Oral ulcers part 2

5/30/2021 Ossama El-Shall
ULCERATIVE,VESICULAR,
AND BULLOUS LESIONS
Part 2
Professor Dr. Ossama El-Shall
Professor, Oral Medicine & Periodontology Dpt,
Al-Azhar University, Cairo, Egypt.
E-mail: oelshall@

Oral Ulcers due to immunologic reaction.

Let us to remembers Oral Ulcers
Classification according to Etiology
1- Physical and chemical agents.
2- Microbial agents.
3- Neoplasm.
4- Immunologic reactions.
5- Blood disorders.
6- Drugs.
7- Gastrointestinal disease.

1- Physical and chemical agents:
(Reactive ulcers):
A- Traumatic.
B- Thermal.
C- Chemical.
D- Electrical.
E- Radiation.

2-Microbial agents.
A-Bacterial:
1- Necrotizing ulcerative gingivitis.
2- Tuberculosis.
3- Syphilis.
B-Fungal:
1- Histoplasmosis.
2- Blastomycosis
C-Viral:
1- Herpes simplex.
2- Herpes Zoster.
3- Herpangina
4- Hand foot and mouth disease.

3-Neoplasm
4- Immunologic reactions.
a- Aphthous ulcers.
b- Behcet’s syndrome
c- Pemphigus vulgaris
d- Mucous membrane pemphigoid.
e- Lupus erythematosus.
f- Epidermolysis bullosa.
G- Drug eruption.
Squamous cell carcinoma

1- Pemphigus vulgaris.
2- Bullous Pemphigoid.
3- Benign mucous membrane pemphigoid.
4- Erythema multiform.
5- Mucocutanous-occular syndromes.
6- Recurrent Aphthous ulcers.

Also let us to remembers the Oral Ulcers
Classification According to its
occurrence:
A- Primary Ulcers:
Not preceded by
Vesiculo-bullous
lesion.
B-Secondary ulcers:
Preceded by
Vesiculo-bullous
lesion

A-Primary Ulcers: Not preceded by
Vesiculo-bullous lesion.
1- Traumatic.
2- Infective: Bacterial and fungal.
3- Neoplastic.
4- Systemic: GIT and blood disorders.
5- Aphthous ulcer.
6- Behcet’s syndrome.
7- Reiter’s syndrome.

B-Secondary ulcers: Preceded by
Vesiculo-bullous lesion
I-Intra-epithelial vesicles:
1- Herpes simplex.
2- Herpes Zoster.
3- Herpangina.
4-Hand, foot and mouth
disease.
5- Pemphigus vulgaris
II-Subepithelial vesicles
1-Bullous pemphigoid.
2-Mucous membrane
pemphigoid
3-Erythema multiform.
4-Bullous erosive lichen
planus.
5-Epidermolysis bullosa
6-Drug eruption.

Pemphigus vulgaris.

Pemphigus vulgaris.
Definition:
It is a chronic uncommon
autoimmune disease, potentially fatal
and characterized by intra-epithelial
vesicle formation on normal skin and
mucosa.

Etiology and pathogenesis:
1- Auto-antibody (IgG) reacts with
component of epithelial desmosome
tonofilament complex (Pemphigus antigen) will
result in destruction of desmosomal
tonofilament system and epithelial
intercellular substance.
2- This antigen auto-antibody reaction will
activates epidermal intracellular proteolytic
enzymes, leading to loss of adhesion
between epidermal cells (acantholysis) and
degeneration of epidermal cells (acantholytic
Tzank cells)

3- This loss of adhesion between epidermal
cells will be much apparent between basal
cell and prickle cell layers leading to
formation of suprabasillar split, which will
full with exudates products leading to
intraepithelial bulla formation.
4- Tzank cells, which are cells showing signs
of degeneration will seen floating or line
the formed bulla. Their nuclei appears
rounded, swollen hyperchromatic and
surrounded with narrow cytoplasm.

