Oral ulcers part (1)

5/30/2021 Ossama El-Shall
ULCERATIVE,VESICULAR,
AND BULLOUS LESIONS
Part 1
Professor Dr. Ossama El-Shall
Professor, Oral Medicine & Periodontology Dpt,
Al-Azhar University, Cairo, Egypt.
E-mail: oelshall@hotmail.com

Definitions
Vesicles Bullae Pustules
Ulcer
Macules Papules
Plaques Nodules Erosions

Bullae: Large vesicle, Elevated blister
like lesion containing clear fluid that over
1cm in diameter
Pustules: vesicle containing purulent mater
Vesicles: Elevated blisters containing
clear fluid that are under 1cm in
diameter

Intra-epithelial vesicles
Sub-epithelial vesicles

suprabasal separation of
the epithelial cells
Pemphigus Vulgaris
intraepithelial vesicle

Pemphigus Vulgaris

Mucous Membrane Pemphigoid
Subepithelial vesicles

subepithelial vesicle
separation of the full thickness of the
epithelium from the underlying connective
tissue
Mucous Membrane Pemphigoid

formation of
subepithelial vesicle
subepithelial separation of
the epithelium from the
underlying corium

Ulcer
A defect in the epithelium;
it is a well-circumscribed depressed lesion
over which the epidermal layer has been lost.
Or it is a complete loss of epithelium

Macules: Well-circumscribed, flat, lesion
with different color from normal skin. They
may be red due to presence of vascular lesions
or inflammation, or pigmented due to presence
of melanin or drugs.
Melanotic Macule

Papules
Papules: Solid lesions raised above the skin surface
that are smaller than 1cm in diameter

Plaques: Large papules, solid raised lesions
that are over 1cm in diameter
Erosions: Moist red lesion often caused
by the rupture of vesicle or bullae as well
as trauma. Or it is a superficial defect of
epithelium associated with partial loss of
epidermis.

• Nodule: firm lesions present deep in
the dermis, and the epidermis can be
easily moved over them

I-According to its occurrence:
II-According to its etiology:
Classification of Oral ulcers
1- Physical and chemical agents.
2- Microbial agents.
3- Neoplasm.
4- Immunologic reactions.
5- Blood disorders.
6- Drugs.
7- Gastrointestinal disease.
1- Primary ulcers.
2- Secondary ulcers.

I- Classification According ulcer
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.

II-Classification according to Etiology

3- Neoplasm.
5- Blood disorders.
6- Drugs.

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
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

5- Blood disorders:
a- Anemia.
b- Leukemia.
C- Neutropenia

6- Drugs.
Cytotoxic drugs.
a- Coeliac disease.
b- Ulcerative colitis.
c- Crohn’s disease.

Ulcers due to Physical and chemical
agents
Reactive oral ulcers
These ulcers occurs as a result of trauma,
thermal agents, radiation or electrical
source.

Radiation mucositis & ulceration

It should differentiate from malignant
ulcers by, site and shape
in relation to traumatic source and
healing in 1-2 week after cause removal.
Biopsy is indicated if there is a doubt.
It treated mainly by removing of the
causative agent and symptomatic
treatment such as anti-inflammatory
mouthwash and topical steroids.
Traumatic Ulcer

It occurs due to mechanical trauma such as;
A- Uncontrolled biting of soft tissues (lips, cheek….) as
during epileptic attack or after L.A.
B- Self-induced trauma due to abnormal habits such as
cheek or lip biting.
C- Iatrogenic, from the dental instrumentation, such as
bur, saliva ejector, hand instrument and forceful
removal of cotton rolls (cotton roll stomatitis).
D- Over extended dentures margins.
E- Riga’s ulcers :( Riga-Fede disease) appears on lingual
frenum in neonates due to abrasion of the tongue by
lower incisors during sucking.

Traumatic ulcer of the tongue

Look for the cause !!!!

Traumatic ulceration of the lip

Riga’s ulcer

Oral Ulcers due to Bacterial agents
1- Necrotizing ulcerative gingivitis.
2- Tuberculosis.
3- Syphilis.

