This document discusses fungal infections of the oral cavity, specifically those caused by Candida species. It covers topics like the introduction, terminology, morphology and carriage vs infection of Candida. It also discusses the etiology and pathogenesis of Candidal infections, including factors like adherence, invasion, dimorphism and evasion of the host immune system. Predisposing factors to Candidal infections include local changes to the oral mucosa as well as systemic factors that compromise the host's defenses. The document outlines various clinical presentations of oral Candidal infections.

1. {
Fungal infections of
oral cavity
Part 1
Aureus Desouza
1-6-15

2.  Introduction
 Terminology
 Morphology of candida
 Candidal carriage Vs infection
 Etiology and pathogenesis
 Predisposing factors to infection
 Body’s defence against Candida
 Classification
 Clinical presentation
 Erythematous candidiasis
 Psuedomembranous candidiasis
CONTENTS (PART 1)

3. CONTENTS (PART 1)
 Hyperplastic candidiasis
 Angular cheilits
 Denture stomatits
 Candida in HIV
 Candida infection after HAART
 NON Candida ablicans and HIV
 Candida in dysplasia
 Chronic muco-cutaneous candidasis

4.  Classified in their own kingdom (Kingdom Fungi), separate
from
 animals (Kingdom Animalia) and
 plants (Kingdom Plantae)
 Fungi are thought to be evolutionarily closer to animals than
plants
 They belong to Eumycetes groups
 They act as opportunistic infections
FUNGI

5. Fungal infections are known to have occurred since long time,
the fact that it causes disease in humans is mentioned in the
writings of Hippocrates.
The invention of Antibiotics has brought an opportunity for
candida species to shift from commensals to pathogens, now
with emerging immunosuppressive conditions it has found a
way to be an important pathogen in today's world.
Introduction – fungal
infections

6. MYCOSES comprise a series of infectious diseases caused by
the pathogenic action of fungi
Majority: saprophytes
Some: cause diseases in humans
Primary pathogenic fungi: those that cause mycoses in
previously healthy host
Opportunistic fungi : those that causes mycoses in individuals
with diminished defense mechanisms
INTRODUCTION

7. Fungi = eukaryotic microrganisms
2 structural forms; moulds &
yeasts
Important fungus in dentistry =
yeast
Genus = candida, 150 species
identified
Medically important fungi are
fungi imperfecti
Introduction to human mycoses

8. Introduction to human mycoses
Superficial
• Mucosal e.g. oral thrush
• Dermatophyte infection of skin, hair,nails
Subcutaneous
• Result of traumatic implantation of
environmental fungi, e.g. Madura
Systemic
• Internal organ systems
• Spread hematogenously
• Developed world= immunocompromised
• Developing world = healthy( Histoplasmosis)

9. Fungal infections
Opportunistic fungal
infections:
Candidiasis
Aspergillosis
Systemic fungal infections
Histoplasmosis
Blastomycosis
Paracoccidioidomycosis
Coccidioidomycosis
Cryptococcosis
Zygomycosis

10. candida

11.  Genus: Candida which includes a collection of 150 asporogenous yeast
species
 Broad class: Fungi imperfecti
 Class: Deuteromycetes
 Medically important species: C. albicans
 C. tropicalis
 C. glabrata
 C. parapsilosis
 C. guillermondi
 C. krusei
 C. dubliniensis
 C. kefyr
 C. inconspicua
 C. lusitaniae Less common
 C. norvegensis
 C. rugosa
Candida
NCAC

12.  Of the Candida species isolated from humans, Candida albicans
MC in health and disease ~ 50 %, varies acc to population(Shimizu
et al. 2008)
 Mycological studies have shown that C. albicans represents over
80% of isolates from all forms of human candidosis (Pfaller et al.
2007)
EPIDEMIOLOGY
1. Shimizu C, Kuriyama T, Williams DW, Karasawa T, Inoue K, Nakagawa K, Yamamoto E. Association of oral yeast
carriage with specific host factors and altered mouth sensation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008:
105: 445–451.
2. Pfaller MA, Diekema DJ. Epidemiology of invasive candi- diases: a persistent public health problem. Clin Microbiol Rev
2007: 20: 133–163

13. The number of yeasts isolated from the mouth of normal carriers are
usually low although some variation does occur.
 Arendorf and Walker(1980), about 10-20 colony forming units
(CFU)cm2 (N)
 Epstein, Pearsall and truelove (1980), 200-500 CFU in per ml of
normal saliva
 600 CFU/ml were reported by (McKendrick, Wilson and Main (1967)
 Healthy dentate carriers—dorsum of tongue
 Healthy Denture wearers- denture bearing mucosa mostly the palate
Distribution of yeasts within the
mouth

