Neftaha Tazi, Witold Chmielewski, Abdelhabib Semlali, Bouchaib Lamkhioued, Adil Akkouch, Manon Clavette, Mahmoud Ghannoum and Mahmoud Rouabhia
Candida albicans (C. albicans) is the most prevalent fungus in the human oral cavity and has been known as the primary cause of denture-related stomatitis. Candida cells have a high adhering potential to dental material in almost the same manner as to oral tissues, and they are known to form biofilm that leads to C. albicans resistance against antifungal drugs. The aim of this study was to investigate C. albicans adhesion and growth on different restorative dental materials and studied the effect of fluoride on C. albicans growth and morphological transition. To this end, C. albicans (Sc 5314) was cultured on acrylic resins, composite resin, and glass-ionomer materials. Growth was analyzed at various times using scanning electron microscopy analyses and cell proliferation assay. The effect of different concentrations (50 and 100 ppm) of exogenous fluoride on C. albicans growth and yeast-to-hyphae transition was investigated.
Scanning electron microscopy showed that C. albicans adhered to all of the tested restorative materials. Adhesion was greater on diamond D and ivocap than on composite resin and glass ionomer. After 1 to 4 days, C. albicans growth on acrylic resins was two folds that of the composite resin and the glass-ionomer. The latter also displayed the lowest adhesion and growth which may be due to the release of antimicrobial molecules such as fluoride present in this material. This hypothesis is supported by our results showing that exogenous fluoride significantly inhibits C. albicans growth and its morphological changes from blastospore to hyphal form. This study clearly demonstrates that restorative materials are conducive to C. albicans adhesion and growth. Exogenous fluoride was also shown to down-regulate C. albicans growth and morphological changes. Overall data suggest the possible integration of fluoride into dental materials which may control oral microbial pathogenesis.