PRECANCEROUS CONDITIONS OF

THE ORAL CAVITY

 By
Arun
Babu Joseph
Classification ( Bailey)
Lesions considered having a definite risk of
malignancy
 Leukoplakia
 Erythroplakia
 Chronic hyperplastic candidiasis
Conditions that are not themselves premalignant but
which are associated with a higher than normal
incidence of oral cancer
 Oral submucous fibrosis
 Syphilitic glossitis
 Sideropenic dysphagia
Oral conditions about which there is still some doubt
as to whether their association with oral cancer is
causal or casual
 Oral Lichen planus
 Discoid lupus erythematosus
 Dyskeratosis congenita
Types of oral precancer.
Precancerous lesions
 Defined as morphologically altered tissue in which
cancer is more likely to occur than its apparently
normal counterpart.
Example
 Leukoplakia
 Erythroplakia
 Mucosal changes associated with smoking habits.
 Carcinoma in situ
 Bowen disease
 Actinic keratosis, cheilitis and elastosis.
Precancerous conditions
 Defined as generalized state or condition
associated with significantly increased risk
for cancer development.
Example
 Oral sub mucous fibrosis
 Syphilis
 Sideropenic dysphagia
 Oral Lichen planus
 Lupus erythematosus
Leukoplakia

 Any white patch or plaque that cannot be

characterized clinically or pathologically
as any other disease.
 This definition has no histological
connotation.
Forms of leukoplakia.
(WHO 1980)

Homogenous : lesions that are

uniformly white.
Non homogenous : lesions in
which part of the lesion is
white and the rest appears
reddened.
Alternatively
1.) Homogenous
a.) Smooth
b.)Furrowed(fissured)
c.) Ulcerated.
2.) Non homogenous
nodulospeckled:
Well demarcated raised
white areas
interspersed with
reddened areas.
According to risk of future
development of oral cancer.
High risk sites
 Floor of mouth
 Lateral or ventral
surface of tongue.
 Soft palate.
Low risk sites
 Dorsum of tongue
 Hard palate
Intermediate group
 All other sites of
oral mucosa.
Etiology
Local factors
 Tobacco Smokeless and
smoking tobacco.
 Alcohol
 Chronic irritation
malocclusion ill fitting
dentures, sharp broken
teeth, hot spicy food,
root piece etc
 Candidiasis
 Electromagnetic reaction
or galvanism
Etiology (contd.)
Regional & systemic factors.

 Vitamin deficiency
 Sideropenic anaemia
 Nutritional deficiency
 Conditions causing xerostomia ( Salivary gland
diseases, Anticholinergic drugs, Radiation.)
 Drugs ( Anticholinergics, Antimetabolic, Systemically
administered alcohol)
 Virus ( HSV & HPV)
 Idiopathic
 Histopathological
features.