14.  Infections caused by Candida collectively  Candidoses(plural)/
(singular candidosis)
or candidiases (plural)/ candidiasis (singular)
 Both terms used, although candidosis prefered because it denotes a
fungal infection
Candidosis Vs Candidiasis
-iasis -osis
Council for International
Organizations for Medical
Sciences,1982
International Society for Human
and Animal Mycology, 1980
Eg: Filariasis Eg: Histoplasmosis

15.  SPORE: unit of asexual reproduction ,adapted for dispersal , for
survival, in unfavorable conditions
 BLASTOSPORE / BLASTOCONIDIA :an asexual fungal spore
produced by budding
 GERM TUBE: short cylindrical extensions from mother cell
 PSEUDOHYPHAE: elongated yeast cells, appear as filamentous cell
chains, constricted at the site of emergence by a septum
 HYPHAE: elongated yeast cells, first septum 1-2um from mother cell
 CHLAMYDOSPORE: spore during unfavorable condition
Terminology

16. Morphogenesis of candida
mother cell 5 protuberances /germ tube
budding
2 germ tubes remain
filamentous cell chains, constricted at the
site of emergence by a septum
PSEUDOHYPHAE
elongated yeast cells, first septum 1-2um
from mother cell
HYPHAE

17.  Differs in different environmental conditions
 Different forms:
1. Budding yeast cells(Below 33°C)
2. Pseudohyphae
3. True hyphae (elevated temp and neutral Ph)
4. Chlamydospores
Morphology of Candida

18.  Y:M= 1:3
 Increase in chitin from yeast to mycelial form
 Yeast cells in correct nutrient state
 Presence of an inducer
 Elevated temperature (>33°C)
 Near neutral pH
Y to M morphogenesis
Inducers
Serum
N-acteylglucosamine
Proline
Carbon deprivation (competence)
Nitrogen starvation (morphogenesis)

19.  Candida are normal commensals in mouth
 Dividing line between carriage and infection is rather hazy
 (Arendorf & Walker 1980 ) – no of yeasts increase beyond a
specific value considered as infection, number not as yet
quantified
 Same no. may not cause infection in healthy individual
Candidal carriage VS infection

20. PATHOGENESIS OF
FUNGAL INFECTIONS
Fungus
Exogenous spp
Endogenous spp
Compromised host tissue/
and or immune system
HOST FACTORS TRIGGERS ALTER FUNGAL
MORPHOLOGY AND PATHOGENECITY
1. Improved fungal adherence
2. Ability to invade hosts
3. Secretion of antiphagocytic and cytolotic
properties
4. Ability to develop resistance to anit-
fungals
EFFECT ON HOST TISSUES AND IMMUNE
SYSTEM
1. Innate defence less effective
2. Increased fungal load in host tissues
3. phagocytosis./ opsonization impaired
4. Fungal invasion in deep tissues
5. CHRONIC INFLAMMATOR REACTIONS
CELL MEDIATED IMMUNTIY
NORMALDEFECTIVE
CHRONIC INFECTION
ELIMINATION OF THE
FUNGI
1. LOCALLY DESTRUCTIVE
DISEASE
2. SYSTEMIC DISEASE
ACTIVATED MACROPHAGES –
CYTOKINE RELEASE:
ELIMINATION OF FUNGI
RAPID HEALING
RETURN OF FUNGI TO
COMMENSAL NICHE

21. Candidal infection
Epithelial colonization
Adherence to epithelial
cells
Invasion of the host cells
by candida

22. Robin 1853, Bouchut 1867, Parrot 1877
Prior to appearance of lesion
 Dryness/ inflammation of oral mucosa
 Swelling of lingual papillae prior to clinically detectable lesions of thrush
 Destruction on epithelium (Parrot 1877)
 General health as imp as local factors in causing disease (Bouchut 1867)
Gubler 1858, Delafond 1858
 Acidic environment is a contributing factor.
 Healthy children = neutral/ alkaline Ph
 Children with thrush =acidic Ph
 Secretions of major salivary glands (alkaline) , thrush (dec . secretion)
Etiology and Pathogenesis
(early theories..)

23. Quinquaud 1868
 Normal- fermentation process by m/o causes production of carbonic
acid
 Thrush- excessive fermentation process  inc. acidity
Etiology and Pathogenesis
(early theories..)

