1- Lab Infections of the Oral Mucosa

7/28/2019 1- Lab Infections of the Oral Mucosa

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Infections of the Oral

Mucosa

LAB 1

Dr. Tahani Abualteen


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Viral Infections


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The following viruses may cause oral infections or oral manifestations:

1. Herpes viradae (or Human Herpes viruses)

2. Coxsackie A virus causing Herpangina and hand, foot & mouth

disease

3. Paramyxovirus causing measles and mumps (may be associated

with non-specific stomatitis)

4. Human Papilloma Virus (HPV) causing warts/epithelial

hyperplasias

5. Human Immunodeficiency Virus (HIV)

6. Influenza Viruscausing influenza (may be associated with non-specific stomatitis)


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Herpes viradae (or Human Herpes viruses):

Generally speaking, these viruses tend to produce an initial primary infection, get

latent somewhere in the body and then they may be reactivated for a reason or

another to cause recurrent or secondary infections

These viruses include:

1. Herpes Simplex (HSV) type 1 causing herpetic stomatitis (primary/recurrent)

ofskin & oral mucosa

2. Herpes Simplex (HSV) type 2 causing herpetic stomatitis (primary/recurrent)

ofgenitalia3. Varicella Zoster (VZV) causing chickenpox (primary) & shingles"herpes zoster"

(recurrent)

4. Epstein-Barr virus (EBV) causing infectious mononucleosis "glandular fever

(primary) and hairy leukoplakia (recurrent) (may be associated with non-

specific stomatitis)5. Cytomegalovirus (HHV5) causing cytomegalovirus infection(may be

associated with non-specific stomatitis)

6. Human Herpes Virus 6 (HHV6) not common

7. Human Herpes Virus 7(HHV7) not common

8. Human Herpes Virus 8(HHV8) thought to be associated with Kaposis sarcoma


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This 12 years old child is presented to the dental

clinic with Multiple vesicles and ulcers affecting

both keratinized and non-keratinized mucosae and

widespread gingival inflammation

Knowing that the patient is having this situation for

the first time in his lifetime and his little brother hadthe same situation 1 week earlier

The histopathological picture is shown below

1- Whats the most likely diagnosis?!

2- Whats the causative agent?!

3- How did the condition probably spread from thelittle brother to the patient?!

4- Describe the clinical course of the disease?!

5- Is this condition usually clinical or subclinical?!

6- Do lesions only occur intraorally?! And if can occur

extraorally, then where?!

7- Does the immunity gained after this primary

infection protect against farther secondary

infections?!

8- Describe the histopathological appearance?!

9- What happens to the virus at the end of this

primary infection?!10- Whats the treatment?!


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Mild Circumoral crusting


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Herpes virus maybe transmitted to

fingers causing a

primary infection

which is extremely

painful known asHerpetic

whitlow


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Primary herpetic gingivostomatitis


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Tzank cells


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Intraepithelial

vesicle

Multinucleated epithelial cells

Tzanck

Cell


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Balloon cell

degeneration


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This 24 years old female patient is presented to the

dental clinic with clusters of vesicles on the lips

and adjacent skin

She stated that these lesions started to appear

few hours after local Prodromal symptoms ofitching or tingling

Knowing that the patient had this situation before



2- Whats the causative agent?!3- How did the condition probably develop?! And

what factors participate?!

4- Describe the clinical course of the disease?!

5- What can the patient do before these vesicles and

ulcers appear to minimized symptoms?!

6- Do lesions only occur extraorally?! And if can

occur intraorally, then where?!

7- If this patient contacts another patient, will she be

spreading the infection to someone else?!

8- Describe the histopathological appearance?!


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Thi 10 ld hild i d h d l


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This 10 years old child is presented to the dental

clinic with Multiple vesicles and ulcers affecting

the skin & the oral mucosa

Skin lesions are pruritic while mucosal lesions are

asymptomatic

Knowing that the patient is having this situation forthe first time in his lifetime and his little brother

had the same situation 1 week earlier



2- Whats the causative agent?!3- How did the condition probably spread from the

little brother to the patient?!

4- Describe the clinical features of the disease?!

