Infections of the Oral Mucosa 2 (Slide 12 +13)

7/30/2019 Infections of the Oral Mucosa 2 (Slide 12 +13)

1/58

Infections of the Oral Mucosa

2

Dr. Rima Safadi


2/58

Fungal Infections

Candida albicans

Dimorphic

Multiply by budding

Commensal

Others like C.

glabrata, tropicalis,parapsilosis, C. kruseiare also pathogenic


3/58

Fungal InfectionsCandida albicans

Variable carriagerates around 40%...

Mainly on the tongue Candidal counts

overlap betweenpatients (infection)

and carriers Presence of hyphae in

smears is importantfor diagnosis


4/58

Candidosis Opportunistic pathogen

Disturbance of balance between host and

organism (homeostatic balance)

Factors: local and systemic


5/58

Candidosis

Factors predisposing to candidal infection

Local factors: trauma, denture hygiene,

tobacco smoking, carbohydrate-rich dietAge

Drugs: broad spectrum AB, steroids, cytotoxic

drugs Xerostomia

Systemic diseases


6/58

Candidosis

Protection against candidal infection

Non specific factors: shedding ofepithelium, salivary flow, commensalbacteria

Specific:

Serum antibodies: less important

Secretory immunity is more important (itdecreases adherence of candida)

Cell mediated


7/58

Candidosis

Pathogenesis of Candidal infection

Adherence

Secretion of enzymes: proteineases

Invasion of epithelium by hyphae

Secretion of nitrosamine compounds ? Type 4 hypersensitivity to candidal

pathogens


8/58

PAS stain


9/58

Classification of Oral Candidosis

Classifications: acute or chronic, oral or extraoral

Acute:

Psuedomembranous

Erythematous (atrophic)

Chronic

Psuedomembranous

Erythematous (atrophic) Hyperplastic (candidal leukoplakia)


10/58

Classification of Oral Candidosis

Candida associated lesions:

Denture stomatitisAngular cheilitis

Median Rhomboid glossitis

Secondary oral candidosis:

Systemic mucocutanous candidosis


11/58

Acute Pseudomembranous

Candidosis (Thrush) Pain or burning Predisposing:

xerostomia, antibiotics

decreased hostresistance

5 % of infants, 10%of elderly

White plaques and red base


12/58


13/58

Acute Pseudomembranous

Candidosis (Thrush)


14/58

Acute Erythematous (Atrophic)

Candidosis (antibiotic sore

tongue)

Generalized pain,burning, erythema

Prolongedcorticosteroids or

antibiotics Red and painful


15/58


16/58


17/58

Chronic Atrophic Candidosis (Candida-

associated denture stomatitis) Secondary infection by Candida intissues modified by continualwearing of dentures

Poor denture hygiene High carbohydrate diet

May be asymptomatic

Candida colonize the denture

surface Minimal or no candidal invasion of

mucosa


18/58

3 patterns ofinflammation (Newtonsclassification):

1. Pinpointed erythema

2. Diffuse erythema

3. Granular or multinodular(chronic inflammatorypapillary hyperplasia)


19/58

Chronic Hyperplastic Candidosis

(Candidal Leukoplakia) Persistent white patch Speckled/nodular

Most frequent location:buccal mucosa atcommissures

Triangular Bilateral

Associated with angularcheilities?

Strong association withsmoking Local factors?


20/58


(Candidal Leukoplakia) Can be multifocal

Chronic multifocal oralcandidosis


21/58


(Candidal Leukoplakia)


22/58


(Candidal Leukoplakia)


23/58

PAS Stain


24/58

Chronic Hyperplastic Candidosis(Candidal Leukoplakia)

Premalignant?????

50% associated with

epithelial dysplasia

15% progress to true dysplasia

Most of candidal leukoplakias are non homogenous

Candidacan generate carcinogenes like nitrosamine


25/58


26/58

Angular Cheilitis

Fungal or bacterial orcombined


27/58

Angular Cheilitis Multifactorial disease of

infectious origin

Candida or Staph aureus orStreptoccocci

Mainly in denture wearers

30% of patient with

denture stomatitis haveanguar cheilitis


28/58

Angular Cheilitis Cracks, fissures, crusts,

pain in commissure area

Loss of vertical

dimension Deep folds of skin at

angles of mouth

Continual wetting by

saliva Nutritional deficiencies


29/58

PAS stain modified for fungi


30/58

Median Rhomboid Glossitis

Just anterior to foramen

cecum

Red depapillated smooth or

fissured asymptomatic

Etiologic debate Developmental or chronic candidal

infection Opposing lesion on the palate

may be seen Multifocal candidosis


31/58

Chronic mucocutanous candidosis

Persistent superficial infection of: skin,mucosa, nails

Oral mucosa involved in most cases

Orally: similar to candidal leukoplakia

May be multifocal


32/58

Deep fungal infections

Non specificulceration

Or Granulomatous areas

Blastomycosis


33/58

Histoplasmosis


34/58

Zycomycosis


35/58

HIV infection and AIDS

Sero-conversion: detection of HIV antibodies in blood in 3 months May have also acute symptoms

Sero-postitive for many yearslater on Persistent generalized lymphadenopathy AIDS related complex:persisitent pyrexia, lymphadenopathy, diarrhea, weight

loss, fatigue and malaiseFinal Stage: Fully developed AIDS: opportunistic infections,

Kaposi sarcoma, non Hodgekins lymphoma.


