Oral Ulcers and other
benign Oral conditions.
Dr. Maisam Abbas
Objectives :
At the end of this presentation students should be
able to:
Recognize commonly occurring oral ulcers and
other oral pathologies with their initial
management
Differentiate
autoimmune ulcers/oral conditions
from other forms
Know when to order specific investigations
Recognize pre malignant oral conditions.
Case scenario
A 21 year old female presents to
the Outpatient with complains of
an oral ulcer for past 3 days. She
says that it hurts a lot especially
with food intake. Also she is
giving her exams in the coming
days so she needs quick relief.
Examination of oral cavity
reveals:
HOW WILL YOU PROCEED?
Key to Diagnosis
History
Detailed Examination
Specific Investigations
Causes of oral ulcers
IN A TIN
Causes of oral ulcers
Idiopathic
Neoplastic
Autoimmune
Traumatic
Infective
◦ Viral
◦ Fungal
◦ Bacterial
Nutritional Deficiency
APTHOUS ULCERS syn. Stress
ulcers
Apthous Ulcers
Stress Ulcer
? Aetiology
Major vs minor
Herpetiform
Apthous Ulcers
Usuallyidiopathic but may have other
Associated conditions like :
◦ Bechets Disease
◦ Crohns
◦ Ulcerative colitis
◦ Coeliac disease
◦ Iron-folate deficiency
◦ MAGIC Syndrome (mouth, genital ulcers,
inflammed cartilage)
◦ FAPA Syndrome (fever,apthous, pharyngitis,
cervical adenitis)
Investigations
Tailored to history / examination
Includes:
◦ CBC, ESR
◦ Ferritin, Vit B 12 & Folate levels
◦ For Celiac, IBD
◦ Autoimmune screen
Apthous ulcers
Most apthous ulcer disappear
with time (2-4 weeks) and require
only supportive treatment.
Major apthous ulcer may come in
crops and may remain upto 4
weeks.
ANY ULCER STAYING FOR MORE
THAN 4 WEEKS SHOULD BE RULED
OUT FOR “MALIGNANCY”
Infective
HSV,
Actionmycosis,
CMV,
Varicella Zoster,
Coxsackievirus,
Syphilis,
Candidiasis,
Cryptosporidium,
Histoplasma (fungal typically seen in
immunocompromised
Bacterial infection (secondary)
HSV
Primary:
◦ Multiple oral vesicles which rupture in 24
hrs
◦ Fever, arthralgia, malaise,
lymphadenopathy
Reactive
◦ Triggers: stress, UV light,
immunosuppression
◦ Vesicles on mucocutaneous junction of
lips, palate
HSV
Dx:
◦ Hx & Exam
◦ PCR, ELISA
Tx:
◦ Conservative Mx
◦ Acyclovir helps only in prodrome
VZV
Primary v/s secondary (shingles)
Oral involvement on buccal
mucosa and hard palate
Secondary usually involves V3
dermatome
Supportive Tx
Rarely acyclovir in Secondary
Oral Candidiasis
Pseudomembranous candidiasis
(thrush) presents after prolonged
abx use
Whitish plaque screpped – red
beefy base
Mucocutaneous candidiasis - in
immunocompromised
Multiple mucosal surfaces
involved
Thrush
Tx:
◦ Nystatin
◦ Topical clotrimazole
◦ Oral fluconazole
◦ i.v. Ampho B
Bechets Syndrome
Bechets (Oro-oculo-
genito)
Autoimmune disorder affecting:
◦ Mouth: Painful ulcers like apthous are the
most common sign of Behcet's disease. Usually
heal in one to three weeks.
◦ Eyes. Uveitis, typically in both eyes. May recur.
◦ Genitals. Red, open painful sores can occur on
the scrotum or the vulva.
◦ May also affect skin, joints, GI and CNS.
Lupus
LUPUS
Oral involvement:
◦ Erythematous plaques – erosions –
ulceration
◦ White keratotic striae radiating from lesion
Dx:
◦ Clinical, Serologic testing, ANA, SS-A/SS-B
Tx:
◦ Topical / oral Steroids
◦ Cyclophosphamide, azathioprine, mtx
Pemphigoid
Autoimmune: Abodies against
epethelial basement membrane,
intercelllular junctions
Oral involvement more in
cicatrical pemphigoid
Oral inv occur first in pemphigus
vulgaris
Dx: Biopsy
Tx: Steroids and cytotoxic agents
Erythema Multiforme
Reaction to drug or infectious
agent
Range from target lesions to
Steve Johnsons to Toxic Epidermal
Necrolysis
Treatment is supportive
Strawberry tongue – Kawasaki’s
diseasae
XRT induced mucositis
IBD associated oral
lesions
Morsicatio buccarum
Hyperkeratosis found in the line
of the occlusal plane on the
tissue that contacts the teeth. •
The mucobuccal folds are usually
not affected by the trauma –
Inner lip areas may also be
irritated (morsicatio labiorum)
and traumatized by the incisors
History of habitual chewing
What is your diagnosis?
