POTENTIALLY MALIGNANT DISORDER

PRESENTER- DR ANWESHA
BISWAS
POTENTIALLY MALIGNANT DISORDERS

INTRODUCTION
 Oral cancer constitutes an important entity in the field of head and
neck oncology
 The global incidence of oral cancer is 644600 cases per year.
 The incidence of oral cancer In India is 40 % among all cancer and
about 1,00,000 patients suffer from oral cancer in any year.
 Oral cancer is responsible for 7% of all cancer deaths in males
while it is 3 % in females.

 Various potentially malignant lesions, particularly red
lesions(erythroplasias) and some white lesions (leukoplakias) have
a potential for malignant change.
 In that, risk of erythroplasias is exceedingly high.
 The accuracy of predictions about potentially malignant lesions and
conditions is low but the process of identifying “at risk” lesions is
fundamental for diagnosis and treatment planning.
Mortazavi H, Baharvand M, Mehdipour M. Oral potentially malignant disorders: an
overview of more than 20 entities. J Dent Res Dent Clin Dent Prospects. 2014;8(1):6–
14.

DEFINITION
 A potentially malignant lesion is “A morphologically altered tissue in
which oral cancer is more likely to occur than in its apparently
normal counterpart.
-WHO 1978
 A potentially malignant condition is‘a generalized state associated
with a significantly increased risk of cancer’
- WHO 1978

Potentially malignant Lesions
 Leukoplakia
 Erythroplakia
 Mucosal changes associated with smoking habits
 Actinic cheilitis

Potentially malignant Conditions
 Oral submucous fibrosis
 Oral lichen planus
 Lupus erythematosus
 Sideropenic dysphagia

Potentially malignant disorders
 “It is a group of disorders of varying etiologies, usually tobacco
characterized by mutagen associated, spontaneous or hereditary
alterations or mutations in the genetic material of oral epithelial
cells with or without clinical and histo-morphological alterations that
may lead to oral squamous cell carcinoma transformation”.
Warnakulasuriya S. Clinical features and presentation of oral potentially malignant
disorders. Oral Surg Oral Med Oral Pathol Oral Radiol. 2018;125:582‐590

LEUKOPLAKIA
 Oral leukoplakia, as defined by the WHO, as“ A predominantly
white lesion of the oral mucosa that cannot be characterized as any
other definable lesion.”
Parlatescu I, Gheorghe C, Coculescu E, Tovaru S. Oral leukoplakia - an
update. Maedica (Buchar). 2014;9(1):88–93.

ETIOLOGY
ETIOLOGY OF
LEUKOPLAKIA
LOCAL
FACTORS
SYSTEMIC
FACTORS

Local Factors
 Tobacco
 Alchohol
 Chronic irritation
 Candidiasis
 Electromagnetic reaction

Systemic factors
 Syphillis
 Vitamin and nutritional deficiency
 Viruses
 Drugs
 Xerostomia
 Actinic radiation

CLINICAL FEATURES
 Male predilection
 Mostly occurs in 4th to 7th decade of life.
 Oral leukoplakias are found on the Upper and lower
alveolus(36%) buccal mucosa(22 %) , lips (11%), palate (11%),
floor of mouth (9%), gingiva(8%), Tongue(7%), retromolar
trigone(6%)
Warnakulasuriya S. Clinical features and presentation of oral potentially malignant
disorders. Oral Surg Oral Med Oral Pathol Oral Radiol. 2018;125:582‐590

CLINICAL TYPES
 Homogenous
 Non homogenous

HOMOGENOUS
 Uniform white patch lesion with smooth or corrugated surface
sometimes, slightly raised mucosa.
 Usually plaque like, some are smooth, may be wrinkled or criss-
crossed by small crack or fissure.
 Malignant transformation – 1 to 7%.

