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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????
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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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