24. Pathogenesis
CANDIDIASIS
Microbial
Factors
Host
Factors

26. ADHERENCE
 Ability to persist on mucosal epithelium
 Involvement of hydrophobic interactions and electrostatic bonds
Lectin like
proteins of
fungal
cell wall
Terminal sugars
of cell surface
glycoproteins
of human host

27. Proteinases
 Chiefly aspartate proteinases
Candidal proteinase acts as a keratinase in vitro
Involved in invasion of orthokeratinised
epithelium

28. Lipases
 Maybe exclusive for C. albicans
 Phospholipase activity
 Limited to tip of fungal hyphae
 Limited to acidic conditions
 PL-A, B, C, D
 Lysophospholipase
 Lysophospholipase transacylase

29. Persorption
 Reflects action of fungal extracellular hydrolases
 Passage of yeasts from intestinal lumen through intact mucosa
into the blood stream
 Disputed

30. Dimorphism and germ tube
formation
 True hyphae at 37°C
 Blastspores below 30°C
 In between 30-37°C psuedohyphae
form
 Germ tubes mark the onset of
hyphal growth

31. High switching frequency
 Phenotypical shuttle system of most strains of C,albicans
and C.tropicalis
 Differences in colony morphology, involving size, shape
of blastoconidia
 True reversible transition system without recognizable
differences among DNAs

32. Interference with phagocytosis
Produces acidic peptides:
 Inhibits attachment of fungal hyphae to phagocytes
 Inhibits induction of respiratory burst of phagocytes
 Neutrophilic granulocytes may allow the yeast phase C.albicans to
evade intra-cellular killing, if the blastospores are internalised in
“unsealed” phagosomes.
 The internal mileu is acidic and there is a competition between acid
fungal hydrolases and acid hydrolases of the phagosome may
determine the outcome of phagocytosis

33. Interference with immune system
 Seen in chronic mucocutaneous candidiasis
 Polysaccharide fraction of C. albicans:
 Inhibits proliferation of human T-lymphocytes
 Inhibits production of IL-1 and IL-2

34. Interference with complement
 Binding of iC3b and C3d to C.albicans and C.stellaoidea
 Fungal iC3b is non-identical to receptor on human neutrophils.
It binds iC3b non-covalently and impairs phagocytosis of the
fungal cell

35. Microbial factors

37. Local host factors
 Mucosal barrier
 Exogenous epithelial
changes
 Trauma
 Local occlusion
 Maceration
 Endogenous epithelial
changes
 Atrophy
 Hyperplasia
 Dysplasia
 Saliva
 Quantitative changes
 Qualitative changes
 Commensal flora
 High carbohydrate diet

38. Systemic host factors
 Altered physiological states
 Infancy
 Old age
 Altered hormonal states
 Diabetes
 Hypothyroidism
 Hypoparathyroidism
 Hypo-adrenocortism
 Altered nutritional states
 Iron deficiency
 Malnutrition
 Altered immune mechanisms
 Decreased number of
phagocytes
 Intrinsic defects in immune cells
 Defects in cell mediated
immunity
 Due to infective states
 Malignant diseases
 Cytotoxic drugs &
radiotherapy

39.  Keratinized and non-keratinized mucosa first line of defence
 Proteins in the epithelium acts as antifungals
 Continuous wearing of well-fitting/ ill-fitting denture 
variations in thickness of palatal epithelium … TRAUMA ,
LOCAL OCCLUSION (thin, more susceptible)
 Angular cheilitis  constant maceration of skin folds at angle of
mouth due to decreased vertical dimension, iron deficiency
Local Factors Mucosal barrier
(EXOGENOUS EPITHELIAL CHANGES) Trauma , local occlusion,
Maceration

40.  Constant desquamation of epithelium > candida growth rate 
protective
 ATROPHIC epthelium  more conducive to Candidal
invasion
 Candidal infection  promotes hyperplasia, certain situations
cellular atypia and malignant change……. DYSPLASIA
Local Factors Mucosal barrier
(ENDOGENOUS EPITHELIAL CHANGES) Atrophy, Hyperplasia, Dysplasia

41.  Protection against Candida: Secretory IgA ( inhibits candidal
adhesion to host surface), Antifungal factors ( lysozyme,
lactoperoxidase, lactoferrin, histidine rich polypeptides)
 Flushing action of saliva
1. Qualitative effect:
 Pts on broad spectrum antibiotics, corticosteroids and having
diabetes mellitus  more glucose in saliva
 Acidic Ph of saliva:  Sjogrens syndrome
Candidal species are aciduric and acidophilic and attach to epithelial
surfaces and denture acrylic surfaces
2. Quantitative effect:
 Dec. salivary output in Sjogren’s syndrome, pts on cytotoxic and
irradiation therapy
Local Factors Saliva

42.  The normal flora poses a competition for the nutritional
elements to candida
Local Factors (Commensal Microflora)

43.  In presence of inc carbohydrate in saliva, a sticky extrafibrillar
layer is formed which carries Candida and there in inc adhesion
in its presence
 Production of acid, dec in Ph  direct toxicity, activation of
phospholipase, and acid protinase Inflammation of mucosa
 Dec Ph  activation of iC3b receptors in Candida  Inc resistance
of phagocytosis of Candida
Local Factors (Dietary Carbohydrate)