NON HOMOGENOUS
 Ulcerative or Erosive
 Proliferative Verrucous Leukoplakia
 Speckled Leukoplakia

Ulcerative leukoplakia
 It is characterized by red area, giving the appearance of ulceration.
 White patches are present at the periphery of the lesion

Proliferative Verrucous Leukoplakia
 Verrucous leukoplakia can become more exophytic with
development of multiple keratotic plaques with roughened surface
projection.
 It has got strong female predilection
 It can spread and involve adjacent mucosa.
 As the disease progress it transforms into a lesion that is clinically
and microscopically identical to verrucous carcinoma or squamous
cell carcinoma.

 It is a mixed red white lesion in which small keratotic nodules are
scattered
 over an atrophic patch of oral mucosa.
 Nodules may be pinhead sized or even larger
 It has got a high malignant potential.

Classification by Van der Waal et al
 Lx — Size not specified
 L1 — Size of leukoplakia <2 cm
 L2 — Size of leukoplakia 2–4 cm
 L3 — Size of leukoplakia >4 cm
 P — Pathology
 Px — Dysplasia not specified in the pathology report.
 P0 — No epithelial dysplasia
 P1 — Mild to Moderate epithelial dysplasia
 P2- Severe Epithelial dysplasia

Staging of Leukoplakia
 Stage I — L1 P0
 State II — L2 P0
 Stage III — L3 P0 or L1/ L2 P1
 Stage IV — L3 P1 or any LP2

HAIRY LEUKOPLAKIA
 Hairy leukoplakia is a condition that is characterised by irregular
white patches on the side of the tongue and occasionally elsewhere
on the tongue or in the mouth.
 It is a form of leukoplakia often arises in response to chronic
irritation.
 Hairy leukoplakia is associated with Epstein-Barr virus (EBV) and
occurs primarily in HIV-positive individuals.

Clinical features
 Male predilection
 Most common in 40 – 60 years of age
 Recent studies show higher incidences in young adults
 Bilaterally on the lateral borders of the tongue as painless, faint
white vertical streaks or thickened and furrowed areas with a
shaggy keratotic surface with vertical striations imparting a
corrugated appearance.

Investigations
 Toluidine Blue Staining
 Lugol’s iodine Staining
 Vizilite
 Exfoliative Cytology
Lugol’s iodine Staining
Toluidine Blue Staining
Vizilite

 Histopathological examination:- It shows hyperkeratosis of surface
epithelium with acanthosis of the spinous layer. The Cells show
features of dysplasia i.e
 1. Loss of polarity of the basal cells
 2. Presence of more than one layer of cells having a basaloid
appearance
 3. Increased nuclear cytoplasmic ratio
 4. Drop-shaped rete processes

 5. Irregular epithelial stratification
 6. Increased number of mitotic figures
 7. Presence of mitotic figures in the superfi cial half of the
epithelium
 8. Cellular pleomorphism
 9. Nuclear hyperchromatism
 10. Enlarged nucleoli
 11. Reduction of cellular cohesion
 12. Keratinization of single cells or cell groups in the prickle layer

DIFFERENTIAL DIAGNOSIS
 White sponge nevus
 Hypertrophic candidiasis
 Leukoedema
 Lichen planus
 Psoriasis
 Discoid lupus erythematosus
 Electrogalvanic white lesion
 Frictional keratosis

MANAGEMENT
 Vit A -75000- 300000 IU for 3 months.
 13-cis-retinoic acid 1.5 to 2 mg/kg body weight for 3 months.
 Topical Bleomycin – 0.5-1% solution for 2wks
 5-Fluorouracil 50-150 mg/kg Qid

 Surgical Management:-
 Scalpel excision / Stripping
 Electrocautery
 Cryotherapy with liquid nitrogen
 Laser therapy which includes CO2 and Erbium laser

ERYTHROPLAKIA
 Also known as ERYTHROPLASIA OF QUEYART
 A fiery red patch that cannot be characterized clinically or
pathologically as any other definable disease.
- WHO
Etiology:-
 Unknown
 Contributing factors include tobacco use, alcohol
consumption

CLINICAL FEATURES
 Incidence :- It is more common in males and occurs more
frequently in the 6th and 7th decade of life.
 Red, often velvety, well-defined patches.
 Most commonly present on floor of mouth, retromolar area, lateral
tongue.
 Usually asymptomatic
 May be smooth to nodular

