2- Oral Ulceration and Vesiculobollous Diseases

7/28/2019 2- Oral Ulceration and Vesiculobollous Diseases

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Oral Ulceration &

Vesiculobullous diseasesLAB 2

Dr. Tahani Abualteen


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Definition:

Ulcer = localized defect in the surface epitheliumexposingthe underlying connective tissue base leading to inflammation

Most common lesion of the oral mucosa

May be a manifestation of many disease entities (local andgeneral disorders)

Erosion = superficial ulcer (partial loss of epithelial thickness

not exposing the connective tissue base)


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Causes of oral ulceration:

Infective (viral, bacterial, fungal)

Traumatic (mechanical, chemical, thermal, factitious injury, radiation,

eosinophilic ulcer "traumatic granuloma")

Idiopathic (recurrent aphthous stomatitis "major, minor, herpetiform")

Neoplastic (SCC, other malignant neoplasms)

Associated with systemic diseases (GIT diseases, hematological

diseases, Behcets disease, HIV infection)

Associated with dermatologic diseases (lichen planus, chronic discoid

lupus erythematosus, vesiculobullous diseases)

** All these should be kept in mind as differential diagnoses for ulcers


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Traumatic Ulceration


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Mechanical Ulceration

Three criteria for diagnosis1. Define a cause

2. Fit size, shape and location of ulcer

3. Healing within 10 days of cause removal

Chronic ulcers: Deep crater like ulcer with rolled everted margins and Induration

Differentiation of chronic traumatic ulcers from a neoplasticulcer may be difficult

When is biopsy indicated?! If we remove the cause and the presumed chronic

traumatic ulcer does NOT show signs of healing within aperiod of 10-14 days


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Chronic Traumatic Ulcer


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Highly concentrated or caustic materials used in dental practice(e.g. hydrogen peroxide) that may be accidentally applied to oral

mucosa orpreparations used by patients in self-treatment of oral

complaints (e.g. local use of aspirin to relieve toothache, inadequately

diluted mouth washes)

Reaction varies in severity (edema to necrosis), so the concentration

and duration of the irritant is important

Recall:

oLow-grade chronic irritationhyperplasia or hyperkeratosis

oHigh-grade or severe acute traumaulceration or necrosis

Chemical Ulceration


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Caustic action of aspirin is doseand time related

Reactions vary in severity from

edema of epithelium

(resembling Leukoedema) to

necrosis of epithelium

(presenting as white patches

which slough off leaving areas

of ulceration)

Painful

Patients history and location of the lesion are important for

clinical diagnosis

Aspirin Burn


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Formocresol Burn


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Hydrogen peroxide burn


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Anesthetic necrosis

NOT clearly understood!

May be due to tissues being stretched or damaged by giving too much

solution

Or due adrenaline which is a vasoconstrictor in anesthetic solutions


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Factitious ulcers

Self-inflicted ulcers (induced on purpose!)

May be a manifestation of stress, anxiety, or more severe emotionaldisturbance


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Factitious ulceration and keratosis


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Factitious ulcers


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In patients undergoing radiotherapy for head and neck cancer, the oral

mucosa may suffer from:Damage to the epithelium (resulting in Erythema, radiation mucositis,

and ulceration)

Damage to blood vessels (resulting in epithelial atrophy)

Damage to lymphatics (resulting in edema)

Thin atrophic epithelium is prone to traumatic ulcers

Differentiation of radiation ulcers form neoplastic ulcers may be

difficult but radiation ulcers (mucositis) are generally painful while

pain is not a common feature of early malignant disease

Radiation Ulcers


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Radiation mucositis

SCC


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????


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The patient stated

that he had a verysevere severing injury

to the site of the

lesion 3 days earlier

Upon microscopy, the

lesion is found to be

infiltrated withEosinophils and

histiocytes


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Etiology: chronic trauma and crush injury to skeletal muscles

Occurs most commonly in the tongue

Clinical appearance: chronic, well-demarcated ulcer which may

mimic Sequamous cells carcinomaulcer (indurated and fixed due to

histiocytes infiltration)

Histopathological features

Dense chronic inflammatory cell infiltrate in the base of the ulcer

involving underlying damaged muscle

Deeper parts of the lesion are characterized by an infiltrate rich in

histiocytes & Eosinophils

True granulomas aren't present and the condition has no relation to

eosinophilic granuloma of bone

Treatment: remove the cause and follow-up to see signs of healing

Eosinophilic Ulcer


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Healing uponFollow Up


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????


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????


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Diagnosis??

