PREMALIGNANT

LESIONS AND
CONDITIONS

Submitted by-BALJEET KAUR

B.D.S.-3rd year
Roll no.15
 CONTENTS
 Premalignant lesions
1.Dysplasia
2.Leukoplakia
3.Intraepithelial carcinoma
4.Erythoplakia

 Premalignant conditions
1.Oral lichen planus
2.Oral submucous Fibrosis
3.Syphilis
 Premalignant lesions and
conditions
 What is a premalignant lesion?
It is defined by WHO as a morphological altered
tissue in which cancer is more likely to occur than
in its apparently normal counterpart.E.g
Leukoplakia, erythoplakia,mucosal changes
associated with smoking habits,carcinoma insitu.
 What is a premalignant condition?

It is generalized state associated with a

significantly increased risk of cancer. E.g.
Sideropenic dysphagia,oral submucous
fibrosis(OSMF) and lichen planus.
 Dysplasia
• This word is originated from the ancient Greek
word dys- difficulty + plasia-formation.
• It is the loss in the uniformity of the cells, as well
as a loss in their architectural orientation.
• DYSPLASIA is encountered principally in the
epithelium.e.g. epithelial dysplasia in
premalignant and malignant lesions.
 MICROSCOPIC FEATURES
associated with Oral epithelial
Dysplasia
Architectural(tissue) changes:
 Loss of polarity

 Abnormal orientation of

epithelial cells
 Basal cell hyperplasia

 Increased cellular density

 Bulbous drop-shaped rete pegs

 Disordered maturation from basal to squamous cells

 Abnormal stratification of the epithelium.

 Dyskeratosis
Cytologic features of dysplasia
 Loss of polarity and abnormal orientation of
epithelial cells:
Basal epithelial cells are usually cuboidal or short
columnar,They are arranged perpendicular to basement
membrane.In dysplastic lesions this arrangement is
changed.Cells become Haphazardly arranged on the
basement membrane.
 Basal cell hyperplasia:
They are most active cells have capacity to divide.As in
dysplasia there is increased mitosis the basal cells divide to
form a large no. of basaloid cells.
 Increased cellular density:
Because of increased mitosis there in increase in
cellular density in the epithelium
 Bulbous drop-shape rete pegs:
As basal cell proliferation induces the change
and appear very broad gives rete peg bulbous shape.
 Disordered maturation from basal
to squamous cells:
Epithelial cells gradually mature as they move towards the surface.As
they move they differentiate or mature to start forming keratin and
depositing it. in dysplasia this process is hampered cells fails to mature
and retain their basal cell appearance.
 Abnormal stratification of the epithelium:

As maturation is affected different layers of the epithelium are not clearly

demarcated. The cells are not defined in strata and appear almost similar to
each other.
 Dyskeratosis
Epithelium shows dyskeratosis where this process is abnormal
and it may start from the lower level itself. so in such lesion
keratinized epithelial cells may be found in prickle cell layer
where they are usually not present. Keratin pearls may be seen.
Cellular changes
 Abnormal variation in nuclear size (anisonucleosis)
Nucleus become enlarged with prominent nucleoli.
 Abnormal variation in cell size (anisocytosis)
Cytoplasm shows great variation in size and shape. few
cells become very big gaining giant proportions.
 Increased N/ C ratio ,Normal range 1:4 to 1:6.this
 Enlarged nuclei and cells,Hyperchromatic nuclei
 Increased mitotic figures
 Abnormal mitotic figures(abnormal in shape or
location)
• Abnormal Mitosis leading to tripolar or tetrapolar
mitotic figures.sometimes nucleus divides without
division of cytoplasm.upper layer show mitotic figures.
 Nuclear and cellular pleomorphism
 Increased number and size of nucleoli.
 WHO Dysplasia system
Hyperplasia with increased no. of cells: This may be in the
spinous layer(acanthosis) or in basal and parabasal cell
layer( basal cell hyperplasia).The architecture of the epithelium
is preserved and there is no cellular atypia.
Dysplasia with three grades:
1.Mild dysplasia -Architectural disturbance is limited to the lower
third of the epithelium, accompanied by cytological atypia.
2.Moderate dysplasia- architectural disturbance extends into the
middle third of the epithelium,accompined by un upgrading
degree of cytological atypia.
3.Severe dysplasia-Architectural disturbance is greater than two-
thirds of the epithelium with associated cytological atypia.
Carcinoma in situ- Full or almost full thickness of the epithelium
shows architectural disturbance,accompined by pronounced
cytological atypia.Atypical mitotic figures and abnormal
superficial; mitosis are present.
 LEUKOPLAKIA
The term Leukoplakia originates from two Greek words leuko, i.e white and plakia i.e. patch.
It is defined as a predominantly white lesion of the oral mucosa that cannot be characterized
as any other definable lesion.