 It appears as a bright red, soft velvety lesion with straight or
scalloped well demarcated margins, often quite extensive in size,
commonly found on the buccal mucosa and sometimes on the soft
palate, more rarely on the tongue and floor of the mouth.
 Sometimes it appears which is soft, red lesions that are slightly
elevated with an irregular outline and a granular or fine nodular
surface speckled with tiny white plaques

Diagnosis
 Clinical diagnosis
 Toluidine blue examination
 Biopsy

 Erythematous (atrophic) candidiasis
 Kaposi’s sarcoma
 Squamous cell carcinoma
 Contact Stomatitis

MANAGEMENT
 Beta Carotene 20 to 90 mg/day for a period of 3-12 months.
 Vitamin E 800 IU/day from 6 to 9 months
 Topical bleomycin in dosages of 0.5%/day for 12 to 15 days
 Photodynamic therapy with Aminolaevulinic acid 10%, activated by
a laser at 635 nm and 100 J/cm2 per session, for 6 to 8 sessions.
 If proven dysplastic then go for surgical excision.

Actinic cheIlitis
 Actinic cheilitis (AC) is a chronic inflammatory disorder of the lips
that is caused by prolonged exposure to sunlight in susceptible
individuals.
 The word has been derived from the Greek words "aktis" meaning
"ray" and "cheilos" meaning "lips."
 This disorder is considered to be potentially malignant and a
predisposing factor for the development of squamous cell
carcinoma.
Somasundaram E, Gera R, Peethambaran HB. Actinic cheilitis: A review. J Indian Acad
Oral Med Radiol 2015;27:569-71

 Etiology:-
 This disorder manifests itself after prolonged exposure to sunlight
 UV rays with a wavelength of 290-320 nm are held responsible for
the sunlight-induced deleterious changes that occur in the lips.
 The vermilion zone of the lower lip is more susceptible to the
effects of UV rays because of thinner epithelium, lower melanin
content, and lower sebaceous and sweat secretion.

 Pathogenesis:-
 The exact mechanism of development of Actinic cheilitis is unclear.
 The chronic exposure to UV radiation (sunlight) results in
mutational changes in the keratinocytes and progressive
degradation of epithelium and inflammatory responses in the
lamina propria.
Clydesdale GJ, Dandie GW, Muller HK. Ultraviolet light induced injury: Immunological and
inflammatory effects. Immunol Cell Biol 2001;79:547-68

Clinical features
 Age predilection:- 20-80 years of age
 Sex predilection:- Can affect both men and women but ,men are
affected much more commonly than women.
 Although Actinic chelitis is considered to occur commonly in fair-
skinned people, it is also found in dark-skinned people
Cavalcante AS, Anbinder AL, Carvalho YR. Actinic cheilitis: Clinical and
histological features. J Oral Maxillofac Surg 2008;66:498-503.

 It affects the lower lip exclusively because of its anatomic orientation that
exposes it to sunlight.
 It initially occurs as an asymptomatic dry lip affecting the lower lip
vermilion. Advanced lesions may manifest as parallel folds or fissures, a
loss of normally distinct cutaneous vermilion border, mottling, keratotic
plaques, and erosions.
 On palpation, these lesions give the sense of gloved sliding finger on fine
sand paper.

 Squamous cell carcinoma
 Basal cell carcinoma
 Cheilitis Granulomatosa
Picascia DD, Robinson JK. Actinic cheilitis: A review of etiology, differential diagnosis,
and treatment. J Am Acad Dermatol 1987;17:255-64

Investigations
 Biopsy
 Biopsy:- Following features will be seen
 Dysplasia
 Inflammatory infiltrate

 Acanthosis
 Hyperkeratosis,
 Epithelial atrophy

Management
 Topical Application of Diclofenac gel 3% once daily for 1-4
weeks
 Cryotherapy: Liquid nitrogen physically destroys abnormal
cells
 Laser treatment: Commonly used lasers are:-
 CO2 Laser: 10600 nm
 Erbium Laser: 2940 nm
 Vermilionectomy/Surgical excision: preferred treatment
for severe/refractory cases
Picascia DD, Robinson JK. Actinic cheilitis: A review of etiology, differential
diagnosis, and treatment. J Am Acad Dermatol 1987;17:255-64

LICHEN PLANUS
 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”.