1- Necrotizing ulcerative gingivitis:
a-It is inflammatory destructive disease of gingiva
characterized by punched out ulceration with
crater-like depression at the crest of interdental
papillae.
b-Gingival crater is usually covered with
pseudomembranous slough.
c-The lesion may extend to involve marginal gingiva,
attached gingival and finally may exposed the bone.
d-Smear from the lesion reveals presence of
Spirochetes and fusiform bacilli

Ulceration in acute necrotizing gingivitis
destroys the interdental papillae particularly

Necrotizing ulcerative gingivitis

2- Tuberculosis:
a- It is a specific granulomatous disease
caused by Mycobacterium Tuberculosis
and characterized by granuloma formation
in any organ of the body.
b- Oral lesions are secondary to pulmonary
T.B and it appears as chronic indurated
ulcer, with irregular undermined edge and
thick mucous material in its base.

Noticed the mucous material in the Tb ulcer

Oral TB ulcer

3- Syphilis:
It is an infectious disease caused by
T.Pallidum and appears in three general
stages.

Primary syphilis: Chancre; is the lesion of
primary syphilis, began as small macules
which converted to slightly painful ulcer
(2ry infection), with raised margin and
covered with white adherent membrane.
There is local L.N enlarged, which is
rubbery and painless.
Secondary syphilis: Condyloma latum: Painless
white flat warty-like papule with ulcerated
surface.
Tertiary syphilis: Gumma: whish is a localized
granuloma that may breakdown to form
punched out deep ulcer usually on the
tongue.

Syphilitic Chancre of the Tongue

Syphilitic chancre of the lip

Syphilitic chancres

Tertiary syphilis of the tongue

Lecture Number 2
Oral Ulcers due to Viral infection

Remember the classification of oral ulcers
3- Neoplasm.
5- Blood disorders.
6- Drugs.

Lecture Number 2
Oral Ulcers due to Viral infection
Herpes Simplex infection
Varicella Zoster virus infection
Coxsacki virus
All are Secondary ulcers preceded by intra-epithelial
vesicles or bulla

Virus is nucleic acid cores either DNA or
RNA coated with protein and has the
ability to produce certain diseases when
invades human cells.
It consists of:
1-Genome: The inner nucleic acid core,
either D.N.A of R.N.A.
2-Capsid: The protein coat.
3-Envelop: Lipoproteins surround many
viruses.

Herpes Simplex viral Infection

Herpes Simplex viral Infection
1- There are two types of herpes simplex virus;
HSV1 and HSV2.
2- HSV1 is responsible for oral infections namely;
primary herpetic gingivostomatitis, recurrent intra-
oral herpes, recurrent herpes labialis, pharyngeal
infection and meningoencephalitis in addition to
dermatitis above the waist.
3- HSV2 is responsible for occurrence of genital
infection and dermatitis below waist in addition to
infection in newborn infants from infected vagina
during delivery.

4- The primary herpetic infection occurs in the
patient for the first time, i.e. infection by the
virus prior immunity to the virus. It manifested as
herpetic gingivostomatitis, which occurs due to
infection for the first time in a patient with no
prior immunity and it results in local and systemic
manifestations.
5- Recurrent lesion; occurs in the patients
previously infected with primary herpetic infection
as a result of activation of latent virus. It
manifested as Herpes labialis or intra-oral herpes
without any systemic manifestations.

Primary Herpetic gingivostomatitis
(Acute herpetic gingivostomatitis)

(Acute herpetic gingivostomatitis)
Clinically:
1- Most commonly in infants and children up to
10 years but the high peak at 2-3 years.
2- Uncommon before 6 months because of
maternal antibodies (IgG) from mother.
3- Most of cases are sub clinically or missed
diagnosed as teething problems.

4- Predromal signs and symptoms: fever,
headache, malaise, and tender palpable
submandibular and upper deep cervical lymph
nods.
5-Lymphadenopathy occurs before significant
antibody titre is detectable because of
early cellular immune response activation by
the herpes simplex virus.
6- Acute marginal gingivitis. Within few days

Gingivitis & multiple shallow ulcers

Primary herpetic gingivostomatitis

7- Oral and par oral vesiculo-bullous lesions appear
immediately after fever subsides.
8-These lesions appear orally on tongue and gingiva
as small vesicles, which is rapidly ruptured forming
small ulcers that coalesce together resulting in
large irregular ulcer.
9- Tongue appears enlarged, inflamed and scalloped
10-Circumoral, this lesions appears on Vermillion
border of the lip and the skin

1 or 2 days after the prodromal symptoms occur, small vesicles appear
on the oral mucosa; these are thin-walled vesicles surrounded by an
inflammatory base
ORAL HERPES

An important diagnostic criterion in this disease is the appearance of generalized
acute marginal gingivitis. The entire gingiva is edematous and inﬂamed

Acute marginal gingivitis.

