Serious game as oral histology learning strategy for undergraduate dental students; crossover randomized controlled trial.

BACKGROUND: Oral histology is perceived by dental students as a challenging subject and often struggle to recognize the long-term relevance of understanding the cells and tissues at the microscopic level. Serious games have been reported to have a positive effect on student cognitive skills and learning motivation. However, there is still a limited amount of research supporting the effectiveness of serious games as a learning method in dentistry. The present study aimed to evaluate the impact of serious game of HistoRM as a complementary learning strategy for oral histology. METHODS: The study design was a crossover randomized controlled trial. A total of 74 first year dental students of Universitas Indonesia participated in the study and divided into 2 groups. Study intervention included HistoRM game for 3 days followed by a combination of HistoRM and script-based handouts for another 4 days. The groups represented different intervention sequences. Evaluation was performed using pre-test, post-test on day 3 and 7 and a questionnaire. RESULTS: The data showed significant improvement of student cognitive skills (p < 0.001) and it was influenced by the number of game missions completed. Students who completed the whole 15 missions have a higher day-7 post-tests scores (p = 0.03). Perception of dental students on HistoRM was positive in all domains tested, the learning content, games and learning experience domains. Immediate feedback given after each gameplay helped the students understand the subject matters. CONCLUSION: Serious game of HistoRM effectively improved students' understanding of oral histology learning outcome and provided more interesting learning experiences. This innovative learning can be recommended as a complementary learning strategy of oral histology for dental students.

Chitosan as a potential osteogenic factor compared with dexamethasone in cultured macaque dental pulp stromal cells.

Chitosan, a natural biopolymer derived from chitin, is considered a promising scaffold material for bone tissue engineering. The ability of chitosan to promote the osteogenic differentiation of dental pulp stromal/stem cells (DPSCs) is unknown. We have evaluated the potential of chitosan to induce the osteogenic differentiation of macaque DPSCs in comparison with that of dexamethasone. DPSCs were cultured in mineralizing medium supplemented with 5 or 10 µg/ml chitosan or with 1 or 10 nM dexamethasone. The metabolic activity of DPSCs was measured by MTT assay. Their osteogenic differentiation was determined by the number of transcripts of RUNX2, alkaline phosphatase (ALP), and COL1A1 by using real-time polymerase chain reaction, by alizarin red staining for mineral deposition, and by the ALP activity released into the medium for their ability to support biomineralizaton. Addition of chitosan to the mineralizing medium significantly increased DPSCs metabolism after 7 and 14 days of culture (P ≤ 0.0001). Chitosan at 5 µg/ml also significantly enhanced RUNX2 and ALP mRNA but not COL1A1 mRNA; chitosan tended to increase the release of ALP hydrolytic enzyme activity into the medium during the first week. Dexamethasone upregulated the osteogenic markers tested. Mineral deposition was similar in the chitosan and dexamethasone groups and was not statistically different from that of the mineralizing control group. Thus, the potential of chitosan to stimulate DPSCs proliferation and early osteogenic differentiation is comparable with that of dexamethasone, but mineralization remains unaffected by chitosan treatment. In addition to its role as a three-dimensional scaffold for osteogenic cells in vivo, chitosan might also stimulate DPSCs proliferation and early osteogenic differentiation in vitro.

Chitosan exerts anticancer activity through induction of apoptosis and cell cycle arrest in oral cancer cells.

Chitosan, a multipurpose biomaterial, has been shown to exert effects against several types of cancer including oral cancer. However, the mechanisms underlying the anticancer activities of chitosan on oral squamous cell carcinoma (SCC) cells remain largely unknown. The present study aimed to compare the effects of low-molecular-weight chitosan (LMWC) and cisplatin on oral SCC Ca9-22 and non-cancer keratinocyte HaCaT cell lines. Cell viability and cell cycle profiles were measured by MTT assay and laser scanning cytometry, respectively. Apoptosis was examined by TUNEL assay and electron microscopy, followed by analysis of caspase activity. LMWC exhibited cytotoxic effects on Ca9-22, but not HaCaT cells, whereas cisplatin induced apoptosis in both types of cells. Exposure of Ca9-22 cells to LMWC led to G1/S cell cycle arrest and an increase of TUNEL-positive cells accompanied by an early apoptotic cell morphology and subtle increases of caspase activity. Short-term LMWC exposure was less cytotoxic to HaCaT cells than to Ca9-22 cells, and anticancer activity was exerted through induction of apoptosis and cell cycle arrest, suggesting that LMWC could be a promising natural anticancer agent with fewer side effects on normal cells.

Involvement of lysosomal storage-induced p38 MAP kinase activation in the overproduction of nitric oxide by microglia in cathepsin D-deficient mice.

Nitric oxide (NO) and peroxynitrite, which are produced by activated microglia, are responsible for accelerated neurodegeneration in cathepsin D-deficient (CD-/-) mice. To elucidate the mechanisms by which microglia are initially activated in CD-/- mice, we analyzed the possible relationship between lysosomal storage and microglial activation. In CD-/- mice, the microglial NO-generating activity that was closely associated with the induction of inducible NO synthase and the cationic amino acid transporter-2 (CAT-2) coincided well with the lysosomal storage of subunit c of mitochondrial F0F1ATPase and the formation of ceroid/lipofuscin. Furthermore, activated microglia, which are often accumulating subunit c and ceroid/lipofuscin, showed proliferation activity and an activation of p38 mitogen-activated protein (MAP) kinase. In the primary cultured microglia, pepstatin A was found to enhance the generation of NO and superoxide anion radicals. In these pepstatin A-treated microglia, both an increased generation of the intracellular reactive oxygen species (ROS) and an activation of p38 MAP kinase were observed. These results suggest that the ceroid/lipofuscin which form in microglia activate the p38 MAP kinase cascade through the increased intracellular generation of ROS in CD-/- mice. The activated p38 MAP kinase cascade then promotes the expression of iNOS and CAT-2, thereby inducing the overproduction of NO.