Candids / dental implant courses

INDIAN DENTAL
ACADEMY
Leader in continuing
Dental Education
Seminar on
Candidiasis
www.indiandentalacademy.com

CONTENTS
• Introduction
• C.albicans
• Pathogenecity
• Factors affecting Candidal carriage.
• Immunity to Candida.
• Classification of Candidiasis.
• Investigations.
• Treatment.

Introduction
• Samaranayake & Mc Farlane (1990)
described Candidiasis as “DISEASE OF
THE DISEASED”

• It is an opportunistic fungal infection
of the oral cavity.
• Oral candidiasis is caused by an
overgrowth a yeast-like fungus,
candida.
• It is common among the elderly people,
particularly in those who wear
dentures and in many cases is avoidable
with a good oral care.

• Usage of B.S.A and Corticosteroids, and
Common Endocrine Disorders such as
Diabetes mellitus- all have resulted in an
incidence of oral candidosis as a
relatively common Disease.

• Advent of HIV infection has resulted in
an increased incidence of Oral Candidal
Infections.
• Thus, it has been reported that more
than 90% of HIV-infected individuals
develop oral candidosis during some
point of their disease.

Candida
• Candida is present as a commensal in the oral
cavities of up to 40% of healthy individuals.
• Because of their inability to form a sexual
stage, they are most often classified among the
fungi Imperfecti in the class Deuteromycetes.
• The primary oral reservoir for the organism in
carriers is the dorsum of the tongue, where it is
usually found as blastospores.

• Candida is a dimorphic fungus that exists in
both yeast form (Blastospore, Blastoconidia)
and Hyphal form (Mycelial form)
• Candida reproduces by Multilateral Budding
& may develop either as Mycelial form
composed of long branching septe or
Filaments or Spherical or Ovoid Yeast cells.www.indiandentalacademy.com

• For a clinical infection to occur the yeast
must be converted into Pseudohypal form.
• Candida species are assumed to cause
disease by direct tissue invasion either by
inducing a Hypersensitive state or produce
candidial toxins.
• Healthy persons with yeast colonization have
an average of 300 to 500 CFU/cumm3 of
saliva which varies with diurinal variation.

• Most frequently isolated strains of candida
are
• C. albicans
• C. tropicalis
• C. glabrata

I) Factors Affecting Candida Carriage
1. Salivary Factors
• The Quality and the Quantity of saliva and its
constituents play a critical role in modulating yeast
cell populations in the oral cavity.
• Lack of salivary flushing action and the absence of
antifungal salivary constituents such as Lactoferrin
and Lysozyme may help increase oral yeast carriage
and infection seen in xerostomic patients.

• The correlation between Candida
carrier status and pH shows carriage
of yeast is higher in Acidic saliva.

2. Temporal Variations:
• Candida counts increase during sleep but are
reduced by taking a meal and by tooth
brushing.
• Generally, counts are highest early in the
morning.

• The Early Morning saliva sample is also
the most dependable for making a
comparison of the Candida population
within individuals.

3. Smoking
• Some studies have suggested that smoking
does not affect Candida carriage
significantly (Bastiaan 1982)
• While others have reported that smoking
significantly increased carriage by 30 to
70%.

• It has been suggested that cigarette
smoking might lead to localized
epithelial alterations that allow
colonization by Candida .
(Arendorf and Walker, 1980).
• An alternative hypothesis is that
cigarette smoke provides Nutrition for
C. albicans.

• Tobacco smoke increases adrenaline
levels in blood and blood glucose levels
in diabetic smokers significantly higher
than non-smokers due to the effect of
smoke on adrenaline.
(Soysa NS et al. Oral Diseases (2005) 11, 268–273)

• Slavinsky et al, 2002 Smoking in HIV
positive persons has an inhibitory effect on
local immunity (i.e. antigen presentation,
innate resistance and cytokine production)
that systemic CD4 cells, at levels that are
normally considered protective, cannot
overcome.

• Alternatively, smoking together with
HIV infection may adversely affect
the blood CD4 cells resulting in
reduced immunity.
Soysa NS et al. Oral Diseases (2005) 11, 268–273.

4. Oral Topography:
• C. albicans colonizes mainly the posterior
dorsum of the tongue
5. Immune Status:
• Specific antibodies to C. albicans and
decreasing T-cell, helper-to-suppressor
ratios may also influence carriage.

