Prof. dr.

Radosveta Andreeva, DMD,

PhD
Oral candidiasis is a group of diseases with
clinical manifestations on the oral
mucosa caused by yeast-like fungi from
the Candida type.
ž Fungus with a round or oval body;
ž Normally it is a saprophyte in the mouth;
ž In case of overdevelopment, the oral
mucosa becomes filamentous;
ž Produces mycelium.
ž In the mouth,
Candida albicans
grow as a chain of
cylindrical cells -
hyphae or
blastospores (single-
celled).
ž A chain of
blastospores forms
pseudohyphae.
ž Hypha on the surface
of the epithelium;
ž Organelles can be
seen inside the fungal
hypha.
ž A group of hyphae
forms a mycelium.
ž Clearly visible
hyphae
among the
epithelial cells
of the oral
mucosa.
ž 1 - spores of
candida albicans
in the oral mucosa
in candidiasis;
ž 2 - neutrophil
leukocytes in
different stages of
necrobiosis.
ž 1- spores of candida
albicans;
ž 2- pseudomycelium;
ž Their presence is a
diagnostic sign.
žIt is called an opportunistic pathogen
because it is part of the normal oral flora,
but under certain conditions it can
cause disease.
ž C. albicans is the most common isolated
species of fungus in the oral cavity;
ž It is 47% to 75% of all Candida species;
ž The other types are:
ž Candida tropicalis,
ž Candida parapsilosis,
ž Candida krusei,
ž Candida kefyr,
ž Candida glabrata and Candida
guilliermondii.
ž C. dubliniensis is a new species recently
described in the literature, found in severe
oral candidiasis caused by HIV.
ž Together with oral microorganisms and glycoproteins,
Candida albicans can form an adhesive biofilm;
ž Coaggregation of Candida with oral bacteria promotes
the development of candidiasis;
ž C. albicans binds to bacteria such as viridans
streptococci, Fusobacterium and Actinomyces spr .;
ž Mediators between fungi and streptococci in
coaggregation are salivary proteins - the binding of
adhesins to receptors.
ž Oral candidiasis is a manifestation of an
imbalance in the microbial ecosystem;
ž Candida has mechanisms of adhesion
that cause its colonization;
ž Different types of Candida have different
activity to overcome the defense
mechanisms.
ž The pathogenic potential of fungi is due
to their contact with the mucosa and
secreted proteolytic enzymes;
ž Candida can modulate its virulence and
upset the balance between purification
and colonization, leading to candidiasis;
ž Modulation is a response to changes in
the environment and depends on the
qualities of the body's immune system.
Local factors Systemic factors

Mucosal barrier Some physiological conditions

Trauma Endocrine disorders
Changes in the oral Diabetes
environment Hypothyroidism
Endogenous epithelial changes Nutritional deficiency
Atrophy Iron deficiency
Hyperplasia Vit B12 deficiency
Dysplasia Acute leukemia,
Saliva agranulocytosis
Xerostomia, hyposalivation Corticosteroids
Smoking Immune defect
Immune defect HIV infection
РН Thymus aplasia
Glucose concentration
Cytotostatics
ž Quantity and viscosity of saliva;
ž Salivary enzymes (lactoferrin and lysozyme);
ž PH of saliva;
ž Diurnal cycle of salivation;
ž Oral microflora.
ž Norm:
ž oral microorganisms limit the overdevelopment of
Candida through competition and inhibition;
ž Food competition:
ž Change in the microenvironment;
ž Manufacture of toxic and metabolic products;
ž Competitive adhesion on the surface of epithelial
cells.

In pathology:
ž synergism occurs between C. albicans and
Staphylococcus aureus (angular
cheilitis);Modification of the oral microflora
(systemic diseases, hormonal changes,
corticosteroids and antibiotics).
Oral epithelium
ž The oral epithelium acts as a mechanical barrier,
and the epithelial cell cycle provides protection
against Candida.