ETIOLOGY
 Unknown.
 Autoimmune. T cell–mediated disease targeting basal keratinocytes
 Lichenoid changes associated with galvanism, graft-versus-host
disease (GVHD), certain drugs, contact allergen.

Incidence
 Up to 3 to 4% of Indian population has oral lichen planus.
 0.5 to 1% of population has cutaneous lichen planus; 50% also
have oral lesions.
 More common in White females (60%)
 It occurs in 4th to 8th decades of life

PATHOGENESIS
 OLP is a T-cell mediated autoimmune disease in which the auto-
cytotoxic CD8+ T cells trigger apoptosis of the basal cells of the
oral epithelium.
 An early event in the disease mechanism involves keratinocyte
antigen expression or unmasking of an antigen that may be a self-
peptide or a heat shock protein.
 Following this, T cells (mostly CD8+, and some CD4+ cells) migrate
into the epithelium either due to random encounter of antigen
during routine surveillance or a chemokine-mediated migration
toward basal keratinocytes.
Nosratzehi T. Oral Lichen Planus: an Overview of Potential Risk Factors, Biomarkers
and Treatments. Asian Pac J Cancer Prev. 2018;19(5):1161–1167.

 These migrated CD8+ cells are activated directly by antigen binding
to major histocompatibility complex (MHC)-1 on keratinocyte or
through activated CD4+ lymphocytes.
 In addition, the number of Langerhan cells in OLP lesions are
increased along with upregulation of MHC-II expression .
 Subsequent antigen presentation to CD4+ cells and Interleukin (IL)-
12 activates CD4 + T helper cells which activate CD8+ T cells
through receptor interaction, interferon γ (INF – γ) and IL-2.

 The activated CD8+ T cells in turn kill the basal keratinocytes
through tumor necrosis factor (TNF)-α, Fas–FasL mediated or
granzyme B activated apoptosis.
 The normal integrity of the basement membrane is maintained by a
living basal keratinocyte due to its secretion of collagen 4 and
laminin 5 into the epithelial basement membrane zone.
 In turn, keratinocytes require a basement membrane derived cell
survival signal to prevent the onset of its apoptosis.

 Apoptotic keratinocytes are no longer able to perform this function,
which results in disruption of the basement membrane.
 Again, a non-intact basement membrane cannot send a cell
survival signal. This sets in a vicious cycle which relates to the
chronic nature of the disease.

CLINICAL PRESENTATION
 Variants: reticular (most common oral form); erosive (painful);
atrophic, papular,plaque types; bullous (rare)
 Bilateral and often symmetric distribution
 Oral site frequency: buccal mucosa (most frequent), then tongue,
then gingiva, then lips (least frequent)

Reticular type of lichen planus
 Characterized by fine whites lines or striae.
 These striae may form a network or show annular pattern.This arrangment is known
as Wickham’s striae.
 It often displays a peripheral erythematous zone reflecting sub epithelial
inflammation.
 Most frequently seen on buccal mucosa and dorsum of tongue and sometimes on
vermilion border of lips

Papular type
 These are characterized by white elevated lesions seen on
keratanized oral mucosa.
 These lesions are oftenly spaced apart, but sometimes they may
coalesce.
 They are mostly present on the periphery of striae.

Plaque type
 It is seen on dorsum of tongue and buccal mucosa.
 It consists of pearly white or grayish lesions with elevated areas
having irregular peripheries.
 It spreads in a concentric peripheral growth
Mollaoglu N. Oral lichen planus: a review. Br J Oral Maxillofac Surg .2000; 38(4) 370-77

Bullous form
 It contains of bullae which are mostly found on buccal mucosa and
posterior and lateral margins of tongue
 These bullae are often short lived and rupture soon.
 As these bullae rupture, these leave an ulcerated surface
associated with a striae component.
.