44.  INFANCY:
1. Immature immune defenses
2. Antibiotic therapy
3. Congenital Defects like thymic aplasia
4. Maternal Cross infection
5. Cross-infection from nursery staff
6. Low Salivary Ig A levels at birth (Normal)
7. Low birth weight ( inc incidence if other factors are also present)
 Psuedomembranous variety > , delay of 4 days ( activity of candida
more)
OLD AGE:
 Diseases, antibiotic therapy, corticosteroid therapy , denture use
Systemic factors (Altered
physiological states)

45.  Hypothyroidism
 Hypoparathyroidism
 Adrenal insufficiency
Systemic Factors (Altered hormonal
states)

46.  Oral carriage and density more in diabetes and denture
wearers
 Proposed mechanism
Systemic Factors (Diabetes)
1. Increased rate of germ tube formation
2. Intrinsic qualitative cell surface changes in cell
surface receptors modulating yeast adhesion
3. Defects in candidiacidal activity of neutrophils in
presence of glucose
4. Micro-vascular degeneration in capillaries within
lamina propria

47.  Iron deficiency (more susceptible)
 Proposed mechanism
 Vitamin deficeincy
 Folate deficiency, Vit A deficiency, Zinc deficiency derangements
of epithelial cell kinetics
Systemic Factors (Altered
Nutritional Status)
1. Impairment of iron dependent enzyme systems affecting
metabolism of rapidly dividing oral epithelial cells
2. Def- hyperkeratosis and atrophy, suitable for growth
3. Dec. Cell mediated immunity
4. Impaired phagocytosis
5. Inadequate antibody production

48.  An altered immune response:
1. Intrinsic defects in immune cells
2. Decreased number of phagocytes
3. Defects in cell mediated immunity
Systemic Factors (altered
immune response)

49.  Antibiotics
 Locally  Reduce bacterial population
 Systemically  cause changes in immune
response
 Oral contraceptives  Predispose to vaginal
candidosis
Iatrogenic factors (Antibiotics
and Oral Contraceptives
1. Antibiotics like penicillin Enhance immune response
2. Erythromycin, co-trimoxazole,
aminoglycosides
Reduce neutrophil and candidiacidal
activity

50.  More due to topical application of steroids than due to steroid
inhalers
 Steroid inhalers.. Atrophic and psuedomembranous >
 Possible mechanism of action
Iatrogenic factors
(corticosteroids)
1. Generalised immunosuppression
and anti-inflammatory effects
2. Triamcinolone acetonide inc,. Calcium uptake in C.albicans
thus protecting it from econazoles
3. Higher level of glucose in saliva Promotes their growth
4. Dexamethasone Incorporated into outer surface of
the yeast, thus promoting
adherence via surface receptor
interaction (esp. in steroid spray/
inhaler)

51.  Yeast proliferation and initiation of infection is related to both
host and changes caused by the tumor itself and side effects of
therapy
Effect of Cytoxic drugs and
radiotherapy, malignant diseases
1. Neoplastic drugs Neutrophil, lymphocyte-monocyte
interaction is decreased
2. Cytotoxic action of therapeutic
drugs on rapidly dividing mucosal
cells
Atrophy, thinning, inflammation 
inc. susceptibility to trauma and
inection
3. Persorbtion Candida can interact with GI
mucosa

52.  Cigarette Smoke  epithelial alterations that may facilitate
candidal proliferation
 Could catalyze formation of N-nitrobenzyl methylamine
candidal leukoplakia (higher potential for malignant change)
Cigarette smoking and
Oral candidiosis

53.  Non- secretion of blood group antigens in saliva  inc oral
candida carriage
 Reason: it may bind to lectin-like adhesins in yeast and/or host
surface thus, blocking the attachment sites of yeast and/or host
surface
Blood Group, Secretor
status

54. Body’s defence
against Candida

55. Body’s defence against
candida
1. Skin and mucous membrane Continuous de-squamation prevents
attachment
2. Buffering & washing off effects Maintains alkalinity of saliva and
washes off microbes, prevents adhesion
Makes them come in contact with non
specific factors
3. Non specific anti-microbial factors(
lactoferrin, chelating agent)
Competes for iron free radicals which
are essential for bacterial and fungal
infection
Non-specific immunity to candida
Role of commensal bacteria
Normal flora inhibits candida due to competition for nutritional factors

56. 1. Polymorphonuclear leucoytes and
macrophages
Phagocytose and kill bacteria in
absence of opsonizing antibodies
(limited destruction of hyphae and
yeast), damaging to the host when
inflammation against them is not
localised
2. Candia agglutinating factor A non-immunoglobulin factor with
the same binding site as candida
3. Macrophage Fungistatic > fungicidal
4. Natural killer cells Marginally cytotoxic to candida,
5. Complement activation Bind iC3b and C3d
Body’s defence against
candida

