Potentially Malignant Lesions and Conditions

8/3/2019 Potentially Malignant Lesions and Conditions

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POTENTIALLY MALIGNANT LESIONS AND

CONDITIONS

PRESENTED BY

NALEENA JOSEPH

CTAHBDS029KMCT DENTAL COLLEGE

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POTENTIALLY MALIGNANT LESION

Definition:

A morphologically altered tissue in which cancer is more likely to occur

than its normal counterpart

- Shafer

1) Leukoplakia

2) Erythroplakia

3) Palatal Keratosis associated with reverse smoking4) Actinic Keratosis, Cheilitis, & Elastosis

POTENTIALLY MALIGNANT CONDITION

Definition:

A generalized state or condition associated with significantly increased risk

of cancer development

- Shafer

1) Oral Submucous Fibrosis

2) Oral Lichen Planus

3) Discoid Lupus Erythematosus

4) Dyskeratosis Congenita

5) Sideropenic Dysphagia

6) Syphilitic Glossitis

7) Xeroderma Pigmentosum8) Epidermolysis Bullosa

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LEUKOPLAKIA

DEFINITION:

A white patch or plaque that cannot be characterized clinically or

pathologically as any other lesion

-WHO

A predominantly white lesion of the oral mucosa that cannot be

characterized as any other definable lesion. Some oral leukoplakia will

transform into cancer.

-Axell 1996

A predominant white lesion of oral mucosa that cannot be characterized as

any other definable lesion

- Pindborg 1997

EPIDEMIOLOGY

Risk of malignant transformation is 4-6%

Global prevalence of 2.6%

Common in patients above 50 yrs of age

Common in men

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ETIOLOGY

TOBACCO

- Smoking form- Smokeless form

ALCOHOL

CHRONIC IRRITATION

SANGUINERIA

CANDIDIASIS

VIRAL INFECTION

NUTRITIONAL DEFICIENCY

DRUGS

IDIOPATHIC

CLASSIFICATION

LEUKOPLAKIA

1) Mild / Thin Leukoplakia

2) Homogenous Leukoplakia

3) Non homogenous Leukoplakia

HOMOGENOUS LEUKOPLAKIA

Well-defined white patch, localized or extensive, that is slightly elevated and

that has a fissured, wrinkled, or corrugated surface on palpation, these

lesions may feel leathery to dry, or cracked mud-like

NON HOMOGENOUS LEUKOPLAKIA

White patches or plaque intermixed with red tissue elements. Also called

Erythroleukoplakia and speckled leukoplakia

NODULAR

VERRUCOUS

PROLIFERATIVE VERRUCOUS

ULCERATED

ERYTHROLEUKOPLAKIA

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NODULAR LEUKOPLAKIA

Keratotic white nodules or patches are distributed over an Erythematous

background. Associated with higher rate of malignant transformation

VERRUCIFORM LEUKOPLAKIA

Presence of thick white lesions with papillary surfaces in the oral cavity.

These lesions are usually heavily keratinized and are most often seen inolder adults in the sixth to eighth decades of life. Some of these lesions may

exhibit an exophytic growth pattern.

PROLIFERATIVE VERRUCOUS LEUKOPLAKIA (PVL)

Extensive papillary or Verrucoid white plaques that tend to slowly involve

multiple mucosal sites in the oral cavity and to inexorably transform into

Squamous cell carcinomas over a period of many years. PVL has a very high

risk for transformation to dysplasia, Squamous cell carcinoma or verrucous

carcinoma .Verrucous Carcinomas is a slow growing and well-differentiated

lesion that seldom metastasizes.

CLINICAL FEATURES

Asymptomatic

Common sites buccal mucosa, lower lip, Gingiva

Less common sites palate, retro molar area

Lesions on the floor of mouth and lateral borders of tongue are high

risk sites for malignant transformation

HISTOPATHOLOGY

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Epithelial hyperplasia and surface hyperkeratosis

Mild to moderate epithelial dysplasia

Chronic inflammatory changes

DIAGNOSIS

1) Elimination of possible causes

2) Biopsy (gold standard test)

3) Toluidine blue staining

4) Exfoliative cytology (Limited value)

MANAGEMENT

1) MEDICAL topical vitamin A / Retinoid (single and combination

dosages of vitamins A, C, and E; beta carotene; analogues of vitamin A; anddiets that are high in antioxidants and cell growth suppressor proteins (fruits

and vegetables).