Clinically:
1- Age between 40-60 years.
2- Oral lesions:
a- Oral lesions appear first due to weak
intercellular junction than in skin.

b- Flaccid bulla on normal mucosa,
rupture, leaving bright red
ulceration or erosion with large map
likes lesion.
This ulceration is painful, shallow,
covered with yellow exudate and not
surrounded by inflammatory halo unless
it secondarily infected.

bright red ulceration with large map likes lesion.

c- +Ve Nikolsky’s signs: Peeling off of
the superficial epithelial layers on
gentile pressure leaving irregular areas
having denuded base that bleeds easily.
It caused by pulling away the upper
layer of the epithelium from the basal
layer.
d- Symptoms: Pain. Bloody or salty taste
and excessive salivation.

Pemphigus vulgaris
Oral lesions

Pemphigus has involved the gingiva; there is
obvious ulceration around the marginal gingiva.

The ulceration and slough on the patient's tongue is dramatic
testimony to the seriousness of intra-oral pemphigus.

3- Skin lesions
a- Appears on pressure areas as face neck, trunk,
extremities and axilla.
b- Wide spread painless fragile bulla with thin roof
containing a clear fluid on normal looking skin.
(Unless secondarily infected where the fluid is
purulent and the margins are erythematous).
c- The bullae are soon ruptured and the lesions
continue to expand peripherally over a period of
weeks to months to denude a large area of skin.

d- +Ve Nikolsky’s signs: rubbing the palmer
surface of the waist will lead to peeling off
of the epithelium or bulla developed.
e- General constitutional symptoms of weigh
loss, nervousness, anaemia, and pruritis.
f- The disease may terminate in death in
about 10% of the patients (elderly
debilitating). Or healing in slow processes
may take months or years.

Skin lesions of Pemphigus vulgaris.

Diagnosis:
1- History of developing painless vesicle and
bulla that become painful on rupture
associated with systemic findings of loss
weight….
2- Clinical picture: bullous eruption on normal
skin and/or mucosa without inflammatory
haloes around it. +Ve Nikolsky’s signs.
3- Direct smear: Show Acantholytic cells from
the fresh vesicle fluid.

4- Hypoalbuminemia: due to escape of fluid
containing albumin from large areas of skin
covered with bullae.
5- Raised ESR.
6- Biopsy: Fresh bullae 24 h old excised for
biopsy and halved to examine either with light
microscopy or immunofluorescent antibody test.

a- The light microscopy examination
will revel intraepithelial vesicle formation containing
free-floating acantholytic cells.

b- Immunofluorescent antibody test:
1- Indirect:
- It aimed to demonstrate the presence and
concentration of circulating antibodies.
- Is done by incubating normal animal or
human mucosa with serum of a patient and
adding a fluorescin conjugated human
antiglobulin.
- Positive reaction indicates the presence of
circulating immunoglobulin antibodies

2- Direct
- Aimed to demonstrate the presence of
autoantibody attached to the tissue, not
circulating.
- Is done by incubating lesional tissues with
florescin conjugated human antiglobulin.
- Positive reaction in the form of honey
comb pattern indicates the presence of
tissue auto-antibodies.

Treatment:
1- Systemic cortisone.
- Predensone 60-100mg to control the signs
and symptoms then reduced to maintenance
dose.
- The patient may die as a result of side
effects of steroids.
2- High protein diet. If serum albumin is low.
3- Topical Corticosteroids.
4- Antifungal drugs.
5- Systemic antibiotics.

Dental Implications:
1- Handling of the tissue with care because
the epithelium is fragile and excess pressure
may cause erosion.
2- Prolonged use of cortisone may induce
adrenal crises in the dental clinic.
3- Control of the infection.
4- Oral lesions appears early so it easily to
diagnosed first by the dentist.
Last

Bullous Pemphigoid.
Definition:
Pruritic blisters located on the
flexor surface of the extremities,
axilla and lower abdomen

Etiology and pathogenesis:
1-Autoimmune mechanism in which
autoantibodies develops against auto-
antigen.
2-Two types of Bullous pemphigoid
antigens are founds in basement
membrane area, Laminin found in
lamina lucida and other in
hemidesmosomes.