57. 1. Serum Antibodies Candida antigens can
cause a systemic
response
Ig G, IgA, Ig ( inc in
CMC
Serum antibodies act as
opsonins for
macrophages, PNL’s,
stimulant for chemotaxis
2. Complement system C3a, C5a Released after fixation of
the complement by the
antibody
3. Salivary Antibody IgA Prevent adhesion to
epithelium
(some candida produce
IgA proteinases)
4. Cellular response Lymphocyte
proliferation, NK cells,
cytotoxic T cells
Respond to candida
antigen
Body’s defence against
candida

58.  Increased prevalence in the recent decade
 Possible Reasons :
1. Improvements in diagnostic methods (use of primary agars with the ability
to differentiate species, and the introduction of molecular techniques in the routine
diagnosis of fungaemia) (1)
2. Higher level of antifungal drug resistance in NCAC ( elimination of
C.albicans in mixed species infections) when treated with traditional
antifungal agents (1)
3. Use of invasive medical procedures (e.g. use of indwelling
catheters, organ transplants) (2)
4. Immunosuppressive therapy (2)
non - Candida albicans Candida

59. classification
A. BILLIARD 1828
3 categories in infants:
Category 1
Small white lesions on
tongue & oral mucosa
Category 2
Larger scattered plaques
of varying sizes
Category 3
A confluent membranous
lesion completely
covering the tongue
B. BOUCHET 1867
Idiopathic
“Muguet idiopathique”
Symptomatic
“Muguet symptomatique”
C. TROUSSEAU 1869
“Le muguet mixte”
Idiopathic
Symptomatic
Mixed

60. classification
D. LEHNER 1966
(Based on clinical, mycological, histological, serological, therapeutic criteria)
Acute
 Acute pseudomembranous candidiasis (thrush)
 Acute atrophic candidiasis
Chronic
 Chronic atrophic Candidiasis
(Candida associated denture stomatitis, denture sore mouth)
 Chronic hyperplastic candidiasis
 Chronic oral candidosis
 Endocrine candidosis syndrome
 Chronic localized mucocutaneous candidosis
 Chronic diffuse candidosis

61. classification
E. HOLMSTRUP AND BESSEMANN 1983
Acute infections
 Acute pseudomembranous candidiasis
 Acute erythematous candidiasis
Chronic infections
 Chronic pseudomembranous candidiasis
 Chronic erythematous candidiasis
 Chronic plaque-like candidiasis
 Chronic nodular candidiasis

62. classification
Category I : Primary oral candidoses
Category II: Secondary oral candidoses
Subg-
group
Disease state Synonyms Acute
/chronic
1 Acute pseudomembranous Thrush Acute
2 Acute atrophic candidosis Candida glossitis/ glossodynia Acute
3 Chronic hyperplastic candidosis Candida leukoplakia Chronic
4 Chronic atrophic candidosis
( 3 types by Newton)
Candida as denture stomatitis/
denture sore mouth/ denture
induced stomatitis
Chronic
5 Candida as angular chelitis Perleche A/C

63. classification
CATEGORY II:
1. Secondary oral candidosis ( Odds, 1988)
2. CMC with endocrinopathy
3. Familial CMC with endocrinopathy
4. Familial CMC without endocrinopathy
5. CMC due to thymoma
6. Idiopathic CMC with mature onset (>20 yrs)
7. Idiopathic CMC with juvenile onset (<19yrs)
MISCELLANEOUS CANDIDIASIS
1. Cheilocandidosis
2. Juvenile juxta vermillion candidosis
3. Median rhomboid glossitis

64. Classification; samaranayake 1991
M.A.M. Sitheeque,L.P. Samaranayake*, Crit Rev Oral Biol Med, 14(4):253-267 (2003)

66.  SYNONYM: Atrophic candidiasis (Atrophos, ill-fed, Greek)
 May arise de-novo or a successor to psuedo-membranous candidiasis
 PREDISPOSING FACTORS: Inhalational and systemic steroids, broad
spectrum antibiotics, smoking, Diabetes Mellitus
 VARIANTS: Acute and Chronic
 SITE PREDILECTION: Dorsum of tongue and palate (inhalational steroids ),
other mucosal surfaces ( broad spectrum antibiotics)
 APPEARANCE: Diffuse erythema over the mucosal surface (Acute~ chronic)
 SYMPTOM: Asymptomatic or symptomatic (burning sensation)
ERYTHEMATOUS CANDIDIASIS

67. Erythematous candidiasis

68. DIFFERENTIAL DIAGNOSIS
 Eyrthroplakia
 Pernicious anaemia
 Iron deficiency anemia
 Vitamin B deficiency

69.  VARIANTS: Acute
 SYNONYM: Thrush (acute)
 May be considered a precursor to erythematous candidiasis
 PREDISPOSING FACTORS: Antibiotics (acute); HIV, patients with
impaired immune system (eg. elderly, debilitated) (chronic variety),
immature immune system (infants), in patients receiving
immunosuppressant therapy , steroid inhalers
Pseudomembranous candidiasis

