ObjectiveA 37-residue amino acid sequence corresponding to the segment encoded by exon-5 of murine ameloblastin (Ambn), AB2 (Y67-Q103), has been implicated with membrane association, ameloblastin self-assembly, and amelogenin-binding. Our aim was to characterize, at the residue level, the structural behavior of AB2 bound to chemical mimics of biological membranes using NMR spectroscopy. DesignTo better define the structure of AB2 using NMR-based methods, recombinant 13C- and 15N-labelled AB2 (*AB2) was prepared and data collected free in solution and with deuterated dodecylphosphocholine (dPC) micelles, deuterated bicelles, and both small and large unilamellar vesicles. ResultsAmide chemical shift and intensity perturbations observed in 1H-15N HSQC spectra of *AB2 in the presence of bicelles and dPC micelles suggest that a region of *AB2, S6-E36 (murine Ambn S68 – E98), associates with the membrane biomimetics. A CSI-3 analysis of the NMR chemical shift assignments for *AB2 free in solution and bound to dPC micelles indicated the peptide remains disordered except for the adoption of a short, 12-residue α-helix, F10-G21 (murine Ambn F72-G83). In dPC micelles, the NOE NMR data was void of patterns characteristic of long-lived helical structure indicating this helix was transient in nature. ConclusionsA continuum of intrinsic disorder in the membrane-bound state may be responsible for ameloblastin’s ability to dynamically interact with multiple partners at the same site during amelogenesis.

ObjectivesRats are used as animal models for basic and applied research related to orthodontic tooth movement (OTM). The magnitude of mechanical force in OTM rat models mainly depends on the supporting capability of the periodontal ligament (PDL), which is highly associated with the root surface area (RSA). But the size of rat RSA remains unknown, which is the reason why there are still debates on the magnitude of mechanical force in OTM rat models. This study aimed to explore a method for measuring the RSA in rat molars. DesignThe maxillary and mandibular samples of rats were scanned by Micro-CT to generate three-dimensional (3D) images, followed by 3D reconstruction of every molar through Mimics Medical 21.0. Geomagic Wrap 2021 and Unigraphics NX 12.0 were utilized to smooth teeth surface and mark the cementoenamel junction (CEJ). Finally, the RSA in rat molars was measured. ResultsThe results showed that for the six-, eight-, or ten-week-old rats, the average RSA of maxillary first, second, and third molars was 25.90 ± 2.29 mm2, 15.92 ± 2.14 mm2, and 10.34 ± 1.94 mm2. The RSA of mandibular first, second, and third molars was 27.03 ± 2.63 mm2, 17.16 ± 1.61 mm2, and 11.39 ± 2.13 mm2. ConclusionsThrough 3D modelling, we provided data of rat RSA, and observed the trend of increasing RSA mean values with age. These data are pivotal for determining the magnitude of mechanical force required to move rat molars, especially when conducting research related to OTM using rat models.

ObjectiveTo provide a comprehensive summary of the available evidence on the oral microbiota of humans and non-human primates about the etiology of periodontal disease. DesignAn integrative literature review was conducted on 398 clinical and observational articles published between 2010 and 2024 using searches in the MEDLINE/PubMed, Virtual Health Library, and SciELO databases. After the screening, eligibility, data extraction, and methodological quality assessment, 21 studies were selected. ResultsThe results, which reveal striking similarities between the pathogens involved in periodontal disease in humans and NHPs, confirm the potential of NHPs as research models and inspire further research in this area. ConclusionAccording to these studies, Actinomyces spp., Aggregatibacter actinomycetemcomitans, Campylobacter rectus, Capnocytophaga spp., Eubacterium spp., Filifactor alocis, Fusobacterium spp., Leptotrichia spp., Neisseria mucosa, Parvimonas micra, Porphyromonas spp., Prevotella spp., Selenomonas spp., Streptococcus spp., Treponema spp., Tannerella spp., Veillonella parvula, were the genus and/or species of bacteria found in humans. On the other hand, Aggregatibacter acinomycetemcomitans, Campylobacter rectus, Desulfobulbus spp., Dialister invisus, Eikenella corrodens, Filifactor alocis, Fusobacterium spp., Parvimonas micra, Porphyromonas spp., Prevotella spp., Staphylococcus spp., Streptococcus spp., Treponema spp., Tannerella spp., Veillonella spp., were the most reported in NHPs. No study in non-human primates reported the presence of protozoa, unlike studies in humans that reported the presence of Entamoeba gingivalis and Trichomonas tenax. However, its role in periodontal disease still needs to be elucidated, despite the strong association mainly with severe periodontal disease where protozoa are observed in injured tissues.

ObjectiveThis systematic review and meta-analysis (SRMA) aimed to determine whether the presence of H. pylori in dental plaque is associated with gastric H. pylori infection. DesignSearch for the relevant literature was done in various databases: PubMed, Embase, Web of Science and Cochrane till September 21, 2023. The studies were screened for outcome of interest i.e. gastric H. pylori infection and exposure of interest i.e. H. pylori positivity in dental plaque. The pooled results of the study outcomes were evaluated using Odds Ratio (OR), accompanied by a 95% confidence interval (CI). To evaluate the heterogeneity among studies, I2 statistics were utilized, with an I2 exceeding 50% indicating a significant to high variation. In cases where I2 was greater than 50%, a random-effects model (specifically, the Der Simonian and Laird method) was employed. ResultsData from 27 observational studies and 2408 participants were included. The pooled OR of the H. pylori positivity in dental plaque among the patients with H. pylori positivity in stomach was 3.80 (95% CI 2.24; 6.43), with high heterogeneity (I2= 69%, p<0.01). Sensitivity analysis after removing the outliers reduced the heterogeneity significantly (I2=22%, p=0.16). Meta-regression revealed that the strength of association did not vary according to the year of study or the sample size included in the studies. Overall certainty of the evidence was low. ConclusionsThe present meta-analysis showed that the presence of gastric H. pylori infection was higher among patients with H. pylori in dental plaque compared to patients without H. pylori in dental plaque. Presence of H. pylori infection in dental plaque can have implications in the management of H. pylori infection as dental plaque can serve as a reservoir from which the microorganism can recolonize the gastric mucosa.

ObjectiveThe aim of this study was to evaluate the effect of periodontal Porphyromonas gingivalis (P. gingivalis) infection on lung homeostasis and to explore the underlying mechanism. DesignsIn in vivo experiments, twelve mice were divided into two groups. The P. gingivalis infection group received P. gingivalis around the maxillary second molar, and the control group was left untreated. After 12 weeks, the histopathological changes of the lung tissue and the autophagy and apoptosis in the lung tissue cells were detected. In in vitro experiments, alveolar epithelial cell A549 was co cultured with P. gingivalis and treated with autophagy inhibitor chloroquine (CQ). Western blot was then used to detect autophagic markers LC3 and P62, and mRFP-GFP-LC3 was used to observe autophagic flux. Cell viability and apoptosis were also detected. ResultsFor the in vivo experiments, pathological changes were observed in the lung tissue of the P. gingivalis infection group at 12 weeks, along with higher levels of autophagy and apoptosis in the lung tissue cells. For the in vitro experiments, infection of alveolar epithelial cells with P. gingivalis inhibited cell viability and promoted cell autophagy and apoptosis. Interestingly, we found that inhibiting P. gingivalis-activated autophagy significantly improved cell apoptosis and viability damage induced by P. gingivalis. ConclusionPeriodontal P. gingivalis infection can cause pathological changes and abnormal homeostasis in lung tissue, and the up-regulation of autophagy induced by P. gingivalis may play a synergistic role in this process.