3- This reaction wills results in attraction
of neutrophils and eosinophils to the
basement membrane zone.
This inflammatory cells will release of
proteolytic enzymes which participate in
degeneration of the basement membrane
attachment complex leading to formation of
sub epithelium bulla.

sub-epithelium vesicle formation, which
separates the intact epithelial from the
underlying connective tissue.

Clinically:
1- Age: over 60 years both sexes.
2- Skin lesions:
a- Usually at flexor surfaces of extremities,
axillary and abdomen.
b- Localized or generalized pruritis persisting for
several weeks then, development of large blister
(1cm or more) tense, with thick roof on
erythematous or normally looking skin.

c- The blisters stay unchanged for long
time or it may rupture with formation
of eroded surface but it is not
extended as in pemphigus.
d- -Ve Nikolsky’s signs.

Close-up of tense thick roof blisters of
pemphigoid on normally looking skin

Bullous Pemphigoid

3- Oral lesions
a- It may found in the third of the patients.
b- Most commonly at gingiva and palate.
c- Tense vesicles usually rupture leaving
painless non-expanded ulcer.
d- Occasionally there is a localized form of
desquamated gingivitis with +ve Nikolsky’s
sign.

Diagnosis:
1- History.
2- Clinical picture.
3- Biopsy:
a- Light microscopy: revealed sub-epithelium
vesicle formation, which separates the intact
epithelial from the underlying connective tissue.
This in addition of presence of both acute and
chronic inflammatory cell infiltration according to
the stage of the disease
b- +Ve immunofluorescent antibody tests either
direct or indirect.

Sub-epithelium vesicle formation in
Bullous pemphigoid

sub-epithelium vesicle formation, contain
exudates, separates the intact epithelial from the
underlying connective tissue.

Treatment:
Topical Corticosteroids in mild
cases and systemic types in sever
cases.
Prognosis:
It is a self-limiting condition, but
fatal complications may occur in
oldest debilitating patients.
Last

Benign mucous membrane pemphigoid.
(Occular-cicatrical pemphigoid).

Benign mucous membrane pemphigoid.
(Occular-cicatrical pemphigoid).
Definition:
It is a chronic non-fatal
autoimmune disease characterized by
vesiculo-bullous lesions on mucosa of
mouth, pharynx, larynx, trachea,
and vagina. It is less frequently to
affect skin.

Cicatricial pemphigoid is an autoimmune disease that is characterized by
blistering lesions on mucous membranes.
Areas commonly involved are the oral mucosa and conjunctiva (mucous
membrane that coats the inner surface of the eyelids and the outer surface of
the eye).
Other areas that may be affected include the nostrils, oesophagus, trachea and
genitals.
Sometimes the skin may also be involved where blistering lesions can be found
on the face, neck and scalp.

Etiology:
1- Auto antigen (MMP antigen) located in the
lower area of lamina Lucida of the
basement membrane.
2- It is identical to Bullous pemphigoid in
histological picture and in the
immunofluorescence.
3- They may be simple variants of a single
disease.

In benign mucous membrane pemphigoid the peeling away of the
epithelium from c.t. is obvious. This change results in what pathologists
call "sub-basalar clefting."

Clinically:
1- Age: 50-70 more in female.
2- It affects any mucosal surface in the
body and began with a bullae and end with
scar.
3- Involvement of trachea, larynx and
esophagus will lead to difficulty in
breathing and swallowing due to scaring.

4- Eyes may be affected with shallow
conjunctival erosion that heals with scaring,
scaring of lacrimal ducts, which lead to
xerophthalmia, corneal damage and
blindness.

5- Skin lesions appear only in 20% of cases as
bulla and ulcerated crusted lesions.

6- Oral lesions:
a-Desquamated gingivitis: Developed at 90%
of the cases and appears as Erythema of
marginal and attached gingiva with +Ve
Nikolsky’s signs.

b-Vesiculo-bullous ulcerated lesions: Appears on the palate and gingiva, the
bulla is of thick walls, it ruptures after a long time forming a slightly painful
slowly growing ulcer surrounded by erythema. Healing rarely to occur with scar
formation in opposite to eye lesions.

Exposed c.t. appear as red areas; epithelium about to slough appears as
white areas. This is a typical appearance of benign mucous membrane
pemphigoid.