70. Pseudomembranous candidiasis
SITE: buccal mucosa, tongue (MC), tongue, palate, gingiva, floor of the mouth
APPEARANCE: Soft , white, slightly elevated, loosely adherent plaques
Plaques described as cottage cheese or curdled milk

71. If the pseudo membrane is peeled off--- Underlying mucosa either
appears normal appearing / erythematous
Pseudomembranous contains thick zone of sloughed
 Epithelial cells
 Fibrin
 Keratin
 Food debris
 Leucocytes
 Bacteria
 C. albicans ( hyphal form)
Pseudomembranous Candidiasis

72. Differential diagnosis
P. Candidiasis Papular lichen
planus
Chemical burn
/Thermal burn
Diptheria Mucous
Patches of
syphilis
May coalesce to
form larger
plaques
May intermingle
with reticular
striae during
course of disease
May have a
pseudomembran
e over the ulcer
Will have an
erythematous
margin
Strictly adherent
papular or
plaque like
Raised grayish
white, glistening
patches on
mucous
membrane,
Affects oral
cavity,
oropharyngeal
and oesophageal(
severe cases)
Affects buccal
mucosa MC
At the site of
application of
causative agent
Affects usually
soft palate and
oropharynx
Soft palate ,
tonsil,
cheek,palate
If removed, it
leaves a normal
appearing
mucosa or
erythematous
region
Cannot be
removed by
mechanical force
If removed, it
leaves a necrotic
appearing area
If removed ,
leaves a raw
bleeding surface

73.  Synonym: Candidal Leukoplakia ,Lehner (1964, 1967)
 Sex predilection: M>F:: 2:1
 Predisposing factor: smoking
 Important points:
More likely to be a/w epithelial dysplasia ~ 15%(Samaranayake and
MacFarlane, 1990)
Hyperplastic candidiasis

74. Hyperplastic Candidiasis
SITE PREDILECTION: Buccal mucosa, tongue, commissures, lip
APPEARANCE: Thick, white, leathery, adherent white plaques or nodules
Cannot be pealed off

75. Classification (Chronic Hyperplastic candidiasis)
Type I CHC Type II CHC
Candidal leukoplakia CHC of chronic
mucocutaneous candidosis
syndromes
Adult onset Childhood onset
No other immune
disorders
2 to uncommon , inherited
immune disease Like Di
George Syndrome
M.A.M. Sitheeque, L.P. Samaranayake Chronic hyperplastic candidosis/candidiasis
(candidal leukoplakia). Crit Rev Oral Biol Med.14(4):253-267 (2003)

76.  Acanthosis with hyperplasia of rete pegs
 Microabscesses (collections of
polymorphonuclear leukocytes)
 Cellular atypia may be present
Hyperplastic candidiasis
Candida Hyphae

77.  Mixed bacterial-fungal infection (Candida + Streptococci +
Staphylococci)
 PREDISPOSING FACTORS: Reduced Vertical dimension,
nutrtional deficiencies ( Thiamine, riboflavin, iron, and folic acid),
immunocompetent host, diabetes, atopic or seborrheic dermatitis,
dry skin, children who frequently lick or suck thumb,
Down’s syndrome, infants who slobber and use pacifier
 SITE: Either or both corners of the mouth (mc), also affect anterior
nostril region (esp when a/w staph.)
Angular cheilitis
Devani A, Barankin B. Answer: Can you identify this condition? Canadian Family Physician. 2007;53(6):1022-1023.

78.  APPEARANCE : erythematous fissuring at the commissures,
often accompanied by a pseudomembranous covering or
crustation
Angular cheilitis

79. Classification (Angular cheilitis)
Mild localized lesion with
minimal skin involvement
Type
1
Type
2
Fissure(s) /rhagades more extensive in length
and depth than type 1
Ohman et al 1985

80. Type
3
Severe fissures radiating from angle into
adjacent skin
Classification (Angular cheilitis)
Ohman et al 1985
No fissures evident but erythematous area
spreading towards vermillion border
Type
4

81. After clinical inspection and the extent of the disease is
determined
 Mild (type 1)
 Moderate (type 2)
 Severe (type 3).
Classification (Angular cheilitis)
Warnakulasuriya KA, Samaranayake LP, Peiris JS. Angular cheilitis in a group of Sri Lankan adults: a clinical and
microbiologic study. J Oral Pathol Med. 1991;20(4):172–5. [PubMed]
Warnakulasuriya KA, Samaranayake LP (1991

82.  SYNONYM: median rhomboid glossitis , Glossite losangique
mediane de la face dorsale de la langue
 EPIDEMIOLOGY: prevalence of less than 1%
 GENDER PREDILECTION: Men> women 3:1
 PREDISPOSING FACTORS: Smoking, inhalational steroids
 Occurs due to the loss of filiform papillae
Central papillary atrophy of tongue