Clinical Diagnosis:

Recurrent aphthous stomatitis,exacerbated by orthodontic appliances


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Accounts for80% of RAS

1-5ulcers (that are shallow,

round or oval, with grey/yellow

base and an erythematous

margin)

Affect non keratinized mucosa

Less than 10 mm in diameter

Heal without scarring within

10 daysRecur in 1-4 month intervals

Minor RAS


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1-10 ulcers

Affect any area in the mouth

(keratinized & non-keratinized

mucosa)

** Common sites: lips, soft palate,tonsils, oropharynx

Greater than 10 mm in diameter

Heal with scarring within 4-6

weeks

Major RAS


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Major RAS-scarring

H if RAS


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The least common

Affects older age group

Hundreds of small pin point ulcersresembling herpetic ulcers

Affect any area in the mouth

(keratinized & non-keratinized mucosa)

1-2 mm in diameter

When several ulcers are clusteredtogether, coalescence can result in larger

areas of ulceration of irregular outline

Heal in 2-3 weeks (large coalesced ulcers

may take longer time to heal and may heal

with scarring)Recur in less than 1 month (in severe

cases, ulceration of the oral cavity is

continuous and may be associated with

severe discomfort and with difficulty in

eating & speaking)

Herpetiform RAS


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Etiology of RAS:

Most likely immune mediated (there is increasing

evidence that damaging immune responses are involved)

A number ofCo factors (local and general factors)

may play a contributory role in a proportion of cases


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In the pre-ulcerative stage, there is infiltration of the laminapropria by lymphocytes

Small number of lymphocytes also infiltrate the epithelium

As the ulcerative stage approaches, there's increased infiltration

of the tissuesby lymphocytes (especially the epithelium)associated with damage to epithelial cells leading eventually to

theirdeath and the formation of an ulcer

In the healing phase, the number of lymphocytes decreases

Histopathological features

Hi t th l i l fi di


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epithelium

Loss of surface epithelium

Inflammatory infiltrate

Histopathological finding


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Recurrent Aphthous Stomatitis

Treatment

Steroids

Topical*

Systemic Intralesional


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Triamcinolone acetonide 0.1% aqueous

suspension, mouthrinse and expectorate QID,

No food or drink until hour after use

Clobetasol 0.05% ointment, apply thin film tooral ulcers QID, No food or drink until hour

after use

Use only Biotene toothpaste

SLS (Sodium Lauryl Sulphate) can induce

aphthous ulcers

Advised to contact you in 2 weeks to report on

condition

Recurrent Aphthous Stomatitis

Management


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What is your differential diagnosis?!?!

Chronic

ulcer with

rolledeverted

margins and

Induration

on

palpation?!?


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Differential Diagnosis of Chronic Oral

Ulcerative Lesions

Sequamous cell carcinoma Deep fungal infection

Histoplasmosis, cryptococcosis, mucormycosis

Chronic viral infection Herpes simplex, cytomegalovirus

Oral tuberculosis

Trauma

Eosinophilic ulcer, factitious ulcer

Syphilis

Major aphthous


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Diseases that result in collection of clear fluid (blisters)

within or below the epithelium

Blisters are classified into (vesicles and bullae)

Vesicles:

Fluid filled lesion

Smaller in size

Mostly arise intra-epithelially

Bullae:

Fluid filled lesionLarger in size

Mostly arise sup- epithelially

Vesiculobullous diseases are present as oral ulceration

following rupture of the vesicles & bullae

Vesiculobullous diseases


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Classification of vesiculobullous diseases

Vesiculobullous diseases are classified into 2 major groups depending on the

histological location of the lesions:

Intraepithelial vesiculobullous diseases (lesions form within the epithelium)

Pemphigus Vulgaris (Acantholytic)

Herpes Simplex infection (Non-acantholytic)

Subepithelial vesiculobullous diseases(lesions form between the epithelium

& lamina propria)

Pemphigoid

Erythema multiforme

Dermatitis herpetiformisLinear IgA disease

Epidermolysis bullosa

Angina bullosa hemorrhagica (oral blood blisters)

Bullous lichen planus


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oTarget "iris"


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oTarget "iris"

lesions consist of

concentric rings of

varying Erythema,in the center of

which may be an

intact or rupturedand crusted bulla

oCharacteristic

diagnostic Feature

oHands & Feet


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Erythematous patches are

quickly followed by

vesiculobullous eruptions

which rapidly breakdown

into erosions as the bullae

disintegrate

Erosions on the lips areassociated with bleeding and

crusting

Circumoral crustinghemorrhagic lesions are an

important sign to reach clinical

diagnosis


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Erythema Multiforme Wide range of clinical presentation