INCIDENCE AND PREVALANCE:

 Dysplastic epithelium or frankly invasive carcinoma =5%-25% of biopsies of Leukoplakia.
 4% Leukoplakia can transform into malignancy.

 Specific clinical subtypes=47%

 May be artificially low

because many lesions are

surgically removed at the
beginning of follow up.
 Leukoplakia is the

most common oral precancer=85%

 Males are more affect

then females 70%.

 3% of white adults are also

affected.
 ETIOLOGY
6-S : sunlight,smoking,syphilis,spices
,Spirit & sepsis.
1.Tobacco: >80% of patient is smokers.
smokers > Non-smokers
Other then smoking tobacco , some people have habit
of chewing coarsely cut tobacco or holding fine ground
tobacco leaves( snuff) in the mandibular vestibule is
one the common cause of leukoplakia. This is known
as Tobacco pouch keratosis.This is not a true
leukoplakia.
2.Alochol: Alcohol has synergistic effects with tobacco
relative to oral cancer production.
People who use mouth rinses with >25% alcohol content
have grayish buccal mucosa plaque.
3.Sanguinaria
Person who use toothpaste or mouth rinses containing herbal
extract sanguinaria develops true leukoplakia and is known
as sanguinaria associated keratosis.It usually occurs on
max. vestibule and on alveolar mucosa of the maxilla.
4.U.V. radiations
Mainly cause leukoplakia of vermillion border of lower lip i.e.
usually associated with actinic cheilosis..mainly
immunocompromised person , transplant patients.
5.Micro-organisms
The microorganisms candida albicans can colonize the
superficial layer of oral mucosa producing a thick granular
plaque with mixed white and red coloration is known as
candidal leukoplakia.
HPV16 has been shown to induce dysplasia like changes in
normal differentiating squamous epithelium.
6.Trauma
Nicotine stomatitis is generalized white palatal
alteration.

CLINICAL FEATURES
 It usually affects person more than 40 years of age
 Males are more commonly affected then females.
 Apx. 70% of leukoplakia occurs on vermillion border of
lip, buccal mucosa, gingiva, tongue, floor of mouth.
CLINICAL VARIANTS OF LEUKOPLAKIA

1.Mild leukoplakia
Presents as elevated gray white plaque which may
be translucent , fissured or wrinkled.
They are soft and flat and be sharply demarcated or
bled into the normal tissue.
2.Homogenous
As the lesion progress it becomes thicker , it may be
leathery to palpation and fissures may deepen.
3.Granular or nodular
More severe lesions that develops surface
irregularities.
4.Verrucous leukoplakia
Lesions that shows Sharpe or blunt projections.
5.Proliferative verruous leukoplakia.
It is characterized by development of multiple
keratotic plaque with roughened surface
projections.
6.Erythoplakia
In this the lesion become dysplastic even invasive
and some lesions demonstrates scattered
patches of redness called erythoplakia.
 STAGING
L: extent of leukoplakia
 L0, no evidence of lesion

 L1, ≤ 2 cm

 L2, 2–4 cm

 L3, ≥ 4 cm

 Lx, not specified

S: site of leukoplakia
 S1, all sites excluding FOM, tongue

 S2, FOM and/or tongue

 Sx, not specified

C: clinical aspect
 C1, homogenous

 C2, nonhomogeneous

 Cx, not specified

Definitive (histopathologic) diagnosis

P: histopathologic features
 P1, no dysplasia

 P2, mild dysplasia

 P3, moderate dysplasia

 P4, severe dysplasia

 Px, not specified

 Histopathology
 Hyperkeratosis with or without acanthosis
 Atrophy of epithelium

 Chronic inflammatory cell infiltration

 Keratin layer may be para keratin or ortho

keratin.
H/P alteration of dysplastic epithelial cell
o Enlarge nuclei an cells

o Altered nucleic cytoplasmic ratio

o Hyperchromatism
LEUKOPLAKIA
 Large and prominent nucleoli
 Dyskeratosis
 Pleomorphic nuclei and cells
 Inc. mitotic activity
 Bulbous or tear shape drop rete ridges
 Loss of polarity
 Keratin or epithelial pearls
 Loss of cell cohesiveness
 Abnormal mitotic figures.
 TREATMENT
 Biopsy can be done that will guide the course of
treatment.
 Habit sessation that is recommended
 Complete removal is accomplished by surgical
excision, lasor ablation , cryosurgery.
 Carcinoma insitu
 It is a condition which arises frequently on skin
but also occurs on mucous membrane including
those of oral cavity.
It represents a precancerous dyskeratotic process
or a intraepithelial type of superficial
carcinoma.
 If it is develop from Leukoplakia it would be

