BackgroundIt is widely accepted that oral health plays an important role in overall health. Both dental and medical students are expected to possess good oral health awareness and work together for public oral health promotion especially in developing countries like China. The aim of this study was to assess the oral health knowledge, behavior and status of dental and medical undergraduate students in the first (fresh) and third year (before specialized courses) study.MethodsA self-administered structured questionnaire with 13 questions was designed based on oral health knowledge, behavior and status and a cross-sectional study was conducted among the 1st, 3rd year dental students (1DS, 3DS) and medical students (1MS, 3MS) of Sichuan University in Chengdu, China, in the period of September–December 2017. The data was analyzed by chi-square test using IBM SPSS Statistics v. 21.0.ResultsThe oral health behavior, consciousness and status of the 1st, 3rd year medical and dental students were not optimistic. Dental freshmen were slightly superior to the medical ones in terms of the brushing methods and the awareness of oral disease-systemic disease relationship. The junior dental students showed highly significant improvement than their counterparts, mainly in the items about frequency of brushing teeth, brushing methods of vertical scrub or Bass technique (66.3%), usage of floss or mouth wash (49.7%), causes of caries, periodontal diseases and system diseases (56.9–83.4%). The rates mentioned above were 36.1, 15.8%, 26.7–43.6% among 3MS, respectively. In terms of oral health status, significant differences were only observed in junior students. The prevalence rates of bad breath, gum bleeding, and tooth discoloration among 3DS were obviously lower than those of 3MS. However, only a total of 17.2% junior students had a good oral health, including 23.8% dental students and 11.4% medical students.ConclusionsOur study provided a new understanding of oral health knowledge, behavior and status among dental and medical students, which may help to promote the reform of oral health education and establish a model for clinicians and dentists to work together for improving oral health.

The biodiversity of the mycobiome, an important component of the oral microbial community, and the roles of fungal–bacterial and fungal–immune system interactions in the pathogenesis of oral lichen planus (OLP) remain largely uncharacterized. In this study, we sequenced the salivary mycobiome and bacteriome associated with OLP. First, we described the dysbiosis of the microbiome in OLP patients, which exhibits lower levels of fungi and higher levels of bacteria. Significantly higher abundances of the fungi Candida and Aspergillus in patients with reticular OLP and of Alternaria and Sclerotiniaceae_unidentified in patients with erosive OLP were observed compared to the healthy controls. Aspergillus was identified as an “OLP-associated” fungus because of its detection at a higher frequency than in the healthy controls. Second, the co-occurrence patterns of the salivary mycobiome–bacteriome demonstrated negative associations between specific fungal and bacterial taxa identified in the healthy controls, which diminished in the reticular OLP group and even became positive in the erosive OLP group. Moreover, the oral cavities of OLP patients were colonized by dysbiotic oral flora with lower ecological network complexity and decreased fungal–Firmicutes and increased fungal–Bacteroidetes sub-networks. Third, several keystone fungal genera (Bovista, Erysiphe, Psathyrella, etc.) demonstrated significant correlations with clinical scores and IL-17 levels. Thus, we established that fungal dysbiosis is associated with the aggravation of OLP. Fungal dysbiosis could alter the salivary bacteriome or may reflect a direct effect of host immunity, which participates in OLP pathogenesis.

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The ability of mannose receptor (MR) to recognize the carbohydrate structures is well-established. Here, we reported that MR was crucial for the immune response to a Ganoderma atrum polysaccharide (PSG-1), as evidenced by elevation of MR in association with increase of phagocytosis and concentrations of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in normal macrophages. Elevation of MR triggered by PSG-1 also led to control lipopolysaccharide (LPS)-triggered inflammatory response via the increase of interleukin-10 (IL-10) and inhibition of phagocytosis and IL-1β. Anti-MR antibody partly attenuated PSG-1-mediated anti-inflammatory responses, while it could not affect TNF-α secretion, suggesting that another receptor was involved in PSG-1-triggered immunomodulatory effects. MR and toll-like receptor (TLR)4 coordinated the influences on the TLR4-mediated signaling cascade by the nuclear factor-κB (NF-κB) pathway in LPS-stimulated macrophages subjected to PSG-1. Collectively, immune response to PSG-1 required recognition by MR in macrophages. The NF-κB pathway served as a central role for the coordination of MR and TLR4 to elicit immune response to PSG-1.

The aim of the present study was to examine the role of Ganoderma atrum polysaccharide (PSG-1) in reactive oxygen species (ROS) generation and mitochondrial function in hyperglycemia-induced angiopathy. In this work, ROS scavenger, oxidizing agent tert-butylhydroperoxide (tBH), mitochondrial permeability transition pore (mPTP) blockers, and caspase inhibition are used to investigate whether PSG-1 may promote survival of human umbilical vein cells (HUVECs) through preventing the overproduction of ROS and mitochondrial dysfunction. Experimental results show that exposure of HUVECs to 35.5 mmol/L glucose increases the proportion of cells undergoing apoptosis. PSG-1, mPTP blocker, or caspase inhibition can reduce apoptosis and ROS generation. PSG-1 also increases mitochondrial Bcl-2 protein formation and mitochondrial membrane potential (ΔΨm) but inhibits Bax translocation, cytochrome c release, and caspase activation. In summary, vascular protection of PSG-1 can be mediated by a mitochondria-ROS pathway. ROS generation and mPTP induction are critical for high glucose-mediated apoptosis. PSG-1 ameliorates endothelial dysfunction by inhibiting oxidative stress and subsequent mitochondrial dysfunction.