Oral Pathology I Third Year

1. Oral pathology 1
DR. Aiman A. Ali
A
28
Hussain AL - hasan
Vesiculo-Bollous
Vesiculo-Bollous Diseases :
Diseases
Viral
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Associated with immunologic defects
Hereditary
Viral infections of significance to clinical dentistry:
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Herpes Simplex Virus (HSV) infection
Varicella-Zoster infections
Hand, Foot, and Mouth Disease
Herpangina
Measles (Rubeola)
1-HSV Infection
pathogenesis:
DNA virus.
Two types HSV1 & HSV2.
Transmitted by physical contact with an infected person.
Virus travels through the trigeminal nerve to the t. ganglion .
Virus becomes latent in the neural tissue.
With reactivation it travels to the epithelial surface.
Reactivation by exposure to sunlight [fever blister] or exposure to cold [cold blister] or other factors.
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clinical features:
A - clinical features - primary:
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Primary herpetic gigivostomatitis
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Usually affects children
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Vesicular eruption may appear on the skin vermilion
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In the oral cavity, lesions may appear on any part of the oral mucosa
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Viremia symptoms: fever, arthralgia, malaise, headache and cervical lymphadenopathy
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After 7 to 10 days the lesions heal without scar
B
- clinical features - secondary:
• Usually on the lip and rarely on gingiva or palate
• Prodromal symptoms
• Within hours multiple fragile vesicles appear
• Lesions ulcerate and coalesce
• Lesions heal without scaring in 1 to 2 weeks
• Rarely become secondarily infected
• Recurrence vary from 1 per year to 1 per month

2. C
- clinical features - whitlow:
 Typically occur in dental practitioners who don’t use gloves and had physical contact
with infected individuals.
 Either primary or secondary HSVI involving the fingers.
 Recurrent lesions if occurred, would be expected on fingers.
 Pain, redness, vesicles that break to become ulcers.
 Duration vary from 4 to 6 weeks.
Histopathology :
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Vesicles are intraepithelial
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Some virus-infected epithelial cells are seen
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After several days these features
disappear
Differential diagnosis:
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Primary HSV infection
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Streptococcal pharyngitis
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Erythema multiform
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ANUG
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Secondary HSV infection
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Recurrent aphthous stomatitis
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Virus culture, monoclonal antibodies or DNA hybridization
Treatment :
Time is very important.
Acyclovir.
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Oint 5% 5t. daily when symptoms first appear.
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Tab 200 to 400 mg 5t daily is effective.
Vidarabine or Idoxuridine are effective on ocular HS but not LHS.
Primary HSV infection is best managed with supportive therapy [fluid, rest, oral lavage and
antipyretics].
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2-Varicella-Zoster Infection:
Etiology & Pathogenesis:
VZV is one of the herpes virus.
Cause primary infection (varicella or chickenpox) and secondary disease (herpes zoster or
shingles).
After primary infection, virus remain latent in a sensory ganglia.
Reactivation of latent VZV usually follows immunosuppressive status, drug administration,
irritation or local trauma.
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3. Clinical features :
A- Clinical features-vericella :
Common among children.
Fever, chills, malaise and headache .
Rash involves the trunk, head & neck including oral mucosa.
It develops into vesicles pustular ulcerations.
Lesions heal after several weeks.
Secondary infection is common.
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B-
Clinical features-herpes zoster :
• Involvement of 5th nerve result in unilateral oral, facial, and ocular lesions
• Prodromal symptoms of pain or paresthesia maculo-papular rash vesiculo-bullae ,
Ulcerations heal after several weeks
• Complications include:
• Secondary infection
• Post-herpetic neuralgia
• Motor paralysis
• Ocular inflammation
* Hunt’s Syndrome:
A special type of herpes zoster infection with involvement of the external ear and oral
mucosa (facial and auditory nerves).
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Histopathology :
* Varicella-Zoster Infection:
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The same as those seen in HSV.
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Virus infected epithelial cells.
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Homogenous nuclei .
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In uncomplicated cases, epithelium regenerates with little or no scar.
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Differential diagnosis:
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HSV infection.
Treatment :
A -Varicella:
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Supportive therapy.
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In immunocompromised patients more substantial measures are indicated.
B - Herpes zoster:
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The same for HSV but in high dose .
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Acyclovir 800 mg x 5 x 7 to 10 days.
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Analgesics.
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Corticosteroids are contraindicated.