Cicatrical pemphigoid

Diagnostic techniques:
1- antibodies (IgG) precipitates complement (C3) in the lamina lucida of the
basement membrane.
2-Circulating auto-antibodies to BP-1 antigen (located in hemidesmosome).
3- Negative Nikolsky sign.
4- IgG, C3 deposition at BM creating smooth line in immunofluorescent
analysis.

Treatment:
1- Gingival and oral hygiene
instructions after scaling and
root planning.
2-Topical or intra-lesion steroids.
3-Systemic Corticosteroids.

Lecture number 5
In Oral Ulcers

Let us to remembers oral ulcers due to
immunological reactions
1- Pemphigus vulgaris.
2- Bullous Pemphigoid.
3- Benign mucous membrane pemphigoid.
4- Erythema multiform.
5- Mucocutanous-occular syndromes.
6- Recurrent Aphthous ulcers.

Erythema multiform.
Definition:
It is an acute self-limiting
vesiculo-bullous inflammatory disease
with multiple skin lesions and
sometimes mucosal involvement.

Etiology:
It is of unknown etiology,
but it has been suggested that the
disease is mediated by deposition of
immune complex mostly (IgM and C3) in the
superficial microvasculature of skin and
mucous membrane.
Many factors may help such immune
complexes, such as:
1- Drugs: like sulphonamids, antibiotics or
barbiturates.
2- Infection: bacterial or viral such as
herpes simplex or histoplasmosis.
3- Radiation.

Clinically:
Erythema multiform may appears in
one of the following forms:
1- Minor form.
2- Major form: This include
a- Steven Johnson syndrome.
b-Toxic epidermal necrolysis (TEN).
3- Chronic form: Rare, may seen in
immunocompromised patients.

4-Herpes associated erythema multiform:
a-It is a form of erythema multiform
initiated by cell mediated immune reaction
to recurrent herpes simplex infection.
b-Such patients developed erythema
multiform 10-14 days after recurrent of
herpes simplex infection. They should place
on acyclovir prophylactic-maintenance dose.

Herpes associated erythema multiform

Minor form
1- Skin lesions: Various types of eruptions,
such as macule, papules, vesicle, or bullae
all found on erythematous base. Most
commonly on the back of the hands,
forearms, feet and legs knees.
2- Any of these eruptions are with iris, target
or bull’s eye appearance. This means
concentric rings like appearance. This due to
various shades of erythema with clean
healed center.

Erythema multiform at hands

3-Orally; non-specific eruption on erythematous
base.
But if it occurs at lip it gives a characteristic
appearance: (Blood crusted appearance).
If affected tongue it resulted in enlargement of
the tongue with indentation and non-specific
ulceration of anterior and lateral border.
4-It may accompany with pain, discomfort and
inability to eating and swallowing due to extension
of the lesion to the oropharynx.
5-It heals with no scar formation within 3 weeks.

Drug induced Erythema multiform
(Blood crusted appearance).

Blood crusted appearance And non-specific eruption of erythema multiform on labial
mucosa

Enlargement of the tongue with indentation and non-specific ulceration
of anterior and lateral border

non-specific eruption of erythema multiform on labial
mucosa

Erythema multiform

Erythema multiform
Last

Major form
1- Steven Johnson’s syndrome.
2- Toxic epidermal necrolysis, (TEN),
(Lyell’s syndrome)

Steven Johnson’s syndrome
It is one of the mucocutenous-Occular syndromes.
Erythema multiform,+ eye lesions + genital lesions.
1-Age: infants, children and young adults of both
sexes.
2-Sudden onset with general constitutional
symptoms, (fever, headache, anorexia…) and then
patient may developed sever vesiculobulous lesions
within 24-48 days.
3-Oral lesions: Erythema Multiform.

4- Skin lesions : Erythema Multiform.
5-Eye lesions: Diffuse conjunctivitis
with corneal ulceration, which may
lead to scarring and blindness.
6-Urogenital: Non-specific urethritis,
Balanitis in male and vaginal ulcers in
female.