6. Oral Microflora:
• A number of studies have indicated
that Candida can be isolated from the
oral cavity with greater prevalence and
in greater numbers during broad
spectrum antibiotic therapy.

II. Host oral defenses against candida
infection:
A. Microbial interactions:
• Include nutritional competition, change in
Microenvironment and Elaboration of toxic
and Metabolic byproducts.

• Samaranayake(1990)The oral bacterial
flora can decrease colonization by C.
albicans by competing for adherence
sites on epithelial cells.
• In contrast, Candida may also maintain
synergistic relationships with
pathogenic flora.

B. Salivary Nonimmune Factors
1. Iron
• Iron is an essential nutrient of both bacteria
and fungi.
• Weinberg (1974) showed evidence that
increased susceptibility to infectious agents
was associated with elevated levels of iron in
serum.
• Iron-binding proteins, including Lactoferrin,
have been shown to inhibit growth of C.
albicans (Nikawa et al., 1993).

2. Lysozyme:
• Lysozyme is a low-mol wt protein present
in relatively high concentration in the oral
cavity, saliva, GCF,PMN’S
• Lysozyme :
– Stimulate phagocytosis in association with IgA.
– The hydrolytic action of lysozyme on cell wall
structural proteins, cytoplasmic membranes
– agglutination of Candida species.

3. Lactoferrin:
• Its antifungal activity is believed to be
because of binding of iron (Soukka et al., 1992).
• Lactoferrin has been postulated to enhance
the antibacterial activity of lysozyme by
attenuating the inhibitory effect of iron.
• Lactoferrin may confer structural changes
on the cell walls of Candida.

4. Lactoperoxidase:
• Significant candidacidal activity was
demonstrated when Candida organisms
were incubated with a conjugate of
lactoperoxidase, Xanthine oxidase and
specific antibody against Candida.
(Okuda et al., 1980).

Immune factors in host defense
against candida
1. Granulocytes:
• Neutrophils are crucial to the natural
resistance to C. albicans.
• Individual granulocytes can phagocytose up
to 10 yeasts but the proportion killed
remains constant at about 20 to 30%.

• The candidicidal activity of human
neutrophils has been shown to be enhanced
independently by interferon (IFN- γ ) and
tumor necrosis factor (TNF).

2. Cell mediated immunity
• Candida infections are consistently seen
when cell-mediated immunity is depressed.
• (IFN-γ) is the only lymphokine known to
– Increase the microbicidal activities of
macrophages
– It also initiates TNF synthesis
• In the presence of suboptimal levels of IFN-
γ, Candida killing by neutrophils is markedly
enhanced by TNF.

3. Humoral Immunity:
• Serum antibodies can affect the growth of
C. albicans.
• The major specific immunologic factor in
saliva is IgA, which may be a primary
defense against oral candidosis by :
»Aggregating the organisms
»Preventing their adherence to mucosal
epithelium

• Mucocutaneous and systemic candidosis
are typically associated with defects in
the CMI response.
• These can be caused by
»Deliberate immunosuppression
(as in transplant patients)
»Cancer patients treated with
cytotoxic drugs
» (HIV) infection

Pathogenic factors of candida
• The indigenous oral flora may interfere with
adherence and colonization by Candida
organisms.
• Normal resident bacterial flora suppresses
fungal colonization.
• Alteration and reduction in surface bacteria,
such as is seen after antibiotic therapy, are
associated with fungal colonization and often
symptomatic disease (Saigh et al., 1978).

• The pathogenicity of candida depends on
various factors.
A. Enzymes of Candida
• It has been suggested that C. albicans
produces an "Endotoxin“ but the levels of
endotoxin found in vivo may not be sufficient
to produce toxic effects.
• Alternatively, the organisms may produce
enzymes that facilitate penetration of the
mucous membranes.

• Candida has the ability to produce
phospholipases that are concentrated at the
tips of fungal hyphae and localized in the
vicinity of host cells where active invasion is
occurring.
• Extracellular proteinases have also been
implicated in the pathogenicity of C. albicans.

• Proteinase-deficient strains are
noninvasive.
• Salivary proteins, including IgA, can be
almost completely degraded by acidic
proteinases of Candida especially under
low pH conditions.

