Oral candidiasis

ORAL CANDIDIASIS
Dr. Nikitha Sree. K
Lecturer
Malabar Dental College and Research Centre

 Oral candidiasis is the most prevalent oppurtunistic
infection affecting the oral mucosa.
 The lesion is mainly caused by Candida albicans.
 Pathogenesis is not fully understood, but a number
of predisposing factors convert normal commensal
flora to pathogenic organism.
 It is divided in to primary and secondary infections.
 Primary infections restricted to oral and perioral
regions. Secondary infections are accompanied by
systemic mucocutaneous manifestations.
 Table 1

ETIOLOGY AND PATHOGENESIS
 Candida albicans, C. tropicalis and C. glabrata comprise
together over 80% of the species isolated from human
Candida infections.
 To invade the mucosal lining, the microorganisms must
adhere to the epithelial surface; therefore, strains of
Candida with better adhesion potential are more
pathogenic than strains with poorer adhesion.
 The yeast penetration of the epithelial cells is facilitated
by their production of lipases, and for the yeasts to
remain with in the epithelium, they must overcome
constant desquamation of surface epithelial cells.
 Table 2

EPIDEMIOLOGY
 More frequently isolated from women, and an
increase during the summer months.
 Hospitalized patients have higher prevalence of
Candida.
 In healthy subjects, blood group O and cumulative
risk factors for oral carriage of C.albicans.
 In denture wearers, the prevalence of denture
stomatitis varies, but in population studies, it has
been reported to be approximately 50%

CLINICAL FINDINGS
PSEUDOMEMBRANOUS CANDIDIASIS
 The acute form of pseudomembranous candidiasis
is grouped with the primary oral candidiasis and is
recognized as the classic Candida infection.
 Predominantly affects patients medicated with
antibiotics, immunosuppressant drugs, or a disease
that suppresses the immune system.
 It presents with loosely attached membranes
comprising fungal organisms and cellular debris,
which leaves an inflamed, sometimes bleeding area
if the pseudomembrane is removed.

 The chronic form emerged as a result of human
immunodeficiency virus (HIV) infection as patients
with this disease may be affected by a
pseudomembranous candida infection for a long
period of time.
 Patients treated with steroid inhalers may also
acquire pseudomembraneous lesions in chronic
nature.
 Patients infrequently report symptoms from their
lesions, although some discomfort may be
experienced from the presence of the
pseudomembranes.

ERYTHEMATOUS CANDIDIASIS
 The erythematous form of candidiasis was
previously referred to as atrophic oral candidiasis.
 An erythematous surface may not just reflect
atrophy but it can also be explained by increased
vascularization.
 The lesion has diffuse border, which helps
distinguish it from erythroplakia, which has a
sharper demarcation.
 It may be considered a successor to
pseudomembraneous candidiasis.

 Predominantly encountered in the palate and the
dorsum of the tongue of patients who are using
inhalation steroids.
 Other predisposing factors are smoking and
treatment with broad spectrum antibiotics.
 Acute and chronic forms present with identical
clinical features.

CHRONIC PLAQUE TYPE AND NODULAR
CANDIDIASIS
 The chronic plaque type of oral candidiasis
replaces the older term,candidial leukoplakia.
 The typical clinical presentation is characterised by
a white plaque, which may be indistinguishable
from an oral leukoplakia.
 Chronic plaque type nodular candidiasis have been
associated with malignant transformation,but the
probable role of yeasts in oral carcinogenesis is
unclear.

DENTURE STOMATITIS
 More prevalent site for denture stomatitis is the
denture bearing palatal mucosa.
 The denture serves as a vehicle that protect the
microorganisms from physical influences such as
salivary flow.
 Three types:
 Type l- localised to minor erythematous sites
caused by trauma from the denture.
 Type ll- effects a major part of the denture covered
mucosa.
 Type lll- in addition to type ll features, type lll has a
granular mucosa in the central part of the palate.

ANGULAR CHEILITIS
 It is infected fissures of the commissures of the
mouth, often surrounded by erythema. The lesions
are frequently coinfected with both Candida and
Staphylococcus aureus.
 Vitamin B12, iron deficiencies, and loss of vertical
dimensions have been associated with its formation
along with dry skin.

MEDIAN RHOMBOID GLOSSITIS
 Clinically characterised by erythematous lesion in the
center of the posterior part of the dorsum of the tongue
with an oval configuration.
 This area of erythema resulting from atrophy of filiform
papillae and the surface may be lobulated.
 Lesion frequently shows mixed bacterial/fungal
microflora.
 Smokers,denture wearers and patients using inhalation
steroids have an increased risk of developing.
 Sometimes a concurrent erythematous lesion may be
observed in the palatal mucosa (kissing lesion)
 Asymptomatic and the management is restricted to a
reduction in predisposing factors.
 The lesion does not entail any risk of malignant
transformation.