Oral lesion
Diffuse conjunctivitis
with corneal ulceration
Skin lesion
E.M
Blood crusted appearance

Eye lesions: scarring
and blindness
Oral lesions:
Erythema Multiform with
Blood crusted
appearance of the lips

Toxic Epidermal Necrolysis, (TEN),
(Lyell’s syndrome)
1- It is the most severs form of E.M.
2- Drug reaction may play an important role in its
occurrence.
3- It characterized with generalized E.M of skin and
mucous membrane.
4- +Ve Nikolsky’s sign, with peeling of large areas of
the skin leaving painful exudative surface
5- Fever, and high morbidity rate due to loss of body
fluids and secondary infection.

+Ve Nikolsky’s sign, with peeling of large
areas of the skin leaving painful
exudative surface
Oral manifestation as
E.M
Toxic epidermal necrolysis, (TEN), (Lyell’s syndrome)

Mucocutanous-occular syndromes
1- Steven Johnson’s syndrome.
2- Behcet’s syndrome.
3- Reiter’s syndrome.

Behcet’s syndrome
It is a multi-system syndrome with inflammatory
nature with unknown etiology.
1-Age: Young adults, and more commons in males.
2-Orally: Aphthous like ulcers.
3-Genital lesions: Recurrent genital ulceration
(scrotum, penis, labia).
4-Eye lesions: Conjunctivitis, keratitis and optic
atrophy.

5-Skin lesions: Seen on the limbs, trunk and
around genitals in one form of the following;
a-Erythema nodosum: Inflammatory skin
disease marked by tender red nodules.
b-Acneform lesions: Inflammatory changes
with formation of pustule.
c-Large pustule lesions: induced by
trauma.
6-+Ve Pathergy test: Pustule formation in the
site of oblique insertion of needle into the
skin.

The pathergy phenomenon is considered
an outstanding feature of Behcet disease.
Following a needle prick or intradermal
injection with saline or dilute histamine, the
puncture site becomes inflamed and
develops a small sterile pustule due to
hyperactivity of the skin to any
intracutaneous insult.
The pustular reaction of the skin is
thought to denote increased neutrophil
chemotaxis. The presence of pathergy
strongly suggests the diagnosis of Behcet
disease.

Pathergy
Ulceration from blood test

7- Arthritis: involving one or two large
joints without involving small joints.
8- CNS lesions.
9- GIT ulceration.
10-Deep venous thrombosis.

Aphthous like ulcers on labial mucosa of a case of
Behcet’s syndrome

Reiter’s syndrome.
1- Age: 30-40 years, males.
2- It considered an important cause of
non-gonococcal urethritis and it often
acquired sexually
3- It characterized with acute onset
and fever, polyarthritis, urethritis
and conjunctivitis.

4- Oral lesions:
a-Painless red macules with white raised
border on buccal mucosa, lips and gingiva.
b-Geographic tongue.
c-Painless Aphthous like ulcers.
5- Skin lesions:
a- Keratoderma blenorrhagica: red or yellow
Keratotic macules on palms and soles.
b- Circinate Balanitis: Red glans penis with
raised white irregular lesions

Keratoderma blennorrhagicum of Reiter’s syndrome

6-Arthritis: which is chronic or
recurrent migratory.
7-Non specific urethritis.
8-Self-limiting disease

Lecture number 6
Oral Ulcers
The final one

Recurrent Aphthous ulcers
Recurrent Aphthous Stomatitis
(RAS)
canker sores

Recurrent Aphthous ulcers.
1-It is a common painful single or multiple recurring
ulcerations commonly affecting non-keratinized
mucosa.
2-It seen at any age, but become less frequent as
the patient enters the 40th decade
3-It affects females more than males.
4-It is probably represents the most common lesions
of the mouth after caries and periodontal
diseases.

It can divided into three clinical forms
Minor Aphthous ulcers. 80%
Major Aphthous ulcers. 10%
Herpetiform Aphthous ulcers, 10%

shallow ulcer, small in size (<1cm) with slightly raised irregular margins
on erythematous base

Minor Aphthous ulcers:
1- Proceeded by prodromal symptoms, up to
(24H) with burning sensation and tingling at
the site where the lesion will develop.
2- This is followed by painful erythematous
macules or papules formation with necrosis
in its center.
3- The central necrotic epithelium begun to
slough with ulcer formation.

