Oral precancerous lesions and anatomy of oral cavity

Anatomy and premalignant conditions of oral cavity

sumeryadav2004@gmail.com

1. Oral Vestibule

- lies between the gums, teeth and

inner lips, inner cheek .

2. Oral Cavity Proper

- lies behind and within the arch of

teeth.

Oral Vestibule

Boundaries:

1. Anteriorly by the lips,

2. Laterally by the cheeks,

3. Superiorly by the mucolabial and mucobuccal folds, and

4. Posteriorly and medially by the teeth and gums. sumeryadav2004@gmail.com

Boundaries:1. Anteriorly and laterally by

the teeth and gums,

2. Superiorly by the palate (hard and soft),

3. Inferiorly by the tongue and the floor of the mouth, and

4. Posteriorly by the opening into the pharynx.

BLOOD SUPPLY

Mouth is supplied by branches from

Facial Artery

Inferior Alveolar

Artery

Maxillary Artery

Infraorbital Artery

Postero superior

alveolar arteries

Lymphatic Supply

PALATE

The palate forms thesuperior wall or theroof of the oral cavityproper.

It is composed of thehard palate which hasan osseous base, andbehind, a soft palatecomposed of fibroustissue.

SOFT PALATE

Tensor veli

palatini

Tenses the soft palate; opens

the pharyngotympanic tube

Levator veli

palatini

Only muscle to elevate the soft

palate above the neutral position

Palatopharyngeus

Depresses soft palate; moves

palatopharyngeal arch toward

midline; elevates pharynx

Palatoglossus Depresses palate; moves

palatoglossal arch toward midline;

elevates back of the tongue

Musculus uvulae

Elevates and retracts uvula;

thickens central region of soft

palate

FUNCTION

A. Tensor veli palatini muscles and the palatine aponeurosis. B. Levator velipalatini muscles. C. Palatopharyngeusmuscles

Blood supply of Soft palate

VENOUS DRAINAGE AND LYMPHATICS

NERVE SUPPLY OF PALATE

• All muscles of soft palate are supplied by Vagusnerve [X] via pharyngeal branch to pharyngeal plexus

• Except Tensor palatini muscle which is supplied by Mandibular nerve.

• Sensory supply is derived from lesser palatine branches of the sphenopalatine ganaglion and from the branches of glossopharyngeal nerve.

• Secretomotor from Suprior salivary N. through greater petrosal nervesumeryadav2004@gmail.com

tongue

“A mobile mass of muscles lying on the floor of the

mouth and associated with the function of taste,

chewing, swallowing, and speaking”.

TONGUE CONSISTS OF

• Mucous membrane

• Mucous glands

• Lymphoid tissue

• Fat

• Striated muscle fibres

• Fibrous tissuesumeryadav2004@gmail.com

PAPILLAE

Circumvallate papillae are arranged in a

row parallel to and in front of sulcus

terminalis

Fungiform papillae are numerous at the

tip and margin of the tongue.

Filliform papillae are prevalent on the

dorsum of the tongue arranged in rows

parallel to sulcus terminalis

Muscles of the tongue

INTRINSIC MUSCLES

MUSCLE FUNCTION

SUPERIOR Shortens tongue;

curls apex and sides

of tongue

INFERIOR Shortens tongue;

uncurls apex and

turns it downward

TRANSVERSE Narrows and

elongates tongue

VERTICAL Flattens and widens

tongue All intrinsic muscles are supplied by Hypoglossal nerve

EXTRINSIC MUSCLES

GENIOGLOSSUS

Protrudes tongue; depresses center of tongue

HYOGLOSSUS

Depresses tongue

STYLOGLOSSUS

Elevates and retracts tongue

PALATOGLOSSUS

Depresses palate;Moves palatoglossal fold towardmidline;

Elevates back of the tonguesumeryadav2004@gmail.com

Arteries:

Lingual artery

Tonsillar branch of facial

artery

Ascending pharyngeal artery

Veins:

Lingual vein, ultimately

drains into the internal

jugular vein Hypoglos

sal nerve

Lingual

artery &

lingual

Dorsal

lingual artery

& vein

BLOOD AND NERVE SUPPLY

Tip:• Submental nodes

bilaterally & then deep cervical nodes

Anterior two third:• Submandibular

unilaterally & then deep cervical nodes

Posterior third:• Deep cervical nodes

(jugulodigastricmainly)

NERVE SUPPLY OF TONGUE

Precancerous

Lesions & Conditions

Introduction

• Precancerous lesion

• “Morphologically altered tissue in which cancer is more

likely to occur, than in its apparently normal

counterpart”

• Precancerous condition

• “Generalized state of the body, which is associated with a

significantly increased risk of cancer”

