Candida albicans is frequently isolated from the human mouth, yet few
carriers develop clinical signs of candidiasis. Oral candidiasis prese
nts clinically in many forms. This reflects the ability of the yeast t
o colonize different oral surfaces and the variety of factors which pr
edispose the host to Candida colonization and subsequent infection. Co
lonization of the oral cavity appears to be facilitated by several spe
cific adherence interactions between C. albicans and oral surfaces whi
ch enable the yeast to resist host clearance mechanisms. Thus, Candida
has been shown to adhere to complement receptors, various extracellul
ar matrix proteins, and specific sugar residues displayed on host or b
acterial surfaces in the oral cavity. Oral candidiasis results from ye
ast overgrowth and penetration of the oral tissues when the host's phy
sical and immunological defenses have been undermined. Tissue invasion
may be assisted by secreted hydrolytic enzymes, hyphal formation, and
contact sensing. While these and other phenotypic characteristics may
endow certain Candida species or strains with a competitive advantage
in the oral cavity, it is the host's immune competence that ultimatel
y determines whether clearance, colonization, or candidiasis occurs.