The objective of this study is to determine the therapeutic efficacy of allicin against Candida albicans (C. albicans) and Staphylococcus aureus (S. aureus), the common etiological agents for denture stomatitis (DS). The minimum inhibitory concentration (MICs), minimum bactericidal concentrations (MBCs) and minimum fungicidal concentration (MFCs) of allicin were determined by the broth microdilution method followed by checkerboard microdilution method for a synergistic interaction between allicin + nystatin and allicin + CHX. The potential of allicin to eradicate C. albicans and S. aureus biofilms was assessed by treating biofilm formed on self- polymerized acrylic resin with allicin at a sub-MIC concentration for 5 min. The commercial denture cleanser (brand X) was used as a positive control. A Kruskal-Wallis test followed by the post-hoc Mann-Whitney U test was applied (SPSS 20.0), and the level of significance was set at P < 0.05. Allicin exhibited antimicrobial activity against C. albicans (MIC:8 µg/ml and MFC:16 µg/ml) and S. aureus (MIC:8 µg/ml and MBC:8 µg/ml). A synergistic interaction was observed between allicin + nystatin and allicin + CHX (FICI ≤ 0.5). Allicin exhibited significant biofilm eradication against C. albicans and S. aureus biofilms with percentages of 50.0% and 52.6%, respectively. The results of this study suggest a possible application of allicin in treating C. albicans and S. aureus infection in DS.

This study aims to determine the paracrine effects of Candida auris phenotypic switching in mono- and co-culture with Staphylococcus aureus on oral epithelial homeostasis and oncogenic progression in phenotypically normal (hTERT TIGKs) and malignant (ORL-48) oral keratinocytes. C. auris switched phenotype was scored using Phloxine B, and mono- and co-culture biofilms with S. aureus were developed. hTERT TIGKs and ORL-48 cell lines were independently seeded into 6-well and 96-well plates for dispase and viability test, respectively. The oral cell lines were exposed to phenotypically switched C. auris mono- and co-culture biofilm test cell growth medium (TCGM) for 24 h. Outcomes included cell morphology, metabolic activity/viability (CCK-8), and cell-cell adhesion (dispase assay). Microscopic observation revealed that the biofilm induced damage and disrupted epithelial cell integrity in a paracrine manner. The mono- and co-culture TCGM suppressed the growth of normal cells while promoting the metabolic activity of cancer cells. The adhesion analysis of hTERT TIGKs indicated a strong intercellular cohesion, while ORL-48 cells downregulated intercellular adhesion and compromised cell-cell cohesion. C. auris biofilms promote the development of a malignant phenotype by regulating cell viability, promoting epithelial-mesenchymal transition, and adhesion in a switched generation-dependent manner.

Cancer which synonymously known as neoplasia is a genetic disorder of cell growth that is triggered by acquired or less commonly inherited mutations affecting a single cell and its clonal progeny. The aims of this scoping review was to investigate the role of sugar and sugar substitutes in breast, lung, and oral cancers with a hypothesis that sugar promoted carcinogenesis. Three databases (EBSCO, PubMed, and Scopus) were searched from January 2010 to December 2021 to identify the preclinical studies eligible for this scoping review. The review was performed according to the Preferred Reporting Items for Systematic reviews and Meta-Analyses for Scoping Reviews (PRISMA-ScR) guidelines. A total of 361 articles were reviewed and the qualitative synthesis used 12 of these articles. Based on the qualitative synthesis, four studies reported dietary sugar (glucose- and/or sucrose) induced cancer progression, one study revealed sugar substitute (aspartame) induced cancer proliferation, seven studies reported that sugar substitutes inhibit cancer proliferation, and one study reported that sucrose promotes cancer while xylitol inhibits cancer. In addition., it was reported that D-allose and cisplatin have a synergistic effect in treating cancer. In conclusion, simple sugar intake is associated with an increased risk of carcinogenesis. In contrast, sugar substitutes inhibit cancer cell line progression, subsequently acting as a potential cancer therapy, thus supporting the study's hypothesis.