lia session 3 vesiculobulous diseases - viral

8/13/2019 Lia Session 3 Vesiculobulous Diseases - Viral

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t the end of the session student have to beable to explain the various virus infections oforal and perioral diseases

Learning objectives

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Diagram of the

oral tissues,

illustrating the

component

tissues and their

relativepositions.

1. Stratified squamous

epithelium.

2. Lamina propria

3. Loose connective

tissue

4. Mucous glands

5. Serous glands

(occasionally)

6. Sebaceous glands(Fordycs granuless)

7. Nerve

8. Bone

9. Cartilage

10. Skeletal muscle


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List as much as possible vesiculo-bulous

viral infections of the oral diseasesTimes 10 mnt.

Viral infection of the oral diseases

1

2

3

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Infection

Hard tissue J a w s

Dental pulpitis

Periapical abssess

Acute osteomyelits Chronic osteomyelitis

Osteitis

Oral tissue

Oral Mucosa Lips

Gingival

Palate mucosa

Tongue

Pharynx

Floor of the mouth

Sub mucous swelling

Gingival

Floor of mouth

Lips & buccal mucous

Tongue

Palate

Neck

Mucosal surface lesion Vesiculobulous diseases

Ulcerative condition White lesions

Red blue lesions

Pigmented lesions

Verrucal papillary lesion

Differential diagnosis approach

to jaw lesions

Cyst of the Oral Region

Odontogenic Tumors

Benign Non Odontogenic Tumor

Inflamatory Jaw Lesions

Malignant Non-odont Neoplasm

Metabolic and Genetic Jaw Diseases

Soft tissue

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Example 1


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odontogenicTeeth component

Pulpitis

Pericoronitis

Periapical absess

Periostitis

Subperiosteal absess

Sub mucous abscess

Cellulitis

Phlegmoon

Subcutan absess

Bacterial infection

Actinomycosis

NUG

Pericoronitis

Syphylis

Gonorhoue Sinusitis maxillaris

Tbc

Leprosi

Noma

Sinus cavernosus

thrombosis

Viral infection

Vesiculobulosa

Herpes simplex

Recurrent herpes

Varicellazoster virus

Hand foot mouth dis

Herpangina

Measeles

Mumps

Fungal infection

Candidiasis

Deepfungus infection Subcutaneus fungus inf.

Sporotricosis

Opportunistic Infection

Mucor mycosis

Aspergillosis

Infection

Non odontogenic

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Example 2


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Viral diseases

Herpes simplex

infection

Varicella infection

Hand foot mouth

disease

Herpangina

Measles

Vesiculo-bulous diseases

Condition related with

immunology defect.

Pemphigus vulgaris

Mucous membrane

pemphigoid

Bullous pemphigoid

Dermatitis

herpetiform

Linear Ig A disease

Heriditary diseases

Epidermolysis

bullosa

Example 3


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Viral diseases

Herpes simplex infection

Varicella infection

Hand foot mouth disease

Herpangina

Measles



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Virus groupDNA virus RNA virus

1 Poxvirus

Small pox

Molluscum contagi

Vaccina

1 Myxovirus Influensa

2Herpes

Virus

Herpes simplex

Herpes zoster/

varicellaCytomegallo

2Paramyxo

virus

Rabies

3Adeno

virus

Pharyngoconj.tiva

Epidemic keratocon

junctivitis

3 Rhabdovirus Rabies

4 Papo virus 4 ArbovirusEncephalitis

Yellow fever

5Parvo

virus5 Rheovirus ISPA

6 Picornavirus HFM


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Schematic representation of herpes simplex virus


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Schematic diagram of the productive (lytic) replication of herpes

simplex virus type 1 (HSV-1)


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HSV-1 is an obligate, intracellular parasite

Requires a healthy host mammalian cell to produce new

progeny viruses through a productive (lytic) replication

cycle

Following attachment of the virion to the host cell by

specific receptors (viral envelope glycoproteins gB and gC

and cell surface heparin sulfate),


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The nucleocapsid gains entry to the cell by fusion of the

envelope with the plasma membrane.

