This document discusses oral candidiasis, caused by an overgrowth of Candida species in the oral cavity. It begins with an introduction to candidiasis and the most common Candida pathogens. It then covers the classification of oral candidiasis, including acute and chronic forms. Predisposing factors are discussed. The document delves into the clinical features and management of various types of oral candidiasis such as pseudomembranous candidiasis and denture stomatitis. Laboratory tests for diagnosis are also summarized, followed by an overview of antifungal drugs used to treat oral candidiasis.

1. Presented by: Shweta
JR II
Seminar
OralCandidiasis

2. Introduction:
• Candidiasis, a common opportunistic fungal infection of
oral cavity
• Candida species are responsible for a wide range of
systemic as well as superficial opportunistic infections.
• Genus CANDIDA is oral commensal microflora of
healthy individuals, & c. albicans among most common
pathogens

3. • Change from harmless commesal existence of Candida
to a pathogenic state can occur following alteration in
oral environment .
• Infections are mostly superficial and associated with
moist mucosal surface
• In immunocompromised patients systemic infection is
prevalent and so higher rate of mortality is associated

4. • Most frequently isolated strains of candida
are
• C. albicans
• C. tropicalis
• C. glabrata
• The other pathogenic Candida species are
• C. parapsilosis
• C. stellatoidea
• C. guilliermnondii
• C. krusei
• C. pseudotropicalis.

5. Classification
ACUTE
Acute pseudomembraneous candidiasis
Acute atrophic candidiasis
• antibiotic sore mouth
CHRONIC
Chronic atrophic candidiasis
•Denture stomatitis
•Angular chelitis
•Median rhomboid glossitis
Chronic hyperplastic candidiasis
1966

6. REVISEDCLASSIFICATIONBY
LEHNERIN1967 PRIMARY ORAL CANDIDOSIS SEC. ORAL CANDIDOSIS
• acute forms Oral manifestations of
psuedomembranous Systemic mucocutaneous
ertyhmatous candidosis
• chronic forms
pseudomembranous
erythmatous
hyperplastic(nodular/plaque
J. Of marmara university institute of health sciences vol: 1, no. 2,2011
• candida assoc.
denture stomatities
median rhomboid glossities
angular chelities
• keratinized pri. Lesions
superinfected with candida
leukoplakia
lichen planus
lupus erythmatous

7. AxellT.,HolmstrupP
1990
Acute
Pseudomembraneous
erythematous
Chronic type
Pseudomembraneous
Erythematous
Plaque- type
Nodular
Candida – associated lesions
Angular chelitis
Denture stomatitis
Median rhomboid glossitis

8. Classification based on clinical
appearance:
PRIMARY FORM;
acute form psuedomembranous (most acute)
erythmatous (acute)
Chronic erythmatous/ atrophic (resolving)
hyperplastic (deep seated infection)

9. Predisposing factors
Local
Mucosal barrier
Phagocytosis
morphogenesis
saliva
systemic
Immunocompr
omised
individuals
Altered
nutritional
states
Iatrogenic
Antibiotic
therapy
Corticosteroid
therapy
Cytotoxic therapy
& radiotherapy
Cigarette/
tobacco smoking
Ref: South afr.J.Epidemiol infect 2011;26(1):18-21

10. Acute pseudomembranous candidiasis
(Thrush).
Clinical Features.
• superficial infection of the outer layers of the
epithelium,
• patchy white plaques or flecks on the mucosal
surface.
• Scrapable & reveals an area of erythema or
even shallow ulceration.
• easily recognized; diagnosis based on
appearance of the lesion.

11. • infants - soft white adherent patches on the oral
mucosa,painless and can be removed
• Prodromal symptom - rapid onset of a bad
taste and the loss of taste discrimination
• Burning sensation of the mouth and throat
may also precede

12. • in children and in adults of all ages
• Transient episodes ; lesions disappear
spontaneously with minimal or no
treatment.
• usually unrelated to any recognized
predisposing factor and are common in
neonates and young children.

