Candida–streptococcal interactions in biofilm-associated oral diseases

Bacterial-fungal interactions and oral diseasesThe oral cavity contains up to 700 different species of microorganisms, including both bacteria and fungi [1].The interactions of these communities of different organisms has become of increasing interest, particularly with respect to cross-kingdom interactions involving fungi and bacteria, which have been associated with severity of dental caries (tooth decay) and mucosal infections.Here, we provide a short review of the significance and mechanisms for the interactions between C. albicans and streptococci, the most common fungal and bacterial organisms in the oral cavity [2][3][4][5].Candida albicans and oral streptococci coinfections are associated with enhanced virulence of dental caries and more severe oropharyngeal diseases (Fig 1) [6,7].Specifically, C. albicans partners with Streptococcus gordonii, S. oralis, and S. sanguinis to enhance bacterial colonization and biofilm formation.In addition, C. albicans becomes more invasive, exacerbating mucosal tissue infection and destruction [8,9].Mixed C. albicans-bacterial infections are also associated with denture stomatitis, the inflammation of the oral mucosa under dentures.Furthermore, C. albicans-bacterial communities have been clinically found in other oral niches, including periodontal pockets and endodontic canals [6].C. albicans-streptococcal biofilms are an important contributor to the development of early childhood caries that affects toddler-age children [10][11][12].Severe childhood caries is a particularly virulent form of caries that causes extensive and painful tooth destruction, induced by protracted consumption of sucrose containing foods and beverages [11].Typically, C. albicans is usually absent on teeth of healthy, caries-free children [10].Furthermore, C. albicans does not interact strongly with S. mutans (a caries-causing pathogen), nor is it an efficient colonizer of mineralized tooth enamel by itself.However, the high level of sucrose in the oral cavity increases the physical coadhesion between the C. albicans and S. mutans as well as tooth surface colonization and drastically enhances the microbial burden, aciduricity, and production of extracellular matrix.Ultimately, the extensive mixed-kingdom and acidogenic biofilm leads to severe tooth decay in a process that can be recapitulated in a rodent model under sugar-rich diets [12].