Radioactive caries is the most common complication of head and neck cancer after radiotherapy. It is a rapidly progressing and widespread destructive disease of tooth tissue after radiotherapy. It is currently believed that salivary gland dysfunction and direct damage to teeth by radiation are the main pathogenic factors of radiation caries. In this paper, the pathogenesis of radiation caries, especially the effect of radiotherapy on oral caries-related microorganisms, are reviewed, and future research directions are proposed. Existing research has revealed that the structures of oral microorganisms change significantly after radiotherapy. The number and proportion of some dental caries-related microorganisms such as Streptococcus mutans, Lactobacillus lactis and Candida albicans increased, and their virulence increased. This indicated that the changes in oral microorganisms caused by radiotherapy played an important role in radioactive caries.

Oral potentially malignant disorders (OPMDs) refer to all epithelial lesions and conditions with an increased risk for malignant transformation, including oral leukoplakia, oral submucous fibrosis, oral lichen planus, erythroplakia, etc. Additionaly, oral infection of Candida albicans is considered to be closely related to the development of OPMDs. It was demonstrated in previous studies that the detection rate of Candida albicans was higher in the oral mucosa with OPMDs; in addition, Candida albicans showed high virulence by adhering to and destroying the epithelium. Moreover, Candida albicans was able to induce the immune response and cause chronic inflammation in the epithelium, producing carcinogenic products such as acetaldehyde. The factors mentioned above play a key role in the occurrence and development of OPMDs. Furthermore, the oral mucosa is highly susceptible to Candida albicans. The present review provides an introduction to the relationship between Candida albicans and OPMDs.

Oral cancer is one of the most common cancers that occur in the head and neck and can seriously affect the life span and living standard of oral cancer patients. Candida albicans (C. albicans) is the most common opportunistic pathogenic fungus in the oral cavity, shows pathogenicity and easily causes Candida infection when the host′s immune function is low. Recent studies have shown that C. albicans infection is closely related to oral cancer. This paper reviews the epidemiology of C. albicans infection in oral cancer patients, the influence of C. albicans infection on the occurrence and development of oral cancer and research on its mechanism. Existing studies have shown an increased risk of C. albicans infection in oral cancer patients, while C. albicans infection may promote the occurrence and development of oral cancer through mechanisms such as damaging the oral epithelium; producing carcinogens, including nitrosamine and acetaldehyde; and inducing a chronic inflammatory response and T helper cell 17 immune response. However, these mechanisms are still relatively superficial and lack sufficient direct evidence. In the future, additional in-depth studies are still needed to further clarify the cancer-promoting mechanisms of C. albicans and provide new ideas for the prevention and treatment of oral cancer.

Candida albicans is the most abundant fungal species in oral cavity. As a smart opportunistic pathogen, it increases the virulence by switching its forms from yeasts to hyphae and becomes the major pathogenic agent for oral candidiasis. However, the overuse of current clinical antifungals and lack of new types of drugs highlight the challenges in the antifungal treatments because of the drug resistance and side effects. Anti-virulence strategy is proved as a practical way to develop new types of anti-infective drugs. Here, seven artemisinins, including artemisinin, dihydroartemisinin, artemisinic acid, dihydroartemisinic acid, artesunate, artemether and arteether, were employed to target at the hyphal development, the most important virulence factor of C. albicans. Artemisinins failed to affect the growth, but significantly inhibited the hyphal development of C. albicans, including the clinical azole resistant isolates, and reduced their damage to oral epithelial cells, while arteether showed the strongest activities. The transcriptome suggested that arteether could affect the energy metabolism of C. albicans. Seven artemisinins were then proved to significantly inhibit the productions of ATP and cAMP, while reduced the hyphal inhibition on RAS1 overexpression strain indicating that artemisinins regulated the Ras1-cAMP-Efg1 pathway to inhibit the hyphal development. Importantly, arteether significantly inhibited the fungal burden and infections with no systemic toxicity in the murine oropharyngeal candidiasis models in vivo caused by both fluconazole sensitive and resistant strains. Our results for the first time indicated that artemisinins can be potential antifungal compounds against C. albicans infections by targeting at its hyphal development.