13. • In the adult,
inflammation, erythema,
and painful eroded areas
are more often associated
with this disease, and the
typical pearly white
plaque like lesions.
• entire oral mucosa or
localized areas where
normal cleansing
mechanisms are poor.

14. • broad-spectrum antibiotics,
immunodeficiencies, such as those
suffering from AIDS or hematologic
malignancies, - susceptible to this form of
candidiasis.
D/D
• flecks of milk
• Habitual cheek biting
• White sponge nevus

15. Acute Erythematous (Atrophic)
Candidosis:
• Synonym: Antibiotic sore mouth
• Holmstrup and Axell (1990) - "atrophic
candidosis“ should be replaced by
"erythematous candidosis“ in a new
classification of oral candidosis

16. • Precipitating factors:
• corticosteroids and topical or systemic broad
spectrum antibiotics or HIV disease.
• persistent acute pseudomembranous
candidosis

17. Clinical features:
• characterized by erythematous
areas and painful mucosa, with
minimal evidence of the white
pseudomembrane
• palate, or buccal mucosa.
• Dorsum of the tongue -
depapillated areas.
• Red areas in the palate in HIV
disease.
• associated angular stomatitis.

18. • Antibiotic sore mouth- oral burning, bad taste,
or sore throat during or after therapy with
broad-spectrum antibiotics.
• Patients with chronic iron deficiency anemia
may also develop atrophic candidiasis

19. Chronic Atrophic Candidiasis.
• Denture stomatitis (denture sore mouth),
angular cheilitis, and median rhomboid
glossitis.
Denture Stomatitis (Denture Sore Mouth)
• common form of oral candidiasis
• diffuse inflammation of the maxillary denture-
bearing areas and associated with angular
cheilitis.

20. • Most likely results from yeast colonization of
the oral mucosa, combined with bacterial
colonization.
• Act as an endogenous infecting agent on
tissue predisposed by chronic trauma to
microbial invasion.
• reported in HIV-positive and AIDS patients.

21. Clinical stages of denture
sore mouth
• First stage - numerous palatal
petechiae /pinpoint hyperaemia
• Second stage - diffuse erythema of
denture-covered mucosa
• Third stage - tissue granulation or
nodularity (papillary hyperplasia)
commonly involving the central
areas of the hard palate and
alveolar ridge.

22. • Rarely found under a mandibular denture.
Close adaptation of
maxillary denture
Negative pressure under
maxillary denture
Exclude salivary
antibodies
Yeast develops
undisturbed

23. Pathogenesis of denture associated
candidiasis:
Denture worn
at night
Altered
microflora
Compromised
blood supply
Anaerobic
environment
candidiasis

24. Angular Cheilitis
• Infection involving the lip commissures.
• Coexistent with denture stomatitis, and angular cheilitis
• Uncommon in patients with a natural dentition.
Possible etiologic cofactors include:
• Reduced vertical dimension
• Nutritional deficiency (iron deficiency anemia and vitamin B or
folic acid deficiency) sometimes referred to as perlèche.
• Diabetes
• Neutropenia
• AIDS
• Co-infection with Staphylococcus and beta-hemolytic
Streptococcus.
• Habitual lip sucking
Chelio- candidosis
& juvenile
juxtavermillion
candidosis

25. Clinical features:
• Young children and adults
• Characterized by feeling of dryness and a
burning sensation at corner of the mouth.
• angles of the mouth, characterized by soreness,
erythema, and fissuring which do not bleed.

26. • These fissures do not involve the
mucosal surface of the commisures
inside the mouth, but stop at the
mucocutaneous junction.

27. Median Rhomboid Glossitis
• Synonym: Midline glossitis, glossal central
papillary atrophy
• an area of papillary atrophy ;elliptical or
rhomboid in shape
• symmetrically placed centrally at the midline of
the tongue, anterior to the circumvallate
papillae.
• Occasionally, median rhomboid glossitis
presents with a hyperplastic exophytic or even
lobulated appearance.