11- The oral ulcers are small, painful, superficial,
surrounding with erythema and covered by
grayish membrane.
12- Increase salivary secretion that may result in
extension of the infection to the skin.
13- The lesions are self-limiting and resolves within
10-14 days.
14- Sever form of the disease may seen in newborn
infants, malnourished children and patients with
malignancy or immunosuppressive drugs.

Herpetic ulcers coalesce together

Pathogenesis
1- The viruses invade and destroy the epithelial cells resulting in
intra-epithelial vesicles formation.
2- The intraepithelial vesicles contain: exudates, inflammatory
cells and virus infected epithelial cells.
3- Virus invade the epithelial cells itself forming inclusion bodies,
(Lipschutz bodies).
4- There is ballooning degeneration of nucleus of epithelial
cells,(appears homogenous with migration of chromatin)
5- Presence of multinucleated epithelial cells especially at
epithelial cells lining the vesicle due to division of the nucleolus
without division of cytoplasm or fusion of infected cell to non
infected one.

Diagnosis
1- Case history: prodromal symptoms positive history
of contact with other patients, first time of
infection.
2- Clinical examination: Gingivitis, multiple small
shallow ulcers on both keratinized and non-
keratinized mucosa, L.N.
3- Special investigations: rarely to perform except in
patients with less obvious clinical manifestation.
A- Cytology: Multinucleated giant cells and others with
ballooning degeneration.
B- HSV Isolation: using tissue culture e.g. rabbit kidney.
C- Antibody titre: After 7 days of infection.

Virus invade the epithelial cells forming inclusion bodies, (Lipschutz
bodies).

Herpes simplex eye infection

Treatment
1- Mild cases: it is a self-limiting
disease, so it need:
A- Bed rest.
B- Liquid balanced diet.
C- Analgesics and antipyretics.
D- Antiseptic mouth washes.

2-Sever oral cases.
A-Rifampicin:
10mg/kg body weight. T.d.s. orally.
In adult used as mouth rinse then
swallowed, while in infants as dropper.
It gives both topical and systemic actions
and has both antibacterial and antiviral
actions.

B- Acyclovir.(Zovirax):
1- It used in Sever oral involvement in either healthy
or immuno-compromised patients.
2- Also used in disseminated disease in infants.
3- Healthy patient dose;
-Above 12 years: 200mg 5times/day/5days.
-Below 12 years: 100mg 5 times/day/5days.
4-Immunocompromised patients:
400mg/5times/day/healing.
5- Advantage; It inhibit DNA replication in HSV
infected cell without affecting of the normal cells.

6- It is phosphorylated (activated) by herpes
specific enzyme (DNA polymerase) and then
becomes inhibitory to the virus.
7- The drug is inactive unless it activated by the
virus so it is inactive in un-infected cell so it is
non toxic
8- From its mechanism of action it should be used
in the early stages of the disease to prevent
virus replication because its late administration
is of less value.

Recurrent herpetic lesions

1- After resolution of the primary lesion, the viruses
migrate to remain latent in the trigeminal ganglion,
until it reactivated by any local or systemic
predisposing factors.
2- At activation, the virus spread along the trunk of
the nerve to infect oral-skin epithelial through
formation of intra-epithelial vesicles.
3- Predisposing factors are: trauma, common cold,
exposure to sun, fever, stress, GIT disturbance
and immuno-suppression.

Occurs in the patients previously infected
with primary herpetic infection as a result
of activation of latent virus.
It manifested as
Herpes labials or Intra-oral herpes
without any systemic manifestations.

Recurrent herpes labialis.
1- Prodromal symptoms; burning or tingling
sensation at the location of the vesicle
development, then followed by local
erythema, edema and vesicle formation.
2- The vesicles are small in size (1mm), tend
to coalesce forming a large lesion,
surrounded with erythema usually on the
Vermillion border of the lips.

3- The vesicle rupture to forming ulcers
covered with crust of purulent exudates
due to secondary infection.
4- It is a self-limiting lesion heals without
scar formation within 7-14 days.
5-Recurrent attacks may occur once
monthly, once bimonthly, once per year
or once or twice per life.

