Oral pathology 1
DR. Aiman A. Ali
Hussain AL - hasan
Vesiculo-Bollous Diseases :
Associated with immunologic defects
Viral infections of significance to clinical dentistry:
Herpes Simplex Virus (HSV) infection
Hand, Foot, and Mouth Disease
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.
A - clinical features - primary:
Primary herpetic gigivostomatitis
Usually affects children
Vesicular eruption may appear on the skin vermilion
In the oral cavity, lesions may appear on any part of the oral mucosa
Viremia symptoms: fever, arthralgia, malaise, headache and cervical lymphadenopathy
After 7 to 10 days the lesions heal without scar
- 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
- 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.
Vesicles are intraepithelial
Some virus-infected epithelial cells are seen
After several days these features
Primary HSV infection
Secondary HSV infection
Recurrent aphthous stomatitis
Virus culture, monoclonal antibodies or DNA hybridization
Time is very important.
Oint 5% 5t. daily when symptoms first appear.
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
Etiology & Pathogenesis:
VZV is one of the herpes virus.
Cause primary infection (varicella or chickenpox) and secondary disease (herpes zoster or
After primary infection, virus remain latent in a sensory ganglia.
Reactivation of latent VZV usually follows immunosuppressive status, drug administration,
irritation or local trauma.
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.
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).
* Varicella-Zoster Infection:
The same as those seen in HSV.
Virus infected epithelial cells.
Homogenous nuclei .
In uncomplicated cases, epithelium regenerates with little or no scar.
In immunocompromised patients more substantial measures are indicated.
B - Herpes zoster:
The same for HSV but in high dose .
Acyclovir 800 mg x 5 x 7 to 10 days.
Corticosteroids are contraindicated.
3- Hand foot & mouth disease:
CV type A
CV type B
A16, and occasionally A5, A9, A10, B2 and B5 cause HFM disease
HFM is a highly contagious infection
Virus transmission: through airborne spread or oral-fecal contamination
• 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
Vesicles are intraepithelial
The vesicle cavity filled with proteinaceous debris and inflammatory cells
Diffretial Diagnosis :
1- Primary HSV infection and varicella:
• Milder symptoms
• Cutaneous distribution
• Virus culture or detection of antibodies
2- Aphthous stomatitis.
Etiology & Pathogenesis
Coxsackie type A (A1-6, A8, A10, A22, B3 and possibly others)
Transmission through contaminated saliva
* Common in summer and in children
* Pain, malaise, fever, dysphasia and sore throat
* Oral vesicular eruption on the soft palate, faucial pillars and tonsils
* Lesions last less than 1 week
HSV infection, HFM and varicella
Treatment is usually not required
5-Measles (Rubeola) :
Measles virus (DNA paramyxovirus).
Commonly affect children in winter and spring
incubation period of 7 to 10 days
Fever, malaise, conjunctivitis and cough
After 2 days small macules with white necrotic center (Koplik’s spots) appear in the buccal
After 2 days skin rash appear initially on the head and neck followed by the trunk and then
Warthin-Frankeldey giant cells are seen in lymphoid tissue.
Infected epithelial cells which become necrotic.
M. Rubeola But,
Usually made on:
• Clinical signs and symptoms.
• Prodromal symptoms.
• Koplik’s spots.
• If necessary, serologic test for antibodies to measles virus.
• Bed rest
• Adequate diet
Differential diagnosis between :
M. Rubeola :
• Paramyxovirus Family
• (sever) Fever respiratory symptoms and rash
• Koplik's spots
• Does not cause develop-mental abnormalities in the fetus
Rubella (German M.) :
(mild) Fever, respiratory symptoms and rash
no Koplik's spots
Cause developmental abnormalities in the fetus
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
Activate epithelial intracellular
1- Pemphigus Vulgaris
Reactive IgG against epithelial desmosome-tonofilament complexes
Loss of cell-to-cell adherence (acantholysis)
Skin lesions appear after OL in a period of 1
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.
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
Appear in 80% of Pemphigus Vulgaris patients.
To assess the severity of the lesion.
* Differential diagnosis:
Pemphigoid (bullous or cicatricial)
Bullous lichen planus
Paraneoplastic pemphigus syndrome
In small lesions, aphthous stomatitis
2- Pemphigus vegetans:
Skin, vermilion and oral mucosa
Histopathologically: epithelial hyperplasia with intraepithelial abscess formation
High dose of corticosteroids.
Immunosuppressant agents to reduce complications of SAIDs as (osteoporosis,
When SAIDs are contraindicated Gold
therapy is recommended.
3- Cicatricial Pemphigoid :
Benign mucous membrane pemphigoid, ocular pemphigus, childhood pemphigoid, and
Idiopathic autoimmune disease
Deposit of IG and complement components along the basement zone
Usually no circulating antibodies
* Clinical features:
More common among adult women.
Chronic lesions appear as vesiculo-bullous eruptions involve oral mucosa, which heal with
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.
Sub-basal clefting with clear cut separation at the basement membrane.
No evidence of acantholysis.
Variable infiltration with lymphocytes, plasma cells and occasionally eosino- and
Blood vessels often are dilated.
Direct IF of intact oral mucosa demonstrate linear pattern of IgG fluorescence.
Occasionally IgA may detected.
Complement components are commonly found.
Indirect IF studies are usually negative.
* Differential diagnosis:
Erosive lichen planus.
Topical corticosteroids (betamethasone dexamethasone…etc).
In severe cases systemic SAIDs with immunosuppressive agents.
4- Bullous pemphigoid
Similar to cicatricial pemphigoid.
There are circulating autoantibodies to basement membrane zone antigen.
Degeneration of basement membrane attachment complexes.
Separation occur at the lamina lucida plane.
* Clinical features:
Very common in the 7th and 8th decades.
Lesions affect the skin.
Normal MS: the same of CP
Ultrastructurally: the basement membrane is cleaved at the level of lamina lucida
There is a detectable level of circulating antibodies in 70% of cases.
However, no correlation with the level of clinical disease.
IF findings corresponding to those in CP.
5- Dermatitis herpetiformis
Deposits of IgA in the skin and mucosa.
No circulating autoantibodies in the patient’s serum .
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.
Accumulation of neutrophils and eosinophils producing dermal micro- abscess
Connective tissue become necrotic and the overlying epithelium separate
Formation of subepithelial vesicle
Immunofluorescent staining is positive at the epidermal-dermal junction.
Almost IgA alone or in combination with IgG or IgM.
It dose not respond to SAIDs.
Sulfapyridine is the treatment of choice.
6 -Linear IgA Disease
(Read it from the book)