B. Temperature Variations:
The virulence of C. albicans can also be
influenced by the temperature at which it is
grown in culture.
Virulence is associated with increased germ
tube production by yeast grown at the lower
temperature.
Yeasts grown at room temperature are more
resistant to killing by polymorphonuclear
leukocytes

• There are two surface types of Candida
adhesion:
• Floccular and Fibrillar:
• Floccular Layer mediates adhesion to Oral Mucosal
Epithelium
• Fibrillar Surface layer increases adhesion to ACRYLIC.

• However, at low pH of 3 to 4, the adherence of
Candida to both epithelial and acrylic surfaces is
significantly increased (Samaranayake et al., 1980).
• Secretory immunoglobulin A (IgA) can inhibit the
adherence of C. albicans to human oral epithelial
cells .
• Chitin derivatives can inhibit the adherence of C.
albicans to acrylic .

Switching Phenomena
• C. albicans frequently exhibits variant
colonial forms when grown in vitro.
• It is known that switching can be triggered
by low doses of UV radiation, and once
triggered, they exhibits high rates of
alterations in colony morphology.

• It has been postulated that the switching
mechanisms of Candida may help potentiate its
pathogenic features:
(1) during invasion of different body
Environments
(2) by invading the immune system by altering
its surface Antigenicity,
(3) by escaping the action of Antifungals.

Mechanisms of Pathogenicity
• The yeast proliferation as well as the
subsequent infection is related to the host
factors.
• Host defenses that are critical to shield
against the development of candidiasis, are
an adequate number of circulating
neutrophils, functional Lymphocyte–
monocyte axis.

• A study by Bergmann et al, patients
with Hematological Malignancies
revealed severe granulocytopenia
associated with acute oral candidiasis.

• During Antineoplastic therapy salivary
flow rate is also reduced, thus doubling
the microbial load of saliva.
• Hence chemotherapy induced
Xerostomia plays a significant role in
pathogenesis of acute oral infections in
general and candidal infections in
particular.

• It is well established that B.S.A such as
Tetracycline or combination therapy with
antibiotics suppress the oral bacterial flora
thereby providing the growth of commensal
Candida species to a very high degree.

• Factors Predisposing to Oral
Candidosis
»Chronic local irritants
»Ill-fitting appliances
»Inadequate care of
appliances
»change in the oral microbial
flora by antibiotics,
corticosteroid intake.
»xerostomia

»Immunological and endocrine
disorders
»Malignant and chronic diseases
»Severe blood dyscrasias
»Radiation to the head neck
»Age
»Hospitalization
»Oral epithelial dysplasia
»Heavy smoking

• A. Prostheses
• Chronic local irritants
• Ill-fitting appliances
• Inadequate hygiene are concerned
• High salivary yeast counts are much
more common in full-denture wearers
than in dentate subjects.

B. Drug Therapy and Radiation Therapy:
• Patients on broad spectrum antimicrobial therapy
may be predisposed to alterations in the oral flora.
• Topical, systemic, and aerosolized corticosteroids
• Drugs with xerostomic side effects also predispose
to oral candidosis.

C. Dietary Factors:
• A variety of nutritional factors, including
deficiencies of iron, folic acid, vitamins and diets
rich in carbohydrates, have been implicated in the
pathogenesis of oral candidal infections.
• Candida is thought to block fungistatic property of
transferrin.
• Moreover, iron may also affect the local host
defenses via its modulating role in the activity of
lysozyme and lactoferrin (Samaranayake, 1990).

• Iron deficiency may produce an impairment
of iron-dependent enzyme systems, thereby
affecting the metabolism, kinetics of the
rapidly dividing oral epithelial cells.
• Such alterations may result in an epithelial
surface more conducive for the adhesion,
growth, and invasion of Candida.

Endocrine disorders
• Candida species are more prevalent in the
oral cavity of diabetic patients than in those
of healthy nondiabetic individuals.

Immunologic disorders
• Fungal infections, particularly
pseudomembraneous and atrophic form are
common in patients with HIV & other
immunodeficiencies due to depressed cell
mediated immunity or phagocytic immunity.

Malignant Diseases
• Host defense mechanisms are impaired by
the malignant process and its chemotherapy,
which in turn can lead to dysfunction of
neutrophils & lymphocytes.
• Acute forms of oral mycoses are frequent in
patients with myeloproliferative disease and
provide potential sources for fungal
septicaemia.

