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Learning objectives
At the end of the session student have to be able to explain the various virus infections of oral and perioral diseases

Diagram of the oral tissues, illustrating the component tissues and their relative positions.

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 diseases

Times 10 mnt.

Viral infection of the oral diseases

1 2 3

Example 1
Hard tissue Oral tissue

Jaws
Oral Mucosa Lips Gingival Palate mucosa Tongue Pharynx Floor of the mouth
Dental pulpitis Periapical abssess Acute osteomyelits Chronic osteomyelitis Osteitis

Infection
Soft tissue Mucosal surface lesion
Vesiculobulous diseases Ulcerative condition White lesions Red blue lesions Pigmented lesions Verrucal papillary lesion

Sub mucous swelling

Gingival Floor of mouth Lips & buccal mucous Tongue Palate Neck

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
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Example 2

odontogenic

Teeth component Pulpitis Pericoronitis Periapical absess Periostitis Subperiosteal absess Sub mucous abscess Cellulitis Phlegmoon Subcutan absess

Infection Non odontogenic

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
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Example 3

Vesiculo-bulous diseases

Viral diseases Herpes simplex infection Varicella infection Hand foot mouth disease Herpangina Measles Condition related with immunology defect. Pemphigus vulgaris Mucous membrane pemphigoid Bullous pemphigoid Dermatitis herpetiform Linear Ig A disease 10

Heriditary diseases Epidermolysis bullosa

Vesiculo-bulous diseases

Viral diseases
Herpes simplex infection Varicella infection Hand foot mouth disease Herpangina Measles

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Virus group

DNA virus
1 Poxvirus Small pox Molluscum contagi Vaccina Herpes simplex Herpes zoster/ varicella Cytomegallo Pharyngoconj.tiva Epidemic keratocon junctivitis

RNA virus
1 Myxovirus Influensa

Herpes Virus

Paramyxo virus

Rabies

Adeno virus

3 Rhabdovirus

Rabies Encephalitis Yellow fever ISPA HFM

4 Papo virus
5 Parvo virus

4 Arbovirus
5 Rheovirus 6 Picornavirus

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 virusspecific transcripts by host ribosomes.

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Pathogenesis of herpes simplex infections

HOSPES
Seronegative

Primary infection: direct contact with HSV

Virus

Primary disease
Primary Herpetic Gingivostomatitis PHG Herpetic Withlow

Subclinical infection

Secondary disease
Secondary or Recurrent Herpes Simplex Infections Herpes Labialis, Herpetic Withlow (lips, palate, gingiva, hand finger)

Reactivation
Sunlight, fever, mechanical trauma, allergy, worry

resolution

HOST CARRIER
Seropositive
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Vesiculo-bulous diseases
Group viral infections 1. Herpes simplex virus infection, HSV o Is a vesicular eruption of the skin and mucosa

o Pathogenesis : (previous slide)

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 Gingivostomatitis, PHG

The classical clinical presentation of PHG with markedly swollen interdental papillae and bleeding areas.

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A. Acute Primary Herpetic Gingivostomatitis, PHG Prodromal period :

One single virus can not produce disease To achieve a substantial number of viruses intracellular replication take place One week, during which the patient does not present any symptom.

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A. Acute Primary Herpetic Gingivostomatitis, PHG 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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A. Acute Primary Herpetic Gingivostomatitis, PHG 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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A. Acute Primary Herpetic Gingivostomatitis, PHG The ulcers are seen in any of the oral mucosas and the oropharynx. 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.
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A. Acute Primary Herpetic Gingivostomatitis, PHG

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A. Acute Primary Herpetic Gingivostomatitis, PHG 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 with advanced 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. Acute Primary Herpetic Gingivostomatitis, PHG

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 Recurrent Herpes Simplex Infection, Herpes Simplex Labialis, HSL

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B. Secondary Or Recurrent Herpes Simplex Infection, Herpes Simplex Labialis, HSL 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 the peripheral 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 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 the junction 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- rences may vary from 1 to several a year.

Secondary lesions also heal without scar formation.

The oral recurrent lesions generally occur in the lip's vermilion, but lesions may also develop in the attached gingiva and/or hard palate.
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B. Secondary Or Recurrent Herpes Simplex Infection, Herpes Simplex 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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Recurrent Herpetic Infection, HS Labialis

RHS lesions which have been secondarily infected. Note pus inside of the vesicles and also areas of ulceration on the vermilion.
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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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Herpetic Whitlow (HW) Another form of herpes simplex infection: a herpetic whitlow (HW) Generally acquired as a contagious disease. HW mostly affects the fingers of dentists and dental hygienist 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.

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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 for indefinite periods after a primary infection is quite the same.
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2. Varicella-Zoster Virus Infection

A cutaneous or mucosal vesiculoulcerative eruption following reactivation of latent virus is also same typical. Serious complications from chickenpox include bacterial infections which can involve many sites of the body including the skin, tissues

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Varicella - Zoster 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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Varicella (chickenpox)

Chickenpox which involve many sites of the body including the skin, tissues and mucosa
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Varicella (chickenpox)
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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Varicella (chickenpox)
Clinical features Chills, malaise and headache may accompany rash that involves primarily the trunk and head and neck Rash vesicular eruption pustular and eventually ulcerates

Crops of new lesion appear owing to repeated waves of viremia

Self limiting and last several weeks.

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Varicella (chickenpox)
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

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Herpes- Zoster
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 and eventually ulcerated follows. Local cutaneous hyperpigmentation may also be noted on occasion

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Herpes- Zoster

Herpes zoster of around the neck

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Herpes- Zoster
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.
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Herpes- Zoster
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.