The nonenveloped nucleocapsid is transported via

cytoskeletal elements of the host cell to the nuclear pores

where the viral DNA is released into the nucleus.

A tegument protein of the parental virus rapidly inhibits host

protein synthesis to allow for efficient translation of virus-specific transcripts by host ribosomes.


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Primary infection: direct contact with H SV

HOSPESSeronegative

Primary disease

Primary Herpet ic

Gingivostomat i t is PHG

Herpet ic With low

Subclinical infection Secondary disease

Secon dary or Recurrent

Herpes Sim plex Infect ions

Herpes Labial is, Herpetic

Withlo w (l ips , palate,

gingiva, hand f inger)

HOST CARRIER

Seropositive

Virus

Reactivat ion

Sunlig ht, fever,

mechanicaltrauma, allergy,

worry resolut ion

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Pathogenesis of herpes simplex infections


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Group viral infections

1. Herpes simplex virus infection, HSV

o Is a vesicular eruption of the skin and mucosa

o Pathogenesis : (previous sl ide)

o 2 forms : primary

acute primary herpetic gingivostomatitis,

PHG

: secondary

secondary or recurrent herpes simplex

infection, herpes labialis, HSL


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A. Acute Primary Herpetic Ging ivostomati t is, PHG

The classical clinical presentation of PHG with markedly swollen

interdental papillae and bleeding areas.


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Prodromal period :

One single virus can not produce disease

To achieve a substantial number of viruses intracellularreplication take place

One week, during which the patient does not present

any symptom.



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Prodromal period :

The initial symptoms are a lack of sensation or a tingling

sensation in the affected areas which are usually

keratinized (masticatory) mucosa.

Vesicles, are the basic manifestations of the disease, follow

the initial sensation.

Bullae and ulcer forming: ..



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Bullae and ulcer forming :

These vesicles are intraepithelial in location, and they

eventually coalesce forming bullae which extend to the

dermis becoming subepithelial

Vesicles and bullae break, especially in intraoral locations,

mostly associated to mastication.

Upon opening the vesicles leave painful superficial ulcers.



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The ulcers are seen in any of the oral mucosas and theoropharynx.

Occasional crusting over these ulcers, especially on the

lip, is also seen in the late stage of the infection.

PHG is essentially an ulcerative gingivitis.

The gingiva is characterized by marked erythema,

especially of the interdental papillae.

There is increased body temperature, regional

lymphadenopathy and incapacity to eat properly due to the

painful lesions.

A. Acu te Primary Herpetic Gingivos tomati t is, PHG


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The primary infection lasts up to two weeks and resolves

itself without leaving scars or sequelae.

The clinical manifestations are more severe in

immunocompromised patients especially those withadvanced AIDS, leukemia or transplant patients.

After the clinical and/or sub clinical infection subsides the

virus goes into latency by reaching the regional ganglion,

such as the Gasser ganglion, migrating through the nerve

axon. The affected patient then becomes a carrier.



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A severe case of PHG with a secondary superimposed infection. Note the

sero-purulent exudate. The photo shows several ulcers on the lower lip

mucosa of the same patient.


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B. Secondary Or Recu rrent Herpes Simplex Infect ion,

Herpes Simp lex Labial is, HSL


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Excitants such as: GI upsets, stress, menses, solar radiation,

extreme cold or other infections, will reactivate the virus in

around 40% of carriers.

This reactivation induces migration from the ganglion to theperipheral epithelial cells where the virus replicate.

This new viral load will produce recurrent lesions which are

generally less severe than the primary ones.

The recurrent lesions on the lips go through several clinical

stages which are: burning sensation, erythema of the

affected area, vesiculation, ulceration and crust formation.

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B. Secondary Or Recu rrent Herpes Simp lex Infect io n,

Herpes Simp lex Labial is, HSL


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B. Secondary Or Recurrent Herpes Simplex Infection, Herpes

Simplex Labialis, HSL

Recurrent herpes simplex, also known as recurrent herpes

labialis (cold sores)

As the name implies, develops on the lips, generally at thejunction of the vermilion and the skin.

It begins as a burning sensation which last several hours to

one day.

Erythema is the second stage which is followed by small

coalescing vesicles, which are short lived.