Acute pseudomembranous
candidiasis (Thrush).
Clinical Features:
• It is a superficial infection of the outer layers of the
epithelium, and it results in the formation of patchy
white plaques or flecks on the mucosal surface.
• Removal of the plaques by gentle rubbing or
scraping usually reveals an area of erythema or
even shallow ulceration.

• Because of their prevalence,
characteristic appearance, and ease of
removal, the lesions of thrush are easily
recognized, and a diagnosis of thrush is
frequently made on the basis of the
appearance of the lesion.

• Thrush is seen in children and in adults of all ages
whenever the number of Candida organisms in the
oral cavity increases significantly.
• When Candida is reduced or eliminated by the
administration of antifungal agents, the lesions of
thrush rapidly disappear.

• Alternatively, the lesions may promptly
recur following treatment, suggesting the
persistence of a predisposing factor, as is
often seen in adult patients with
candidiasis.

• The typical lesions in infants are described as
soft white adherent patches on the oral
mucosa.
• The intraoral lesions are generally painless and
can be removed with little difficulty.

• A prodromal symptom of a rapid onset of
a bad taste and the loss of taste
discrimination is described by some
adults.
• A burning sensation of the mouth and
throat may also precede the appearance
of the white pseudomembranous lesions.

• The lesions may involve the entire oral
mucosa or may involve relatively localized
areas where normal cleansing mechanisms
are poor.

• Any mucosal surface may be involved, and
Erythematous or White areas often develop
beneath partial or complete dentures.
• Symptoms of this type in a patient receiving
broad-spectrum antibiotics are strongly
suggestive of thrush or other forms of oral
candidiasis.

• Patients with immunodeficiencies, such as
those suffering from AIDS or hematologic
malignancies, are also especially
susceptible to this form of candidiasis.

Erythematous (Atrophic)Candidosis:
Synonym: Antibiotic sore mouth
• Holmstrup and Axell (1990) noted that the term
"atrophic" used to describe the red areas could be a
misnomer, as redness may be caused not only by
reduced epithelial thickness atrophy but also by
increased vascularity.
• Hence, they suggested that the term "atrophic
candidosis“ should be replaced by "Erythematous
candidosis“ in a new classification of oral candidosis

Precipitating factors:
• Corticosteroids and topical or systemic broad
spectrum antibiotics or HIV disease.
• It may arise as a consequence of persistent
acute pseudomembranous candidosis when the
pseudomembranes are shed or HIV infection
may precede pseudomembranous candidosis.

Clinical features:
• Characterized by Erythematous
areas and painful mucosa, with
minimal evidence of the white
pseudomembranous lesions
observed in thrush.
• Generally seen on the dorsum of
the tongue, palate, or buccal
mucosa. Lesions on the dorsum
of the tongue present as
depapillated areas.
• Red areas are often seen in the
palate in HIV disease.

• Antibiotic sore mouth, a common form of
atrophic candidiasis, should be suspected in a
patient who develops symptoms of oral burning,
bad taste, or sore throat during or after therapy
with BSA’S.
• Patients with chronic iron deficiency anemia
may also develop atrophic candidiasis

Chronic Atrophic Candidiasis.
• Chronic atrophic candidiasis includes Denture
stomatitis (denture sore mouth), Angular Cheilitis, and
Median rhomboid glossitis.
Denture Stomatitis (Denture Sore Mouth):
• Denture stomatitis is a common form of oral
candidiasis that manifests as a diffuse inflammation of
the maxillary denture-bearing areas and that is often
(15 to 65% of cases) associated with angular cheilitis.

• At least 70% of individuals with clinical signs of
denture stomatitis exhibit fungal growth, and
this condition most likely results from yeast
colonization of the oral mucosa, combined with
bacterial colonization.
• Lesions of chronic atrophic candidiasis have
also been frequently reported in HIV-positive
and AIDS patients.

Clinical stages of denture sore mouth:
• The 1st stage consists of numerous
palatal Petechiae / pinpoint Hyperemia.
• The 2nd stage displays a more diffuse
erythema involving most of the denture-
covered mucosa.
• The 3rd stage includes the development
of tissue granulation or nodularity
(papillary hyperplasia) commonly
involving the central areas of the hard
palate and alveolar ridge.www.indiandentalacademy.com

• The Stage 2 and 3 of denture-induced stomatitis are
most often caused by the accumulation of microbial
plaque (Bacteria Or Yeasts) on and in the fitting
surface of the denture and the underlying mucosa.
• Denture sore mouth is rarely found under a
mandibular denture.