EROSIVE LICHEN PLANUS
 It presents as chronic multiple ulcers which occur after the rupture
of bullae.
 The Patient may complain of burning sensation and pain.
 The common site is buccal mucousa and ventral surface of tongue
 It is seen as eroded and ulcerated lesions which are irregular in
size and shape.
 The surface is erythematous and may bleed upon slight
provocation. Sometimes the surface may be covered by a fibrinous
plaque.

ETIOLOGY OF EROSIVE LICHEN PLANUS
 Drugs like hydrocholrthiazide, penicillamine, ACE inhibitors
 Reaction to dental restorations
 Graft vs Host disease
 Systemic conditions like chronic hepatitis
 Stress

ATROPHIC TYPE
 It often presents a smooth, red, poorly defined area.
 The attached gingiva is most frequently involved in this type of
lichen planus, and this condition is called as desquamative
gingivitis.
 At the margins of atrophic zones, whitish keratotic areas are seen.
 The patient complains and burning sensation in the area of
involvment.

INVESTIGATION
 Examination of oral mucosa, skin
 Biopsy
 Direct-immunofluorescence– fibrinogen and cytoid bodies at
interface help confirm

 Lichenoid drug eruptions
 Erythema multiforme
 Lupus erythematosus
 Contact stomatitis
 Mucous membrane pemphigoid

MANAGEMENT
New cases:-
Topical Corticosteroid therapy:-
Triamicinalone acetonide 0.1% 3 times a day for a maximum period
of one month
Flucinolone 0.025% 3 times a day for 2 months
Clobetasone 0.05% twice a day for 2 months

 Combination therapy:-
 Prednisolone 10 mg 3 times a day for 2 weeks, + Topical
Triamicinolone acetonide 0./1% three times a day till symptoms
improve.
 Recalcitrant cases
 Intralesional injections of Triamcinolone 0.5 ml with once/week for 4
weeks
 Chloroquine 250 mg twice daily for 3 months

 Azathioprine 1mg/kg/day for one month
 Cyclosporine 8 mg per kg for 8 weeks
 Prednisolone 5 mg + levamisole 50 mg for 3 weeks

ORAL SUBMUCOUS FIBROSIS
 This condition was first described by Joshi (1952) and by Schwatz
among East Indian Women.
 This is an insidious chronic disease affecting any part of oral cavity
including pharynx.
 It is considered to be POTETIALLY MALIGNANT DISORDER

DEFINITION
 According to Pindborg et al it is defined as:-
 “It is an insidious chronic disease affecting any part of the oral
cavity and sometimes the pharynx. Although occasionally preceded
by or associated with vesicle formation ,it is always associated with
juxta-epithelial inflammatory reaction followed by a fibro-elastic
changes of the lamina propria with epithelial atrophy leading to
stiffness of the oral mucosa and causing trismus and inability to
eat.”

EPIDEMIOLOGY
 OSMF is seen commonly in India and Indian subcontinent.
 Sporadic cases are seen in Malaysia, Nepal, Thailand and South
Vietnam.
 Population between 20 to 40 years of age are most commonly
affected.

ETIOLOGY
 Exact etiology is unknown.
 The predisposing factors are,
 Chronic Irritation-Due to Chilies, Lime, Areca nut, Tobacco.
 Defective iron metabolism
 Bacterial Infection
 Collagen disorder
 Immunological disorders
 Genetic disorder.

PATHOGENESIS
 Areca Alkaloids Causing Fibroblast Proliferation:-
 Among the areca alkaloids such as arecoline, arecadine,
guvacoline, guvacine, arecoline is the main agent responsible for
fibroblast proliferation.
 Under the influence of slaked lime (Ca(OH) 2 ), arecoline get
hydrolyzed to arecadine, which has pronounced effects on
fibroblasts.
Wollina U, Verma SB, Ali FM, Patil K. Oral submucous fibrosis: an update. J.Clin
Cosmet Investig Dermatol. 2015;8:193–204

 Stablization of Collagen Structure by Tanins and Catachins:-
 Areca flavonoids tannins and catechins can cause increased fibrosis by
forming a more stable and non soluble collagen structure by inhibiting
collagenase enzyme activity.
 Studies have shown that there is 1.5 fold increase in collagen production
by OSMF fibroblasts and with the progression of disease type 3 collagen
is completely replaced by type 1 collagen which is more resistant to
degradation.
 Also there has been an excess of alpha 1 (1) chains relative to alpha 2(1)
chains, suggesting an alteration of collagen molecule during the disease
progression.