4. 3- Hand foot & mouth disease:
Pthogenesis:
Coxsackie virus:
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CV type A
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CV type B
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A16, and occasionally A5, A9, A10, B2 and B5 cause HFM disease
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HFM is a highly contagious infection
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Virus transmission: through airborne spread or oral-fecal contamination
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clinical features:
• Affect children under the age 5 years
• Resolve spontaneously after 1 to 2 weeks
• Signs and symptoms of viremia (low grade)
• Oral lesions: multiple vesicles ulcers covered by yellow membrane surround by erythema
• Occur anywhere of the oral cavity
• Hand and feet lesions are maculopapular with or shortly after the oral lesions vesicles ulcers
Histopathology :
Vesicles are intraepithelial
The vesicle cavity filled with proteinaceous debris and inflammatory cells
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Diffretial Diagnosis :
1- Primary HSV infection and varicella:
• Milder symptoms
• Cutaneous distribution
• Virus culture or detection of antibodies
2- Aphthous stomatitis.
Treatment :
Symptomatic therapy
4- Herpangina:
Etiology & Pathogenesis
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Coxsackie type A (A1-6, A8, A10, A22, B3 and possibly others)
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Transmission through contaminated saliva

5. clinical features:
* Common in summer and in children
* Pain, malaise, fever, dysphasia and sore throat
* Oral vesicular eruption on the soft palate, faucial pillars and tonsils
* Pharyngitis
* Lesions last less than 1 week
Differential diagnosis:
HSV infection, HFM and varicella
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Clinically
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Short duration
Streptococcal Pharyngitis
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Vesicular eruption
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Summer presentation
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Mild symptoms
Aphthous stomatitis
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Systemic symptoms
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Treatment is usually not required
5-Measles (Rubeola) :
pathogenesis:
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Highly contagious.
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Measles virus (DNA paramyxovirus).
clinical fetures:
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Commonly affect children in winter and spring
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incubation period of 7 to 10 days
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Fever, malaise, conjunctivitis and cough
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After 2 days small macules with white necrotic center (Koplik’s spots) appear in the buccal
mucosa.
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After 2 days skin rash appear initially on the head and neck followed by the trunk and then
the extremities.
histopathology:
Warthin-Frankeldey giant cells are seen in lymphoid tissue.
Infected epithelial cells which become necrotic.
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6. Diagnosis:
M. Rubeola But,
Rubella (German
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Usually made on:
M.)
• Clinical signs and symptoms.
• Prodromal symptoms.
• Koplik’s spots.
• If necessary, serologic test for antibodies to measles virus.
Treatment:
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Supportive treatment:
• Bed rest
• Fluids
• Adequate diet
• Analgesics
Differential diagnosis between :
M. Rubeola :
• Paramyxovirus Family
• Contagious
• (sever) Fever respiratory symptoms and rash
• Koplik's spots
• Does not cause develop-mental abnormalities in the fetus
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Rubella (German M.) :
Togavirus Family
Contagious
(mild) Fever, respiratory symptoms and rash
no Koplik's spots
Cause developmental abnormalities in the fetus

7. ‫محاضرة جديدة‬
Vesiculo-Bollous Diseases Associated with immunologic defects:
1. Pemphigus Vulgaris
2- Pemphigus vegetans
3. Cicatricial pemphigoid
4. Bullous pemphigoid
5. Dermatitis herpetiformis
6. Linear IgA Disease
Pemphigus antibody
+
Activate epithelial intracellular
protolytic enzyme
Desmosome-tonofilament complex
1- Pemphigus Vulgaris
Etiology
 Reactive IgG against epithelial desmosome-tonofilament complexes
 Loss of cell-to-cell adherence (acantholysis)
* Clinically:
 Mucocutaneuos disease.
 Skin lesions appear after OL in a period of 1
year.
 Ulcers preceded by bullae.
 60% of cases the first appearance in the oral cavity.
 More common in the 4th and 5th decade.
 Nikolsky sign is positive.
* Histopathologically:
 Acantholysis
 Tzanck cells [free-floating rounded or spherical SSC]
 Basal layer remains attached to the basement membrane
 Bulla or vesicle are filled with fluid, Tzanck cells and neutrophils
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Immunofluorescence:
Immunofluorescence
Direct
Target antigen
Indirect
Acantholysis