keratinized but if arises Renovo it will be non-

keratinized.
 CLINICAL FEATURES
o Carcinoma insitu can have clinical appearance
of leukoplakia 45%
o erytholpkia 16%
o combination of leukoplakia and erythoplakia
9%
o ulcerated lesions 13%
o White + ulcerated lesions 5%
o Red + ulcerated lesions 1%
 COMMON SITES
•Floor of mouth 23%
•Tongue 22%

•Lips 20%

•It commonly occurs predominantly in females

with ratio of 1.8:1

•More commonly in

elderly person.
 HISTOPATHOLOGY
-Keratin may or may not present but if present it
may be parakeratin or orthokeratin.
-Dyskeratosis and keratin pearl formation is rare.
 There may be hyperplasia of altered epihelium

and in some cases there may be atrophy.

 increased N/C ratio.

 Nuclear hyperchromatism
 Cellular pleomorphism is uncommon.

 One of the most common alteration is loss of

orientation of cells and loss of normal polarity.

CARCINOMA INSITU
 Mitotic activity is variable
 There is clear line of demarcation between
normal and altered epithelium.
 All these changes occur within the surface
epithelium which remains confined by
basement membrane.

TREATMENT
-Surgical excision.
-irradiation
-cauterization
-exposure to solid Co2.
 Oral submucous fibrosis
 It is a chronic,progressive lesion that affects the
oral cavity and URT which is caused due to
juxta-epithelial hyalization and is preceded by
formation of blisters due to
 chills,

 fibroelastic changes

which further leads to

leathery appearance ,
stiffness, trismus.
 Etiology
 Habitual chewing of arecanut (bettlenut)
 Chillies
 Tobacco
 Lime
 Nutritional deficiency
 Defective iron metabolism
 Bacterial infection
 collagen disorders
 Immunological disorders
 Genetic suceptibility
Clinical features
 Onset is incisidious over
2-5 years.
1.) Early or prodromal
symptoms- burning sensation,
blisters on palate,ulceration/inflammation of oral
mucosa,excessive salivation,defective gustatory
sensation ,dryness of mouth, small vesicles on
cheeks and palate.
 22% petechaie mostly on tongue followed by

labial and buccal mucosa.

 -Pain in area where submucosal fibrotic bands

are developing when palpated.

2.) Advanced osmf- blanched, opaque, white fibrous
bands appears.
-oral mucosa involved symmetrically and fibrous
bands on buccal mucosa run in vertical direction.
-Variation of fibrous deposit from slight whitish
area on soft palate to dense fibrosis causing
fixation ,shortening or deviation of soft palate or
uvula.
-The fibrosis may extend to pharynx anddown to
piriform fossae.
-impairment of tongue movement.
-Difficulty in opening the mouth
and in swallowing.
 Histopathology
 Epithelium :- marked atrophy of epithelium
that exhibits signet cells and epithelial atypia
and associated with hyperorthokeratosis and
pyknotic changes in nuclei of basal cell layer.
> Retepegs are completely lost.
 Connective tissue :- It shows vesicles which are
caused by sub epithelial accumulation of fluid
and shows inflammatory cell infiltration.
 It also shows dysplastic changes.
ORAL SUBMUCOUS FIRBOSIS
 Management
 Stoppage of all causative agents
 Nutritional support :- Vitamin b complex and
increased protein diet.
 Immunomodulatory drugs :- Glucocorticoids and
placental extracts.
 Physiotherapy :- Forceful mouth opening and
heat therapy.
 Local drug delivery
 Combined therapy :- Vasodilators + vit -D,E & B
complex + iodine + corticosteroids
 Surgical management :- Submucosal
resectioning of fibrotic band and mucosal grafts.
 ERYTHROPLAKIA
It is the term used for chronic red mucosal macule
which cannot be given any other specific
diagnostic name and cannot be attributed to
traumatic, vascular or inflammatory.
It is also called Erythroplasia of Queyrat. It was
Queyrat who coined the term erythroplasia which
is used to describe a precancerous red lesion that
develops on the penis.Erythroplakia is a
persistent velvety red patch. Reddish color results
from absence of surface keratin layer and due to
presence of connective tissue papillae containing
enlarged capillaries projected close to the surface.
ETIOLOGY
It can be idiopathic caused by
1. Smoking: Pipe smokers
2. Trauma