Maculopapular, vesiculobullous, target Iris

lesions

Orally: lips and anterior parts

Target


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Erythema Multiforme Sudden onset

Skin and mucous membranes

Pathogenesis is not clear

Hypersensitivity rxn, type 3 hypersensitivity

And consequenses

Ag - Ab complexes have been detected in EM and HSV infn

Precipitating factors include Drugs: sulphonamides, penicillin

Viral infections: herpes simplex infection (Recurrent Erythemamultiforme is associated in particular with recurrent attacks ofherpes simplex virus infection)

Spontaneously


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Erythema Multiforme

Microscopic features: not diagnostic

Diagnosis is primarily clinical

No autoantibodies, so negative direct & indirect

immunoflourescence Treatment and prognosis

Remove causative drugs, if any

Topical and systemic corticosteroids

May be recurrent

May benefit from prophylactic acyclovir


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54 years old man

Chronic gingivitis, 18

months duration


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Clinical diagnosis for the gingival condition?!

Desquamative gingivitis

Wh diff i l


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What are your differential

diagnoses?

1- Mucous membrane Pemphigoid

2- Pemphigus Vulgaris3- Erosive lichen planus

4- Allergic reaction

5- Drug Induced

Gentle lateral pressure by blunt instrument


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Gentle lateral pressure by blunt instrument

Nikolsky's signinduced bullous formation/


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Immunoflourescence


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Immunoflourescence

was done .

IgG deposition and C3

Epithelium

Di i ??


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Diagnosis??

Mucous membrane

Pemphigoid


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Pemphigoid

2 clinical groups:

Mucous membrane Pemphigoid

Mainly mucosal

Bullous Pemphigoid

Mainly skin

MUCOUS MEMBRANE (CICATRICIAL)


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MUCOUS MEMBRANE (CICATRICIAL)

PEMPHIGOID

Etiology: antibodies against BP Ag2

Women>men

Tense bullae

Oral Lesions of Mucous Membrane


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Oral Lesions of Mucous Membrane

Pemphigoid

Heal with scarring (cicatritial)

90% involve gingiva,

Chronic desquamative gingivitis may bethe only oral manifestation

Nikolsky's sign


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MMP


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MMP


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MMP


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MUCOUS MEMBRANE PEMPHIGOID:


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MUCOUS MEMBRANE PEMPHIGOID:

MICROSCOPIC

Subepithelialvesicle

No subepithelial inflammation first

Later, inflammation and perivascular infiltrate

Eosinophils are involved

Release of proteases


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MUCOUS MEMBRANE PEMPHIGOID

Treatment: topical and/or systemic

corticosteroids

Prognosis: good, but monitor eye lesions


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And this was your


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IgG and C3

epithelium

And this was your

Immunoflourescence results?

Diagnosis??


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Diagnosis??

Pemphigus Vulgaris

P hi


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Pemphigus

Vulgaris is the most common type

Female more than male

Ethnic groups: Ashkenazi Jews

P hi


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Pemphigus

Pathogenesis: auto Ab against desmosomes

Desmoglein 3

Desmoglein 1 and 3 in skin and oral

Activation of proteinases


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Pemphigus vulgaris


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Pemphigus vulgaris

Direct immunoflourescence: biopsy from peri-lesional tissue

IgG autoantibodies can be detected within the

epithelial thickness producing a characteristicfish-net pattern

Indirect immunoflourescence

Disease monitoring

Autoantibodies to desmosomes

Titer correlates with severity

Not present in early stages? Or all patients

P hi l i


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Pemphigus vulgaris

Histopathology

Intra epithelial

separation

Little subepithelial

inflammation

Tzanck cells


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Immunoflourescence


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was done .

granular deposition of IgA at BM


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What if this was your


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y

Immunoflourescence results? ?

Linear deposition of IgA at BM

Subepithelial

separation


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LIMITED MOUTH OPENING


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LIMITED MOUTH OPENING

Bullae rupture to leave painful erosions and

subsequent scarring can restrict the opening

of the mouth, movement of lips and tongue


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Epidermolysis Bullosa


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Epidermolysis Bullosa

Complex group of syndromes Gene mutations coding for keratins in basal

layer or collagens

Keratin: intraepithelial bullae

Basement membrane : subepithelial bullae


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What is your clinical diagnosis?


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Epidermolysis Bullosa aquista


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2- Oral Ulceration and Vesiculobollous Diseases

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