2) SURGICAL

Cold knife surgical excision

Laser ablation & cryosurgery - preferred because of their

Precision and rapid healing

MANAGEMENT OF LEUKOPLAKIA

PROVISIONAL CLINICAL DIAGNOSIS

Elimination of possible causes No possible causes

(2-4 weeks observation) (Definitive clinical diagnosis)

---------------------------------

Biopsy

Good response No response

(Definitive clinical diagnosis)

___________________________

Definable lesion

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(Management accordingly) No definable lesion Definable lesion

(Treatment/ (Management

Observation/ accordingly)

Follow up)

PROGNOSIS

Long term follow up necessary

Malignant changes occur 2-4 yrs after onset

ERYTHROPLAKIA

DEFINITION

A fiery red patch that cannot be characterized clinically or pathologically as

any other definable lesion - Pindborg 1997

Less common than Leukoplakia

High frequency of pre-malignant & malignant changes

Often associated with heavy smoking with or without concomitant

alcohol use

CLASSIFICATION

ERYTHROPLAKIA

- Homogenous Erythroplakia

- Granular / Speckled Erythroplakia

- Erythroleukoplakia

CLINICAL FEATURES

Seen in older men

Irregular outline

Common sites floor of mouth, Ventral aspect of tongue, soft palate

Histopathology lack of Keratin production and Atrophic Epithelium

Treatment same as Leukoplakia

Recurrent rate less than 5%

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PALATAL CHANGES ASSOCIATED WITH REVERSE SMOKING

Peak incidence 55-64 yrs

CLINICAL CHANGES

Keratosis Diffuse whitening of entire Palate

Patches Well defined, elevated white Plaques

Excrescences 1-3mm elevated white Plaques

Red areas Well defined reddening of the Palatal Mucosa

Ulcerated areas Crater like areas covered by Fibrin

Non pigmented areas Areas of Palatal Mucosa that are devoid of

Pigmentation

HISTOLOGICAL FINDINGS

Hyperorthokeratosis

Epithelial Dysplasia

Inflammatory cells in connective tissue

Melanin deposits in Lamina Propria

Malignant changes were seen in 0.3% of the palatal lesions

ACTINIC KERATOSIS

Also called Solar Elastosis, Senile Elastosis or Actinic Elastosis

It is Dermatological disease which is a degenerative condition of skin Also called Sailors or Farmers skin

ETIOLOGY

1. Hereditary factors skin pigmentation or its absence

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2. Exposure to elements sunlight and wind

CLINICAL FEATURES

Common in elderly patients

Site lips

Affected skin appears wrinkled, dry, atrophic and flaccid

On lips there is mild Keratosis and subtle blending of the lip

vermillion with skin surface

HISTOPATHOLOGY Increase in amount of elastic connective

tissue fibers

TREATMENT No treatment

ORAL SUBMUCOUS FIBROSIS

DEFINITION

A insidious and chronic disease affecting mucosa of any part of oral cavityand occasionally extend into pharynx and esophagus ,although sometimes

preceded by and / or associated with vesicle formation . It is always

associated with a juxta epithelial inflammatory reaction followed by fibro-

elastic change of lamina propria with epithelial atrophy leading to stiffness

of oral mucosa causing trismus and inability to eat.

