Expert consensus on odontogenic maxillary sinusitis multi-disciplinary treatment

Odontogenic maxillary sinusitis (OMS) is a subtype of maxillary sinusitis (MS). It is actually inflammation of the maxillary sinus that secondary to adjacent infectious maxillary dental lesion. Due to the lack of unique clinical features, OMS is difficult to distinguish from other types of rhinosinusitis. Besides, the characteristic infectious pathogeny of OMS makes it is resistant to conventional therapies of rhinosinusitis. Its current diagnosis and treatment are thus facing great difficulties. The multi-disciplinary cooperation between otolaryngologists and dentists is absolutely urgent to settle these questions and to acquire standardized diagnostic and treatment regimen for OMS. However, this disease has actually received little attention and has been underrepresented by relatively low publication volume and quality. Based on systematically reviewed literature and practical experiences of expert members, our consensus focuses on characteristics, symptoms, classification and diagnosis of OMS, and further put forward multidisciplinary treatment decisions for OMS, as well as the common treatment complications and relative managements. This consensus aims to increase attention to OMS, and optimize the clinical diagnosis and decision-making of OMS, which finally provides evidence-based options for OMS clinical management.

Porphyromonas gingivalis bacteremia increases the permeability of the blood-brain barrier via the Mfsd2a/Caveolin-1 mediated transcytosis pathway

Bacteremia induced by periodontal infection is an important factor for periodontitis to threaten general health. P. gingivalis DNA/virulence factors have been found in the brain tissues from patients with Alzheimer’s disease(AD). The blood-brain barrier(BBB) is essential for keeping toxic substances from entering brain tissues. However, the effect of P. gingivalis bacteremia on BBB permeability and its underlying mechanism remains unclear. In the present study, rats were injected by tail vein with P. gingivalis three times a week for eight weeks to induce bacteremia. An in vitro BBB model infected with P. gingivalis was also established. We found that the infiltration of Evans blue dye and Albumin protein deposition in the rat brain tissues were increased in the rat brain tissues with P. gingivalis bacteremia and P. gingivalis could pass through the in vitro BBB model. Caveolae were detected after P. gingivalis infection in BMECs both in vivo and in vitro. Caveolin-1(Cav-1) expression was enhanced after P. gingivalis infection.Downregulation of Cav-1 rescued P. gingivalis-enhanced BMECs permeability. We further found P. gingivalis-gingipain could be colocalized with Cav-1 and the strong hydrogen bonding between Cav-1 and arg-specific-gingipain(RgpA) were detected.Moreover, P. gingivalis significantly inhibited the major facilitator superfamily domain containing 2a(Mfsd2a) expression. Mfsd2a overexpression reversed P. gingivalis-increased BMECs permeability and Cav-1 expression. These results revealed that Mfsd2a/Cav-1 mediated transcytosis is a key pathway governing BBB BMECs permeability induced by P. gingivalis, which may contribute to P. gingivalis/virulence factors entrance and the subsequent neurological impairments.

The dimension and morphology of alveolar bone at maxillaryanterior teeth in periodontitis: a retrospective analysis usingCBCT

The morphology of the alveolar bone at the maxillary anterior teeth in periodontitis patients was evaluated by cone-beam computed tomography(CBCT) to investigate the distribution of alveolar defects and provide guidance for clinical practice. Ninety periodontitis patients and 30 periodontally healthy individuals were selected to determine the morphology of the alveolar bone at the maxillary anterior teeth according to the degree of bone loss, tooth type, sex and age. The differences in the dimensions between periodontitis patients and healthy individuals were compared, and the distribution of alveolar bone defects was analyzed.A classification system was established regarding the sagittal positions and angulations of the teeth. The buccal residual bone was thicker and the lingual bone was thinner in the periodontitis patients than in the periodontally healthy individuals, and there were differences between the different tooth types, sexes and age subgroups. The buccal undercut was close to the alveolar ridge, while fenestration was reduced and the apical bone height was higher in periodontitis patients than in periodontally healthy individuals.The apical bone height increased with the aggravation of bone loss and age. The proportions of different sagittal positions changed with the aggravation of bone loss. Moreover, the teeth moved more buccally regarding the positions of the maxillary anterior teeth.The morphology of the alveolar bone at the maxillary anterior teeth differed between periodontitis patients and healthy individuals,and the differences were related to the degree of bone loss, tooth type, sex and age.

Porphyromonas gingivalis infection promotes mitochondrial dysfunction through Drp1-dependent mitochondrial fission in endothelial cells

Porphyromonas gingivalis(P.gingivalis),a key pathogen in periodontitis,has been shown to accelerate the progression of atherosclerosis(AS).However,the definite mechanisms remain elusive.Emerging evidence supports an association between mitochondrial dysfunction and AS.In our study,the impact of P.gingivalis on mitochondrial dysfunction and the potential mechanism were investigated.The mitochondrial morphology of EA.hy926 cells infected with P.gingivalis was assessed by transmission electron microscopy,mitochondrial staining,and quantitative analysis of the mitochondrial network.Fluorescence staining and flow cytometry analysis were performed to determine mitochondrial reactive oxygen species(mtROS)and mitochondrial membrane potential(MMP)levels.Cellular ATP production was examined by a luminescence assay kit.The expression of key fusion and fission proteins was evaluated by western blot and immunofluorescence.Mdivi-1,a specific Drp1 inhibitor,was used to elucidate the role of Drp1 in mitochondrial dysfunction.Our findings showed that P.gingivalis infection induced mitochondrial fragmentation,increased the mtROS levels,and decreased the MMP and ATP concentration in vascular endothelial cells.We observed upregulation of Drp1(Ser616)phosphorylation and translocation of Drp1 to mitochondria.Mdivi-1 blocked the mitochondrial fragmentation and dysfunction induced by P.gingivalis.Collectively,these results revealed that P.gingivalis infection promoted mitochondrial fragmentation and dysfunction,which was dependent on Drp1.Mitochondrial dysfunction may represent the mechanism by which P.gingivalis exacerbates atherosclerotic lesions.