83.  Rhomboid-shaped hypertrophic or atrophic plaque in the mid-dorsal
tongue anterior to the circumvallate papillae
 Associated “kissing lesion” on the hard palate, resulting from direct
inoculation that occurs when the dorsal tongue makes contact with the
hard palate during deglutition.
Central papillary atrophy of tongue

84.  SYNONYM: Denture sore mouth, chronic atrophic candidiasis
 PREDISPOSING FACTOR: denture use, overclosure, reduced
vertical dimension, improper hygiene of the denture
 PATHOGENESIS :
 1. Porous acrylic allows for fungal and bacterial contamination in
the denture.
 2. Relatively acidic and anaerobic microclimate underneath
 3. Denture shields the mucosa from the saliva and salivary
functional properties of local immunity. Serves as a continuous
inoculation source
Denture stomatitis

85. Classification (denture stomatitis) Newton 1962
Type
1
localized simple
inflammation or pinpoint
hyperemia
An erythematous or generalized simple
type seen as more diffuse erythema
involving a part or the entire denture
covered mucosa
Type
2

86. Classification (denture stomatitis) Newton 1962
A granular type (inflammatory papillary hyperplasia)
commonly involving the central part of the hard palate
and the alveolar ridges
Type
3

87.  Type III often is seen in association with type I or type II
 Type III denture stomatitis involves the epithelial response
to chronic inflammatory stimulation secondary to yeast
Denture stomatitis

88.  Uncommon
 Characteristic chronic, ulcerative, granulating lesion of the
vermillion area of the lower lip
 May result from irritative lesions of lower lips becoming infected
with Candida spp.
 Does not come under the classical classification
CHEILOCANDIDOSIS

89.  Bouquot & Fenton 1988 = self limiting form
 Erythema and pruritits
 Yellow crusting plauqes of juxtavermillion skin
 Desqamation of vermilion zone may or may not occur
 Does not come under the classfication
Juvenile juxtavermilion
candidiasis

90.  Impairment of systemic defense mechanisms ( dec. CD4+ T cells below
protective levels )
 Impairment of local immunity (dec. Salivary iga, defensins, or
epithelial cell-mediated cytokines in the saliva )
 Conversion of commensal microorganisms, e.G., Candida, to
microorganisms with increased pathogenicity,
 Causing an imbalance in the host oral microbial composition
 Increased risk for opportunistic infections
Candida and HIV

91.  Oral candidiasis was found to be the most common (71.25%)
opportunistic fungal infection.. Anwar KP et al.
 B.C. Pruthvi et al. reported candidiasis in 71% of HIV positive
patients
 Nagalingeswaran K et al. in 70%,
 A. Singh et al. in 59%
 Anupriyawadhwa et al. 50% of the HIV positive patients.
Candida and HIV

92.  Documented by Pruthvi B.C et al. in N.R.13th International Congress on
Infectious Diseases. 2006. Spectrum of Clinical Presentation and Opportunistic Infections in HIV:
An Indian Scenario
 Enwuru CA et al. in his study found ~ 25% of HIV infected patients
may be colonized with the yeast and C. dubliniensis has been
isolated from the oral cavity of approximately 30% of patients with
AIDS and oral candidiasis
Non-Candida albicans
Candida and HIV

93.  Risk of many HIV-related diseases varies with the patient's degree of
immunosuppression
 Increased risk once CD4+ T lymphocyte counts fall below 200 cells/µl
 Acc. To Yang Y-L et al. HAART markedly decreases mortality and morbidity
as well as the incidence of AIDS-defining opportunistic infections which is in
confluence with other studies in literature
 However, frequency of oropharyngeal colonization by Candida, was not as
dramatically decreased. Possible reason being most patients receiving
HAART continue to be colonized by Candida, but do not develop oral
candidiasis. (among other factors like patient compliance, failure to reduce
viral load etc)
Candida and HAART

94. Candidal infection in
AIDS (clinical features)
 Oropharyngeal candidiasis more prevalent
 Erythematous > Pseudomembranous > Hyperplastic
 Angular cheilitis
 Lesions are more widespread and of a chronic nature

95. Candida in dysplasia
 15% of the CHC lesions dysplastic lesions
(Samaranayake and MacFarlane, 1990)
 7 to 50% of all leukoplakias
(Jepsen and Winther, 1965 Daftary et al., 1972)
POSSIBLE ETIOLOGY
 Role of yeast in oral carcinogenesis is unclear.
 Increased colonization and infection associated with
dysplasia are entirely coincidental
 Reflects a change in the environmental conditions
conducive to the proliferation of ubiquitous commensals.