PREMALIGNANT LESIONS

• Leukoplakia

• Erythroplakia

• Carcinoma in situ

• Bowens disease

• Actinic keratosis & chelitis

• Dyskeratosis follicularis

PREMALIGNANT CONDITIONS

• Oral submucous fibrosis

• Oral lichen planus

• Syphilitic glossitis

• Sideropenic dysphagia

• Dyskeratosis congenita

Leukoplakia

• The term LEUKOPLAKIA was first coined by a Hungarian

Dermatologist SCHWIMMER in 1877

• Originates from Greek words – “leucos” - white and “plakia” -

• WHO 1978

• “A white patch or plaque in the oral cavity which cannot be

scrapped off or stripped off easily & more over, which cannot be

characterized clinically or pathologically as any other disease”sumeryadav2004@gmail.com

Epidemiology

1. Prevalence

• Represents 85% of all oral precancers

2. Incidence

3 – 4 % of adult population

3. Age

Usually in the 4th – 6th decades of life

4. Sex

Males have the highest incidence, with the trend changing gradually

Classification of leukoplakia(Axell & Pindborg et al 1983)

• Based on CLINICAL TYPE:

Homogenous

Non homogenous

• Based on ETIOLOGY:

Tobacco associated

Idiopathic

• Based on EXTENT:

Localized

Diffusesumeryadav2004@gmail.com

• Based on risk of MALIGNANT TRANSFORMATION

High risk sites

Floor of mouth

Lateral/ventral surface of tongue

Soft palate

Low risk sites

Dorsum of tongue

Hard palate

• Based on HISTOLOGY:

Dysplastic

Non dysplastic

Sharp’s staging of leukoplakia

• Stage I- Earliest lesion-non palpable, faintly translucent,

white discoloration

• Stage II- Localized or diffuse, slightly elevated plaque of

irregular outline. It is opaque white & may have a fine

granular texture

• Stage III- Thickened white lesion showing induration and

fissuring

Etiopathogenesis

• Tobacco – most imp offending agent

• Alcohol

• Chronic irritation

• Syphilis

• Nutritional deficiency

• Actinic radiation

• Most studies have reported mortality ratios for smokers

versus never smokers of about 5:1, with several reporting

ratios in excess of 10:1. Furthermore, the risk for death

from oral cancer is consumption related

• Male cigarette smokers had a relative risk for oral cancer

27.7 times greater than that of a male never smoker

• These studies have found that after 3 to 5 years of smoking

abstinence, oral cancer risk decreased by about 50%

Clinical presentation

• Any mucosal surface, solitary or multiple,

“White patches”

• Varies from a non-palpable faintly

translucent white area to a thick fissured,

papillomatous or indurated lesion

• Colour varies from white, grey or yellowish

white, sometimes brownish-yellow

• 70% in buccal mucosa, commissural areas, followed by lower lip,

floor of the mouth, palate & gingivasumeryadav2004@gmail.com

SYMPTOMS

• Patients may report with a feeling of increased thickness of

mucosa

• Those with ulcerated or nodular type may complain of

burning sensation

• Enlarged cervical lymph nodes may signal occurrence of

metastasis

Clinical variants of leukoplakia

Homogeneous/ Leukoplakia Simplex Speckled/Nodular

Ulcerative

Histopathological features

• Keratinization pattern

• Thickness of epithelium

• Changes in underlying

connective tissue

• Waldron & Shafer (1975)

80% lesions show benign hyperkeratosis with/without acanthosis &

17% represent CIS

Dysplastic changes typically begin in basal & parabasal zones of

epithelium sumeryadav2004@gmail.com

• Five clinical criteria for high risk of malignant change

– The nodular type

– Erosion or ulceration within lesion

– Presence of a nodule indicates malignant potential

– A lesion that is hard in its periphery

– Lesion of anterior floor of mouth & undersurface of tongue

• In all cases, relative risk of malignant potential is determined

by presence of epithelial dysplasia upon histological

examinationsumeryadav2004@gmail.com

Diferential diagnosis

• Leukoedema

• Lichen planus

• Chemical burn

• Morsicatio buccarum

• Lupus erythematosus

• White sponge nevus

Conservative management

• Elimination of etiological factor

• Restraining from smoking or chewing tobacco

• To remove sharp broken down teeth

• Correction & replacement of overhanging or faulty metal

restorations with a metal bridge

CHEMOPREVENTION

1) Isotrenitoin / 13- cis- retinoic acid –

2) Beta carotene -30mg TID

3) Topical Bleomycin – 0.5-1% solution/2wks

4) 5-Fluorouracil & Cisplatin

• Surgical Excision: entire lesion excised if it is >1cm in size,

following modalities used:

a) Scalpel – surgical stripping

b) Cryosurgery – with liquid nitrogen

c) Electrocautery

d) Laser ablation

Erythroplakia

WHO DEFINITION:

“Any lesion of the oral mucosa that presents as a

bright red velvety patch or plaque, which cannot be

characterized clinically or pathologically as any other

recognizable condition”

Reported by Querat in 1911

CLASSIFICATION

• Clinical variants

1. Homogenous erythroplakia

2. Erythroplakia interspersed with patches of leukoplakia

3. Granular or Speckled erythroplakia

• Etiology : Same as oral leukoplakia

• Age : Mainly middle age, peak 65-74 years

• Gender : Predilection for men

• Location/size

- Soft palate, floor of the mouth & buccal mucosa & tongue

- Typical lesion < 1.5 cm in diameter but >4cm also

observed

- Smooth and granular/nodular, well defined

- May have an irregular, red granular surface interspersed

with white or yellow foci

- Soft on palpation

• Highest risk for malignant transformation - 14-50%

• Based on the fact that on histology 80-90% of cases

present as-

- Carcinoma In Situ

- Severe epithelial dysplasia

- Microinvasive carcinoma

Management

• Biopsy should be performed

• Treatment guided by histopathologic diagnosis

• Recurrence , multifocality common

• Careful long term follow up

Intraepthelial carcinoma (Ca in Situ)

• Arises frequently on the skin, but also on mucous membranes,

including oral cavity

• Most severe stage of epithelial dysplasia

• Striking feature – dysplastic epithelial cells donot invade into

connective tissue

• Common among elderly, with a male prdiliction

• Present as white plaques or ulcerated, & reddened areas

• Site – floor of the mouth, tongue, lips

• Has combined features of leuko & erythroplakiasumeryadav2004@gmail.com

• Histopathology

• Keratin may or may not be present on the surface, but if present it

is usually parakeratin

• Individual cell keratinization or keratin pearl formation are rare

• Consistent finding – loss of orientation & normal polarity of cells

• Treatment

• No accepted treatment

• Surgical excision, irradiation & cauterization

Precancerous conditions

Oral lichen planus

• Named by E Wilson ( British physician) 1896

Lichen – latin for primitive plants (symbiotic algae & fungi)

Planus – latin for flat

• Definition

• “A common chronic immunologic inflammatory mucocutaneous

disorder that varies in appearance from keratotic (reticular or plaque

like) to erythematous and ulcerative, affecting the stratified squamous

epithelium”

• Affects 0.5% to 1% of world's population

• Approx half patients with cutaneous LP have oral

involvement

• Mucosal involvement, sole manifestation in up to 25%

• Peak incidence - middle age, F:M- 2:1

• Characteristically associated with persistent clinical

course & resistance to most conventional treatments

• On skin-

• Flat-topped purple polygonal & pruritic papular rash

Etiology & pathogenesis

• Both antigen-specific & non-specific mechanisms may be involved

in pathogenesis of OLP

• Antigen-specific mechanisms:

– antigen presentation by basal keratinocytes and

– antigen-specific keratinocyte killing by CD8+ cytotoxic T-cells

• Non-specific mechanisms:

– mast cell degranulation and

– matrix metalloproteinase (MMP) activation

• These mechanisms may combine to cause

T-cell accumulation in superficial lamina propria

Basement membrane disruption

Intra-epithelial T-cell migration &

Keratinocyte apoptosis

Clinical features

• Lesions usually symmetrical

• Frequently affects buccal mucosa,

tongue, gingiva, lip and palate

• Extra-oral mucosal involvements -

anogenital area, conjunctivae,

oesophagus/larynx

• Approx 1.2% - 5.3% lesions undergo

malignant changes

• Hence regular follow up mandatory sumeryadav2004@gmail.com

Clinical variants

Reticular (92%) Atrophic (44%) Plaque (36%)

Erosive (9%) Bullous (1%)

Clinical features

Asymptomatic

• Reticular – Wickham’s striae + discrete erythematous border

• Plaque-like – Resemble leukoplakia, common in smokers

Symptomatic

• Atrophic – Diffuse red patch, peripheral radiating white striae

• Erosive – Irregular erosion covered with a pseudomembrane

• Bullous – Small bullae / vesicles that may rupture easily

Histology

Shklar -3 classic microscopic

features of OLP

• Overlying hyperkeratinization

• A bandlike layer of chronic

inflammatory cells within

underlying connective tissue

• Liquefaction degeneration of basal

cell zone

Diagnosis

• The characteristic clinical aspects of OLP - sufficient for

correct diagnosis

• An oral biopsy - to confirm clinical diagnosis

(exclude dysplasia & malignancy)