Immunological protective factors

ž IgA-S is the first line of defense;
ž Humoral and cellular immunity are the second
and third line of defense against C. albicans.
ž Enzymatic factors - "endotoxins";
ž Phospholipases, extracellular proteinases
- help penetration;
ž Acid proteinases - at low pH salivary
proteins, including IgA-S, are destroyed.
ž Through this mechanism, Candida
avoids protection by changing its
morphology and physiology according
to the environment;
ž Its adhesive properties change;
ž Its pathogenicity changes;
ž Bacterial forms of colonization change.
ž Direct stimulation of candida albicans;
ž Suppression of the normal oral flora;
ž Suppression of the normal intestinal flora;
ž Inhibition of phagocytosis;
ž Suppression of the immune response;
ž Direct tissue damage.
ž In the mouth - 13-76%;
ž Vaginal - 8-76%;
ž Anorectal tract - 8-60%;
ž Normal - balance between protection
and pathogenicity of the fungus;
ž Under changed conditions, the normal
occupant becomes pathogenic.
ž Colonization;
ž Adhesion;
ž Invasion;
ž Occurrence of an inflammatory
response;
ž Damage to the defense mechanisms of
the macroorganism to other infections.
ž It begins at birth;
ž Most often in early childhood and lasts a
lifetime;
ž There is no clinical manifestation in the
colonization itself.
ž Yeast factors:
› Concentration, growth phase, species,
strain and others;

ž Factors of the environment:

› Temperature, acidity, presence of
bacteria, antibodies;

ž Factors of the epithelial cells:

› Interaction between the protein part of
the yeast and the receptors of the
epithelial cell.
1. Yeast forms germ tubes that penetrate the
cell membrane;
2. Having penetrated the cells and
intercellular spaces, the yeast continues to
develop and divide;
3. They pass into the mycelial phase;
4. Damage cellular structures.
ž Occurs as a result of released toxins;
ž From the interaction of the immune system of
the macroorganism and the surface
glycoprotein antigens of yeast;
ž At initial reaction - neutrophils;
ž In chronic inflammation - round cell infiltration;
ž Possible mechanism - specific immune response
and allergy to yeast antigens.
ž In the presence of Candida,
neutrophil function and chemotaxis to
other microorganisms are reduced;
ž The macroorganism opposes its own
barrier-protective function - skin,
mucosal barrier, humoral factors,
phagocytic cells and others.
ž ACUTE
ž CHRONIC
ž MULTIFOCAL
§ Pseudomembranous oral candidiasis - soor;
§ Atrophic (erythematous) oral candidiasis:
§ Antibiotic stomatitis
Chronic oral candidiasis
§Atrophic:
-Prosthetic stomatitis;
-Angular cheilitis;
-Median rhomboid glossitis.

-Hyperplastic:
-Candida leukoplakia;
-Papillary hyperplasia of the palate;
-These two hyperplastic forms of
oral candidiasis are not
characteristic of childhood
-Median rhomboid glossitis
(nodular form)
Multifocal candidiasis
- Mucocutaneous candidiasis;
- Candidiasis associated with
syndromes;
- Endocrine candidiasis syndrome
(familial candidiasis);
- Candidiasis in thymic aplasia.
- Candidiasis can be localized or
generalized (diffuse) forms.
ž 1. LOCAL CANDIDIASIS;