28. Chronic hyperplastic candidosis/candidiasis
(Candidal leukoplakia)/ Chronic plaque
type & Nodular candidiasis
• Lehner (1964, 1967) - "candidal leukoplakia".
• Confusion prevailed, since chronic mucocutaneous
candidal lesions, encountered in patients with
endocrine and immune defects, and affecting the
skin and other mucosae, were also described by
some as chronic hyperplastic candidosis.

29. Clinical Features
• Well-demarcated, palpable, raised lesions; vary
from small translucent whitish areas to large
opaque plaques that cannot be rubbed off.
• plaque may have a smooth, homogenously
white surface, and if this feature predominates,
the lesion is referred to as a homogenous
leukoplakia.

30. • 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

31. Histopathologically:
• Candidal hyphae infiltrate the superficial layers
of the parakeratotic epithelium.
• Mitotic activity inc. – stratum spinosum
• Polymorphonuclear leukocyte infiltrate and
lymphocyte infiltration in the corium seen
• Elongated hyperplastic rete ridges
• Dysplastic changes evident (more than
leukoplakia)

32. CHRONIC MUCOCUTANEOUS
CANDIDIASIS
• defect in cell-mediated immunity/iron deficiency.
• Two categories of CMC have been described:
• 1) syndrome-associated CMC : it is further divided into
– Familial/ chronic.
• 2) localized and diffuse CMC.
Familial form, candidiasis endocrinopathy syndrome
(CES)
• autosomal recessive
• onset - infancy or early childhood.
• hypoparathyroidism, hypoadrenocorticism, and other
endocrine anomalies.
• persistent oral candidiasis and hyperplastic of the nail
folds at an early age.

33. • CMC of late onset- associated with thymoma,
which appears with other autoimmune
abnormalities such as myasthenia gravis,
polymyositis, bullous lichen planus, and
hypogammaglobulinemia.

34. Localized CMC
• associated with chronic oral candidiasis and
lesions of the skin and nails.
• first two decades of life.
• diffuse variant -widespread skin involvement and
development of Candida granulomas.
• associated with other opportunistic fungal and
bacterial infections.
(Burket’s 10th ed)

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

36. Candida & oral cancer
• Confirmed link not yet established
• In vitro, yeast generates nitrosamine N
nitrsobenzylmethylamne
• Is a precursor for oral cancer

37. Virulence factor:
VIRULENCE FACTOR EFFECTS
ADHERENCE PROMOTES RETENTION
• Cell surface hydrophobicity • non-specific adherence
•Expression of adhesins •Specific adherence
EVASION OF HOST DEFENCE PROMOTES RETENTION
•Phenotypic switching •Antigenic modification
•Hyphal development •Reduces phagocytosis
•Secreted aspartyl proteinase
production
•Secretory IgA destruction
•Binding of complement •Antigenic masking
INVASION & DESTRUCTION OF
HOST TISSUE
ENHANCES PATHOGENICITY
•Hyphal development •Invasion in epithelium
•Hydrolytic enzyme production •Host cell & extracellular matrix
production

38. ADHERENCE
Flushing action of saliva & sloughing of epith. Is host
defence
Adherence is initiated through weak & reversible
interactions involving hydrophobic & electrostatic
forces
 Promoted by mannose, C3d receptor, mannoprotein,
saccharins
 Candidal genes ALS & HWP1 encodes for cell wall
assoc. proteins that promotes adhesion
 Association with oral bacteria in biofilm promotes

39.  Production of true hyphae decreases their
phagocytosis & increase pathogenicity.
 It invades host tissue and cause damage

40. HIGH FREQUENCY PHENOTYPIC SWITCHING
MECHANISM
• Have greater virulence
• Aid in evading recognition by acquired
immune response & biofilm formation

41. EXTRACELLULAR ENZYME SECRETION
SAPS( SECRETED ASPARTYL
PROTEINASES)
 Are 10 in nos.
 Are of same class as HIV aspartyl proteinase, human
pepsin & rennin
 Activity range pH 2-7; aids in candida survival
 Directly induce damage to host cells
 Aids in hyphal growth
 Increases adherence
 Degrades host Ig

