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 sumeryadav2004@gmail.com

Lymphatic Supply

PALATE
The palate forms the
superior wall or the
roof of the oral cavity
proper.
It is composed of the
hard palate which has
an osseous base, and
behind, a soft palate
composed of fibrous
tissue.

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
MUSLE
FUNCTION
A. Tensor veli palatini muscles and the
palatine aponeurosis. B. Levator veli
palatini muscles. C. Palatopharyngeus

Blood supply of Soft palate

VENOUS DRAINAGE AND LYMPHATICS

NERVE SUPPLY OF PALATE
• All muscles of soft palate are supplied by Vagus
nerve [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 tissue sumeryadav2004@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 toward
midline;
Elevates back of the tongue

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 &
vein
Deep
lingual
vein
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
(jugulodigastric
mainly)

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” -
patch
• 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”

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
 Diffuse

• 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
examination

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%
cases
• 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 mandatorysumeryadav2004@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 features
Age
• Range wide & regional; even prevalent among teenagers in India
Ranges from 11-60 years
Sex
• From 0.2 - 2.3% in males to 1.2 - 4.5% in females in Indian
communities
Race
• South-East Asian countries, in Indian immigrants to other
countries

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

Management
1. 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 significantly

Thank You

Oral precancerous lesions and anatomy of oral cavity

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Oral precancerous lesions and anatomy of oral cavity

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