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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.
sumeryadav2004@gmail.com
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.
sumeryadav2004@gmail.com
BLOOD SUPPLY
Mouth is supplied
by branches from
 Facial Artery
 Inferior Alveolar
Artery
 Maxillary Artery
 Infraorbital Artery
 Postero superior sumeryadav2004@gmail.com
Lymphatic Supply
sumeryadav2004@gmail.com
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.
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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
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Blood supply of Soft palate
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VENOUS DRAINAGE AND LYMPHATICS
sumeryadav2004@gmail.com
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
sumeryadav2004@gmail.com
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
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EXTRINSIC MUSCLES
GENIOGLOSSUS
Protrudes tongue;
depresses center of tongue
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HYOGLOSSUS
Depresses tongue
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STYLOGLOSSUS
Elevates and
retracts tongue
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PALATOGLOSSUS
Depresses palate;
Moves palatoglossal fold toward
midline;
Elevates back of the tongue
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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
sumeryadav2004@gmail.com
BLOOD AND NERVE SUPPLY
sumeryadav2004@gmail.com
Tip:
• Submental nodes
bilaterally & then
deep cervical nodes
Anterior two third:
• Submandibular
unilaterally & then
deep cervical nodes
Posterior third:
• Deep cervical nodes
(jugulodigastric
mainly)
sumeryadav2004@gmail.com
NERVE SUPPLY OF TONGUE
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Precancerous
Lesions & Conditions
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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”
sumeryadav2004@gmail.com
PREMALIGNANT LESIONS
• Leukoplakia
• Erythroplakia
• Carcinoma in situ
• Bowens disease
• Actinic keratosis & chelitis
• Dyskeratosis follicularis
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PREMALIGNANT CONDITIONS
• Oral submucous fibrosis
• Oral lichen planus
• Syphilitic glossitis
• Sideropenic dysphagia
• Dyskeratosis congenita
sumeryadav2004@gmail.com
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”
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
sumeryadav2004@gmail.com
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
sumeryadav2004@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
sumeryadav2004@gmail.com
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
sumeryadav2004@gmail.com
Etiopathogenesis
• Tobacco – most imp offending agent
• Alcohol
• Chronic irritation
• Syphilis
• Nutritional deficiency
• Actinic radiation
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• 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%
sumeryadav2004@gmail.com
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
sumeryadav2004@gmail.com
Clinical variants of leukoplakia
Homogeneous/ Leukoplakia Simplex Speckled/Nodular
Ulcerative
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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
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Diferential diagnosis
• Leukoedema
• Lichen planus
• Chemical burn
• Morsicatio buccarum
• Lupus erythematosus
• White sponge nevus
sumeryadav2004@gmail.com
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
sumeryadav2004@gmail.com
CHEMOPREVENTION
1) Isotrenitoin / 13- cis- retinoic acid –
2) Beta carotene -30mg TID
3) Topical Bleomycin – 0.5-1% solution/2wks
4) 5-Fluorouracil & Cisplatin
sumeryadav2004@gmail.com
• 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
sumeryadav2004@gmail.com
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
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CLASSIFICATION
• Clinical variants
1. Homogenous erythroplakia
2. Erythroplakia interspersed with patches of leukoplakia
3. Granular or Speckled erythroplakia
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• 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
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- Smooth and granular/nodular, well defined
- May have an irregular, red granular surface interspersed
with white or yellow foci
- Soft on palpation
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• 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
sumeryadav2004@gmail.com
Management
• Biopsy should be performed
• Treatment guided by histopathologic diagnosis
• Recurrence , multifocality common
• Careful long term follow up
sumeryadav2004@gmail.com
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
sumeryadav2004@gmail.com
Precancerous conditions
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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”
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• 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
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• On skin-
• Flat-topped purple polygonal & pruritic papular rash
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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
sumeryadav2004@gmail.com
• These mechanisms may combine to cause
 T-cell accumulation in superficial lamina propria
 Basement membrane disruption
 Intra-epithelial T-cell migration &
 Keratinocyte apoptosis
sumeryadav2004@gmail.com
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%)
sumeryadav2004@gmail.com
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
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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
sumeryadav2004@gmail.com
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