• One possible explanation for this is that the
negative pressure that forms under the
Maxillary Denture excludes salivary antibody
from this region, and yeast may reproduce
undisturbed, in the space between the
Denture and mucosa.

Pathogenesis of denture associated
candidiasis:
• When the dentures especially upper are worn
overnight the oral flora may be altered and plaque
collects between the mucosal surface of the denture
and the palate.
• The tissues underneath the denture bearing area is
compromised of Blood Supply due to compressed
Blood vessels.
• An anaerobic environment is created between the
Denture and the tissues and the presence of food
debris on tissue bearing area of denture add to the
condition.

• In addition, the Saliva that is present between the
maxillary denture and the mucosa may be Thick &
have a Lower pH than usual.
• Patients with denture-induced stomatitis do not have
any serious cell-mediated immune defects, but they
may be deficient in migration inhibition factor and may
have overactive suppressor T cells or other T-
lymphocyte/phagocyte defects.
Samarnayake et al. Critical Reviews in Oral Biology
and Medicine, 5(2):125-157 (1994)

Scanning electron photomicrograph of the
adherent yeast cells to the irregularities in
dentures.
Crit Rev Oral Biol Med. 1999: 10:99-116www.indiandentalacademy.com

Angular Cheilitis:
(perleche)
• Angular cheilitis is the term used for an infection
involving the lip commissures.
• There is frequently a coexistent Denture
Stomatitis and Angular Cheilitis is uncommon in
patients with a natural dentition.

Possible etiologic include:
• Reduced vertical dimension
• Nutritional deficiency (iron deficiency anemia
and vitamin B or folic acid deficiency)
• Diabetes
• Neutropenia
• AIDS
• Co-infection with Staphylococcus and
Streptococcus.
• Habitual lip sucking

Clinical features:
• Perleche occurs in both young children and
adults and is characterized by feeling of
dryness and a burning sensation at corner of
the mouth.
• This is a clinical diagnosis of lesions that affect
the angles of the mouth, characterized by
soreness, erythema, and fissuring which do not
bleed.

• These fissures do not involve the mucosal
surface of the commisures inside the mouth,
but stop at the mucocutaneous junction.
• Few authors consider that the lesion results due
to deep, occlusive folds of skin at the mouth
angles in individuals with facial height reduced
by old age or edentulous condition.

Chronic hyperplastic candidosis/candidiasis
(Candidal leukoplakia):
HISTORY:
Lehner (1964)
• recognized the presentation of chronic candidal
infection in the form of leukoplakia and introduced the
term "Candidal leukoplakia".
• The terms "chronic hyperplastic candidosis“ (CHC)
and "candidal leukoplakia" (CL) appear to have been
synonymously used until the mid-1980s.

Clinical Features:
• CHC presenting as Leukoplakia appears as
well-demarcated, palpable, raised lesions that
may vary from small translucent whitish areas
to large opaque plaques that cannot be rubbed
off.

• Some or all areas of the plaque may
have a smooth, homogenously white
surface, and if this feature predominates,
the lesion is referred to as a homogenous
leukoplakia

• the most common site for these lesions is the
buccal mucosa, especially the commissural
areas.
• The palate and tongue may also be involved.
. Sitheeque M.A.M et al. crit rev oral biol med 2003; 14: 253-267

Median Rhomboid Glossitis:
• Synonym:
Midline glossitis, glossal central papillary
atrophy
• Occasionally, median rhomboid glossitis
presents with a hyperplastic exophytic or even
lobulated appearance.

It is characterized by an
area of papillary atrophy
that is elliptical or rhomboid
in shape, symmetrically
placed centrally at the
midline of the tongue,
anterior to the circumvallate
papillae.

CHRONIC MULTIFOCAL CANDIDIASIS:
• Patients may present with multiple areas of
chronic atrophic candidiasis.
• These are most often seen in
Immunocompromised individuals or in patients
with predisposing factors such as ill-fitting
dentures.

• The changes frequently affect the dorsum
of the tongue and midline of the Hard
Palate (kissing lesions), Commissure area
(angular cheilitis), and Denture Bearing
mucosal surfaces.
• Smoking may also play an important role in
immunocompetent patients.