36/58

Infection by the virus means: virus binds to:CD4 T lymphocytes, macrophages, CNS cells,

endothelial cells

CD4 cells die leading to decrease number of T

helper

Impaired immunity particularly against: viruses,

fungi and encapsulated bacteria.

Table 11.5 in your text book groups the lesionsassociated with AIDS


37/58

Oral Manifestations of HIV infection

Oral candidosis Most frequent oral manifestation Azole resistant species Psuedomembranous and erythematous are most

frequent types. Chronic, multifocal May involve any part of the oral mucosa

Hyperplastic type involves buccal mucosa rarely

commissures Prevalence:

20% of HIV seropositve positive patients 70% of AIDS have oral candidosis

Prev. decreasing with introductions of HAART


38/58

Viral Infections

HSV, HZV: more severe and extensivethan HIV negative pts

Dissimenated CMV infection

Kaposi sarcoma and HHV8

EBV and Hairy leukoplakia

Oral Warts is increasing.


39/58

Hairy Leukoplakia Common in late stage

HIV infection indicatingAIDS

Vertical white folds onlateral border of thetongue, bilaterally

White patch that can not

be removed May have smooth flat

surface

May have candidal

hyphae but as secondary


40/58

Hairy Leukoplakia

Opportunistic infection oforal epithelium by EBV

After primary infectionshedding from oropharynxor salivary glands persists

Minor trauma to tongue

facilitates infection withvirus

Marked reduction oflangerhans cells


41/58

Hairy leukoplakia

In 20-25% of patients

May indicate the development of AIDS

Can occur in pts receivingimmunosuppressive medications

NOT pre malignant


42/58

Hairy leukoplakia

Acanthosis

Parakeratosis

Finger like surface projectionsof parakeratin

Absence of inflammatory cellsin epithelium and laminapropria

Swollen or balloon cells withprominent cell boundaries in

pricke cell layer belowparakeratin

Perinuclear vaculization, smalldrak nuclei: koilocyte-like cells


43/58

HIV associated periodontal

diseases 1. Linear gingival erythema

2. NUG

3. NUP

HIV Gi i iti


44/58

HIV-Gingivitislinear gingival erythema

Linear band of erythema -free gingival margin

Not responsive to plaquecontrol

Gingival hyperaemia due torelease of vasoactivecytokines rather thaninflammation

Has been associated with C.albicans


45/58

Necrotizing Ulcerative Periodontitis

Severe rapidly destructiveprocess

Necrosis of gingival andperiodontal tissues

Exposure of alveolar boneand sequestration

Due to sever impairmentof local defensivemechanisms likereduction in CD4 cells

Defects usually localized

Not responsive toconventional periodontal

therapy


46/58

ANU periodontitis

Acute Necrotizing Ulcerative


47/58

Acute Necrotizing UlcerativeGingivitis


48/58

Kaposis sarcoma

Clinical features

Commonest tumor associated with AIDS

But with low prevalence especially with medications

Male more than females

Associated with HHV8

Multifocal tumor: skin and mucosa

Mainly palatal lesion, tip of the nose


49/58

Kaposis Sarcoma


50/58

Kaposis sarcoma

Clinical: Kaposis sarcoma can be a surface lesion or a

soft tissue enlargement.

red purple patch

macular

Plaque

Nodular Multiple lesions common


51/58

Kaposi sarcoma

Proliferating endothelialcells

Cleft like vascularchannels

Extravasated RBC Inflammation Occasional atypical cells

Later stages more atypical

cells Early stages difficult to

differentiate it from othervascular lesions

Slit-like vessels


52/58

Oral manifestations of HIV infection

Non Hodgkins lymphoma

Neurological disturbances: HIV is neurotropic may directly involve CNS

Facial nerve palsy Atypical ulceration: resemble aphthous stomatitis may be

associated with CMV

Salivary gland disease: xerostomia

Salivary gland enlargement associated with lymphocytic infiltrate

Lymphoepithelial cysts


53/58

HIV associated HSV infection


54/58

HIV associated HZV infection


55/58

HIV thrombocytopenic purpura,autoimmune response


56/58

HIV oral ulceration


57/58

HIV lymphoma


58/58

????

Infections of the Oral Mucosa 2 (Slide 12 +13)

Documents

Transcript of Infections of the Oral Mucosa 2 (Slide 12 +13)