sumeryadav2004@gmail.com
IMMUNOFLUORESCENCE
• Direct immunofluorescence – shaggy band of fibrinogen
in the basement membrane, IgM stained cytoid bodies
are also seen in dermal papilla or peribasilar area
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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
sumeryadav2004@gmail.com
• 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
sumeryadav2004@gmail.com
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”
sumeryadav2004@gmail.com
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
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%
sumeryadav2004@gmail.com
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
sumeryadav2004@gmail.com
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
sumeryadav2004@gmail.com
• 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)
sumeryadav2004@gmail.com
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
sumeryadav2004@gmail.com
• 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
sumeryadav2004@gmail.com
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
sumeryadav2004@gmail.com
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
sumeryadav2004@gmail.com
• Advanced stage shows “homogenization” and
“hyalinization” of collagen fibers (important feature)
• Degeneration of muscle fibers and chronic inflammatory
cell infiltration in the connective tissue
sumeryadav2004@gmail.com
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
sumeryadav2004@gmail.com
Thank You
sumeryadav2004@gmail.com

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Oral precancerous lesions and anatomy of oral cavity

  • 1. Anatomy and premalignant conditions of oral cavity sumeryadav2004@gmail.com
  • 2. 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. sumeryadav2004@gmail.com
  • 3. 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
  • 4. 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. sumeryadav2004@gmail.com
  • 5. BLOOD SUPPLY Mouth is supplied by branches from  Facial Artery  Inferior Alveolar Artery  Maxillary Artery  Infraorbital Artery  Postero superior sumeryadav2004@gmail.com
  • 7. 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. sumeryadav2004@gmail.com
  • 8. 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 sumeryadav2004@gmail.com
  • 9. Blood supply of Soft palate sumeryadav2004@gmail.com
  • 10. VENOUS DRAINAGE AND LYMPHATICS sumeryadav2004@gmail.com
  • 11. 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
  • 12. 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
  • 13. 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 sumeryadav2004@gmail.com
  • 14. 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 sumeryadav2004@gmail.com
  • 15. EXTRINSIC MUSCLES GENIOGLOSSUS Protrudes tongue; depresses center of tongue sumeryadav2004@gmail.com
  • 18. PALATOGLOSSUS Depresses palate; Moves palatoglossal fold toward midline; Elevates back of the tongue sumeryadav2004@gmail.com
  • 19. 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 sumeryadav2004@gmail.com
  • 20. BLOOD AND NERVE SUPPLY sumeryadav2004@gmail.com
  • 21. Tip: • Submental nodes bilaterally & then deep cervical nodes Anterior two third: • Submandibular unilaterally & then deep cervical nodes Posterior third: • Deep cervical nodes (jugulodigastric mainly) sumeryadav2004@gmail.com
  • 22. NERVE SUPPLY OF TONGUE sumeryadav2004@gmail.com
  • 24. 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” sumeryadav2004@gmail.com
  • 25. PREMALIGNANT LESIONS • Leukoplakia • Erythroplakia • Carcinoma in situ • Bowens disease • Actinic keratosis & chelitis • Dyskeratosis follicularis sumeryadav2004@gmail.com
  • 26. PREMALIGNANT CONDITIONS • Oral submucous fibrosis • Oral lichen planus • Syphilitic glossitis • Sideropenic dysphagia • Dyskeratosis congenita sumeryadav2004@gmail.com
  • 27. 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” sumeryadav2004@gmail.com
  • 28. 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 sumeryadav2004@gmail.com
  • 29. 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 sumeryadav2004@gmail.com
  • 30. • 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 sumeryadav2004@gmail.com
  • 31. 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 sumeryadav2004@gmail.com
  • 32. Etiopathogenesis • Tobacco – most imp offending agent • Alcohol • Chronic irritation • Syphilis • Nutritional deficiency • Actinic radiation sumeryadav2004@gmail.com
  • 33. • 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% sumeryadav2004@gmail.com
  • 34. 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
  • 35. 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 sumeryadav2004@gmail.com
  • 36. Clinical variants of leukoplakia Homogeneous/ Leukoplakia Simplex Speckled/Nodular Ulcerative sumeryadav2004@gmail.com
  • 37. 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
  • 38. • 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 sumeryadav2004@gmail.com
  • 39. Diferential diagnosis • Leukoedema • Lichen planus • Chemical burn • Morsicatio buccarum • Lupus erythematosus • White sponge nevus sumeryadav2004@gmail.com
  • 40. 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 sumeryadav2004@gmail.com
  • 41. CHEMOPREVENTION 1) Isotrenitoin / 13- cis- retinoic acid – 2) Beta carotene -30mg TID 3) Topical Bleomycin – 0.5-1% solution/2wks 4) 5-Fluorouracil & Cisplatin sumeryadav2004@gmail.com
  • 42. • 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 sumeryadav2004@gmail.com
  • 43. 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 sumeryadav2004@gmail.com
  • 44. CLASSIFICATION • Clinical variants 1. Homogenous erythroplakia 2. Erythroplakia interspersed with patches of leukoplakia 3. Granular or Speckled erythroplakia sumeryadav2004@gmail.com
  • 45. • 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 sumeryadav2004@gmail.com
