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Betaine, known as trimethylglycine, is a non-toxic natural substance reported to affect cancer cell responses. This study delves into the impact of betaine on the survival, proliferation, and invasion of oral squamous cell carcinoma (OSCC) cells in vitro. Human OSCC cells (HSC-4 and HSC-7) were subjected to varying concentrations of betaine, and their viability and proliferation were assessed through colourimetric MTT and colony-forming unit assays. Cell cycle progression and cell apoptosis were also investigated using flow cytometry, while cell migration and invasion were examined using a transwell migration assay, and the mRNA expression was evaluated by a quantitative polymerase chain reaction. Finally, proteomic analysis was conducted through liquid chromatography-tandem mass spectrometry on the extracted protein component of the cells. Results indicate that betaine effectively suppressed OSCC proliferation and colony formation. It triggered early apoptosis without disrupting cell cycle progression, reduced cell migration, and inhibited invasion. Betaine exposure led to significantly decreased mRNA levels of MMP1, MMP2, and MMP9 while downregulating FN1, a gene linked to epithelial-to-mesenchymal transition. Proteomic analysis revealed 9240 differentially expressed up/downregulated proteins in cells treated with betaine. The significantly upregulated proteins were associated with ATP-binding cassette (ABC) transporters, while the down-regulated proteins were associated with G protein-coupled receptors (GPCR) ligand binding. In conclusion, betaine exhibits potent anti-cancer properties by attenuating OSCC cell proliferation and mitigating invasion. Exploring this natural product as an adjunct for managing oral squamous cell carcinoma shows promise, although further investigations are needed to fully elucidate its functionality. [ABSTRACT FROM AUTHOR]

Objectives: To compare, in vitro, the efficacy of three proprietary silver diamine fluoride (SDF) products in mitigating progression of dentinal caries induced by an inter-kingdom, dual-species, bacterial-yeast biofilm. Methods: Human dentin blocks were demineralized to create artificial caries lesions and randomized into three SDF test groups: Saforide, Topamine, T-SDF, and an aqueous control (n = 26 per group). After application of foregoing SDF variants, the blocks were incubated with Streptococcus mutans and Candida albicans for 24 h for biofilm development, and subsequently subjected to a microbe-induced, pH-cycling process for 7 days, to mimic the oral eco-system. The biofilm cell viability and surface topography were assessed by colony-forming units (CFUs) and scanning electron microscopy respectively. The lesion depth and mineral density were evaluated by micro-computer tomography. SDF precipitate and matrix-to-mineral ratio were evaluated by X-ray diffraction and Fourier transform infrared spectroscopy, respectively. Standard, accepted methodology was used for all these evaluations and procedures. Results: After pH cycling, the SDF groups demonstrated comparable inhibition of the biofilm relative to the control. the log CFU of S. mutans for Saforide, Topamine, T-SDF, and control were 6.69±0.73, 6.48±0.56, 6.63±0.66, and 8.01±0.45, respectively. For C. albicans, the log CFU were 4.86±0.44, 4.72±0.53, 4.92±0.29, and 5.60±0.27, respectively. The log CFU of S. mutans and C. albicans in the SDF groups were significantly lower than the control group (p<0.001). Further, the lesion depth decreased by approximately 14.79±7.00% in the SDF groups, while it increased by 11.07±8.61% in the control (p<0.001), and the mineral density increased by 16.36±4.58% in the SDF group, as opposed to a 5.59±2.64% reduction in the control (p<0.001) implying their caries mitigating effect. These findings were corroborated by SEM images of the lesions. Conclusion: SDF significantly mitigated dentin caries due to an assault by a polymicrobial plaque biofilm whilst arresting mineral loss and lesion growth. There was no difference in the caries-arresting efficacy of the compared SDF variants. [ABSTRACT FROM AUTHOR]

Objective: Endodontic microbiota appears to undergo evolutionary changes during disease progression from inflammation to necrosis and post-treatment. The aim of this study was to compare microbiome composition and diversity in primary and post-treatment endodontic infections from a cohort of patients from the UAE. Design: Intracanal samples were collected from primarily infected (n = 10) and post-treatment infected (n = 10) root canals of human teeth using sterile paper points. Bacterial DNA was amplified from seven hypervariable regions (V2–V4 and V6–V9) of the 16S rRNA gene, then sequenced using next-generation sequencing technology. The data was analyzed using appropriate bioinformatic tools. Results: Analyses of all the samples revealed eight major bacterial phyla, 112 genera and 260 species. Firmicutes was the most representative phylum in both groups and was significantly more abundant in the post-treatment (54.4%) than in primary (32.2%) infections (p>0.05). A total of 260 operational taxonomic units (OTUs) were identified, of which 126 (48.5%) were shared between the groups, while 83 (31.9%) and 51 (19.6%) disparate species were isolated from primary and post-treatment infections, respectively. A significant difference in beta, but not alpha diversity was noted using several different indices (p< 0.05). Differential abundance analysis indicated that, Prevotella maculosa, Streptococcus constellatus, Novosphigobium sediminicola and Anaerococcus octavius were more abundant in primary infections while Enterrococcus faecalis, Bifidobacterium dentium, Olsenella profusa and Actinomyces dentalis were more abundant in post-treatment infections (p <0.05). Conclusion: Significant differences in the microbiome composition and diversity in primary and post-treatment endodontic infections were noted in our UAE cohort. Such compositional differences of microbiota at various stages of infection could be due to both intrinsic and extrinsic factors impacting the root canal ecosystem during disease progression, as well as during their therapeutic management. Identification of the key microbiota in primarily and secondarily infected root canals can guide in the management of these infections. [ABSTRACT FROM AUTHOR]