Oral candidiasis is caused by Candida species, a saprophytic
yeast that is a commensal in the oral cavity. Candida
albicans is the most common agent, with others such as C.
krusie and C.tropicalis also being implicated. The presence
of oral candidosis should prompt a search for local or
systemic predisposing factors.
Clinical presentation of oral candidiasis can take distinct
1 Diet rich in carbohydrates
2 Tobacco smoking
3 Denture hygiene and wearing
5 Topical steroid use (most commonly steroid inhalers
1 Physiological factors: infancy, old age, pregnancy
2 Drug therapy: antibiotics
3 Endocrine disease
a Diabetes mellitus
b Autoimmune polyendocrinopathy
a Primary immune deficiency
b Steroids, cancer chemotherapy
c Radiation therapy
d HIV infection
• Pseudomembranous oral candidiasis (thrush). Patches of
curd-like white pseudomembrane occur on the cheek,
gums, and the palatal mucosa. These are easily removed
and reveal an erythematous base. It may involve the
tongue in immunocompromised patients.
• Acute erythematous oral candidiasis usually occurs
following antibiotic treatment and in immunosupression,
marked by erythema on the dorsum of the tongue.
• Chronic erythematous stomatitis (denture stomatitis) is
characterized by redness in the denture bearing area in
the palate. Soreness is not a prominent
• Chronic hyperplastic oral candidiasis (candidal
leukoplakia) presents with white plaques on the cheek or
tongue that are not easily removed, with little or no
symptoms. It is nearly always seen in smokers and
regression may follow smoking cessation. An incisional
biopsy is indicated to determine the presence of dysplasia.
This lesion can be classed as a premalignant one.
• Median rhomboid glossitis shows an erythematous area
devoid of papilla of the tongue in the midline just anterior
to the circumvallate papillae.
• Angular stomatitis presents as erythema and fissuring of
the angles of the mouth. These lesions may also be
caused by a staphylococcal infection or may also be an
indicator of underlying vitamin deficiency, anaemia, or
even diabetes, hence appropriate screening is warranted.
The varied presentation of oral candidiasis permits many
differentials. All keratotic lesions can be ruled out easily as
they do not rub off on examination. Chemical burns,
superficial bacterial infections, lichen planus, white sponge
nevus syndrome, and necrotic ulcers from systemic disease
should be considered.
As a first-line drug, topical miconozole or nystatin is
recommended; if a response does not occur with one of
them, the other can be tried. Oral imidazoles (fluconazole
and itraconazole) are licensed for use in oral candidiasis
where first-line measures have been unsuccessful.
Identification and removal of predisposing factors is
essential. Avoiding sleeping with dentures in place, tobacco
cessation and rinsing of the mouth following steroid inhaler
use are examples of simple advice that may be given when
indicated. In the absence of obvious predisposing factors,
screening for systemic risk factors may be warranted.
Recurrent infections in the immunocompromised patient
may warrant prophylaxis.