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B. Secondary Or Recurrent Herpes Simplex Infection, Herpes

Simplex Labialis, HSL

Eventually the ulcer becomes covered by a dark red-brown

crust.

As a rule these episodes last 10 to 14 days. Recur- rencesmay vary from 1 to several a year.

Secondary lesions also heal without scar formation.

The oral recurrent lesions generally occur in the lip'svermilion, but lesions may also develop in the attached

gingiva and/or hard palate.

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B. Secondary Or Recurrent Herpes Simplex Infection, HerpesSimplex Labialis, HSL

All these intraoral locations are covered by keratinizing

epithelium.

The gingival and palatal lesions resemble intraoral burns and

are quite painful.

As well as the primary lesions, the recurrent ones are also

highly contagious.

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RHS lesions which have been secondarily infected. Note pus inside of

the vesicles and also areas of ulceration on the vermilion.

Recu rrent Herpetic Infect ion, HS Labialis


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Differential Diagnosis

Erythema Multiformis EM

Recurrent Aphthous Stomatitis, R A U

Herpangina

NUG

HFM

Pemphigus

Pemphigoid


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Herpetic whitlow (HW)


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Another form of herpes simplex infection: a herpetic whitlow

(HW)

Generally acquired as a contagious disease.

HW mostly affects the fingers of dentists and dentalhygienist which had become in contact

Vesicles and bullae were present on the index finger which

accidentally injured herself while working on a patient with

PHG.

Herpetic Whit low (HW)


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2. Varicella-Zoster Virus Infection

Primary, varicella-zoster virus (VZV) infection in

seronegative patient is varicella or chickenpox

Secondary, or reactivated disease is known as herpes

zoster or shingles.

VZV is very similar to HSV: DNA core, protein capsid and

lipid envelop.

The ability of the virus to remain in sensory ganglia forindefinite periods after a primary infection is quite the

same.


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A cutaneous or mucosal vesiculoulcerative eruption

following reactivation of latent virus is also same typical.

Serious complications from chickenpox include bacterialinfections which can involve many sites of the body

including the skin, tissues

2. Varicella-Zoster Virus Infection


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Varicella - Zos ter V

Primary disease ( varicella, chickenpox)

Self-limiting

Common in children, vesicular eruption of trunk and head

and neck occures in crops

Systemic signs symptoms , fever, malaise

Symptomatic treatment

Secondary disease (herpes zoster, shingles)

Self limiting

Adults

Rash, vesicles, ulcers unilateral along dermatome

Post herpetic pain can be severe

Immunocompromised and lymphoma patients, at risk

Treated with acyclovir


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Varicel la (chickenpox)

Chickenpox which involve many sites of the body including the skin,

tissues and mucosa


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Varicella (chic kenpox )

Pathogenesis

Transmission through the inhalation of contaminated

droplets.

Rapidly spread among child to child Incubation in 2 weeks, virus proliferates within

macrophages

Viremia and dissemination to the skin and other organs

Systemic sign and symptom develop Reside in a latent undetectable form in sensory ganglia


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Clinical features

Chills, malaise and headache may accompany rash that

involves primarily the trunk and head and neck

Rashvesicular eruptionpustular and eventuallyulcerates

Crops of new lesion appear owing to repeated waves of

viremia

Self limiting and last several weeks.

Varicella (chickenpox)


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Clinical features

Oral mucous membranes my be involved in primary

disease and usually demonstrate multiple shalow ulcers

that are preceded by vesicles.

Healing on skin with scar formation

Complication including pneumonitis, encephalitis and

inflammation

Varicella (chic kenpox )


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Herpes- Zos ter

Prodromal symptom of pain or paresthesia develop

and persist for several days as the virus infects the

sensory nerve of a dermatome of trunk ,head and neck

A vesicular skin eruption that becomes pustular andeventually ulcerated follows.

Local cutaneous hyperpigmentation may also be noted

on occasion


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Herpes- Zos ter

Herpes zoster of around the neck


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Clinical features

Basically a condition of the older adult population and

of individuals who have compromised immune

responses.

