Oral dysbiosis in the onset and carcinogenesis of oral epithelial dysplasia: A systematic review.

OBJECTIVE: This systematic review aims to investigate possible connections between the oral microbiome and the onset and carcinogenesis of oral epithelial dysplasia (OED). METHODS: A systematic search was performed on PubMed, Embase, Cochrane Database, and SCOPUS by two authors independently, addressing the focused question- "Has oral microbiome dysbiosis been involved in the onset and carcinogenesis of oral epithelial dysplasia?" We used the Newcastle-Ottawa scale to assess the quality of studies included in the review. RESULTS: Out of 580 references screened, ten studies were found eligible for inclusion. All studies were case-control studies, and only qualitative analysis was conducted due to heterogeneous characteristics. The overall risk of bias in the eligible studies was considered as high. Microbiome diversity indices showed inconsistent evidence among studies. A significant increase of phylum Bacteroidetes in OED patients was reported in five studies. Five studies reported an increase of genus Fusobacterium in both the OED and oral squamous cell carcinoma (OSCC) patients and six different studies respectively reported a reduction of genus Streptococcus in both the OED and OSCC groups when compared to normal controls. Other predominant bacteria that were specific to different patient groups varied in each study. CONCLUSIONS: The results of the included studies showed that the composition of the oral microbiome in patients with OED compared to healthy controls and OSCC patients was inconsistent. However, all ten studies showed non-negligible heterogeneity in the type and size of the sample, and the comparability between groups, which strongly limited the external validity of results. Further studies are strongly recommended.

2D→3D Polycatenated Cu(I) Coordination Polymer: Photocatalytic Property and Protective Activity on COPD by Reducing the INF-γ Production.

Reported here is a new [Cu4I4] cluster-based coordination polymer, namely [Cu4I4(bib)2]n·n(DMF) (1, bib = 1,4-bis(imidazolyl)butane, DMF = N,N'-dimethylformamide), which was synthesized by the self-assemble reaction of CuI, bib and KI under solvothermal conditions. Remarkably, compound 1 shows promising photocatalytic performance toward to the degradation of MB solution under visible light irradiation. For the COPD treatment, the ELISA detection kit was conducted to determine the content of INF-γ released by the respiratory tract mucosal epithelial cells. In addition to this, the activation levels of the NF-κB signaling pathway were still need to be assessed by the real time RT-PCR after the compound treatment.

Associations of Salivary BPIFA1 Protein in Chronic Periodontitis Patients with Type 2 Diabetes Mellitus.

AIMS: To explore the differences in salivary BPI fold containing family A, member 1 (BPIFA1) concentration among type 2 diabetes mellitus (T2DM) subjects with various severities of chronic periodontitis and to determine whether BPIFA1 in saliva can be used as a potential biomarker of T2DM. METHODS: Unstimulated saliva samples were collected from 44 subjects with T2DM and 44 without T2DM (NDM). Additionally, demographic data and general health parameters, including fasting blood glucose (FBG) and body mass index (BMI), were collected. We also detected full-mouth clinical periodontal parameters including probing pocket depth (PPD), clinical attachment level (CAL), bleeding index (BI), and plaque index (PLI). Salivary BPIFA1, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) concentrations were also detected. RESULTS: BPIFA1 in saliva was detected at relatively high levels. T2DM subjects had decreased salivary BPIFA1 concentrations (P = 0.031). In T2DM subjects with nonperiodontitis or severe periodontitis, the level of BPIFA1 was significantly lower compared with that of NDM. Salivary TNF-α concentration displayed a similar trend to BPIFA1 in the NDM group. CONCLUSIONS: BPIFA1 protein is rich in saliva and might be used as a potential predictive biomarker of T2DM, especially in patients with severe periodontitis and nonperiodontitis. This trial is registered with ChiCTR-ROC-17010310.