42. PHOSPHOLIPASES (PLs)
 cause hydrolysis of ester linkage degrade host
membrane
Degrades cell membrane of host cell causing lysis &
death
Promotes adherence & penetration in tissue
EXTRACELLULAR LIPASE AND ESTERASE
Hydrolyze ester bonds in glycerides
Cytotoxic effect
HAEMOLYSIN produced by Candida may be
predisposing factor in diabetics

43. HOST RESPONSE TO ORAL CANDIDOSIS
• Candidal mucosal infection is prevented by
innate immunity
• Neutrophils & macrophages kills Candida by
identifying pattern recognition
receptors(PRRs)
• Interaction of dentritic cells with Candida
leads to dentritic activation and phagocytosis

44. Dentritic cell(professional phagocytes) candida
(pattern recognition receptors) (PAMP)
Release cytokines & chemokines
DCs activation & phagocytosis
lymph nodes antigen processed DC with antigen+CD4 Tcells
mature T cells
mucosal protection (Th1, Th2, Th17, regulatory T cell)

45. Ref: South afr.J.Epidemiol infect 2011;26(1):18-21

46. Laboratory investigations
in
orapharyngeal candidiasis.
48

47. Microbiology
• swab, sputum -microscopy or culture
• Quantitative assessment is an important factor in the
differentiation between carriers and infected patients.
• Frequently, Sabouraud's dextrose agar is used as a
primary culture medium.
49

48. Staining
• Gram stain and periodic acid Schiff (PAS)
technique.
50

49. Swab
• Rubbing a sterile cotton-tipped swab over the
lesional tissue or all surfaces irrespective of the
clinical signs is a useful assay for the presence
or absence of Candida.
51

50. Imprint culture
• Imprint culture: sterile foam pads dipped in
Sabouraud’s broth are placed for 30 seconds on the
lesion and then placed on Sabouraud’s agar containing
chloramphenicol for an hour after which they are
incubated, have also been used for identification of
Candida spp.

51. Management:
• A priority in the treatment of oral candidosis is the
alleviation of any identifiable predisposing factor
• Improve oral hygiene & both physical & chemical
reduction of candida in oral cavity
• the regular and frequent use of a denture cleanser
with anti-candidal properties

52. • mouthwashes exhibit anti-candidal activity including
triclosan, chlorhexidine gluconate, and essential oil
formulations.
• The latter tend to contain natural plant extracts such
as thymol, eucalyptol, and bioflavanoids and these
can have a direct anti-candidal activity in vitro
through cell membrane disruption and enzyme
inhibition

53. • Denture disinfection: coated with antifungal and kept in
mouth for few mins.
• Mucosal surface should be also brushed regularly
• After disinfection, dentures should be allowed to air dry
* Postgrad Med J 2002;78: 455-459

54. ANTIFUNGAL DRUGS
• POLYENES (amphotericin B & nystatin)
• MOA: directly binds to ergosterol in fungal cell
membrane causing leakage& cell death
• It can also bind to cholesterol of mammalian cell but in
lower affinity
• Toxic at higher therapeutic concentrations
PROPERTIES:
• poor gut absorption
• Used effectively topically
• Nystatin can b used in refractory candidosis

55. drug Mode of
action
Mode of
administrati
on
use Trade name
polyenes Binds to
ergosterol &
disrupts cell
membrane
1. nystatin topical Chr.
erythmatous
Nystaleb
syrup
2.
Amphoterici
n B
topical Chr.
erythmatous
Ampholip
10 mg;
100mg; 50
mg.
Both nystanin oral rinses & cotrimazole torches have high sucrose
content & if tooth decay is concern ,or steroids & diabetic complication
present or immunocompromised state, TRIAZOLES is effective
* Postgrad Med J 2002;78: 455-459

56. AZOLES (FLUCONAZOLE & ITRACONAZOLE)
• Are fungistatic
• MOA: inhibit enzyme lanosterol demethylase that is a
cytochrome P-450 3 – A dependant enzyme for synthesis
of ergosterol
• Cause inhibition of fungal growth & impairment of
membrane permeability
• Complete inhibition aided by managing of predisposing
factor
PROPERTIES:
• Readily absorbed through gut
• Secreted in high levels in saliva