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Herpes- Zoster

Herpes zoster of the lingual

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Herpes- Zoster
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 at the midline and post herpetic neuralgia are favor a clinical diagnosis of herpes zoster. Herpetic gingivostomatitis Necrotizing ulcerative gingivitis Varicella Erythema multiforme
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3. Hand-Foot and Mouth Disease

Etiology and pathogenesis

HFM is an acute endemic viral infection

One of the subdivisions of the family of viruses known as picornavirus is Coxackie group virus cause oral vesicular eruptions: HFM disease and Herpangina HFM is highly contagious caused by Coxackie type A5, A10, A16. Transmission through airborne spread or fecal-oral contamination Virus exhibits a predilection for mucous membranes of the mouth and cutaneous regions of hands and feet. 52

Hand-Foot and Mouth Disease

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Hand-Foot and Mouth Disease

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Hand-Foot and Mouth Disease 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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Hand-Foot and Mouth Disease

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
Skin

Buccal mucosa, tongue and palate are most frequently affected. Small vesicles with a narrow red halo lateral and dorsal surfaces f the fingers and toes , palms
soles and buttock are the sites of predilection
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o
o

Hand-Foot and Mouth Disease

Differential diagnosis Aphthous ulcers Herpetiform ulcers Primary herpetic gingivostomatitis Secondary herpes Herpangina

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

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Herpangina palatum molle

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Herpangina
Clinical features

Usually endemic with occurring typically in summer or early autumn

Complain of malaise, fever, dysphagia and sore throat after a 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.
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Herpangina
Differential diagnosis PHG Aphthous ulcers FAPA syndrome EM HFM

Gonococcal oropharyngitis
Streptococcal pharyngitis
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5. Measles, Rubeola
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

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Measles, Rubeola

Kopliks spot : Pathognomonic small erythematous macules with blues white necrotic centers appear in the buccal mucosa opposite molar
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Measles, Rubeola
Clinical features Is predominantly a disease of children, fever, malaise, conjunctivitis, photophobia and cough develop

Pathognomonic small erythematous macules with white necrotic centers appear in the buccal mucosa the Kopliks spot Complication is encephalitis and thromocytopenic pupura. pneumonia.
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Additional virus related to dentistry

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Mumps, Parotitis (not included in vesiculous-bulous disease)

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
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Mumps, Parotitis
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.
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Mumps, Parotitis
Salivary gland involvement Parotid tenderness with overlying facial edema Painful swelling of one or both of the parotids that last for about 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

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Mumps, Parotitis
Differential diagnosis

Acute suppurative parotitis

Calculi in the parotid ducts Buccal cellulitis Sjogren syndrom Mikulicz syndrome

Sarcoidosis
HIV infection Neoplasma
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Oral Manifestations Of HIV Infection: Clinical Characteristics, Diagnosis, And Treatment Recommendations
Joan A. Phelan, DDS

June 2000

Diagnosis Of HIV Related Oral Lesions

Oral examination procedures are the same for HIV patients as for all dental patients Diagnostic procedures must be appropriate to the identified problem Treatment should be based on either a provisional or definitive diagnosis Diagnosis should be re-evaluated if treatment is not effective

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.

June 2000

HIV-related Oral Lesions

Infections Fungal, Viral, Bacterial

Neoplasms Kaposis Sarcoma, Non-Hodgkins Lymphoma Other Non-specific or Aphthous-like Ulcers, Lichenoid or Drug Reactions, Salivary Gland Disease

June 2000

Oral Candidiasis
Pseudomembranous Erythematous Hyperplastic Accompanying angular cheilitis

June 2000

Hyperplastic Candidiasis
Appearance: as a leukoplakia (a white lesion that does not rub off) Definitive diagnosis requires:

Identification of fungal hyphae in the lesion Response of the lesion(s) to antifungal therapy If unresponsive to antifungal therapy, biopsy must be considered

June 2000

HIV AIDS hyperplastica candidiasis

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June 2000

HIV AIDS hyperplastica candidiasis

Angular Cheilitis

Appearance: erythema and/or fissuring at the corners of the mouth

Frequently accompanies intraoral candidiasis

June 2000

June 2000

Kaposis Sarcoma

Is an unusual neoplasm first describe 1872 by Moritz Kaposi. Early 1980 it has become quite common because 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

June 2000

Kaposis Sarcoma

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

painless or painful, rapidly or slowly growing swelling or mass the mass may be soft or semi-hard or hard on palpation with or without ulceration.

the color may be red, blue red, or normal

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

June 2000

bony swelling, loosening of teeth and paresthesia

Kaposi sarcoma palatal-bucal

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Kaposis Sarcoma

Appearance: Oral lesions appear as reddish purple, raised or flat Size ranges from small to extensive Behavior is unpredictable Definitive diagnosis: biopsy and histologic examination No curative therapy--radiation treatment, chemotherapy and sclerosing agents have been, used to control oral lesions

June 2000

Kaposis Sarcoma

KS typically evolves through 3 stages. 1. Patch (macular): characterized by proliferation of miniature vessels. The lesional endothelial cells have a bland appearance and may be associated with scattered lymphocytes and plasma cells

2. Plaque 3. Nodular
June 2000

Kaposis Sarcoma

KS typically evolves through 3 stages. 2. Plaque : demonstrates further proliferation of vascular channels along with the development of a significant spindle cell component 3. Nodular : the spindle cells increase to form a nodular tumorlike mass that may resemble a fibrosarcoma or other spindle cell sarcomas.

June 2000

Kaposi sarcoma dorsal

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Kaposi sarcoma palatal-bucal

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Kaposis 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

June 2000

End session

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