Oral candidiasis is a significant health problem in terms of both morbidity and economic outlay. Infections are predominantly caused by the commensal C. albicans, and affect immunocompromised individuals, including HIV-positive and AIDS patients, organ transplant recipients and chemotherapy patients. The molecular and cellular immune mechanisms involved in protection from and responses to oral candidiasis are overlapping, but distinct from those associated with other manifestations of the disease, including systemic, vaginal and gastric candidiasis. In oral candidiasis, clinical observations and experimental mouse models suggest a critical role for cell-mediated immunity. In mice, CD4+ T-cells and the p40 subunit of interleukins 12 and 23 are strict prerequisites for resistance; however abrogation of IFN-gamma does not confer susceptibility. Here, we discuss this apparent inconsistency, and review the experimental evidence that clarifies which immune pathways are specifically involved in resistance and responses to candidiasis of the oral cavity. We also highlight deficiencies in the literature, particularly concerning the putative roles of some relatively new elements in immunobiology: interleukin-23, interleukin-17 and T helper (Th)17 cells.

The present study demonstrates that the use of CHX as an antimicrobial agent is effective in reducing the overall number of bacterial colonies in the oral cavity. Rinsing is a more effective method of doing this.

These data suggest that iNOS-derived NO is not required for resistance to oral candidiasis in vivo, and that bone marrow-derived macrophages may have iNOS-independent means of generating reactive nitrogen species.

Candida species are ubiquitous opportunistic pathogens, causing significant morbidity and mortality in humans. C. albicans can asymptomatically colonise the skin and mucosal surfaces in healthy and immunologically competent individuals without causing disease.