Porphyromonas gingivalis exacerbates ulcerative colitis via Porphyromonas gingivalis peptidylarginine deiminase

Abstract:Ulcerative Colitis(UC)has been reported to be related to Porphyromonas gingivalis(P.gingivalis).Porphyromonas gingivalis peptidylarginine deiminase(PPAD),a virulence factor released by P.gingivalis,is known to induce inflammatory responses.To explore the pathological relationships between PPAD and UC,we used homologous recombination technology to construct a P.gingivalis strain in which the PPAD gene was deleted(Δppad)and aΔppad strain in which the PPAD gene was restored(comΔppad).C57 BL/6 mice were orally gavaged with saline,P.gingivalis,Δppad,or comΔppad twice a week for the entire 40 days(days 0-40),and then,UC was induced by dextran sodium sulfate(DSS)solution for 10 days(days 31-40).P.gingivalis and comΔppad exacerbated DDS-induced colitis,which was determined by assessing the parameters of colon length,disease activity index,and histological activity index,butΔppad failed to exacerbate DDS-induced colitis.Flow cytometry and ELISA revealed that compared withΔppad,P.gingivalis,and comΔppad increased T helper 17(Th17)cell numbers and interleukin(IL)-17 production but decreased regulatory T cells(Tregs)numbers and IL-10 production in the spleens of mice with UC.We also cocultured P.gingivalis,Δppad,or comΔppad with T lymphocytes in vitro and found that P.gingivalis and comΔppad significantly increased Th17 cell numbers and decreased Treg cell numbers.Immunofluorescence staining of colon tissue paraffin sections also confirmed these results.The results suggested that P.gingivalis exacerbated the severity of UC in part via PPAD.

Meeting report: a close look at oral biofilms and microbiomes

The "Biofilms, Microbiomes and Oral Diseases: Challenges and Future Perspectives" symposium jointly organized by Penn Dental Medicine and West China School of Stomatology was held on 30 September 2017 at Penn Wharton China Center(PWCC) in Beijing,China. The topics included the pathogenicity of oral biofilms, novel strategies for the control of biofilm-related diseases, oral microbiome and single-cell approaches, and the link between oral diseases and overall health. Researchers from a number of disciplines, representing institutions from China and Penn Dental Medicine, gathered to discuss advances in our understanding of biofilms, as well as future directions for the control of biofilm-related oral and systemic diseases.

Identification of Methylosome Components as Negative Regulators of Plant Immunity Using Chemical Genetics

Nucleotide-binding leucine-rich repeat （NLR） proteins serve as immune receptors in both plants and animals. To identify components required for NLR-mediated immunity, we designed and carried out a chemical genetics screen to search for small molecules that can alter immune responses in Arabidopsis thaliana. From 13 600 compounds, we identified Ro 8-4304 that was able to specifically suppress the severe autoimmune phenotypes of chs3-2D （chilling sensitive 3, 2D）, including the arrested growth morphology and heightened PR （Pathogenesis Related） gene expression. Further, six Ro 8-4304 insensitive mutants were uncovered from the Ro 8-4304-insensitive mutant （rim） screen using a mutagenized chs3-2D popula- tion. Positional cloning revealed thatriml encodes an allele of AtlCIn （I, currents; CI, chloride; n, nucleotide）. Genetic and biochemical analysis demonstrated that AtlCIn is in the same protein complex with the meth- ylosome components small nuclear ribonucleoprotein D3b （SmD3b） and protein arginine methyltransferase 5 （PRMT5）, which are required for the biogenesis of small nuclear ribonucleoproteins （snRNPs） involved in mRNA splicing. Double mutant analysis revealed that SmD3b is also involved in the sensitivity to Ro 8-4304, and the prmt5-1 chs3-2D double mutant is lethal. Loss of At/C/n, SmD3b, or PRMT5 function results in enhanced disease resistance against the virulent oomycete pathogen Hyaloperonospora arabidopsidis Noco2, suggesting that mRNA splicing plays a previously unknown negative role in plant immunity. The successful implementation of a high-throughput chemical genetic screen and the identification of a small-molecule compound affecting plant immunity indicate that chemical genetics is a powerful tool to study whole-organism plant defense pathways.

Construction of a recombinant yeast strain converting xylose and glucose to ethanol

Candida shehatae gene xyl1 and Pichia stipitis gene xyl2,encoding xylose reductase(XR)and xylitol dehydrogenase(XD)respectively,were amplified by PCR.The genes xyl1 and xyl2 were placed under the control of promoter GAL in vector pYES2 to construct the recombinant expression vector pYES2-P12.Subsequently the vector pYES2-P12 was transformed into S.cerevisiae YS58 by LiAc to produce the recombinant yeast YS58-12.The alcoholic ferment indicated that the recombinant yeast YS58-12 could convert xylose to ethanol with the xylose consumption rate of 81.3%.