5- Does the immunity gained after this primary

infection protect against farther secondary

infections?!6- Describe the histopathological appearance?!

7- What happens to the virus at the end of this

primary infection?!

8- Whats the treatment?!


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Intraepithelial

vesicle

Multinucleated epithelial cells

Tzanck

Cell


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Pharyngitis lymphadenopathy

Petechia


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Bacterial Infections

This 25 years old male is presented to the


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This 25 years old male is presented to the

dental clinic with this unique clinical

appearance of the gingiva

1- Describe the clinical presentation?!2- Whats the most likely diagnosis?!


4- Describe the clinical features of the

disease?!

5- What are the predisposing factorsinvolved in the etiology of this condition?!

6- How to diagnose such condition?!

7- Give me one differential diagnosis?!

8- What is the possible complication?!

9- Whats the treatment?!


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Noma (Cancrum Oris)

Severe and rapidly destructive gangrene of the

orofacial tissue and jawsUsually preceded by NUG followed by rapid spread of

necrosis from gingiva to cheeks

Almost all cases appear in developing countries

(especially Africa) particularly in malnourished

children whose resistance has been lowered by

concurrent infections such as measles or malaria(i.e. immunosuppressed individuals)


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Actinomycosis


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Neutrophils Actinomyces colonies

Actinomycosis


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Primary Syphilis (Chancre)


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Secondary Syphilis (Mucous Patches)


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Secondary Syphilis (Snail-track ulcers)

Snail-track ulcers flat areas ofulceration that coalesced


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Tertiary Syphilis (Atrophic Glossitis)


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Congenital Syphilis (Dental anomalies)

Hutchinsons

Incisors

Mulberry Molars

This 45 years old male is presented to


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y p

the dental clinic with indurated painless

undermined ulcer affecting his tongue

He is also present with granulating

gingival hyperplasia in the lowerright quadrant and granulating

cervical lymph nodes



3- How does the causative agent usually

infect the mouth?!

4- Describe the clinical features of this

condition?!

6- How to diagnose the condition?!7- Whats the treatment?!


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Tuberculosis

Granulating

gingival

hyperplasia

Tuberculous

Lymphadenitis

This 60 years old male is presented to


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the dental clinic with nodular masses of

the skin which cause facial deformity

and tend to ulcerate occasionally

Similar masses are found on anterior

maxillary Gingivae, tongue and palate



3- How many forms of the condition are

there?!4- Within which form oral lesions

occur?!

How does the causative agent usually

infect the mouth?!

4- Describe the clinical features of this

condition?!

6- How to diagnose the condition?!

7- Whats the treatment?! are


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Gonorrhea Neisseria gonorrhea

Mainly Tonsillar and soft palatal lesions Oral lesions are non-specific, presenting as:

Erythema, vesicles, ulcers, pain on speaking

and swallowing

Granulomatous infections:


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Actinomycosis:

Endogenous polymicrobial infection

Submandibular swelling

Chronic suppuration

Multiple sinuses draining pus

Sulphur granules in pus

Syphilis:

Primary chancre

Secondary snail-track ulcers, mucous patches

Tertiary Gumma, lingual leukoplakia

Congenital Hutchinson incisors, mulberry molars, dished face


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Tuberculosis:

Oral usually secondary to pulmonary Painless chronic lingual ulcer

Leprosy:

Oral lesions in Lepromatous type

Secondary to nasal involvement

Nodular masses on palate/anterior maxillary gingiva



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chronic ulcer:InfectiousDifferential diagnoses of an

1. Syphilis

2. TB

3. Cytomegalovirus in immune-compromised patients4. Deep fungal infection


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specific oral lesions:-Causes of non

1. Gonorrhea

2. Infectious mononucleosis (Glandular fever)

3. Cytomegalovirus infection4. Paramyxovirus infection

5. Influenza


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Fungal Infections

Fungal infections of oral mucosa frequently encountered are those


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Fungal infections of oral mucosa frequently encountered are those

due to species of the genus " Candida"

" Candida albicans"is the principle species associated with oral

infection,but other species such as: C. glabrata, C. tropicalis, C.

parapsilosis, C. krusei are also pathogenic

Candida species (especially C. albicans) is characterized by the

following:

Commensal microorganism in the mouth of about 40% of the

population

** Commensalism = benefiting from living in the oral cavity

without harming the host or the flora present there

Dimorphic (exists in two forms; the bud form "present as small

oval yeasts in carriers", and hyphal form "present as elongatedrod-like or ribbon-like structure in patients)Multiply bybudding (production of buds from ovoid yeast cells,

buds then separate and grow to form hyphae)

Variable carriage rates

Candida species (especially C albicans) is characterized by the following:


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Candida species (especially C. albicans) is characterized by the following:The primary oral reservoir for the organism in carriers is the posterior

dorsum of the tongue (probably due to its rough surface)

There is overlap in the candidal counts in saliva from carriers and from

individuals showing infection and so isolation of Candida from the mouth of

an adult is not confirmatory evidence of fungal infectionIt is presumed that Candida has a direct etiological relationship with a

lesion if hyphae are present in smears or in histological sections of the

lesion** The pathogenic form of Candida is the hyphal form that if noticed in theoral cavity it indicates active fungal infection

** The presence of yeasts alone "bud form" not being regarded as

confirmatory evidence for fungal infection but it might indicate a carrier

state

** So to diagnose a patient with fungal infection (candidosis) we cantsimply rely on the presence of Candida nor on their count, BUT insteadwe

need to see the hyphal form histologically and the lesion clinicallyOpportunistic pathogen that is waiting for a chance to cause infection

whenever the balance between the host and the organism is disturbed by

different local or systemic factors


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Factors predisposing to candidal infection:

Local factors: trauma, denture hygiene, tobacco

smoking, carbohydrate-rich diet

Age neonates or elderly people they may not have a

competent immune system

Drugs: broad spectrum Antibiotic (kill the bacteria anddisturb the balance between bacteria and fungi and this favors

candidal growth and proliferation), steroids (cause immunesuppression and disturb the balance between host and fungi

and this favors candidal growth and proliferation), Cytotoxic

drugs

Xerostomialeads to decreased washing effects ofsaliva and this might enhance the adherence of Candida

to the oral mucosa

Systemic diseases


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Protection against candidal infection

Non specific factors: shedding of epithelium,

salivary flow, Commensal bacteria (oral flora)

Specific factors (targeting the Candida specifically):

Serum antibodies is less important

Secretory antibodies (e.g. IgA) is more

important (it decreases adherence of Candida to

oral epithelium)

Cell mediated immune responses


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Pathogenesis of Candidal infection:

Adherence

Secretion of enzymes (such as proteineases)

which enable the hyphae to invade the oral

epithelium

Invasion of epithelium by hyphae

Secretion of nitrosamine compounds which

may play a role in oral carcinogenesis

? Type 4 hypersensitivity to candidal pathogens

Classifications of oral and Perioral candidosis:


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Classifications of oral and Perioral candidosis:

Group 1: primary oral candidosis (candidosis confined to oral & Perioral

tissues)

Acute:PsuedomembranousErythematous (atrophic)ChronicPsuedomembranousErythematous (atrophic)Hyperplastic (candidal leukoplakia)Candida associated lesions:Denture stomatitisAngular cheilitisMedian Rhomboid glossitis** In here Candida may be found in association with these mucosal lesions, but acausal relationship has not been fully established

Group 2: secondary oral candidosis (oral candidosis is a manifestations of a

generalized systemic candidosis)Systemic mucocutaneous candidosis

This 45 years old female is presentedt th d t l li i ith thi k hit


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to the dental clinic with thick white

plaque/coating on the buccal mucosa,

that can be wiped away/scraped off

leaving a red inflamed & bleeding base

The patient complains ofpain and

burning sensation sometimes

The patient is diabetic


2- Whats the causative agent?!3- What are the predisposing factors?!

4- What do we call these white

plaques?! And what are they made

from?!


Acute Psuedomembranous


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Acute Psuedomembranous

candidosis (Thrush)

Thick white plaque/coating (psuedomembrane) on affected

mucosa, that can be wiped away/scraped off leaving a red

inflamed & often bleeding base


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PAS stain

PAS (Periodic Acid Schiff) stain is a special dye that stains the

carbohydrate-rich wall in Candida with a red or pink color

This 40 years old female is presentedt th d t l li i ith ddi h


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to the dental clinic with reddish

painful depapillated dorsum of the

tongue

The patient complains ofgeneralized

pain, discomfort and burning

sensation most of the time

The patient is on antibiotic regimen

since 2 years

1- Whats the most likely diagnosis?!2- Whats the causative agent?!