3. Dental irritation

TYPES
1.Homogenous form:
 Which appears as a bright red, soft, velvety

lesions and quite extensive in size

 Site: Commonly found in buccal mucosa and soft

palate
2. Speckled erythroplakia:
 These are soft, red lesions, slightly elevated with

an irregular outline.
 Surface being granular—These are often referred

to as speckled Leukoplakia/erythroplakia
Common Site: Anywhere in the oral cavity.
3.Erythroplakia interspersed with patches of
Leukoplakia:
 In this erythematous patches are not as bright

as the homogenous form

Common Site: Tongue and floor of the mouth.
 CLINICAL FEATURES
1. Age and sex predilection -Erythroplakia has
been observed to show male predilection and
most common in 6th and 7th decade of life.
2.Location-It occurs on all mucosal surfaces of the
head and neck area. Half of all cases, however ,
are found on the vermillion or intraoral
surfaces (lower lip , tongue, floor , soft palate),
with the rest being evenly divided between the
larynx and the pharynx.
3.Appearance-It is non-elevated , red macule or
patch on epithelial surface.
Affected tongue Vermillion surface

Soft palate
HISTOPATHOLOGICAL FEATURES

 The epithelium shows lack of keratin

production and is often atrophic, but it
may be hyperplastic.This lack of
keratinization, especially when combined
with epithelial thinness, allows the
underlying microvasculature to show
through, thereby causing the red color.
 The underlying C.T. often demonstrates
chronic inflammation.
 Treatment
 Removal of cause – elimination of suspected
irritant should be carried out.
 Incisional Biopsy – it is always preferred
method for establishing a microscopic
diagnosis of suspicious intra oral lesion .
 Laser ablation, cryotherapy proved to be
effective.
 Surgical excision gives excellent results and
recurrence rate of less than 5% is reported.
 ORAL LICHEN PLANUS
Oral lichen planus is a common mucocutaneous
disease.It was first described by Wilson in 1869.
The condition can affect either the skin or mucosa
or both.It can cause bilateral white striations,
papules , or plaques on the buccal mucosa ,
tongue , and gingivae , erythema , erosions and
blisters may or may not be present.
 EPIDEMIOLOGY
The overall prevalence of oral lichen planus among
 Indians - 1.5%
 mixed oral habits -3.7%
 Nonuser of tobacco-0.3%

 Inc. incidence among smoked and chewed tobacco-13.7%

ETIOLOGY:
GRINSPAN SYNDROME :It refers to the triad of lichen
planus , diabetes mellitus and vascular hypertension . It
was described by Grinspan . This association of OLP &
systemic diseases may be coincidental as the lichen
planus commonly occurs in older adults.
ETIOLOGY
 CLINICAL FEATURES
 Females are more affected then man (1.4:1)
 Adults >40 years
 Skin lesions of OLP appear as small, angular,
flat- topped papules
 Discrete or coalesce into larger plaques which is
covered by a fine glistening scale.
 Papules are sharply demarcated.
 Early lesions appear red , but soon take on a
reddish , purple or violaceous hue.
 Later on dirty brownish color develop. Center-
umblicated.
The oral lesion is generally characterized by
radiating white velvety thread like papules in
angular or retiform arrangement. Surface is covered by
very fine grayish-white lines k/as Wickham’s striae.
Bilateral involvement : flexure surface of wrist , fore arms,

inner aspects of knees and thighs, trunk especially the sacral

area.
Six P associated with it are planer, polygonal, purple,

pruritis (1st sign), papules, plaques

 ORAL MANIFESTATIONS
In oral cavity ,lesions consisting of radiating white or
gray , velvety, thread like papules in a linear , annular
or retiform arrangement forming lacy, reticular
patches , rings and streaks over buccal
mucosa.vesicles and bulla formation .
Bullous-Appearing as fluild filled vesicles,which project
from surface
Atrophic-smooth red, poorly defined areas, not always
associated with peripheral straie.
Hypertrophic-well –circumscribed elevated white
lesion.
Erosive/ulcerative-characterized by oral ulcers,
irregular areas of redness, raw painful area.
 Papular type : initially Plaque : Seen as Atrophic : characterized
present as small white homogenous well by Homogenous red area
dots demarcated white plaque