  • 46. - Smooth and granular/nodular, well defined - May have an irregular, red granular surface interspersed with white or yellow foci - Soft on palpation sumeryadav2004@gmail.com
  • 47. • 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 sumeryadav2004@gmail.com
  • 48. Management • Biopsy should be performed • Treatment guided by histopathologic diagnosis • Recurrence , multifocality common • Careful long term follow up sumeryadav2004@gmail.com
  • 49. 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
  • 50. • 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 sumeryadav2004@gmail.com
  • 52. 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” sumeryadav2004@gmail.com
  • 53. • 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 sumeryadav2004@gmail.com
  • 54. • On skin- • Flat-topped purple polygonal & pruritic papular rash sumeryadav2004@gmail.com
  • 55. 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 sumeryadav2004@gmail.com
  • 56. • These mechanisms may combine to cause  T-cell accumulation in superficial lamina propria  Basement membrane disruption  Intra-epithelial T-cell migration &  Keratinocyte apoptosis sumeryadav2004@gmail.com
  • 57. 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
  • 58. Clinical variants Reticular (92%) Atrophic (44%) Plaque (36%) Erosive (9%) Bullous (1%) sumeryadav2004@gmail.com
  • 59. 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 sumeryadav2004@gmail.com
  • 60. 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 sumeryadav2004@gmail.com
  • 61. 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 sumeryadav2004@gmail.com
  • 62. IMMUNOFLUORESCENCE • Direct immunofluorescence – shaggy band of fibrinogen in the basement membrane, IgM stained cytoid bodies are also seen in dermal papilla or peribasilar area sumeryadav2004@gmail.com
  • 63. 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 sumeryadav2004@gmail.com
  • 64. • 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 sumeryadav2004@gmail.com
  • 65. 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
  • 66. 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” sumeryadav2004@gmail.com
  • 67. 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 sumeryadav2004@gmail.com
  • 68. 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% sumeryadav2004@gmail.com
  • 69. 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 sumeryadav2004@gmail.com
  • 70. 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 sumeryadav2004@gmail.com
  • 71. • 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) sumeryadav2004@gmail.com
  • 72. 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 sumeryadav2004@gmail.com
  • 73. • 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 sumeryadav2004@gmail.com
  • 74. 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 sumeryadav2004@gmail.com
  • 75. 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 sumeryadav2004@gmail.com
  • 76. • Advanced stage shows “homogenization” and “hyalinization” of collagen fibers (important feature) • Degeneration of muscle fibers and chronic inflammatory cell infiltration in the connective tissue sumeryadav2004@gmail.com
  • 77. 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 sumeryadav2004@gmail.com

Editor's Notes

  1. WHY WHITE LESIONS APPEAR WHITE? Increased thickness of the epithelium Increased and abnormal production of surface keratin Imbibition of fluid by surface layer Coagulation of surface tissue leading to necrosis Reduced vascularity in underlying lamina propria Sub mucosal deposit of ectopic sebaceous tissue
  2. Hairy Leukoplakia Definition Hairy leukoplakia is one of the most common and characteristic lesions of human immunodeficiency virus (HIV) infection. Rarely, it can also appear in immunosuppressed patients after organ transplantation. Etiology Epstein–Barr virus seems to play an important role in the pathogenesis. Clinical features Hairy leukoplakia presents as a white asymptomatic, often elevated and unremovable patch. The lesion is almost always found bilaterally on the lateral margins of the tongue, and may spread to the dorsumand the ventral surface (Fig. 3). Characteristically, the surface of the lesion is corrugated with a vertical orientation. However, smooth and flat lesions may also be seen. The lesion is not precancerous. Laboratory tests Histological examination, in situ hybridization, polymerase chain reaction (PCR) and electron microscopy. Differential diagnosis Chronic biting, lichen planus, frictional keratosis, cinnamon contact stomatitis, uremic stomatitis, candidiasis. Treatment Not required; however, in some cases aciclovir or valaciclovir can be used with success
  3. Size varies from a small, well localized patch measuring from a few mm in dia to a diffuse large lesion, covering a wide mucosal surface
  4. Retinoids They decrease cohesiveness of abnormal hyperproliferative keratinocytes & may reduce potential for malignant degeneration. They modulate keratinocyte differentiation. Nystatin therapy- it is given in candidal leukoplakia 500,000 IU twice daily plus mouth rinses with chlorhexidine solution Vitamin B complex- it is given as a supplement in cases of commissural and lingual lesions
  5. High risk factors for malignant transformation smoking, excessive alcohol intake, atrophic, ulcerative or erosive clinical types, presence of erythroplakic lesions and Sites involving the tongue, gingiva or buccal mucosa
  6. Specific findings of stage 2 include the following:   Reduction of the mouth opening (trismus) Stiff and small tongue Blanched and leathery floor of the mouth Fibrotic and depigmented gingiva Rubbery soft palate with decreased mobility Blanched and atrophic tonsils Shrunken budlike uvula Sinking of the cheeks, not commensurate with age or nutritional status