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Pathology and clinical correlates in oral candidiasis and its variants: a review
Author(s) -
Reichart PA,
Samaranayake LP,
Philipsen HP
Publication year - 2000
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/j.1601-0825.2000.tb00106.x
Subject(s) - immune system , systemic candidiasis , candida albicans , immunology , pathological , biology , pathology , delayed hypersensitivity , antigen , corpus albicans , medicine , microbiology and biotechnology
Although Candida albicans is well recognised as the major agent of oral candidiasis, it is not clear why several variants such as pseudomembranous (PC), erythematous (EC) and hyperplastic candidiasis (HC) manifest in different individuals, sometimes singly and on other occasions, in combination. The present review focuses on recent histopathologic and immunocytochemical studies as well as the pathogenic attributes of the yeast, in an attempt to address the following queries.(1) Do histopathologic studies of the different variants of candidiasis in immuno‐competent and immunocompromised individuals help explain these varying manifestations? (2) Under what circumstances does oral candidiasis manifest as a pseudo‐membranous rather than an erythematous lesion or vice versa? (3) Are there differences in immunoreactivity in closely adjacent mucosae so that the variable presentation of such lesions reflect differences in the local mucosal immune system? Recent studies of PC, EC and HC offer some insights into the pathogenic mechanisms involved. 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 against Candida antigens in the latter. Hyper‐plastic candidiasis on the other hand could be considered a superficial cellular reaction against the pathogen, which cannot entirely be eradicated by the systemic or local host immune response. The virulent attributes of the fungus, such as the production of extracellular proteinases, do significantly differ within and between species and thereby play a contributory role in the genesis of the clinical variantS. Although the available data do give a tantalising glimpse of the contributory mechanisms for the aetiopathology of PC, EC and HC, further research is warranted to elucidate response of the host to this ubiquitous fungal pathogen.

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