Sometimes patients "sense" an impending apthous ulcer. Soon, an ulcer will
appear in the red area. Application of ice or some medication may abort
ulcer formation

Minor Aphthous ulcer

4- The ulcer is shallow, small in size
(<1cm) with slightly raised irregular
margins on erythematous base.
5- Its floor covered by grayish white
exudates.
6- It is shape is rounded on the lips and
cheek and elongated on the vestibule.
7- Commonly at non-keratinized mucosa.

Minor Aphthous ulcer of the
tongue????????????

8- Chief complaint: at first, sever pain
due to tissue distraction, then 4-6
days, discomfort.
9- It heals by epithelization from the
margins, leaving a small erythematous
area that fade in few days.
10- It heals without scare formation
within 10-14 days.

Typical appearance of aphthous ulcer.

11- It recurs as every month or few
months.
12- Recurrence rate may be every
month, every few months, once or
twice per year
or in some patients there is no ulcer
free period between the attacks, ie.
New set of ulcers overlaps a previous
group.

Typical aphthous ulcer. The yellow color is due to fibrin
coating the exposed surface.

Aphthous ulcer

Aphthous ulcer at floor
of mouth

Aphthous ulcer of soft palate

Major Aphthous ulcer

It is the same as minor form but with some
following differences:
1-Larger in size > 1cm and located deep in
connective tissues, minor salivary glands or
facial muscle.
2-Raised erythematous and shiny margins due
to edema.
3-Floor is covered by gray slough.
4-Solitary.

5-Regional lymphadenopathy.
6-Site: gland bearing areas, such as
soft palate, tonsillar areas.
7-It destroys the deeper tissues and
heals with scar formation within
months.

Major aphthous ulcer is located in the floor of the mouth

Major aphthous ulcer

8- A cobblestone appearance may be
seen on the oral mucosa due to
recurring scars.
9-As a result of slowly healing process
and scar formation, there is difficulty
in tongue movement and uvula
mobility.

Major aphthous ulcer at lower lip

Major palatal aphthous ulcer

Major aphthous ulcer post ttt

Herpetiform Aphthous ulcers

1- Multiple tiny pinheads sized may coalesce
forming large irregular ulcer.
2- Very painful, interfere with eating and
speech.
3- Usually appears on the non-keratinized
mucosa, commonly on lateral margins and
tip of the tongue and floor of the mouth.

Herpetiform Aphthous ulcers of the tongue
& palate

4- Quick healing within 3-4 days.
5- In some patients recurrence is so
frequent that new set of ulcers
overlaps a previous group with nearly
no intervals between remissions.
6- Not proceeded by vesicles. (Unlike
herpes simplex)

Histopathology of Aphthous ulcer
1- Preulcerative stage: T4 lymphocytes are
found in submucosa and around blood
vessels.
2- Ulcerative stage: T8 lymphocytes.
3- Extravasation of RBCs and nutrophils.
4- Mast cells and macrophages in the base
of the ulcer.

Etiology of Aphthous ulcers
The primary cause is unknown but it
may be attributed to
1-Hereditary pattern: It occurs more
frequently in related persons

2- Immunologic factors
a-Cell mediated cytotoxic reaction
B- Immune regulatory imbalance
C-Local immune complex reaction:
d-Increase of adhesion molecules:

2- Immunologic factors
a-Cell mediated cytotoxic reaction: patients
with recurrent Aphthous ulcers have
increased cell mediated cytotoxic activity
against oral epithelia cells during the active
period of ulceration.
B- Immune regulatory imbalance: patients with
recurrent Aphthous ulcerations may have
decreased T-suppressor or increased T-
helper cells.

C-Local immune complex reaction: Antigen-
antibody reaction around blood vessels, will
results in complement activation which end by
inflammation and tissue destruction directly
or indirect by chemotaxis of neutrophils that
release lysosomes at the site of reaction.
d-Increase of adhesion molecules: The
adhesion molecules increased significantly in
recurrent Aphthous ulceration. This results
from activation or vascular damage of
endothelial cells. The adhesion molecules
mediate adhesion of leukocytes to endothelial
cells of blood vessels.

