Lab Oral Infections (Lab 4)

7/31/2019 Lab Oral Infections (Lab 4)

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Lab Oral Infections

Dr. Rima Safadi


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Primary herpetic gingivostomatitis

Mild circumoral crusting

Ulcers on gingiva


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Herpes Simplex Virus

Extraoral spread ofinfection: skin, fingers, nailbed, eyes

Herpetic whitlow


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Microscopic features

Intraepithelial vesicle Ballooning degeneration:

swollen , eosinophiliccytoplasm, pale vesicularnuclei

Enlarged, multinucleatedepithelial cells

Tzanck cell:

Access to nerve axons

Due to ruptured epithelialcells

Intraepithelialvesicle

Multinucleated epithe. cells


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Balloon cell degeneration


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Recurrent herpes infection

Small pinpointed vesicles/ulcers

Vesicles at vermilion border,junction with skin


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Recurrent herpes infection

Small pinpointed vesicles/ulcers


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Recurrent herpes labialis


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Chicken pox


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Microscopicfeatures:

identical to HSV

Prognosis forvaricella is usuallymild in children.

vaccine isavailable.

Acyclovir inimmunocompro

mised


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Shingles

Unilateral vesicles and ulcers followingtrigeminal nerve branches


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Infectious mononucleosis

pharyngitis

lymphadenopathy

petechei


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Herpangina


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Hand foot mouth disease


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ANUG

ClinicallyUlceration of interdental papilla and gingival marginsGrey-green psuedomembraneHalitosis, salivation, lymphadenopathy


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Actinomycosis


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Actinomycosis

Etiologyfilamentous branching

Commensal organism

Diagnosis

Culture, biopsy

TreatmentLong term high dose

antibiotics

Penicillin or tetracycline


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Actinomycosis

neutrophilsActinomyces colonies


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Primary herpetic gingivostomatitis


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Tzank cells


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Syphilis

Clinical features

PrimaryChancre occurs at

site of infection andis highly

contagious


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Syphilis

Clinical featuresSecondary

Diffuse painless,maculopapular muco-cutaneous rash

30% have grayish

mucosal necrosiswhich are calledmucous patches


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Syphilis

Treponema pallidum

Primary: chancre : shallow ulcer

Indurated base

Associated with lymphadenopathy

Heals spontanously


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SyphilisMucous patch


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6 weeks later

Secondary syphilis: skin rash and mucouspatch

Snail track ulcers, flat areas of ulceration

that coalesced


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Years later

Tertiary :

Gumma: Necrosis and type IV hypersensitivity

Perforation of palate Atrophic glossitis:

due to endarteritis obliterance Followed by:

Syphilitic leukoplakia Hyperkeratosis Followed by:

Squamous cell carcinoma


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SyphilisTertiary - Gumma on hard palate


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Congenital Syphilis

Miscarriage, still birth or neonatal infection

Collapse of nasal bridge

Hutchinson triad: blindness, deafness, dentalanomalies

Hutchinson incisors (notched teeth) Screw driver teeth

Peg shaped laterals Mulberry molars

Constricted atrophic cusps

Globular masses of

hard tissue


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Classical TB ulcer:

Painless

Undermind

On the tongue


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TB lymphadenitis and granulatinggingival hyperplasia


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Leprosy


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Gonorrhoea

Neisseria gonorrhea

Mainly tonsillar and soft palatal lesions

Erythema, vesicles, ulcers, pain


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Acute PseudomembranousCandidosis (Thrush)

Pain or burning

Predisposing:

xerostomia,

antibiotics

decreased hostresistance

5 % of infants, 10%of elderly

White plaques and red base


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PAS stain

A P d b


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Acute Erythematous (Atrophic)Candidosis

(antibiotic soretongue)

Generalized pain,burning, erythema

Prolongedcorticosteroids orantibiotics

Red and painful


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Median Rhomboid glossitis


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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


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Chronic Hyperplastic Candidosis(Candidal Leukoplakia)

Persistent white patch Speckled/nodular

Most frequent location:buccal mucosa atcommissures

Triangular Bilateral

Associated with angularcheilities? Strong association with

smoking Local factors?

Ch i H l i C did i


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Ch i H l i C did i


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PAS Stain

Neutrophils microabscess

hyphae


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Chronic Hyperplastic Candidosis

(Candidal Leukoplakia)Premalignant?????? Is candida a secondary

infection of a pre existing

leukoplakia?

Some lesions respond toantifungal

therapyetiologic role


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Angular Cheilitis

Fungal or bacterial orcombined


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Angular Cheilitis

Multifactorial disease ofinfectious origin

Candida or Staph aureus orStreptoccocci

Mainly in denture wearers

30% of patient with denturestomatitis have anguarcheilitis


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Chronic mucocutanous candidosis

Persistent superficial infection of: skin,mucosa, nails

Oral mucosa involved in most cases

Orally: similar to candidal leukoplakia

May be multifocal


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Deep fungal infections

Non specificulceration

Or

Granulomatous areas

Blastomycosis


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Histoplasmosis


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Zycomycosis


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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 malaise

Fully developed AIDS: opportunistic infections, Kaposisarcoma, non Hodgekins lymphoma.

HIV- ingivitis


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HIV ingivitislinear gingival erythema

Linear band of erythema -free gingival margin

Not responsive to plaquecontrol

Gingival hyperaemia due torelease of vasoactivecytokines rather thaninflammation

Has been associated withC. albicans


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Necrotizing Ulcerative Periodontitis

Severe rapidly destructiveprocess

Necrosis of gingival andperiodontal tissues

Exposure of alveolarbone and sequestration

Due to sever impairmentof local defensivemechanisms like

reduction in CD4 cells Defects usually localized

Not responsive toconventional periodontal

therapy

Acute Necrotizing Ulcerative


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Acute Necrotizing UlcerativeGingivitis


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Hairy Leukoplakia

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


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Hairy leukoplakia

Acanthosis Parakeratosis

Finger like surface projectionsof parakeratin

Absence of inflammatory cells

in epithelium and laminapropria

Swollen or balloon cells withprominent cell boundaries inpricke cell layer belowparakeratin

Perinuclear vaculization, smalldrak nuclei: koilocyte-like cells

parakeratin

Superficial prickel cell layer

Koilocyte like cells


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Kaposis Sarcoma


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Kaposi sarcoma

Proliferating endothelialcells

Cleft like vascularchannels

Extravasated RBC Inflammation Occasional atypical cells

Later stages more atypicalcells

Early stages difficult to

differentiate it from othervascular lesions

Slit-like vessels


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HIV associated HSV infection


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HIV associated HZV infection

HIV thrombocytopenic purpura


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HIV thrombocytopenic purpura,autoimmune response


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HIV oral ulceration


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HIV lymphoma

Lab Oral Infections (Lab 4)

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