Also called Atrophica Idiopathica Mucosae Oris , idiopathic

scleroderma of mouth, diffuse oral submucous fibrosis

ETIOLOGY

a) Areca nut chewing

b) Chillies

c) Genetic

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d) Tobacco

e) Autoimmune disorders

PATHOGENESIS

Alkaloids like Arecolin modulate matrix metallo proteins, lysyl

oxidases & collagenases which the affects collagen metabolism and

leads to increased fibrosis

Increased fibrosis results in decrease in water retaining proteoglycans

which favor increased collagen type 1 production

Polymorphism in gene coding for TNF

Aberrations of TGF beta and Interferon gamma

CLINICAL FEATURES

Age group 4-75 yrs

Common in middle & old age

Female predilection

3.3% risk of malignant transformation

PRODROMAL SYMPTOMS/ EARLY OSF

Burning sensation while consuming spicy food

Blisters ,ulcerations ,altered salivary flow, defective gustatory

sensation

Appearance of vesicles, petechiae, pain

ADVANCED OSF

Blanching of mucosa and appearance of white fibrous vertical bands

Buccal mucosa and lips are affected first

Dense fibrosis of Pterygomandibular raphe results in trismus

Restricted tongue movements and depappilation also seen

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OTHER SYMPTOMS

Obstruction of Eustachian tube

Nasal intonation of speech

TMJ pain Inability to blow

HISTOPATHOLOGY

Early stage there is Epithelial Hyperplasia and later stage there is

epithelial atrophy

Sub-mucosal deposition of extremely dense and avascular collagenous

tissue also seen

Chronic inflammatory cells seen in connective tissue such as

Lymphocytes and Plasma cells

DIAGNOSIS

Clinical examination and history of betel chewing habit

At least one of the following should be present

Palpable fibrous band

Mucosa tough and leathery

Blanching of mucosa and Histopathological features

TREATMENT

PREVENTION By stoppage of chewing habits

EXERCISE In mouth opening

MEDICAL Topical or systemic steroids

- Vitamin and nutrient supplements

- Placentrex

- Fibrinolytic agents

- Colloidal Iodine- Antioxidants

SURGICAL

- Surgical excision of bands

- Surgical removal of affected mucosa

followed by repair with grafts

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ORAL LICHEN PLANUS

Oral Lichen Planus (OLP) is a common chronic immunologic inflammatory

mucocutaneous disorder that varies in appearance from Keratotic (reticular

or plaque like) to Erythematous and ulcerative. The skin lesions are flat

violaceous papules with a fine scaling on the surface. Unlike oral lesions,

skin lesions are usually self-limiting, lasting only 1 year or less.

ETIOLOGY

Cell mediated immune response

Autoimmune disease

Stress

Hepatitis C Virus

CLINICAL FEATURES

Radiating white or grey, velvety, thread like papules in a linear,

annular or retiform arrangement with Wickhams striae

0.3-3% rate of malignant transformation. Common in erosive and

atrophic form

The Buccal mucosa is the most common site.

TYPES OF LICHEN PLANUS

a) RETICULAR

b) PLAQUE

c) ERYTHEMATOUS

d) BULLOUSe) PAPULAR

f) EROSIVE

RETICULAR-Fine white striae or lines which form a network or annular

pattern with peripheral Erythematous Zoneand usually seen bilaterally in

buccal mucosa.

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PLAQUE TYPE- Homogenous well demarcated white plaque. Common in

smokers

ERYTHEMATOUS FORM- Homogenous red area and striae seen in

periphery

BULLOUS FORM Appear as bullous structures surrounded by a reticular

network

PAPULAR FORM- seen in initial phase of disease, small white dots are

seen which intermingle with reticular form

EROSIVE FORM disabling form of OLP, fibrin coated ulcers surrounded

by an Erythematous zone with radiating white striae

HISTOPATHOLOGY

Hyperparakeratosis

Saw tooth rete pegs

Subepithelial band of mononuclear infiltrate

Civatte bodies degenerated basal Keratinocytes

Max-Joseph space

TREATMENT

Topical and systemic steroids

Calcineurin inhibitors (Cyclosporine & Tacrolimus)

Retinoid & UV phototherapy

DYSKERATOSIS CONGENITA

Also called Cole Engman Syndrome

Rare Genodermatosis, inherited as x-linked recessive trait

characterized by

Cutaneous reticulated hyper-pigmentation

Nail dystrophy

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Pre-malignant leukoplakia of oral mucosa

Progressive pancytopenia

Striking male predilection is seen

ETIOLOGY

Mutations in DKC1 gene

CLINICAL FEATURES

First manifestation is nail changes that is Dystrophic and shedding of

nails at the age of 5yrs

Grayish brown pigmentation appear at same time in trunk, neck and

thighs

Skin becomes atrophic & teleangiectactic.

Face becomes red

OTHER MINOR FEATURES

Frail skeleton

Mental retardation

Small Sella Turcica

Dysphagia

Transparent tympanic membrane, deafness

Eyelid infections

ORAL MANIFESTATIONS

Mucosal Leukoplakia buccal mucosa, tongue & oropharynx

Can become verrucous or ulcerative

Dysphagia and Dysuria

Increased incidence of malignant neoplasms,dental caries,and tooth

loss

HISTOLOGICAL FINDINGS

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Mild hyperkeratosis

Epidermal atrophy

Teleangiectasia of superficial BV

TREATMENT

Allogenic bone marrow transplant

DISCOID LUPUS ERYTHEMATOSUS

Chronic, scarring, atrophy producing, Photosensitive Dermatosis

ETOLOGY Genetic predisposition

PATHOGENESIS - heat shock proteins is induced in Keratinocyte

following UV exposure or stress and this protein act as target for T

cell mediated epidermal cell cytotoxicity

CLINICAL FEATURES

Third and fourth decade of life and common in women Common sites are face, oral mucous membrane,chest,back and

extremities

Slightly elevated red or purple macules covered by grey or yellow

scales

Carpet tack lesions caused by forceful removal of scales

Malar rash

ORAL MANIFESTATIONS

Begin as Erythematous raised or depressed area, without indurations

and with white spots

Superficial painful ulceration with crusting or bleeding is seen

Central healing result in scar formation

Common site are vermillion border of lower lips

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Malignant transformation can occur

