Pathology and clinical correlates in oral candidiasis and its variants: a review

Although Candida albicans is well recognised as the major agent of oral can didiasis, it is not clear why several variants such as pseudomembranous (PC ), erythematous (EC) and hyperplastic candidiasis (HC) manifest in differen t individuals, sometimes singly and on other occasions, in combination. The present review focuses on recent histopathologic and immunocytochemical st udies as well as the pathogenic attributes of the yeast, in an attempt to a ddress the following queries. (1) Do histopathologic studies of the differe nt variants of candidiasis in immunocompetent and immunocompromised individ uals help explain these varying manifestations? (2) Under what circumstance s does oral candidiasis manifest as a pseudomembranous rather than an eryth ematous lesion or vice versa? (3) Are there differences in immunoreactivity in closely adjacent mucosae so that the variable presentation of such lesi ons reflect differences in the local mucosal immune system? Recent studies of PC, EC and HC offer some insights into the pathogenic mechanisms involve d, Histopathologic and immunohistochemical finding in cases of PC and EC in HIV-infected patients and controls appear to be comparable, with a marked reduction or even an absence of CD4+ cells. The latter phenomenon is marked in PC compared with the EC, and explicable in terms of a breakdown of the local immune response in the former, and a hypersensitivity reaction agains t Candida antigens in the latter. Hyperplastic candidiasis on the other han d could be considered a superficial cellular reaction against the pathogen, which cannot entirely be eradicated by the systemic or local host immune r esponse. The virulent attributes of the fungus, such as the production of e xtracellular proteinases, do significantly differ within and between specie s and thereby play a contributory role in the genesis of the clinical varia nts. Although the available data do give a tantalising glimpse of the contr ibutory mechanisms for the aetiopathology of PC, EC and HC, further researc h is warranted to elucidate response of the host to this ubiquitous fungal pathogen.