Chronic multifocal candidiasis

CHRONIC MUCOCUTANEOUS CANDIDIASIS:
• Persistent infection with Candida usually occurs as a
result of:
- a defect in CMI
-may be associated with Iron deficiency.
• In many cases, persistent and significant
predisposing factors can be identified.
Two categories of CMC have been described:
1) syndrome-associated CMC : it is further divided
into
– Familial/ chronic.
2) localized and diffuse CMC.

CMC showing adherent white
plaques that represent speckled
leukoplakia.
Localized granulomas and nodules on the
tongue.
Localized granulomas and nodules on skin.

Oropharyngeal Candidiasis in HIV
Infection:
• Oropharyngeal candidiasis (OPC) is the most
frequent opportunistic fungal infection among
HIV-infected patients.
• It has been estimated that more than 90% of
HIV-infected patients develop this often
debilitating infection at some time during
progression of their disease.

• Although the incidence of OPC in HIV
infection has been significantly reduced
since the introduction of highly active
antiretroviral therapy (HAART), it remains
a common opportunistic infection in HIV-
infected patients.

Clinical features:
• The pseudomembranous form of HIV
associated OPC is characterized by the
presence of multifocal smooth white papular
lesions that can usually be rubbed away,
leaving a red surface.
• The Erythematous form of OPC typically
presents as diffuse and multiple foci of macular
erythema involving the palate, oropharynx,
buccal mucosa, and dorsal tongue, but hyphae
are frequently absent.

• OPC is frequently complicated by esophageal
candidiasis and symptoms may include:
• Burning pain
• Altered taste sensation
• Difficulty swallowing liquids and solids

Laboratory investigations
in
Candidiasis.

Laboratory Diagnosis Of Oral
Candidosis
• Identification of C. albicans is best
accomplished by using a combination of
morphologic features and biochemical
characteristics.

Immunologic Tests
• Immunity in superficial candidosis and in oral
candidosis is predominantly cell mediated.
• Cell-mediated immunity to C. albicans antigens can
be demonstrated in most human subjects both by
the appearance of delayed skin hypersensitivy to
Candida antigens.
• In vitro tests of cellular immunity such as inhibition
of leukocyte migration or stimulation of lymphocyte
transformation to Candida antigens

Immuno Histochemistry:
• With the recent development and availability of
monoclonal antibodies (Mabs) to various Epitopes of
C. albicans.
• Mab 3H8 which recognizes a mannoprotein, it is
now possible to identify Candida in human tissue
biopsies.

• Immunohistochemical studies using
this antibody have demonstrated its
usefulness in specifically recognizing C.
albicans in the kidney, lung, thyroid,
esophagus, small bowel and gingival
tissues.
• The sensitivity of IHC using a
monoclonal antibody was superior to
PAS stain or plaque culture in
detection of Candida in tissues.
Oral Diseases (2006) 12, 428–433.

Hematologic Investigations
• Because oral candidosis is associated
frequently with predisposing factors such
as:
– Nutritional deficiencies
– Blood dyscrasias
– HIV disease
• Estimates of hemoglobin, lymphocyte and
WBC counts, whole blood folate, vitamin B
12 and serum ferritin can be important.

Treatment
for
Candidiasis

Chlorhexidine:
• Since its introduction in the 1970s, chlorhexidine has been used
as an adjunct in the management of oral candidosis.
• Chlorhexidine gluconate has a bimodal action on Candida.
– It is fungicidal, even at very low concentrations,
– It is capable of significantly suppressing candidal adhesion
to both Inorganic and Organic substrates.
• 0.2% chlorhexidine gluconate has been successfully used as a
mouthrinse in the treatment of Candida-associated denture
stomatitis and in Pseudomembranous candidosis.
• while 2% suspension is used as an overnight denture
disinfectant.

• Due to its anti-candidal action, mouthrinses
containing chlorhexidine have been proposed
as an appropriate alternative to conventional
antifungals in the management of oral
candidosis.
• “Chlorhexidine and Nystatin should not be used
simultaneously, since they interact, forming
chlorhexidine-nystatin complexes, rendering
both agents ineffective against Candida”.
Samaranayake LP et al. Crit Rev Oral Biol Med 2000 11:172-98.

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