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Oral pathology 1
DR. Aiman A. Ali

A
28

Hussain AL - hasan

Vesiculo-Bollous
Vesiculo-Bollous Diseases :
Diseases
Viral




Associated with immunologic defects
Hereditary

Viral infections of significance to clinical dentistry:






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.








clinical features:
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
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
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 :

Vesicles are intraepithelial

Some virus-infected epithelial cells are seen

After several days these features
disappear
Differential diagnosis:

Primary HSV infection

Streptococcal pharyngitis

Erythema multiform

ANUG

Secondary HSV infection

Recurrent aphthous stomatitis

Virus culture, monoclonal antibodies or DNA hybridization
Treatment :
Time is very important.
Acyclovir.
•
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
antipyretics].






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.





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.







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).


Histopathology :
* 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.
•

Differential diagnosis:
o
HSV infection.

Treatment :
A -Varicella:
•
Supportive therapy.
•
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.
•
Analgesics.

Corticosteroids are contraindicated.
3- Hand foot & mouth disease:
Pthogenesis:
Coxsackie virus:
•
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


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



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

Coxsackie type A (A1-6, A8, A10, A22, B3 and possibly others)

Transmission through contaminated saliva
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
•
Clinically
•
Short duration
Streptococcal Pharyngitis
•
Vesicular eruption
•
Summer presentation
•
Mild symptoms
Aphthous stomatitis
•
Systemic symptoms






Treatment is usually not required

5-Measles (Rubeola) :

pathogenesis:

Highly contagious.

Measles virus (DNA paramyxovirus).
clinical fetures:

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
mucosa.

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.


Diagnosis:
M. Rubeola But,
Rubella (German

Usually made on:
M.)
• Clinical signs and symptoms.
• Prodromal symptoms.
• Koplik’s spots.
• If necessary, serologic test for antibodies to measles virus.
Treatment:

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
•
•
•
•
•

Rubella (German M.) :
Togavirus Family
Contagious
(mild) Fever, respiratory symptoms and rash
no Koplik's spots
Cause developmental abnormalities in the fetus
‫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
•

Immunofluorescence:
Immunofluorescence
Direct

Target antigen

Indirect

Acantholysis



Direct
Indirect Immunofluorescence:

Appear in 80% of Pemphigus Vulgaris patients.

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:

Skin, vermilion and oral mucosa

Histopathologically: epithelial hyperplasia with intraepithelial abscess formation

Abundant eosinophils
* Treatment:

High dose of corticosteroids.

Immunosuppressant agents to reduce complications of SAIDs as (osteoporosis,
hyperglycemia, hypertension).

When SAIDs are contraindicated Gold
therapy is recommended.

3- Cicatricial Pemphigoid :
* Etiology:

Benign mucous membrane pemphigoid, ocular pemphigus, childhood pemphigoid, and
mucosal pemphigoid

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
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.








* Histopathology:

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
neutrophils.

Blood vessels often are dilated.



* Immunofluorescence:

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:

Pemphigus vulgaris.

Erosive lichen planus.

* Treatment:

Topical corticosteroids (betamethasone dexamethasone…etc).

In severe cases systemic SAIDs with immunosuppressive agents.

4- Bullous pemphigoid
* Etiology:

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.

* Histopathology:

Normal MS: the same of CP

Ultrastructurally: the basement membrane is cleaved at the level of lamina lucida
* Immunopathology:

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.
* Treatment:

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
(Read it from the book)

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Vesiculo

  • 1. Oral pathology 1 DR. Aiman A. Ali A 28 Hussain AL - hasan Vesiculo-Bollous Vesiculo-Bollous Diseases : Diseases Viral    Associated with immunologic defects Hereditary Viral infections of significance to clinical dentistry:      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.        clinical features: 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 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 :  Vesicles are intraepithelial  Some virus-infected epithelial cells are seen  After several days these features disappear Differential diagnosis:  Primary HSV infection  Streptococcal pharyngitis  Erythema multiform  ANUG  Secondary HSV infection  Recurrent aphthous stomatitis  Virus culture, monoclonal antibodies or DNA hybridization Treatment : Time is very important. Acyclovir. • 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 antipyretics].     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.    
  • 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.       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).  Histopathology : * 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. • Differential diagnosis: o HSV infection. Treatment : A -Varicella: • Supportive therapy. • 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. • Analgesics.  Corticosteroids are contraindicated.
  • 4. 3- Hand foot & mouth disease: Pthogenesis: Coxsackie virus: • 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  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   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  Coxsackie type A (A1-6, A8, A10, A22, B3 and possibly others)  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 • Clinically • Short duration Streptococcal Pharyngitis • Vesicular eruption • Summer presentation • Mild symptoms Aphthous stomatitis • Systemic symptoms    Treatment is usually not required 5-Measles (Rubeola) : pathogenesis:  Highly contagious.  Measles virus (DNA paramyxovirus). clinical fetures:  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 mucosa.  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.  
  • 6. Diagnosis: M. Rubeola But, Rubella (German  Usually made on: M.) • Clinical signs and symptoms. • Prodromal symptoms. • Koplik’s spots. • If necessary, serologic test for antibodies to measles virus. Treatment:  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 • • • • • 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 • Immunofluorescence: Immunofluorescence Direct Target antigen Indirect Acantholysis
  • 8.   Direct Indirect Immunofluorescence:  Appear in 80% of Pemphigus Vulgaris patients.  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:  Skin, vermilion and oral mucosa  Histopathologically: epithelial hyperplasia with intraepithelial abscess formation  Abundant eosinophils * Treatment:  High dose of corticosteroids.  Immunosuppressant agents to reduce complications of SAIDs as (osteoporosis, hyperglycemia, hypertension).  When SAIDs are contraindicated Gold therapy is recommended. 3- Cicatricial Pemphigoid : * Etiology:  Benign mucous membrane pemphigoid, ocular pemphigus, childhood pemphigoid, and mucosal pemphigoid  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 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.       * Histopathology:  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.  Blood vessels often are dilated.   * Immunofluorescence:  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:  Pemphigus vulgaris.  Erosive lichen planus. * Treatment:  Topical corticosteroids (betamethasone dexamethasone…etc).  In severe cases systemic SAIDs with immunosuppressive agents. 4- Bullous pemphigoid * Etiology:  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.
  • 10.  Lesions affect the skin. * Histopathology:  Normal MS: the same of CP  Ultrastructurally: the basement membrane is cleaved at the level of lamina lucida * Immunopathology:  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. * Treatment:  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)