Hallmark
 Surface
hyperkeratosis
 Epithelial
hyperplasia
 Epithelial dysplasia
Keratinization pattern
Keratinization of the mucosal epithelium which is normally
non-keratinized.
Hyperorthokeratosis
 Orthokeratosis:
In normal state , superficial epithelium, is nearly
homogenous, eosinophilic and anuclear with stratum
granulosum always present.
 Hyperorthokeratosis:
abnormal increase in thickness of the orthokeratin layer of
stratum corneum in a particular location.
Hyperparakeratosis
 Parakeratosis:
superficial epithelium is flat and acidophilic with pyknotic
nuclei. Stratum granulosum may or may not be present.
 Hyperparakeratosis:
Increased thickness of parakeratotic layer, exceeding the
normal thickness.
Epithelium
Epithelial thickness
 Hyperplasia
 Atrophy
 Vacuolar degeneration
 Acanthosis
 Basal cell hyperplasia
 Intra-epithelial edema
Epithelial dysplasia
 Drop shaped rete ridges
 Nuclear hyperchromatism
 Nuclear pleomorphism
 Altered nuclear-
cytoplasmic ratio
 Excess mitotic activity
 Loss of polarity of cells
 Deep cell keratinisation
 Loss of differentiation
 Loss of intercellular
distance
 Epithelial dysplasia
seen in 3% of snuff
induced leukoplakias
and 16% of smoking
habit related
leukoplakia.
 Nodular leukoplakia
shows higher
frequency of epithelial
dysplasia
 Grading
Connective tissue
 Chronic inflammatory cell infiltration
is seen in 50% cases.
 Submucosal, homogenous
eosinophilic material is usually seen
in the connective tissue.
 Hyaline degeneration seen in 10 %
cases
Malignant potential
 0.3% - 10% cases
 Higher in women (6%) than men
(3.9%) due to involvement of
endogenous factors
 Leukoplakia associated with chewing
habit of tobacco shows higher rate of
malignant transformation.
 Nodular dysplasia has higher risk of
malignant transformation than other
clinical types.
 High risk if
 Elderly patient
 Persistence of lesion for
several years
 Female patient
 Lesion situated on the
margins, base of tongue,
floor of mouth
 Erosive lesions
Differential diagnosis
 Lichen planus
 Chemical burns
 Syphilitic mucus patches
 White sponge nevus
 Discoid lupus erythematosus
 Psoriasis
Differential diagnosis (contd.)
 Leukoedema
 Hairy leukoplakia
 Verruca vulgaris
 Cheek biting lesion
 Electrogalvanic white lesion
Management
 Elimination of the etiological factor
 Conservative treatment
 13 cis retinoic acid
 Antioxidant therapy
 Nystatin therapy
 Surgical management
 Biopsy taken for microscopic examination from
areas with greater surface irregularities.
 Conventional Surgery
 Cryosurgery
 Electrocautery
 LASER
 Guidelines for treatment
 Biopsy should be done
 Elimination of etiological factors
 Conservative /Surgical management
if not heal in 2-3 weeks
 Conservative treatment applied to
large incipient lesions & verrucous
lesions
 Surgical treatment if conservative
treatment fails in 3 months
 Excision of nodular leukoplakia &
follow up
 All patients , re-examination twice a
year
 Re-biopsy after 5-6 months
 ERYTHROPLAKIA
 Also called erythroplasia of Queyrat.

 Def: Area of reddened, velvety textured mucosa

that cannot be identified on the basis of clinical
& histopathologic examination as being caused
by inflammation or any other disease
process.
Etiology
 Idiopathic
 Alcohol
 Smoking
 Secondary
infection or
superinfection with
candidiasis
Clinical features
Seen as a non elevated red macule on an
epithelial surface.
Otherwise asymtomatic.
 Age and sex
Male predilection 6th & 7th decade
 Sites
 All mucosal surfaces of head & neck area
 50% found on vermilion or intraoral
surfaces rest evenly divide between larynx
& pharynx
 Intraorally lateral & ventral tongue, oral
floor & soft palate are more frequently
involved.
Hisopathological features

 Epithelial dysplasia
 Cause for the red colour
 Spinous layer contains cells showing
atypia, hyperchromatism,
pleomorphism, & increase in the
number of mitotic figures.
Differential diagnosis.
 Candidiasis
 Denture stomatitis
 Tuberculosis
 Histoplasmosis
 Area of mechanical irritation
 Macular hemangioma
 Telengiectasia.
 Traumatic lesion
Management
 1 % toluidine blue test.
 Incisional biopsy for microscopic diagnosis.
 Conservative surgical procedure such as
mucosal stripping
 Destructive techniques such as
electrocoagulation, cryotherapy, laser
ablation also effective.
 Extended clinical follow up.
 Elimination of a suspect irritant
 PIPE SMOKERS’ KERATOSIS