History
Small vesicle which increases in
size and bursts….. Becomes
normal….. Then regrows.
For about 2 years
No pain or tenderness
No addictions
No other lesions or systemic
diseases
Neck nodes not palpable
Diagnosis is……
Mucocele
Upper pic is mucocele of lower lip
Lower one is mucocele of tongue
Pre malignan
lesions of
ORAL CAVITY
Dr. Maisam Abbas
Topics to discuss
Lukoplakia
Lichen Planus
SMF
Erythroplakia
Lukoplakia
Clinical
Diagnosis
Unexplained white patch
Homogenous &
Non-homogenous
◦ Verroucous pattern
◦ Speckled pattern
DIAGNOSIS
History
◦ Tobacco
◦ Alcohol
◦ Candidal infection
Examination
Histopathology
Risk of malignant transformation
high in non-smokers as compared
to smokers *
Lesions of FOM, tongue – high risk
* Einhorn J,Wersäll J. Incidence of oral carcinoma in patients with leukoplakia
of the oral mucosa.Cancer 1967;20:2189-2193.
Bánóczy J. Follow-up studies in oral leukoplakia.J Maxillofac Surg 1977;5:69-75.
LEUKOPLAKIA
LICHEN PLANUS
T-Cell destruction of basal
epidermal layer
Assoc. with Hep C
1-5% chance of oral malignancy
Lesions appear as: whitish striae,
leukoplaktic, erosive
LICHEN PLANUS
Chronic inflammatory disorder
with immune pathology appears
as:
◦ White striaform lesions, bilaterally
symmetrical and usually
asymptomatic
◦ Plaque
◦ Atrophic or erythematous
◦ Erosive (painful)
Cell mediated, T lymphocytes
accumulate beneath the
epithelium of the oral mucosa
and increase the rate of
differentiation of stratified
squamous epithelium
? Malignant potential
LICHEN PLANUS
Small risk of carcinoma evolving from
proven oral lichen planus – in conjunction
with the atrophic or erosive form.
Lichenoid dysplasia – Significant degree of
allelic loss in dysplastic oral lichenoid lesions
Degree of dysplasia in association with
lichenoid features should alert the clinician
to either remove the altered mucosa or
follow the patient carefully
References: Wein, RO. O’Leary, M. Chapter 51: Stomatitis. Bailey’s Otolaryngology
Head and Neck Surgery Sclubba, JJ. Chapter 91: Oral Mucosal Lesions. Cummings
Otolaryngology Head and Neck Surgery
ORAL SUBMUCOUS
FIBROSIS
Juxtaposition of atrophic
epithelium and adjacent fibrosis
of the lining mucosa
◦ Failure of collagen remodelling
◦ Loss of tissue mobility
Etiology – areca (betel) nut use
7-15% malignant transformation
CLINICAL PRESENTATIONS
EARLY FORM:
◦ Burning sensation by spicy food
◦ Blanching of mucosa
◦ Leathery mucosa
LATE FORM:
◦ Fibrous bands
◦ Limited mouth opening
◦ Woody changes to mucosa & tongue
◦ Distortion of uvula
ERYTHROPAKIA
Bright red velvety change in oral
mucosa that cannot be defined
as any other lesion.
Upto 50% malignant
transformation rates
May harbor carcinoma in situ
Erythroplakias may harbor
carcinoma in situ and therefore
have to be removed surgically.
SUMMARY
Premalignant lesions of oral cavity are
usually associated with smoking, alcohol
consumption and even viral & fungal
etiology have been ascribed.
All lesions harbor a certain degree of
malignant potential – erythroplakia being
greatest
All have to be confirmed by histopathology.
The treatment for most is removal of
carcinogen and waitful watching except
erythroplakia which should be excised.
CASE
A 55 year old is referred to your
clinic for evaluation of an oral
lesion discovered on routine
dental examination?
HISTORY
Time course surrounding the onset of symptoms
Location
Multiple vs singular
Duration
Pain
Induration
Other mucosal lesions
Cutaneous lesions
Systemic diseases
Medications (esp. recent changes)
Recognized triggers/palliating factors
Aggressiveness of oral hygiene and product use
Prodromal symptoms
Risk factors for malignancy
History reveals
Incidentally discovered 3 weeks
ago •
Left buccal region •
Singular •
Pain - none •
Other mucosal lesions - none •
Systemic diseases - negative •
Recognized triggers/palliating
factors - none
Examination
A full head and neck examination is necessary •
Assess for synchronous findings beyond the oral
presentation •
Dentures should be removed and assessed for
quality of fit while asking the patient about the
original date of manufacture in addition to visits
for modification •
Buccal mucosal lesions, the relationship of the
ipsilateral dentition and any amalgam that
contacts the mucosa in a closed mouth position
should be identified •
Quality of salivary production should be assessed
Querries??