3- What are the predisposing factors?!

4- Where is this condition seen most

commonly?!


Acute Erythematous candidosis


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Acute Erythematous candidosis

(antibiotic sore tongue)

Red atrophic area of oral mucosa causing generalized pain,

discomfort or burning sensation

This 47 years old male is presented to thedental clinic with reddish painless palatal


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dental clinic with reddish painless palatal

mucosa delineated by the outline of upper

removable partial denture

1- Whats the most likely diagnosis?!2- Whats the causative agent?!

3- What are the predisposing factors

increasing the probability of such condition

in denture wearers?!

4- Where is this condition seen mostcommonly?! Upper or lower dentures?!


6- What is the unique thing about the

histopathological findings?!

7- How many patterns are there?!

This 35 years old male is presented to thedental clinic with reddish painless


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dental clinic with reddish painless

depapillated lesion in the middle of the

dorsum of the tongue just anterior to

foramen cecum

The lesion is roughly rhomboidal in shape




increasing the probability of such conditionin denture wearers?!

4- What can we clinically find in some

patients?!


6- Give me one differential diagnosis?!

M di Rh b id Gl i i


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Median Rhomboid Glossitis

Median (occurs in the midline), Rhomboid (due to its shape),

glossitis (inflammation of the tongue)

This 62 years old female is presented tothe dental clinic with cracks fissures


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the dental clinic with cracks, fissures,

crusts, and pain in the commissure area

bilaterally

The patient is denture wearer



3- Whom patients are mainly affected?!

4- What are the types of candidosis thiscondition is usually related to?!


increasing the probability of such

condition?!


A l Ch liti


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Angular Chelitis

Angular (occurs at the corners of the mouth),

chelitis (inflammation of the lips)

This 25 years old female is presented tothe dental clinic with triangular


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the dental clinic with triangular,

bilateral, white patch on the buccal

mucosa at the commissure area

The white patch seems speckled and

cant be scrapped off

The patient is a smoker



3- Whom patients are mainly affected?!4- What is the type of candidosis this

condition is usually related to?!

5- What are the local predisposing

factors increasing the probability of such

condition?!6- Whats the most commonly affected

site?!

7- Can this lesion be multifocal?! Whats

the term used to describe such a case?!

This 50 years old female is presented tothe dental clinic with triangular


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the dental clinic with triangular,

bilateral, white patch on the buccal

mucosa at the commissure area

The white patch seems speckled and

cant be scrapped off

The patient is a smoker

8- Give me one differential diagnosis

clinically?!

9- How to diagnose the condition?!10- Describe the histopathological

presentation?!

11- Is it considered a premalignant

lesion?! Why?!


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This 50 years old female is presented to


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the dental clinic with multiple white

patches affecting oral mucosa, skin and

nails

The white patches cant be scrapped off


2- Is oral mucosa frequently involved in

this condition?!

3- What type of candidosis do orallesions of this condition resemble?!

4- Can this lesion be multifocal?!

Oral manifestations of the deep fungal infection (deep visceral


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Oral manifestations of the deep fungal infection (deep visceral

mycoses):

Oral lesions are uncommon, but may present as non-specificulceration or as nodular granulomatous areas

Lesions are NOT caused by Candida (Candida cause

superficial lesions only)Examples ofdeep fungal infections which may be associated

with oral lesions are:

BlastomycosisHistoplasmosisZycomycosisCoccidiodomycosis

Deep Fungal Infection


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Blastomycosis




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Histoplasmosis



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HIV infection & AIDS

Transmission of the HIV virus may be


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Transmission of the HIV virus may be

followed by the following stages:

Sero-conversion: Detection of HIV antibodies in blood Within 3 months of exposure Few patients may have also acute symptoms

Sero-postitive: Symptom free for many years

Later on: Persistent generalized lymphadenopathy

AIDS related complex: persistent pyrexia, lymphadenopathy,diarrhea, weight loss, fatigue and malaise

Fully developed AIDS: Opportunistic infections, Kaposi sarcoma, non Hodgkin's

lymphoma.