 palatal keratosis due to pipe smoking

is benign.
 Any carcinomas related to pipe-
smoking appears in another site in
the mouth and may not be preceded
by keratosis.
SMOKELESS TOBACCO-RELATED
KERATOSES
 Hyperkeratotic mucosal lesions
Management
 Diagnosis is based on the history of
snuff use and the white lesion in the
area where the tobacco is held.
 Biopsy is required
 Snuff-dippers’ lesions will resolve on
stopping the habit
 Regular follow-up
 Bowens disease
 Localized intra-
epidermoid carcinoma
 Characterized by
progressive scaly or
crusted plaque like
lesion
Causes
 Sun exposure
 Arsenic ingestion
Clinical features
 Sites :male and female genital mucosa
and in oral mucosa as erythroplakia,
leukoplakia or eryhematous lesion.
 Skin: red & slightly scaly area on the
skin, which eventually enlarges and
turns into white or yellowish lesion.
 Signs: when scales are removed a
granular surface without bleeding is
seen.
 Histopathology
 Intraepithelial
features of
malignancy

 Management
 Freezing
technique/diathermy/
cauterization/
radiotherapy/
application of
cytotoxic drugs.
Chronic hyperplasic candidiasis.
 Dense chalky plaques
of keratin
 Plaques thicker & more
opaque than
leukoplakia
 Commonly seen at the
oral commisures,
extending into
adjacent skin & face.
 High degree of
malignant change
 Treatment
 nystatin,
amphotercin, or
miconazole to
eliminate the infection
 Treatment necessary
for many months &
reinfection common
 Surgical excision for
persistent lesions.
Oral Lichen planus
 First described by
Erasmus Wilson in
1869
 Inflammatory
condition of skin
presenting with
characteristic
violaceous , polygonal,
pruritic papules. Lace
like pattern.
 Buccal mucosa ( 84%)
lips, tongue, gingiva,
floor of mouth &
palate.
 Etiology
 Immunology
Cell mediated immune
response
Autoimmunity
Immunodeficiency
 Genetic factors
 Infections
 Drugs & chemicals
 Psychogenic factors
 Habit
 Miscellaneous
Deficiency of vitamin B1, B6, &
C,electric potential difference,
anaemia, & patients with secondary
syphilis.
Trauma & malnutrition
Clinical features
 Burning pain of the oral mucosa
Appearance
 Oral lesion characterized by white & gray
velvety thread like papules in a linear
angular or retiform arrangement forming
typical lacy reticular patterns, rings and
streaks over the oral mucosa.
 Wickham’s striae--- tiny white elevated
dots present at the intersection of white
lines.
Types of oral lichen planus
 Reticular type
 Papular
 Plaque
 Atrophic form
 Bullous form
 Hypertrophic form
 Annular form
Histopathological features of oral
lichen planus
 Hyperkeratosis
 Prominent granular
layer
 Basal cell degeneration
(may form colloid
bodies)
 Heavy lymphocyte
infiltration (T cells) in
the upper epidermis
 Saw tooth dermo-
epidermal junction.
Differential diagnosis
 Leukoplakia
 Candidiasis
 Pemphigus
 Lupus erythematosus
 Drug induced lesion
 White sponge nevus
 Ectopic geographic tongue
 Cheek biting
 Lichenoid drug reaction
Malignant potential

 1.2 % malignant
change (Silverman
et al)
 Association
between LP & oral
cancer seen only
with atrophic or
erosive LP.
Management
 Removal of cause
 Medical therapy
Steroids
In most patients with erosive & ulcerative lesion
topical steroids are commonly used.
If severe, systemic steroids are used.
Topical Antifungal agents.
Vitamin A analogues
Cyclosporine
 Surgical therapy.
Indications
 When the conventional methods fail in
ulcerative lesions
 In case of small solitary lesions
Cryosurgery & cauterization have also
been tried.
Others
 Psychotherapy
 Dapsone therapy
 PUVA therapy
 Symptomatic
Treatment options
Group 1 lichen planus of reticular or atrophic
variety without symptoms.
 No treatment is required
 Regular follow up
 Diazepam for anxiety
Group 2 lichen planus of reticular or atrophic
variety with mild to moderate pain and burning
 Local application of benzocaine 10 % for burning
 2 mg Diazepam
 Topical corticosteroid
 Intralesional steroid for quicker relief.
 Regular follow up.
Treatment options (Contd.)
Group 3 Erosive lichen planus
 Immediate biopsy
 Local control of pain
 Intralesional steroid
 If infected, antibiotics.
Group 4 lichenoid reaction
 Discontinue offending drug
 Local application of benzocaine
Oral submucous fibrosis
 Insidious chronic disease affecting
any part of the oral cavity and
sometimes the pharynx
 Very common in the Indian
subcontinent
 Juxta epithelial inflammatory reaction
fibroelastic changes of lamina propria
+ epithelial atrophy
stiffness of oral mucosa & trismus
Etiopathogenesis