Recurrent herpes labialis

Treatment
1- Sun blocker if the sunlight is the
predisposing factor.
2-Acyclovir ointment 5
times/day/5/days.

Recurrent intra oral herpes.

Recurrent intra oral herpes.
1- Multiple small (1mm) vesicle formation surrounded
with erythema on the keratinized mucosa (tongue,
palate and gingiva).
2-These vesicles tend to rupture forming small
ulcers, which are pinhead sized, surrounded with
erythema. These ulcers tend to coalesce to form
large superficial painful ulcer on erythematous
base.
3- Self-limiting lesion heal without scar formation.
3-treatment: 2% tetracycline mouth bath.

Recurrent herpes

Recurrent intra-oral herpes

This is a patient that was undergoing chemotherapy for carcinoma and their
immune system was compromised. Then they had recurrent herpes on moveable
mucosa which is not seen in a normal, immunocompetent person.

Herpetic Whitlow
1- It is a primary or secondary HSV infection
of the fingers occurring in medical and
dental persons who in contact with HSV
patients.
2- Pain an itching in the infected finger
followed by deep vesicle formation in the
distal segment of the finger.
3- It is a self-limiting lesion within 20 days.

Herpetic Whitlow

Lecture number 3
Oral Ulcers due to Viral infection.

Varicella Zoster Virus infection

Varicella Zoster Virus infection
1- Primary infection with Varicella
Zoster virus causes Chicken pox.
2- Then the virus remains latent in the
dorsal root ganglion of spinal cord or
the extramedullary ganglion of cranial
nerves.
3- Reactivation of the latent virus
leads to herpes Zoster infection

Primary infection
Secondary infection
Herpes Zoster mandibular

• Varicella is specific to humans and causes
chickenpox and shingles.
• intelligent varicella virus
• How can such a simple organism, which is
basically just a small piece of DNA with
protein covers, take control of multiple large
complex cells, such as human T cells,
neurons and skin cells?
• How can varicella know how to use so many
different techniques in sequence?

Chicken Pox
Mode of infection
1- Droplet
2- Direct contact with fresh skin lesion
of patient with chicken pox or
shingles.
3- Incubation period about 2 weeks.

Clinically
1- Age: any age
but more at 5-10 years.
2- Common in winter and spring.
3- Skin lesion consists of skin rashes of
red papules on the trunk, spread to the
face, scalp and extremities.
4-These papules converted into clear
vesicles (tear drops) within hours.

5- The vesicles content become cloudy
then it ruptures converted into crusted
lesions.
6- Finally lesions heal without scar
formation.
7- Intra-orally: lesions are multiple
vesicles, which rupture forming small
painful ulcers.
8- Oral lesions do not present any
symptomatic, diagnostic or treatment
problems.

Chicken Pox vesicles

Treatment:
1- Healthy children: no treatment hence it
is a self-limiting disease.
2- Immunocompromised patients:
a- Passive immunization with Zoster
immunoglobulin.
b- Acyclovir I.V.
- For less than 12 year;
10mg/kg/8h/7days
- For more than 12 years;
5mg/kg/8h/7days.
Last

Herpes Zoster (Shingles)

Etiology:
1- It is the secondary infection of the Varicella
Zoster virus. It occurs due to reactivation of
the latent virus (in dorsal root ganglion of spinal
cord or extramedullary ganglion of cranial
nerves) by predisposing factors.
2- Predisposing factors such as; trauma, surgery,
irradiation, malignancy, immunosuppresion.
3- Virus may involve sensory branches of
trigeminal nerve, or sensory and motor branches
of facial nerve.

Clinically:
1- Affect any age.
2- Rare in children unless; child had Chicken
pox in the first few months of life or
mother has chicken pox during pregnancy.
At the latest case the new born infants
suffers from Congenital Varicella syndrome,
which consists of : limb deformity, ocular
lesions and extensive scarring.
3- Prodromal symptoms: fever, malaise,
headache and unilateral tenderness along
the involved nerve.

4- Unilateral sever itching and neuralgic pain,
which may be: burning or stabbing,
constant or intermittent.
5- 2-5 days latter there is unilateral vesicle
appearance at linear pattern and
erythematous base on the skin or mucous
membrane supplied by the affected nerve.
6- Vesicles rupture within 1 week forming
crust.
7- Healing occurs 3-4 weeks with scar
formation.