Ulcerated : fibrin coated Bullous: Small bullae or Reticular form: shows

ulcers surrounds by vesicles rupture , overlapping white striae
erythematous zone leaving painful seen bilaterally in buccal
(radiating white straie) ulcerated surface mucosa.
 H/L
 Hyperplasia or hyperorthokeratosis.
 Thickening of granular layer.
 Acanthosis with intercellular edema of spinous
cells.
 Saw tooth appearance of rete pegs.
 Infiltrate consisting of T-cells and Histiocytes.
 (Max-joseph spaces) may form and blisters on
oral mucosa. Degeneration of basal keratinocytes
and disruption of anchoring elements of epithelial
basement membrane weakens the epithelial
connective tissue interface resulting in histiological
clefts known as “MAX JOSEPH SPACES”.
LICHEN PLANUS
DIFFERENTIAL DIAGNOSIS
 Leukplakia
 Candidiasis
 Pemphigus
 Syphilis
 Erythema multiformae
 TREATMENT
 Medication
Topical corticosteroids
 0.05% clobetasol proprionate gel

 0.1% betamethasone valerate gel

 Kanacoi ointment
Can be applied directly or mixed with orabase.
 Syphilis
It is caused by bacteria Treponema pallidum.
Syphilis is a highly contagious disease spread primarily by
sexual activity.
• Ass. With high risk of

HIV infection
• It may be acquired or

congenital syphilis.

A.Acquired syphilis
It is primarily a venereal ds. ,after sexual intercourse with
an infected partner, although such as dentists.The ds. If
left untreated manifest 3 stages :-
 1.Primary
 A lesion k/as chancre develop at the site of
inoculation apprx. 3-90 days after contact with
the infection.
 Occur on penis in males and vulva n cervix in
females.
 In dentist the lesion occurs on lips, tongue ,
palate , gingiva, tonsils.
 Develop at site of fresh extraction wound.
 Lesion is elevated , ulcerated nodule showing
local induration.lips may have brownish , crusted
appearance.
2.Secondary
 It usually commencing about 6weeks after primary lesion
and is characterized by diffuse eruptions of skin and
mucous memb.
 On skin-lesion appear as macules or papules which are

painless.
 Oral lesions-mucous patches are multiple. Painless,

grayish white plaques overlying an ulcerated surface.occur

on tongue, gingiva , buccal mucosa.
 Shape-ovoid or irregular ,surrounded by erythematous

zone.
 Explosive and widespread form k/as leus maligna

Characterized by fever, headache, muscle pain followed by

necrotic ulcerations involving face and scalp.
 Last for 1-30years.
 3.Tertiary (Late syphilis)
 It is non-infectious.
 Classic Lesion is gumma
 It results of hypersensitivity rxn. b/w host and
treponemes.
 Gumma occurs-skin n mucous memb., liver, bone.
 It consist of a focal , granulomatous inflammatory
process with central necrosis.
 Intraoral gumma involve tongue n palate.lesion
appears as a firm nodular mass in the tissue ,which
may ulcerate to form a deep painless ulcer.
 Lesion of palate cause-sloughing of necrotic mass
of tissue.
 B.CONGENITAL SYPHILIS
 Is transmitted to offspring only by an infected
mother and is not inherited.
 Not all the infected pregnant women's deliver
children with congenital syphilis.
 1/3rd of pregnancies results in abortion or stillbirth.
 1/3rd deliver normal children n rest with congenital
syphilis
 Congenital syphilis manifest a variety of lesions as-
frontal bossae , short maxilla,saddal nose, mullbery
molar, hutchinson’s triad-hypoplasia of incisor and
molar teeth, 8th nerve deafness, interstitial keratitis.
 TREATMENT
 Wassermann test and Hinton test(based on
flocculation).
 Diagnosis can be made by examining the

exudates of active lesion under dark filed

microscope for spirochetes.
 Penicillin is drug of choice.

Erythromycin or tetracycline is used if patient is

allergic to penicillin.
 Surgical correction of facial defects give good

esthetic results.
THANK YOU