 Chillies
 Tobacco
 Betel nut
 Nutritional
deficiency
 Defective iron
metabolism
Etiopathogenesis (Contd.)

 Bacterial infections
 Collagen disorders
 Immunological disorders
 Genetic susceptibility
 Altered salivary composition
 Clinical features
Age & sex
 Affects both sexes
 Majority between
between 20-40 years.
Site distribution
 Most frequent location
buccal mucosa &
retromolar areas.
 Also commonly involves
soft palate, palatal
fauces, uvula, tongue &
labial mucosa.
Symptoms
Onset is insidious

Early symptoms Late symptoms

Burning sensation of Gradual stiffening of
oral mucosa,
aggravated by spicy the oral mucosa
food Trismus
Vessiculation, Dysphagia
ulceration,
pigmentation, Referred pain in the
recurrent stomatitis ears and deafness
and defective
gustatory sensation nasal voice
may also be present
Signs
 Earliest sign is
blanching of the
mucosa
 Becomes slightly
opaque and white
 Mucosa acquires a
marble like appearance.
 Later mucosa becomes
stiff and vertical fibrous
bands appear.
Clinical stages of oral submucus
fibrosis

 Stage of stomatitis and vesiculation.

 Stage of fibrosis
 Stage of sequelae & complications.
 Histopathological features.
Epithelium
 Most cases oral epithelium is markedly atrophic.
 The atrophic epithelium exhibits intercellular
edema (18 %), signet cells( 13%), and epithelial
atypia (7%).
 Sometimes atrophic epithelium is associated with
hyper-orthokeratosis
 Liquefaction degeneration of the basal cell layer.
 Rete pegs are completely lost
 Connective tissue.
 It shows vesicles which are caused by sub epithelial
accumulation of fluid.
 Inflammatiory cells are mostly mononuclear: eosinophils &
occasionally plasma cells maybe seen.

Pindborg has described the connective tissue changes in 4

consecutive stages
 1.) Very early stage
 2.) Early stage
 3.) Moderately advanced stage
 4.) Advanced stage
Diffuse hyalinization of subepithelial stroma with few, small fibroblastic

nuclei and with pigment incontinence from the overlying epithelial melanin .
Epithelial atypia in OSMF
 Irregular epithelial stratification,
increased number of mitotic features,
nuclear pleomorphism,
hyperchromatism and loss of polarity
of cell.
 Spongiosis especially in the basal cell
layer.
 Signet cells seen in the basal layer.
 Marked reduction in melanin
pigmentation in basal cell layer.
Malignant potential
 From diverse intra oral
locations
 Atrophic epithelium
Hyperkeratotic
Intracellular edema +
Basal cell hyperplasia
Epithelial atypia +
hyperplasia
Carcinoma
Management
 Reduction of habit / behavioral
therapy
 Medical therapy
 Vitamin rich diet along with iron therapy
 Dexamethasone 4 mg (1ml) combined with
hylase, 1500 I.U. in 1 ml is injected into
the affected area biweekly for 8-10 weeks.
 Vitamin E may also be used with the above
combination.
 Placental extract
Surgical treatment
 Aim is to relieve trismus, prevent further
fibrosis & to provide neo vascularization of
fibrous tissue.
 Indications
 Marked limitation of opening of mouth.
 Biopsy reveals neoplastic changes
 Marked dysphagia
Surgical options
 Excision of fibrous bands followed by use
of tongue flaps as a graft