TREATMENT

Corticosteroid Therapy

Pulse intravenous Cyclophosphamide regimen followed by quarterly

infusion for maintenance is the mainstay of modern therapy

EPIDERMOLYSIS BULLOSA

Heterogenous group of inherited mucocutaneous disorders

4 broad categories

* Simplex

* Junctional

* Dystrophic

* Hemidesmosomal

ETIOLOGY

Mutation of gene coding for keratins 5 and 14 causes simplex type

Recurrent nonsensense mutation in the LAMB3 gene causes

junctional type

Mutation of gene encoding for type 4 collagen COL7A1 causes

dystrophic type

CLINICAL FEATURES

EPIDERMOLYSIS BULLOSA SIMPLEX

Occurs shortly after birth. Formation of vesicles and

bullae on hands and feet at sites of friction or trauma. Heals in 2-10 days

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without scarring or pigmentation (generalized form) Localized form occur in

later childhood.Bullae also seen in oral cavity

JUNCTIONAL EPIDERMOLYSIS BULLOSA

Onset at birth with absence of scarring or pigmentation and death occurs

within 3 months of age . Oral bullae are frequent, extremely fragile and

produce feeding problems. Severe disturbance in enamel and dentin

formation of deciduous teeth are also seen

DYSTROPHIC EPIDERMOLYSIS BULLOSA ( DOMINANT )

Blisters develop in ankles, knees, elbows, feet and

head and it heals with scarring/ keloid. Dystrophic nails, palmar plantar

keratosis with hyperhidrosis and hypertrichosis are also seen. Oral bullae

also present

DYSTROPHIC EPIDERMOLYSIS BULLOSA ( RECESSIVE )

Classical form of the disease withonset at birth and

spontaneous bullae formation at sites of trauma, friction or pressure. It also

exhibits Nikolskys sign and heals by scarring. Also dystrophic nails and

sparse hair. Oral bullae initiated by nursing or any simple dental operative

procedure. Scar formation can obliterate sulcus and restrict tongue

movements. It can also result in hoarseness and Dysphagia and dental

defects like congenitally absent teeth, hypoplastic teeth and rudimentary

teeth seen

TREATMENT

Mild form- topical and intralesional steroids

Tetracycline and doxycycline to control desquamative gingivitis

Dapsone therapy

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Long term systemic steroids and immunosuppresive therapy.

XERODERMA PIGMENTOSUM

Genetically determined disorder

Defective DNA repair mechanism due to excessive chronic UV

damage leads to subsequent development of sun related skin tumors

including melanoma

CLINICAL FEATURES

Increased tendency to sunburn and skin changes like atrophy and

freckled pigmentation

Development of Actinic keratosis which progress to squamous cell or

basal cell carcinoma. Melanoma also develops

Oral manifestation squamous cell carcinoma of lower lip and tip of

tongue

TREATMENT

Avoid sun exposure and use protective clothing

Topical chemotherapeutic agents like 5 -Flurouracil to treat actinic

keratosis

Nonmelanoma skin cancers excised conservatively

Genetic counselling

SIDEROPENIC DYSPHAGIA

Also called Plummer Vinson syndrome or Patterson Kelly syndrome

Characterized by iron deficiency anemia, glossitis and dysphagia

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CLINICAL FEATURES

Seen in Scandinavian women between 30-50 yrs of age

Burning sensation of tongue and oral mucosa

Severe angular chelitis Abnormal bands of tissue in esophagus- esophageal web

Koilonychia

TREATMENT

Dietary iron supplements

Esophageal dilation

SYPHILLITIC GLOSSITIS

Seen in tertiary stage

Surface of tongue gets broken up by fissures due to atrophy and

fibrosis of tongue musculature and hyperkeratosis

Exclusively seen in males

High rate malignant transformation

Treatment by intensive antibiotic treatment using Penicillin or

Erythromycin or Tetracycline

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REFERENCE

BURKETS ORAL MEDICINE 11TH EDITION-

GREENBERG,GLICK,SHIP

TEXTBOOK OF ORAL PATHOLOGY 6TH EDITION- SHAFER

ORAL AND MAXILLOFACIAL PATHOLOGY 3RD EDITION

NEVILLE, DAMM, ALLEN, BOUQUOT

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Potentially Malignant Lesions and Conditions