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Direct
Indirect Immunofluorescence:
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Appear in 80% of Pemphigus Vulgaris patients.
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To assess the severity of the lesion.
* Differential diagnosis:
 Pemphigoid (bullous or cicatricial)
 Erythema multiform
 Bullous lichen planus
 Dermatitis herpetiformis
 Paraneoplastic pemphigus syndrome
 In small lesions, aphthous stomatitis
2- Pemphigus vegetans:
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Skin, vermilion and oral mucosa
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Histopathologically: epithelial hyperplasia with intraepithelial abscess formation
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Abundant eosinophils
* Treatment:
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High dose of corticosteroids.
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Immunosuppressant agents to reduce complications of SAIDs as (osteoporosis,
hyperglycemia, hypertension).
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When SAIDs are contraindicated Gold
therapy is recommended.
3- Cicatricial Pemphigoid :
* Etiology:
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Benign mucous membrane pemphigoid, ocular pemphigus, childhood pemphigoid, and
mucosal pemphigoid
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Idiopathic autoimmune disease
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Deposit of IG and complement components along the basement zone
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Usually no circulating antibodies
* Clinical features:
More common among adult women.
Chronic lesions appear as vesiculo-bullous eruptions involve oral mucosa, which heal with
scaring.
When affects gingiva exclusively is referred to as gingivosis or desquamative gingivitis.
Other sites: conjunctiva, larynx, genitalia, and esophagus.
Skin lesions are uncommon.
Nikolsky’s sign is positive.
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* Histopathology:
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Sub-basal clefting with clear cut separation at the basement membrane.

9. No evidence of acantholysis.
Variable infiltration with lymphocytes, plasma cells and occasionally eosino- and
neutrophils.
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Blood vessels often are dilated.
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* Immunofluorescence:
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Direct IF of intact oral mucosa demonstrate linear pattern of IgG fluorescence.
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Occasionally IgA may detected.
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Complement components are commonly found.
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Indirect IF studies are usually negative.
* Differential diagnosis:
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Pemphigus vulgaris.
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Erosive lichen planus.
* Treatment:
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Topical corticosteroids (betamethasone dexamethasone…etc).
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In severe cases systemic SAIDs with immunosuppressive agents.
4- Bullous pemphigoid
* Etiology:
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Similar to cicatricial pemphigoid.
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There are circulating autoantibodies to basement membrane zone antigen.
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Degeneration of basement membrane attachment complexes.
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Separation occur at the lamina lucida plane.
* Clinical features:
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Very common in the 7th and 8th decades.

10. 
Lesions affect the skin.
* Histopathology:
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Normal MS: the same of CP
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Ultrastructurally: the basement membrane is cleaved at the level of lamina lucida
* Immunopathology:
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There is a detectable level of circulating antibodies in 70% of cases.
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However, no correlation with the level of clinical disease.
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IF findings corresponding to those in CP.
* Treatment:
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Systemic corticosteroids.
5- Dermatitis herpetiformis
* Etiology:
 Unknown cause.
 Deposits of IgA in the skin and mucosa.
 No circulating autoantibodies in the patient’s serum .
*Clinical features:
 Chronic disease typically seen in young adults.
 Cutaneous disease, rarely appear in the oral cavity.
 Symmetrical aggregated vesicular lesions of the skin with face and scalp involvement.
 Periods of exacerbation and remission.
 Iodide component exacerbate some cases.
 Orally lesions appear as superficial ulcers with fibrinous base preceded by vesicles.
* Histopathology:
 Accumulation of neutrophils and eosinophils producing dermal micro- abscess
 Connective tissue become necrotic and the overlying epithelium separate
 Formation of subepithelial vesicle
* Immunopathology:
 Immunofluorescent staining is positive at the epidermal-dermal junction.
 Almost IgA alone or in combination with IgG or IgM.
* Treatment:
 It dose not respond to SAIDs.
 Sulfapyridine is the treatment of choice.
6 -Linear IgA Disease
(Read it from the book)
Hereditary:
Epidermolysis Bullosa

11. (Read it from the book)