 Excision of fibrotic bands, followed by

reconstruction using bilateral full thickness
nasolabial flap

 New technique is of bilateral palatal flap to

cover the exposed area, in combination
with bilateral temporalis myotomy &
coronoidectomy
 Laser
 Carbon dioxide laser surgery alleviates the
functional restriction.
 Under GA laser is used to incise the buccal
mucosa and vaporize the submucosal
connective tissue to the level of buccinator
muscle.
 Hemostasis is provided by lased surface itself
and the mouth opening increases
immediately.
 Oral physiotherapy
 Oral exercises are advised in early
and moderately advanced cases.
 Includes mouth opening and
ballooning of the mouth.
 Cryosurgery
 Diathermy
Dyskeratosis Congenita
 Zinssner-Engman-Cole syndrome.
 Rare genokeratosis
 Characterized by 3 typical signs oral
leukoplakia, dystrophic nails and
pigmentation of skin.
 Other features frail skeleton, mental
retardation, small sella turcica ,
dysphagia, transparent tympanic
membrane, deafness, epiphora, eyelid
infection, urethral anomalies, small
testes and hyperhidrosis of the palms
and soles
Oral manifestations
5 and 15 years
 Diffusely distributed vesicles and ulcerations followed
by accumulation of white patches of necrotic
epithelium and sometimes superimposed monilial
infection over tongue & buccal mucosa
14-20 years
 recurrent ulceration and development of erythroplasia
or red mucosal lesion.
20-30 years
 development of erosive leukoplakia and carcinoma.
Histology
 Skin lesion shows increased number of melanin
containing chromatophores and increased vascularity.
 Depending on stage of disease epithelium may show
dysplasia.
Laboratory finding
 Pancytopenia
Radiographic feature
 There maybe severe periodontal bone loss
Management
 No specific treatment.
 Periodic check up.
Discoid Lupus Erythematosus

 Oral lesions consists of circumscribed, somewhat

elevated white patches usually surrounded by a
telengiectatic halo.
 Epithelial dysplasia maybe seen on histological
examination, this may lead onto malignant
transformation.
 Malignant change usually occurs in those lesions
adjacent to vermilion border.
 More often in men than women
 Such patients advised to avoid bright sunlight and
when in open air to apply an ultraviolet barrier cream
to the lips.
Sideropenic dysphagia ( Plummer-vinson
syndrome, Paterson- Kelly syndrome.)
 In 1936, Ahlbom showed
the relationship between
sideropenic dysphagia
and oral cancer.
 Particularly common in
Swedish women.
 Sideropenic dysphagia
leads to epithelial
atrophy which is
excessively vulnerable to
carcinogenic agents.
 Anaemia responds to
iron supplements. But it
is not known whether
such treatment reduces
risk of subsequent
malignant change.
 Syphilitic glossitis.
 Prior to antibiotic era
 Atrophy of overlying
epithelium.
 Atrophic epithelium more
vulneralble to irritants
 Squamous cell carcinoma
can develop in syphilitic
glossitis even in the
absence of oral leukoplakia.
 Active syphilis must be
treated.
 Regular follow up is
required.
Just remember this……
 Common precancerous conditions are
Leukoplakia, erythroplakia, Submucous
fibrosis & Oral Lichen Planus
 High chance of malignancy seen in
speckled leukoplakia, dysplastic
leukoplakia, erythroplakia, submucous
fibrosis etc.
 Etiology of most of the lesions are
chemical irritants such as tobacco,
betel etc.
Just remember this…..
 Management includes :
 Stop any associated habits e.g. betel quid
or smoking
 Treat candidal infection and/or iron
deficiency.
 Biopsy to assess dysplasia
 Assess risk of premalignant change on
clinical & histological findings
 Consider ablation of individual lesions
 Regular follow up