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Classification of oral lesions associated with HIV infection(fully developed AIDS)


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(fully developed AIDS)Group 1 "lesions strongly associated with HIV"

Candidosis (erythematous, psuedomembranous, hyperplastic)

Hairy leukoplakia (EBV) HIV-associated periodontal disease (HIV-gingivitis, NUG, HIV-periodontitis,

necrotizing stomatitis)

Kaposis sarcoma

Non-Hodgkin's lymphoma

Group 2 "lesions less commonly associated with HIV" Atypical ulceration (oropharyngeal)

Idiopathic thrombocytopenic purpura

Salivary glands disorders (dry mouth, decreased salivary flow rate, uni- or bilateral

swelling of major glands)

Viral infections "other than EBV"(HSV, VZV, CMV, HPV)Group 3 "lesions possibly associated with HIV"

Bacterial infections other than gingivitis/periodontitis

Fungal infections other than candidosis

Melanotic hyper-pigmentation

Neurological disorders (facial palsy, trigeminal neuralgia)


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This 55 years old male is presented to thedental clinic with bilateral vertical white


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folds on lateral border of the tongue

The white folds cant be scrapped off

Histopathological presentation is shown

below



3- Whom patients might be affected with

such kind of condition?!4- Describe the clinical features?!

5- What other microorganism can be

isolated from the surface of the lesion?!

What is its role?!

6- Is it premalignant?!7- Describe how does this condition

usually occur?!

8- Give me one factor that might influence

the location of this condition?!

This 55 years old male is presented to thedental clinic with bilateral vertical white


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folds on lateral border of the tongue

The white folds cant be scrapped off

Histopathological presentation is shown

below

9- What serological finding this patient

might have?!

10- Whats the most commonly affected

site?!11- Describe the histopathological

presentation?!


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Kaposis Sarcoma


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Kaposi s Sarcoma

K i


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Kaposi sarcoma

Proliferating endothelialcells

Cleft like vascular channels

Extravasated RBC

Inflammation

Occasional atypical cells Later stages more atypical

cells

Early stages difficult todifferentiate it from other

vascular lesions

Slit-like vessels


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HIV associated periodontal diseases:HIV-gingivitis (linear gingival Erythema)NUGNUP** Prevalence is less than 10% of all cases

(prevelanact is now low, particular for

patients on HAART)

This 25 years old male is presented tothe dental clinic with Linear band ofErythema on the free gingival margin


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Erythema on the free gingival marginthat doesnt appear to be related to theaccumulation of dental plaque (patient

has excellent oral hygiene)The Erythema is NOT responsive toplaque control


2- Whats the mechanism by which this

condition occur?!

3- What microorganism can be

associated with such condition?!

Acute Necrotizing Ulcerative


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Gingivitis

In HIV-infected patients, the lesions may be persistent and

extensive & may NOT respond to conventional treatment

Necrotizing Ulcerative


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g

Periodontitis Severe rapidly destructive

process

Necrosis of gingival andperiodontal tissues

Exposure of alveolar bone

and sequestration Due to sever impairment of

local defensive mechanismslike reduction in CD4 cells

Defects usually localized

Not responsive toconventional periodontaltherapy

Other oral manifestations of HIV


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Non Hodgkin's lymphomaNeurological disturbances:HIV is neurotropic may directly involve CNSFacial nerve palsy

Atypical ulceration: resemble aphthous stomatitis may beassociated with CMV

Salivary gland disease:xerostomiaSalivary gland enlargement associated with lymphocytic

infiltrateLymphoepithelial cysts

Idiopathic thrombocytopenic purpura:

Present as superficial bleeding spots due to reduction in the

platelets count by an autoimmune response

infection

HIV associated HSV infection


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HIV associated HSV infection

HIV associated HZV infection


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HIV associated HZV infection

HIV thrombocytopenic purpura,


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autoimmune response

HIV oral ulceration


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HIV oral ulceration


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1- Lab Infections of the Oral Mucosa

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