96.  Barett A W et al 1998, in 223 patients found :
 Positive association of fungal infection with moderate and severe
epithelial dysplasia, median rhomboid glossitis and squamous
papillomas.
 21.9% dysplasias which were infected with fungi worsened in
histological severity, as compared with 7.6% of dysplasias which
were not infected at any stage
 Singh SK et al. 2014, in their study on 50 patients found
Candida was present in 32% of cases without dysplasia, and 20 %
with dysplasia, and no correlation was observed between
presence of candida & epithelial dysplasia among various oral
lesions.
Candida in dysplasia

97.  Group of rare heterogeneous disorders that are characterised by
persistent superficial candidal infection of the mouth, skin and nail-
beds
 Term coined by: Chilgren et al (1967)
Chronic mucocutaneous candidosis
(CMC) and related syndromes

98.  Chronic candidal infection of the mouth
1. Initially psuedomembranous hyperplastic affecting any
mucosal surface
2. Tongue (enlarged, fissured, hyperplastic nodules on lateral
borders
3. Painful angular cheiltis
4. Oral ulceration (uncommon)
5. May spread into pharynx, larynx, oesophagus, visceral
(rare)
6. Enamel hypoplasia (a/w candidosis endocrinopathy
syndrome)
CMC and related syndromes

99.  Chronic cutaneous candidal infection
1. Begin as papular nappy rash
2. Later presents as asymptpomatic chronic brown-red, scaly
serpiginous plaque affecting scalp, face, neck, upper chest,
dorsum of hands and feet
3. Granulomatous lesions can arise in particularly diffuse CMC
CMC and related syndromes

100.  Nail changes: dystrophic nails with amrked thickening,
distortion, fragmentation, paronychial areas(red, oedmatous) ,
digital tips have bulbous appearance. One or several fingers
affected
 Chronic vulvo-vaginal candidiasis
Curd like patches of thrush, pruritis , redness, swelling.Less
common than oral candidiasis

101. Classification of CMC and
subtypes
Subgroup Onset Inheritance Features
Familial CMC Early(few
months after
birth)
AR Oral and cutaneous
Low serum iron and low levels of iron storage
Granuloma form less
Diffuse CMC Early AR / sporadic Oral and cutaneous
Low serum iron and low levels of iron storage
Granuloma form less
CES Early AR / sporadic
F>M
Mild oral/skin lesions, enamel hypoplasia
Endocrine(hypoparathyroidism, vitiligo, DM,
Late onset
CMC
Late Sporadic Mild skin/oral lesions
Thymoma, myasthenia gravis, polymyositis,
hypogammaglobulinemia, myeloperoxidase
def)
CMC with
other
immunodeficie
ncy
Early Sporadic/ hereditary Oral and skin; variable involvement
A/w SCID, Di George syn, Nezelof Syndrome

102. 1. Nagalingeswaran K, Solomon S, Madhivanan P, Yepthomi T, Venkatesan C,
Amalraj E, et al. Correlation between plasma viral load and CD4+T cell count to
opportunistic infections in persons with HIV in South India. IntConf AIDS. 2000 Jul;9-14:13.
2. Spectrum of opportunistic infections in AIDS cases.Singh A, Bairy I, Shivananda
PGIndian J Med Sci. 2003 Jan; 57(1):16-21.
3. Sanjeypandey, Shyam Sunder, Hasan H, Ravi Shankar, Singh SP. Clinical profile
and opportunistic infections in HIV/AIDS patients attending SS hospital
varanasi. Indian J PrevSoc Medicine. 2008;39(1 & 2)
4. Pruthvi B.C, Vikram S, Suman S.K, Jayaprakash B, Rau N.R.13th International
Congress on Infectious Diseases. 2006. Spectrum of Clinical Presentation and
Opportunistic Infections in HIV: An Indian Scenario; p. e484
5. Anwar KP, Malik A, Subhan KH. Profile of candidiasis in HIV infected
patients. Iranian Journal of Microbiology. 2012;4(4):204-209.
References

103. 6. Barrett AW, Kingsmill VJ, Speight PM. The frequency of fungal infection in
biopsies of oral mucosal lesions. Oral Dis. 1998 Mar;4(1):26–31.
7. Singh SK, Gupta A, Rajan SY, et al. Correlation of Presence of Candida and
Epithelial Dysplasia in Oral Mucosal Lesions. Journal of Clinical and Diagnostic
Research : JCDR. 2014;8(10):ZC31-ZC35.
8. Yang Y-L, Lo H-J, Hung C-C, Li Y. Effect of prolonged HAART on oral
colonization with Candida and candidiasis. BMC Infectious Diseases. 2006;6:8.
doi:10.1186/1471-2334-6-8.
9. Oral Candidosis. Edited by Lakshman P. Samarnayake. T Wallace McFarlane
10. Textbook of Oral Medcinine .Ravikiran Ongole. Prashanth BN.
11.
References

105.  Scrapable lesions of oral cavity
 Non-scrapable lesions of oral cavity
 What are the methods used for differentiating various species of
candida?
 Why are there skin lesions or nail changes in candida infection?
And what other conditions have nail changes?
Questions