ž 2. GENERAL CANDIDIASIS;
ž Candidal stomatitis;
ž Candidal gingivitis;
ž Candidal glossitis;
ž Candidal cheilitis;
ž Angulus infectiosus oris.
ž Stomach;
ž Lungs;
ž Skin;
ž Mucous membranes;
ž Genitals;
ž Kidneys;
ž Eyes.
ž On the tongue;
ž In the corner of the mouth;
ž All over the mucosa;
ž Mucocutaneous candidiasis;
ž Systemic candidiasis;
ž In newborns;
ž In premature and low birth weight babies;
ž Complication - oropharyngeal candidiasis;
ž Sepsis - 10-15% of all sepsis at this age;
ž In preterm and neonates with central venous
catheter, parenteral nutrition and prolonged
urethral catheterization;
ž In immunocompromised children mainly, but also
occurs in normally developing, full-term infants.It
can be combined with anal candidiasis.
ž On the surface of the mucosa, whitish, easily
removable deposits are formed, surrounded
by erythema of the mucosa;
ž The mucosa looks like "sprinkled with milk";
ž Upon mechanical removal, an erythemo-
erosive surface remains;
ž Erosive stomatitis - an alternative
inflammation with superficial erosion of the
mucous epithelium.
ž Pseudomembranou
s plaque on the
cheek mucosa;
ž Located on a
reddish base.
ž Thrush in
infants;
ž Pseudomembr
anous deposit
on the mucous
membrane of
the lips.
ž Pseudomembranous
deposit on the mucous
membrane of the mouth
corner.
ž Child with leukemia
after chemotherapy
and antibiotic
treatment;
ž Pseudomembranous
candidiasis of the
palate.
ž Pseudomembran
ous deposit on
the back of the
tongue on a
reddish base.
ž White pseudomembranous
deposit on the tongue.
ž Severe hyperemia of the mucosa;Severe
pseudomembranous plaque.
ž Confluent pseudo- membranous
plaques.
ž Generalized candidal
stomatitis;
ž Confluent plaques on
the palate;
ž An obese patient with
systemic intake of
corticosteroids.
ž The plaque consists of:
ž A network of hyphae
on the surface of the
epithelium;
ž Empty epithelial cells;
ž Bacteria;
ž Food residues.
ž MICROSCOPIC
ž large number of
hyphae and spores
with superficial
invasion of the
mucosa.
ž During breastfeeding, lactose is retained in the
baby's mouth, which is broken down into acids
and maintains an acidic environment;
ž The acidic environment is a prerequisite for
candidiasis:
ž transitional;
ž Persistent and long-lasting;
ž Poor self-cleansing in infancy;
ž Ignorance of oral hygiene rules for the mother's
age;
ž Candida has an affinity to colonize on plastic
surfaces - on the child's pacifier and to maintain
the infection.
ž Unclear, poorly studied form of
candidiasis
ž Associated with topical corticosteroid or
antibiotic therapy
ž In patients with AIDS
ž Consequence of acute
pseudomembranous candidiasis
ž CLINICAL MANIFESTATION ž MICROSCOPIC
ž Mucosal erythema;
ž Papillary atrophy of the back ž Superficial invasion
of the tongue (depapillary of several or more
fields).
hyphae and spores
ž The term 'atrophic' is used to
describe red fields due to in the epithelium.
thinned epithelial layers due
to epithelial cell atrophy and
increased vascularization.
ž Dry, bright red
mucous membranes
of the lips
ž The mucosa in contact with the orthodontic
appliance is erythematous and edematous;
ž It may be asymptomatic or with burning and
tingling;
ž Three clinical types are described:
ž Type I – localized inflammation or punctate
hyperemia;
ž Type II - diffuse erythema along the entire
mucosa under the apparatus;
ž Type III - granular type - inflammatory papillary
hyperplasia in the central part of the hard
palate. DD with bacterial infection or allergic
reaction to plastic.
ž Candidiasis atrophica (erythematosa) chronic -
stomaitis protetica - localized chronic erythema of
the tissues covered by the prosthesis. These are
usually the palate and upper jaw, but can also
affect the mandibular tissues.
ž Cell-bound immune
deficiency (T cells);
ž Pseudo-membranes on
the tongue;
ž Atrophic candidiasis on
the mucous membrane
of the lips.
ž Microscopic: ž Clinical
› Epithelial manifestation:
hyperkeratosis; ž White plaques,
› Deep or superficial difficult or partially
invasion of hyphae. removable.
ž Rare case of
chronic
hypertrophic
candidiasis in a
child;
ž Candidal
hypertrophy in a
child with immune
deficiency.
ž This is a clinical diagnosis of oral lesions that
affect the corner of the mouth and are
characterized by irritation, erythema, the
formation of cracks in the corners of the mouth;
ž Angular cheilitis can be due to streptococci,
staphylococci or a fungal infection;
ž The most common is a combination of
Staphylococcus Aureus and Candida;
ž It is very often associated with anemia, vitamin B
12 deficiency, iron deficiency.
ž Glossitis mediana rhombica -
chronic, symmetrical lesion of the back of
the tongue with a diamond-shaped or
elliptical shape, starting from its anterior
third and reaching the papillae
circumvallate. This is an area of atrophied
papillae filiforms. In more than 85% of
cases, the biopsy shows the presence of
candida.
ž This term refers to chronic candidal infections
that can occur in the oral cavity and other
parts of the body.
ž Oral lesions lasting more than one month;
ž In the absence of predisposing medical
conditions;
ž In patients undergoing radiotherapy, long-
term antibiotic, immunosuppressive,
cytostatic or psychotropic treatment.
gr conditions Initial Affected body parts and clinic
appearance
1 Chronic familial 1 – 10y Mouth, nails, skin, mainly
mucocutaneous hyperplastic lesions
candidiasis