ORAL CANDIDIASIS ASSOCIATED WITH HIV
 More than 90% of acquired immune deficiency
syndrome patients have had oral candidiasis during
the course of their hiv infection, and the infection is
consicered a potent of AIDS development.
 Most common type is pseudomembraneous
candidiasis, erythematous candidiasis, angular
cheilitis, and chronic hyperplastic candidiasis.

CLINICAL MANIFESTATIONS
 Systemic oral candidiasis is accompanied by
systemic mucocutaneous candidiasis and other
immune deficiencies.
 Chronic mucocutaneous candidiasis embraces a
heterogenous group of disorders,which, in,
additional to oral candidiasis, also effect the skin,
typically the nail bed and other mucosal lining, such
as genital mucosa. Face and scalp may be
involved, granulomatous masses can be seen at
these sites.

 The oral affection may involve the tongue, and
white hyperplastic lesions are seen in conjunction
with fissures.
 CMC can also occur as a result of as a part of
endocrine disorders as hyperparathyroidism and
addison’s disease.
 Impaired phagocytic function by neutrophilic
granulocytes and macrophages caused by
myeloperoxidase deficiency has also been
associated with CMC.

 Chediak-Higashi syndrome, an inherited diseae
with a reduced number of impaired neutrophilic
granulocytes, lends further support to the role of
phagocytic system in Candida infections as these
patients frequently develop candidiasis.
 Severe combined immunodeficiency syndrome
characterised by a defect in the function of the cell
mediated arm of the immune system.
 Patients with this disorder frequently contract
disseminated Candida infections.

 Thymoma is a neoplasm of thymic epithelial cells
that also entails systemic candidiasis.
 thus., both the native and adaptive immune
systems are critical to prevent development of
systemic mucocutaneous candidiasis.

DIAGNOSIS AND LABORATORY
FINDINGS
 The presence of Candida as a member of the
commensal flora complicates the discrimination of
the normal state from infection.
 It is imperative that both clinical findings and
laboratory data are balanced in order to arrive at a
correct diagnosis.
 Sometimes antifungal treatment has to be launched
to assist in the diagnostic process.

 Identification of blastophores and pseudohyphae in
stained smears from a lesion.
 Culture, usually on sabouraud’s or dextrose
sabouraud’s medium
 Occasionally by histology stained by periodic acid
schiff (PAS)

 Tests of immune function are indicated mainly in
HIV disease or chronic mucocutaneous candidiasis.
 Since some endocrine disorders may be associated
with chronic mucocutaneous candidiasis, tests of
thyroid, parathyroid and adrenocortical function are
warranted in selected individuals.
 Since oral candidiasis is occasionally associated
with nutritional deficiencies or blood dyscrasias,
estimates of haemoglobin, white blood cell counts,
corrected whole blood folate, vitamin B12 and
serum ferritin can be important.

MANAGEMENT
 Avoid or reduce smoking.
 Treat any local predisposing cause, such as
xerostomia.
 Improve oral hygiene; chlorhexidine has some
anticandidal activity.
 The most commonly used antifungal drugs belongs
to the groups of polyenes or azoles
 Polyenes such as nystatin and amphotericin B are
the first alternatives in treatment of primary oral
candidiasis and are well tolerated.
 Permanent removal of the denture is an effective
treatment for denture stomatitis.

 Type lll denture stomatitis may be treated with
surgical excision if it is necessary to eradicate
microorganisms present in the deeper fissures of
granulation tissue.
 Topical treatment with azoles such as miconazole is
the treatment of choice in angular cheilitis often
infected by both S. aureus and Candida.
 Fusidic acid (2%) can be used as a complement to
the antifungal drugs.
 If , angular cheilitis comprises an erythema
surrounding the fissure, a mild steroid oinment may
be required to suppress the inflammation.

 Systemic azoles may be used for deeply seated
primary candidiasis, denture stomatitis and median
rhomboid glossitis with a granular appearance, and
for the therapy resistant infections, mostly related to
compliance failure.
 Development of resistance is particularly
compelling for fluconazole in HIV patients. In such
cases itraconazole and ketoconazole have been
recommended as alternatives.
 The azoles are also used in the treatment of
secondary oral candidiasis with systemic
predisposing factors and for systemic candidiasis.

REFERENCE
 BURKET’S ORAL
MEDICINE 11th
EDITION

Oral candidiasis

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