Involvement of the the various branches of the

trigeminal nerve may result in unilateral oral, facial or

ocular lesions

Ramsay Hunt syndrome : facial paralysis, vesicles of

ipsilateral external ear, tinitus, deafness and vertigo.

Herpes- Zos ter


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Clinical features

Prodromal symptoms of pain or paresthesia, a well

delineated unilateral maculopapular rash appears

vesicular- pustular and then ulcerative.

Complication include secondary infection of ulcers

postherpetic neuralgia, motor paralysis and ocular

inflammation.

Herpes- Zos ter


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Herpes- Zos ter

Herpes zoster of the lingual


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Differential diagnosis

Clinically diagnosed by the history of exposure and by

the type and distribution of lesions.

The longer duration, greater intensity of prodromal

symptoms, unilateral distribution with abrupt ending atthe midline and post herpetic neuralgia are favor a

clinical diagnosis of herpes zoster.

Herpetic gingivostomatitis

Necrotizing ulcerative gingivitis

Varicella

Erythema multiforme

Herpes- Zos ter


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Hand -Foot and Mouth Disease


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Clinical features

Affect children and younger than 5 years of age

Incubation: 1-2 weeks

Sign and symptom: mild to moderate in intensity and low

grade fever, malaise, lymhadenopathy and sore mouth

Oral vesicle quickly rupture to become ulcers covered by a

yellow fibrinous membrane surrounded erythematous halo.



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Clinical features

Oral lesion:

o A few (5-20) small vesicles that soon rupture, leaving

slightly painful, shallow ulcers surrounded by a red

halo

o Buccal mucosa, tongue and palate are most

frequently affected.

Skin

o Small vesicles with a narrow red halo lateral and

dorsal surfaces f the fingers and toes , palms

o soles and buttock are the sites of predilection



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Etiology and pathogenesis

Herpangina is an acute viral infection that is caused by

coxsackie type A virus (A1-6, A8, A10, A22)

Transmitted by contaminated saliva and occasionally

through contaminated feces

4. H e r p a n g I n a


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Clinical features

Usually endemic with occurring typically in summer or early

autumn

Complain of malaise, fever, dysphagia and sore throat aftera short incubation period.

Intraorally a vesicular eruption appears on soft palate,

faucal pillars and tonsils, oropharynx and uvula.

Signs and symptoms are mild to moderate and last in a

week.

Herpangina


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PHG

Aphthous ulcers

FAPA syndrome

E M

H F M

Gonococcal oropharyngitis

Streptococcal pharyngitis

Herpangina


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Etiology and Pathogenesis

Is a highly contagious viral infection cause by a member of

the paramyxovirus family

Related structurally and biologically to viruses of the

orthomyxovirus family which cause mumps and influenza.

The virus spread by airborne droplets through the

respiratory tract

5. Measles, Rubeola


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Measles , Rubeola

Kopliks spot : Pathognomonicsmall erythematous macules

with blues white necrotic

centers appear in the buccal

mucosa opposite molar


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Additional virus related to dentistry

Mumps Parotitis (not included in


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Etiology and Pathogenesis

Mumps is an acute, self

limiting infectious disease that

most frequently affect the

parotid gland of children 5-15

years of age.

The causative agent is a

paramyxovirus.

Transmission is by direct

contact with salivary droplets

Mumps, Parotitis (not included in

vesiculous-bulous disease)

Mumps Parot i t is


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Clinical features

Fever malaise, headache and chills and preauricular pain

The parotid swelling tends to be asymmetric at the outset,

reaching maximum proportion within 2-3 days

Stensen s duct may become partially occluded as the

gland swells

Affects males and females equally, especially young adults

and children.

Potentially serious complications is orchitis or oophoritis

can occur in adults.