2 Diffuse Before 5y Mouth, nails, skin, pharynx,

chronicmucocutaneou larynx, chronic hyperplastic
s candidiasis lesions
3 Candidalendocrinopat 10 – 20y Mouth - in combination with
hicsyndrome hypoparathyroidism,
hypothyroidism,hypoadrenoc
orticism, diabetes, chronic
hyperplastic lesions.
4 Family 1y Mouth, nails, scalp, folds,
mucocutaneous mainly hyperplastic lesions.
candidiasis
5а Severe combined In childhood Oral mucosa, skin, nails,
immunodeficiencies pseudomembranous,hyperpla
stic lesions.
5в Di George, s Pseudomembranous,Erythem
syndrome; atous,hyperplasticoral lesions
Chronic with or without skin
granulomatosis; involvement.
AIDS.
ž Immune deficient
patient;
ž Pseudomembranos
deposit on the
tongue;
ž Skin involvement.
ž Pseudomembranes
on the tongue;
ž The child's skin is also
affected.
ž Epithelial hypertrophy;
ž Parakeratosis of the
surface.
ž This group includes oral candidiasis in
combination with cutaneous candidiasis;
ž They can develop in a generalized wayand
lead to candidal sepsis;
ž It can cause death in premature and
underweight infants;
ž In older children, this type of candidiasis can
only develop in highly immunocompromised
individuals.
ž Chronic mucocutaneous candidiasis
includes the group of rare syndromes
characterized by immune defects;
ž Often defects of cellular immunity;
ž In them, candidiasis is not affected by
topical treatment.
ž Persistent pseudomembranous, erythematous and
chireplastic candidiasis:
ž The tongue, soft and hard palate and buccal
mucosa;
ž Serious prognostic indicator for AIDS;
ž Most children with congenital AIDS develop severe
oral mucocutaneous candidiasis in early childhood
up to one year;
ž In these cases, a weak inflammatory reaction is
observed, the epithelium is dotted with hyphae
and pseudohyphae, as well as with a massive
infiltrate of PMNL. The subepithelial inflammatory
response is diffuse and contains little or no
leukocytes.
Oral candidiasis in AIDS
ž Severe
erythematous
candidal mucosa;
ž Single
pseudomembranes.
ž Candidal leukoplakia (keratosis) in 5-10%
can develop into carcinoma;
ž Candida albicans in leukoplakia differs
from the candidate in the oral cavity;
ž It is thought to be involved in
carcinogenesis by making nitrosamine
components that can initiate oral
neoplasia.
ž Material for examination of Candida can be taken by
swab, cotton swab, with an imprint on a plastic surface,
paper pins, saliva, mouthwash with sterile saline;
ž The identification of candida in the oral cavity is done
with the help of tests for morphological and biochemical
characteristics;
ž Subaro dextrose agar is used to cultivate candida;
ž Candida was observed by direct microscopy, and the
preparations were stained by Gram or PAS technique;
ž Commercial systems (Microstix-Candida and Oricult-N)
can also be used for rapid screening in the diagnosis of
oral candidiasis.
ž Histopathological diagnosis - used in
candidal leukopakia;
ž The preparations are stained with PAS and
GMS techniques. In the latter, the candidate
appears pinkish-red.
ž There are blastospores, hyphae and
pseudohyphae in the superficial epithelial
tissue.
ž Immunological tests:
ž Immune reactions in superficial oral candidiasis
are of the cell-related type;
ž A delayed allergic reaction to candidal antigens
is observed;
ž Humoral immunity tests, agglutination test,
precipitation test, complement fixation,
immunofluorescence and ELISA.