• Gingival LP more difficult to diagnose, direct

immunofluorescence of perilesional mucosa for diagnosis

IMMUNOFLUORESCENCE

• Direct immunofluorescence – shaggy band of fibrinogen

in the basement membrane, IgM stained cytoid bodies

are also seen in dermal papilla or peribasilar area

Management

• Reticular type is asymptomatic & treatment often

unnecessary

• Erosive type presents significant management problems

• All patients should optimize oral hygiene

• Oral candidiasis should be excluded/treated

• Cortico steroids, is the treatment of choice eg – Fluocinonide

or Clobetasol gel for 2 weeks, with 3mnths follow-up

• In symptomatic patients with apparent contact dental

factor, patch test with replacement of amalgam

• In those with no apparent contact factor, topical or

intralesional steroid - first line treatment. A short course

of systemic steroid for more rapid control

Lichenoid reaction

• The oral lichenoid eruption is a less specific entity compared with

LP of the skin.

• Best considered as a reaction pattern of oral mucosa to a variety of

insults, including

– OLP itself

– Contact allergy

– Trauma and

– Other inflammatory dermatoses (e.g. oral lupus erythematosus

may look very lichenoid) sumeryadav2004@gmail.com

Oral submucous fibrosis

DEFINITION -

“It is a slowly progressing chronic fibrotic disease of the

oral cavity & oropharynx, characterized by fibroelastic

change and inflammation leading to a progressive

inability to open the mouth, swallow or speak”

Clinical featuresAge

• Range wide & regional; even prevalent among teenagers in India

Ranges from 11-60 years

• From 0.2 - 2.3% in males to 1.2 - 4.5% in females in Indian

communities

• South-East Asian countries, in Indian immigrants to other

countries sumeryadav2004@gmail.com

Mortality/morbidity

• High rate of morbidity - progressive

inability to open mouth, resulting in

difficulty eating & consequent

nutritional deficiencies

• Significant mortality rate - can

transform into oral cancer, particularly

Squamous cell carcinoma 7.6%

Etiology

• Initially classified as idiopathic, now

• Betel quid & it’s components (Arecoline, an active

alkaloid found in betel nuts, stimulates fibroblasts to

increase production of collagen by 150%)

• Capsaicin – Chillies (hypersensitivity reaction)

• Nutritional factors

• Immunological factors

Clinical presentation

• Common site – buccal mucosa, retromolar area, uvula,

palate, etc

• Initially, pain and a burning sensation upon

consumption of hot & spicy foods

• Vesicle & ulcers

• Excessive or reduced salivation & defective gustation

• Hearing loss

• Depapillation & atrophy of tongue and uvula

• Depigmented & loss of stippling over gingiva

• Nasal tone in the voice

• Difficulty in deglutition

• Impaired mouth movements (eg, eating, whistling,

blowing, sucking)

Clinical stages

Three stages (Pindborg, 1989) based on physical findings:

• Stage 1: Stomatitis includes erythematous mucosa, vesicles,

mucosal ulcers, melanotic mucosal pigmentation & mucosal

petechiae

• Stage 2: Fibrosis occurs in ruptured vesicles & ulcers when

they heal, hallmark of this stage

• Stage 3: Sequelae of OSF

– Leukoplakia is found in more than 25% of

individuals with OSF

– Speech and hearing deficits may occur because of

involvement of the tongue and the eustachian tubes

RANGANATHAN K (2001)

• Group I : Only Symptoms, No mouth opening

• Group II : Mouth opening > 20mm

• Group III : Mouth opening < 20mm

• Group IV: Limited mouth opening, precancerous

& cancerous changes throughout mucosa

Histopathology

• Hyperkeratinized, atrophic epithelium with flattening

& shortening of rete pegs

• Nuclear pleomorphism & severe inter-cellular edema

• Finely fibrilar collagen & increased fibroblastic activity

in early stage showing dilated & congested blood vessels

with areas of hemorrhage

• Advanced stage shows “homogenization” and

“hyalinization” of collagen fibers (important feature)

• Degeneration of muscle fibers and chronic inflammatory

cell infiltration in the connective tissue

Management1. Behavioral therapy

- Patient counseling, stoppage of habit

2. Medicinal therapy

-Hyaluronidase: Topically, shown to improve symptoms more

quickly than steroids alone

- Mild cases – intralesional inj Dexamethasone 4 mg to reduce

symptoms & surgical splitting / excision of fibrous bands

- Recent study – intralesional inj of gamma interferon 3 times a

week, improves mouth opening significantlysumeryadav2004@gmail.com

Thank You

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