Mumps , Parot i t is


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Salivary gland involvement

Parotid tenderness with overlying facial edema

Painful swelling of one or both of the parotids that last forabout 7 days

The auricula tend to raised up

Orifice of the Stenson duct is usually red and swollen

Variable swelling and tenderness of submandibular and

sublingual glands


M P ti t i


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Acute suppurative parotitis

Calculi in the parotid ducts

Buccal cellulitis

Sjogren syndrom

Mikulicz syndrome

Sarcoidosis

HIV infection

Neoplasma



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June 2000

Oral Manifestations Of HIV

Infection:Clinical Characteristics,

Diagnosis, And Treatment

Recommendations

Joan A. Phelan, DDS

Di i Of HIV R l d O l


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June 2000

Diagnosis Of HIV Related Oral

Lesions

Oral examination procedures are the samefor HIV patients as for all dental patients

Diagnostic procedures must be appropriate to

the identified problem

Treatment should be based on either aprovisional or definitive diagnosis

Diagnosis should be re-evaluated if treatmentis not effective


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June 2000

Oral Manifestations Of HIV

Infection

Opportunistic diseases--manifestations

of immune deficiency or derangement. Not caused directly by HIV.

The same lesions occur in association

with other immune deficiency disorders.


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June 2000

HIV-related Oral Lesions

Infections Fungal, Viral, Bacterial

NeoplasmsKaposis Sarcoma, Non-Hodgkins Lymphoma

Other

Non-specific or Aphthous-like Ulcers, Lichenoidor Drug Reactions, Salivary Gland Disease


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June 2000

Oral Candidiasis

Pseudomembranous

Erythematous Hyperplastic

Accompanying angular cheilitis


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June 2000

Hyperplastic Candidiasis

Appearance: as a leukoplakia (a whitelesion that does not rub off)

Definitive diagnosis requires:

Identification of fungal hyphae in the lesion

Response of the lesion(s) to antifungaltherapy

If unresponsive to antifungal therapy, biopsymust be considered


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76HIV AIDShyperplastica candidiasis


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June 2000 HIV AIDShyperplastica candidiasis


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June 2000

Angular Cheilitis

Appearance: erythema and/or fissuring at

the corners of the mouth Frequently accompanies intraoral

candidiasis


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June 2000


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June 2000

Kaposis Sarcoma

Is an unusual neoplasm first describe 1872 byMoritz Kaposi.

Early 1980 it has become quite commonbecause of its propensity to develop in

individuals infected by HIV virus causes by herpes virus 8 (associated

herpesvirus)

The lesion arises from endothelial cells

Four clinical presentations are recognized:

1.classic (chronic), 2. endemic (African),

3. iatrogenic 4. AIDS related

Kaposis Sarcoma


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June 2000

Kaposi s Sarcoma

Main clinical features :almost all oral sarcoma presents with similar clinicalsigns and symptoms :

painless or painful, rapidly or slowly growingswelling or mass

the mass may be soft or semi-hard or hard onpalpation with or without ulceration.

the color may be red, blue red, or normal

the tongue, palate, buccal mucosa, gingiva andthe jaws are more frequently affected.

bony swelling, loosening of teeth and paresthesia


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Kaposi sarcomapalatal-bucal


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June 2000

Kaposis Sarcoma

Appearance: Oral lesions appear as reddishpurple, raised or flat

Size ranges from small to extensive

Behavior is unpredictable

Definitive diagnosis: biopsy and histologicexamination

No curative therapy--radiation treatment,

chemotherapy and sclerosing agents havebeen, used to control oral lesions


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June 2000

Kaposis Sarcoma

KS typically evolves through 3 stages.

1. Patch (macular): characterized byproliferation of miniature vessels. Thelesional endothelial cells have a blandappearance and may be associated withscattered lymphocytes and plasma cells

2. Plaque

3. Nodular


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June 2000

Kaposis Sarcoma

KS typically evolves through 3 stages.

2. Plaque : demonstrates further proliferationof vascular channels along with thedevelopment of a significant spindle cellcomponent

3. Nodular : the spindle cells increase to forma nodular tumorlike mass that mayresemble a fibrosarcoma or other spindlecell sarcomas.


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Kaposi sarcomadorsal


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Kaposi sarcomapalatal-bucal

Kaposis Sarcoma


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June 2000

Kaposi s Sarcoma

Differential Diagnosis:

Soft tissue sarcomas

Soft tissue abses

Pyogenic granuloma

Hemangioma

Peripheral giant cell granuloma

Non-Hodgkin lymphoma Salivary gland tumors

Squamous cell carcinoma


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End session

lia session 3 vesiculobulous diseases - viral

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