Herpes zoster rash and blisters

8- These scars are diagnostic in cases of post
herpetic neuralgia.
9- Orally: very painful vesicle formation in unilateral
distribution, which they rupture to form small
painful ulcers, shallow, at erythematous base.

10- The site of lesion is depend on the nerve involved; if the mandibular
division of trigeminal nerve is involved, the lesions will be unilaterally on the
cheek, tongue, vestibule of lower jaw.
If the maxillary division is involved, the lesions will be on the hard palate,
soft palate and vestibule of upper jaw.

Herpes zoster Maxillary, intra-oral

11-Ophthalmic involvements will leads to
unilateral corneal ulcer.

Ophthalmic involvement

Ophthalmic involvement.

12- Herpes sine herpes: (Zoster sine
eruption) It is pain caused by
zoster virus without any clinical
lesion along the course of the
nerve. It usually misdiagnosed as
dental pulpits. Diagnosis only
depends on the serological finding
and clinical symptoms.

Maxillary

mandibular division of trigeminal nerve is involved, the lesions
will be unilaterally on the tongue & lower jaw.

Complications:
Are common in Immunocompromised and
elderly patients.
1- Post herpetic neuralgia: It is persistence
of the pain after rash resolution due to
inflammation and fibrosis of the affected
nerve. It is most commonly in elderly
patients. And it may improve spontaneously
after 24 months.

2-Generalized herpes Zoster
infection: involving internal organs.
3- Motor paralysis.
4- Secondary infection.
5-Blindness due to corneal ulceration.

Affection of maxillary & ophthalmic branches of trigeminal nerve by
Herpes zoster

Treatment:
1- Healthy patients:
a- Mild clinical manifestation:
Sedation, Extreme care to avoid secondary
infection, 0.2% chlorhexidine mouthwash,
and 5% Acyclovir ointment.
b- Sever clinical manifestation: Oral 800mg
Acyclovir tab./5 times/day/7days.

2- Immunosuppressed patients:
Acyclovir I.V. 10mg/kg/8h/10days.
3- Elderly patients: Acyclovir and
prednisone to prevent post herpetic
neuralgia.
Last

Ramsay-Hunt Syndrome
Definition:
It is a special form of Herpes
Zoster infection affecting facial
nerve via infection of Geniculate
ganglion.

Clinically:
1- Herpetic Oticus: Small vesicles eruption around
external auditory canal.
2- Prodrome: headache, fever, malaise and ear pain
which may radiate to the neck and jaws.
3- Unilateral vesicular eruption: at anterior 2/3 of the
tongue and soft palate.
4- Xerostomia: due to disturbance of parotid
secretion.

5-Facial palsy, (identical to facial
paralysis).
6- Loss of taste sensation.
7- Deafness on the affected side.
8- Rapid course of the disease, it resolute
within 7-10 days.
Treatment: As herpes Zoster infection.

Ramsay-Hunt Syndrome

Last

Coxsackievirus infection

Coxsakie Virus infection

1- Coxsackie virus is RNA virus, separated
into groups A and B. each group contain
many types of the virus.
These viruses are responsible for occurrence
of meningitis, pericarditis, myocarditis and
acute respiratory infections.
2- Type A Coxsackie virus is important to
dental professionals, because it can produce
the following infections: Herpangina, Hand,
foot and mouth disease, and acute
lymphonodular pharyngitis.

Herpangina
1- Seasonal but commonly in Summer.
2- Sudden onset commonly in Children.
3- Saliva is the mode of transmission.
4- Symptoms of low-grade infection;
headache, fever.

5- Sore throat and dysphagia due to
vesicle formation.
6- Soft palate affection in addition to
uvula and pharynx.
7- Small vesicles, bilaterally, rupture
to form small shallow ulcers on
erythematous base.
8- Self-limiting within few days.

Herpangina

Hand, foot, and mouth disease

1- Air born spread.
2- Commonly at children or young adult.
3- Low-grade fever, diarrhea, vomiting and
lymphadenopathy.
4- Macule, papules or vesicles on the extensor
surface of hands, fingers, feet and toes.
Hand, foot, and mouth disease

5-Bilateral Vesicles eruption on the hard
palate, tongue, cheek mucosa and tonsils.
6-Vesicles are ruptures into large ulcers,
which are; shallow, multiple and on
erythematous base.
7- Sore mouth and inability to eating.
8- Self-limiting within one week.

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