ž Haematological tests
ž Because candidiasis develops in the presence of
predisposing factors with characteristic
abnormalities in the blood picture (hemoglobin,
erythrocytes, iron, B12, folic acid, lymphocytes,
etc.), they are part of the diagnostic tests.
ž Treatment is local and / or systemic with
antifungal drugs and complementary
symptomatic (antimicrobial, anti-
inflammatory, epithelial, etc.).
ž Cleaning the mouth after each
breastfeeding:
› With diluted hydrogen peroxide 1: 1 and
gauze;
› Alkalizing the environment - with baking soda
› 1 tsp Soda in a glass of water;
› Using a gauze to wash the mouth.
ž Cleaning;
ž Alkalization;
ž NAPA, but without prednisolone
ž Boiling of pacifiers, towels and clothes;
ž Breast cleansing before and after
breastfeeding.
ž Polyenes:
ž Antifungals from streptomycetes;
ž They include nystatin and
amphotericin.
ž Nystatin
ž Dosages - 4 times X 100 000 E daily, per
os / for children 1/3 dose /.
ž Nystatin glycerin - for topical
treatment of oral mucosa
ž Dactarin oral gel
ž Binds sterols from the cell membrane of the
candidiasis cell, thereby reducing the
protective properties of the candidate;
ž It is applied topically in the oral cavity in the
form of a suspension -100 mg / ml, lozenges
10 mg. It is not absorbed in the intestine.
ž Rp/ Nystatin –100 000 I.U. tablets
ž D. scat.orig I
ž S. dissolve one tablet in the mouth 5
times a day for 14 days.
ž To eliminate the pathogenic fungal
organism and restore the normal oral flora:
ž Rp / Nystatin (Mucostatin) 1 ml-100 000 I.U.- 4
times a day

ž ACTION:
ž -Anti-inflammatory;
ž -Antitoxic;
ž -Antifungal.
–
ž Rp/ Nystatin (Mukostatin), pastilles –200
000 I.U.
ž S - dissolve one lozenge in the mouth 4
times a day for 14 days.
 Azoles-synthetic antifungal agents
With fungistatic, not fungicidal action. There is
hepatotoxicity. In chronic candidiasis, resistance
to this type of drug may develop.

Imidazoles;
Triazoles.They cause a change in the
permeability of the cytoplasmic
membrane of the candidiasis cell.
Imidazoles: clotrimazole, miconazole, econazole,
ž Тriazoles: ketoconazole, fluconazole и
itraconazole
ž Clotrimazole - only locally (externally)
because it is neurotoxic;
Miconazole(Daktarin gel) – only external;
ž Ketoconazole(Nizoral gel) – for topical
treatment of oral candidiasis in children
and adults. Systemic therapy up to 2
weeks is possible.
ž the first imidazole agent that could lead
to the required therapeutic level in the
blood when administered orally.
Used to treat immunocompromised
patients. They are hepatotoxic.
ž Fluconazole- Inhibits ergosterol from the cell
wall of the candidiasis cell. It is secreted by
saliva in high concentration and inhibits the
adhesion of the candidate to the epithelial
cells of the oral mucosa. Oral absorption is
rapid and ends in two hours.
ž The daily dose is 50 mg. For the treatment of
oral candidiasis
ž Itraconazole – Orally active bis-triazole;
ž Inhibits ergosterol synthesis in the candidiasis
cell. It is contraindicated in liver diseases.It is
sold in 50 and 100 mg capsules and 10 mg / ml
solution for oral administration.
ž Effective treatment is achieved over a period
of 2 weeks at doses of 100 to 200 mg / day
5-Fluorocytosine

ž DNA analog;
ž Interacts with the nucleic acids of the
candidiasis cell;
ž Used for oral therapy of systemic fungal
infections in a dosage of 50 to 150 mg / kg /
day divided into 4 doses.
ž Rp/ Clotrimazole-10 mg, tablets
ž S - dissolve one tablet in the mouth 5
times a day for 14 days.
ž Rp/ Ketoconazole/Nizoral, 200 mg, tab.
ž S - one tablet daily for 2 weeks
ž Rp/ Amphotericin B – 10 mg
ž S –4 times a day

ž For children - suspension of Nystatin +

Amphotericin
ž Rp/ Prednisoloni 0,06
ž Anaestesini 10,0
ž Vit. A 300 000 UE
ž Nystatini 600 000 UE
Sorbitol 0,02
ž Glicerini 300,0
ž S/locally – 3 times a day
ž Rp/ Thymostimulin;

ž S/1mg per kg of body weight daily for 1

week
For maintenance treatment - 2 times a
week
1. Let's interrupt the input paths
2. To ensure good general condition
3. To ensure optimal nutrition
4. To provide the necessary vitamins
5. To stimulate the immune system
6. To ensure oral hygiene
7. To comply with systemic medication.