3- It may be associated with:
a- Vitamin deficiency: B12, folate zinc or iron.
b- GIT disturbances.
c- Allergic factors: such as drug or food allergy
d- Emotional stress.
e- AIDS.
f- Behcet’s disease.
G-Fever, Aphthous, Pharyngitis Adenitis
syndrome:(FAPA): It affects children less than 5
years, characterized by fever, Aphthous ulcers,
Pharyngitis and hepatospleenomegaly.

4-Recurrence of the ulcers may be
precipitated by:
a-Trauma: of lips or cheek mucosa or even
from highly spiced food may.
b-Hormonal changes: premenstrual,
pregnancy, and menopause.
c-Emotional factors: during exams times.

Diagnosis of aphthous ulcer

By
Exclusion

There is no laboratory investigation is made
to confirm diagnosis only diagnosis of
recurrent Aphthous ulceration usually made
by exclusion.
History and clinical examination should
exclude lesions on the skin, genitalia, and
eyes.

Periodic fever, malaise, and enlarged
cervical lymphnodes are suggestive of
cyclic neutropenia.
Genital, ocular and joint lesions are
suggestive of Behcet’s disease
Opportunistic infection is suggestive
of AIDS.

Treatment
Aphthous ulcers secondary to systemic disease:
1- The underlying systemic diseases should be
treated well first, then the oral ulcerative
lesion can be managed either by
Orabase (Sodium carboxy methyle cellulose),
topical steroids or
tetracycline mouth bath.

Aphthous ulcers unrelated to systemic
diseases:
1-The majority of cases are with no
underlying systemic disease.
2-The treatment in these situations is aimed
at controlling (palliative rather than curing)
or preventing recurrence of the disease.
3-The first concept in the treatment is
patient education concerning the nature of
the disease, its clinical course, recurrence
and the aim of the drug prescribed.

Corticosteroids:
Its better to use the Corticosteroids
therapy during the prodromal period, it
may abort the developing of the ulcer
or decreased its duration.
The therapy may be in one of the
following forms:

a- Topical:
-The dentist should starts with the weakest
concentration and progress to the stronger
one.
-In cases of frequent and persistent ulcers
and there is a long-term topical steroid
usage, an antifungal drug should be
administered.
-Steroids in the form of mouth bath or
aerosol provide better drug

b- Systemic:
it used as a short term of systemic
steroids in the cases of major ulcers.
Such as Prednisone 20-40mg 1.5 hour
after waking up for 5-7 days and then
reduced to 10-20mg for the next few
days.
This rarely results in pituitary adrenal
suppression.

c-Intra-lesion:
May promote healing of ulcers resistant
to healing over 2-6 weeks after topical
and/or systemic steroids.
Used as 10-20mg trimcinolone acetonide
dilated with lidocaine 2% repeated weekly
for 2-3 times.

Tetracycline mouth bath: It is better
to used before topical application of
steroids as tetracycline plus nystatin
dissolved in 5 ml of water.
Ora-base (sodium carboxy methyle
cellulose) it cover and isolate the ulcer
from environment until healing.

Patient should avoid spicy food, and
citrus food and may use topical
analgesics before eating to avoid
pain.
Dentist should avoid usage of phenol
and silver nitrate in the treatment
the ulcers hence they delay healing
and may accompanied with scar
formation.

Ossama El-Shall
നന്ദി धन्यवाद
hvala ti
Salamat

Differential Diagnosis of oral
Ulcers

What is
The Differential Diagnosis

Differential Diagnosis.
It is a possibility of occurrence of a
condition due to 2 or more diseases.
It is a list of two or more diseases with
similar signs and symptoms after collection of
data.
The most likely lesion is put on top of the
list. Then through history, clinical
examination and special investigation, final
diagnosis can be reached via exclusion.

More Examples for Oral
Ulcers

Ossama El-Shall
Salamat
hvala ti

Oral ulcers part 2

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