57. drug MOA ADM. USE
azoles Inhibits
ergosterol
biosynthesis
1. Fluconaz
ole
Syst. PMC, AEC,
CHC
Fluconex,
fluconil
150mg
2.
Miconazole
Topical CEC Miconit skin,
micorid skin,
fungiderm
3.Ketoconazo
le
Topical/sys. PMC, AEC,
CHC
Cinort,
kenacort
4.Clotrimazo
le
Topical CEC Clotriv,
ctzole,
canazole
5.Itraconazol
e
Sys. PMC,AEC,C
HC
Tab. Itra,
knoz,
candistat
6.
voriconazole,
posaconazole
Sys.

58. Drug resistance to azole
• production of lanosterol demethylase
• Alteration of enzyme structure
• Removal of azole from cell by multi drug transporter pumps
• Alternative sterol in place of ergosterol in cell membrane

59. Newer drugs;
• New azoles; ITRACONAZOLE, VORICONAZOLE,
POZOCONAZOLE
• ECHINOCANDIN; caspofungin, micafungin &
anidulafungin
act through inhibition of D-glucan sythase( enzyme for
synthesis of fungal cell wall)
Is non- toxic for mammalian cell
Limited in application because of large molecular size
In invasive fungal infection

60. 5-
flucytosine
Inhibition of
DNA/protein
synth.
Sys.
Combined
with
amphotericin
ECHINOCA
NDINS
Inhibits β 1,3-
glucan synth.
1. Caspofung
in
2. Micafugin
3.Anidulafug
in

61. Additional statergies:
• nutritional deficiency states (iron, folate and
vitamin B12), diabetes mellitus, and any
immunodeficiencies should be excluded
• pharmacologic agents that may contribute should
be identified, and if practical, substituted for an
alternative drug
• Use of corticosteroid inhalers for asthma should be
coupled with rinsing the mouth with water after
each use*J. Of marmara university institute of health sciences vol: 1, no. 2,2011

62. • Biomaterial modification:
denture coating with silanes, chorhexidiene, histatins
incorporation of surface modifying groups
biofilm disruption by exploiting quoram sensing
mechanism
• Probiotics:
induce microbial pressure & promotes local immune
response

63. Nystatin:
• Nystatin oral suspension (100000IU/ml) is used as
a mouth rinse four times a day for approximately 2
minutes, then swallowed (10,28).
• should avoid eating or drinking for 20 minutes
after using Nystatin oral suspension.
• Intraoral appliances should be removed during the
treatment as the medication works topically and
must be in contact with the tissue
• Oral suspension of Nystatin contains abundant
sucrose, so patients with natural teeth should be
advised to brush

64. • Treatment duration varies between 7-14 days, with
therapy continued at least for 2-3 days after the last
clinical signs and symptoms have disappeared.
• contraindicated in the treatment of oral candidosis in
patients with diabetes mellitus
• There are reports of reduced efficacy of Nystatin when
used in combination with chlorhexidine gluconate, it
is often advised to delay Nystatin treatment for 30 min
after the use of chlorhexidine mouthwash

65. Refrences:
• Burket’s oral medicine and diagnosis 9th edn
• Burket’s oral medicine 10th edn.
• Neville’s color atlas of clinical oral pathology 2nd edn.
• Oral disease of tropics, prabhu & daftary
• Pathogenesis and treatment of oral candidosis, David Williams* and
Michael Lewis;Journal of Oral Microbiology 2011, 3: 5771 - DOI:
10.3402/jom.v3i0.5771
• Journal of Oral Microbiology 2011. Citation: Journal of Oral Microbiology
2011, 3: 5771 - DOI: 10.3402/jom.v3i0.5771
• J. Of marmara university institute of health sciences vol: 1, no. 2,2011
• Postgrad Med J 2002;78: 455-459
• South afr.J.Epidemiol infect 2011;26(1):18-21