR while gut microbiota constitution was detected by 16S rRNA gene sequencing. The remaining saliva samples of periodontitis patients and periodontal healthy individuals were applied to detect the expression of tryptophan and indole metabolites themselves.Results:The salivary microbiota of periodontitis patients could induce the expression of interleukin-1β [P group: (162.38±39.46) pg/ml, H group: (82.83±20.01) pg/ml; t=4.40, P=0.001) and tumor necrosis factor-α [P group: (361.16±123.90) pg/ml, H group: (191.66±106.87) pg/ml; t=2.54, P=0.030) in serum of periodontitis mice, and reduce the expression of AhR in colon (P group: 1.18±0.05, H group:1.83±0.47; t=3.09, P=0.015) and ileum (P group: 0.80±0.13, H group: 1.18±0.11; t=4.93, P=0.001). After gavage of salivary microbiota of periodontitis patients to the mice, tryptophan (P group: (18.1±3.8)×10 7, H group: (26.6±6.6)×10 7; t=2.49, P=0.037] and indole lactic acid [P group: (1.9±0.7)×10 7, H group: (3.7±0.6)×10 7; t=4.49, P=0.002) in serum of periodontitis mice were significantly decreased, but was relatively disorder in intestinal tract. However, the expressions of tryptophan and indole metabolites in saliva of periodontitis patients were higher than those of periodontal healthy individuals. There were significant differences in indole propionic acid [P group: (1 239.39±818.72) nmol/L, H group: (56.96±38.33) nmol/L; t=2.83, P=0.022]. What we find noteworthy was that the expressions of indolelactic acid metabolism in saliva, serum and intestinal were consistent, and salivary microbiota of periodontitis patients could reduce the relative abundance of indolelactic acid-producing bacteria in the gut, suggesting that the salivary microbiota of periodontitis patients might affect the expression of AhR through gut microbiota disorder and indolelactic acid downregulation. Conclusions:Salivary microbiota in patients with periodontitis may affect the systemic inflammatory state through down-regulating the expression of tryptophan-AhR signal axis.

Endo-periodontal lesions(EPLs)involve both the periodontium and pulp tissue and have complicated etiologies and pathogenic mechanisms,including unique anatomical and microbiological characteristics and multiple contributing factors.This etiological complexity leads to difficulties in determining patient prognosis,posing great challenges in clinical practice.Furthermore,EPL-affected teeth require multidisciplinary therapy,including periodontal therapy,endodontic therapy and others,but there is still much debate about the appropriate timing of periodontal therapy and root canal therapy.By compiling the most recent findings on the etiology,pathogenesis,clinical characteristics,diagnosis,therapy,and prognosis of EPL-affected teeth,this consensus sought to support clinicians in making the best possible treatment decisions based on both biological and clinical evidence.

Efforts to control inflammation and achieve better tissue repair in the treatment of periodontitis have been ongoing for years. Human β-defensin 3, a broad-spectrum antimicrobial peptide has been proven to have a variety of biological functions in periodontitis; however, relatively few reports have addressed the effects of human periodontal ligament cells (hPDLCs) on osteogenic differentiation. In this study, we evaluated the osteogenic effects of hPDLCs with an adenoviral vector encoding human β-defensin 3 in an inflammatory microenvironment. Then human β-defensin 3 gene-modified rat periodontal ligament cells were transplanted into rats with experimental periodontitis to observe their effects on periodontal bone repair. We found that the human β-defensin 3 gene-modified hPDLCs presented with high levels of osteogenesis-related gene expression and calcium deposition. Furthermore, the p38 MAPK pathway was activated in this process. In vivo, human β-defensin 3 gene-transfected rat PDLCs promoted bone repair in SD rats with periodontitis, and the p38 mitogen-activated protein kinase (MAPK) pathway might also have been involved. These findings demonstrate that human β-defensin 3 accelerates osteogenesis and that human β-defensin 3 gene modification may offer a potential approach to promote bone repair in patients with periodontitis.
Animals ; Anti-Infective Agents ; metabolism ; pharmacology ; Cell Differentiation ; drug effects ; Cells, Cultured ; Humans ; Osteogenesis ; drug effects ; Periodontal Ligament ; drug effects ; metabolism ; Periodontitis ; drug therapy ; Rats ; Rats, Sprague-Dawley ; beta-Defensins ; metabolism ; pharmacology

The aim of this study was to identify whether periodontitis induces gut microbiota dysbiosis via invasion by salivary microbes. First, faecal and salivary samples were collected from periodontally healthy participants (PH group, n = 16) and patients with severe periodontitis (SP group, n = 21) and analysed by 16S ribosomal RNA sequencing. Significant differences were observed in both the faecal and salivary microbiota between the PH and SP groups. Notably, more saliva-sourced microbes were observed in the faecal samples of the SP group. Then, the remaining salivary microbes were transplanted into C57BL6/J mice (the C-PH group and the C-SP group), and it was found that the composition of the gut microbiota of the C-SP group was significantly different from that of the C-PH group, with Porphyromonadaceae and Fusobacterium being significantly enriched in the C-SP group. In the colon, the C-SP group showed significantly reduced crypt depth and zonula occludens-1 expression. The mRNA expression levels of pro-inflammatory cytokines, chemokines and tight junction proteins were significantly higher in the C-SP group. To further investigate whether salivary bacteria could persist in the intestine, the salivary microbiota was stained with carboxyfluorescein diacetate succinimidyl ester and transplanted into mice. We found that salivary microbes from both the PH group and the SP group could persist in the gut for at least 24 h. Thus, our data demonstrate that periodontitis may induce gut microbiota dysbiosis through the influx of salivary microbes.
Animals ; Dysbiosis ; Gastrointestinal Microbiome ; Humans ; Mice ; Mice, Inbred C57BL ; Microbiota ; Periodontitis ; RNA, Ribosomal, 16S/metabolism*