 Inhibition of Collagen Phagocytosis:-
 There is a gross imbalance in the extracellular matrix remodeling in
OSMF.
 In fibrotic connective tissue lesions without marked inflammation such as
OSMF, the main route of collagen degradation is by phagocytosis and not
by extracellular digestion.
 In OSMF, the reduction of phagocytic activity is inversely dose
dependent to levels of arecoline, safrole and nicotine in saliva.
 Arecoline causes a suppression of T cell activity which in turn decreases
the cell mediated immunity and thus results in decreased phagocytic
activity of the cells.

 High Copper Content in Areca Nut and Fibrosis:-
 The Copper causes upregulation of lysyl oxidase enzyme which
plays a crucial role in cross linking of collagen and elastin
molecules.
 Lysyl oxidase is a copper-dependent enzyme which is also an
intrinsic protein of connective tissue.
 It is induced at detectable levels during fibrogenesis and
fibroproliferative process.

 Increased Expression of Fibrogenic Cytokines:-
 It has been postulated that external stimuli such as areca nut may
induce OSMF by increasing the levels of cytokines in lamina
propria and also increasing the production of cytokines by the
peripheral mononuclear cells.
 An upregulation of proinflammatory cytokines i.e IL-6 and IL-8 has
been seen. It may be due to the T-cell activation, which occurs
secondary to the chronic inflammation.
 Also an upregulation of certain fibrogenic cytokines such as TNF-α,
TGF-β, platelet-derived growth factor, basic fibroblast growth
factors is seen in OSMF.

CLASSIFICATION
 Khanna JN and Andrade NN (1995) developed a group
classification system for the surgical management of OSMF:-
 Group I:
 Very early cases: Common symptom is burning sensation in the mouth,
acute ulceration and recurrent stomatitis and not associated with mouth
opening limitation.
 Histology: Fine fibrillar collagen network interspersed with marked
edema, blood vessels dilated and congested, large aggregate of plump
young fibroblasts present with abundant cytoplasm, inflammatory cells
mainly consist of polymorphonuclear leukocytes with few eosinophils. The
epithelium is normal.

 Group II: Early cases—Buccal mucosa appears mottled and marble like,
widespread sheets of fibrosis palpable, interincisal distance of 26 to 35
mm.
 Histology: Juxta-epithelial hyalinization present, collagen present as
thickened but separate bundles, blood vessels dilated and congested,
young fibroblasts seen in moderate number, inflammatory cells mainly
consist of polymorphonuclear leukocytes with few eosinophils and
occasional plasma cells, flattening or shortening of epithelial rete-pegs
evident with varying degree of keratinization.

 Group III: Moderately advanced cases— Trismus, interincisal distance of
15 to 25 mm, buccal mucosa appears pale firmly attached to underlying
tissues, atrophy of vermilion border, vertical fibrous bands palpable at the
soft palate, pterygomandibular raphe and anterior faucial pillars.
 Histology: Juxta-epithelial hyalinization present, thickened collagen
bundles, residual edema, constricted blood vessels, mature fibroblasts
with scanty cytoplasm and spindle-shaped nuclei, inflammatory exudate
which consists of lymphocytes and plasma cells, epithelium markedly
atrophic with loss of rete pegs, muscle fibers seen with thickened and
dense collagen fibers.

 Group IVA: Advanced cases—severe trismus, interincisal distance of
less than 15 mm, thickened faucial pillars, shrunken uvula, restricted
tongue movement, presence of circular band around entire lip and mouth.
 Group IVB: Advanced cases—presence of hyperkeratotic leukoplakia
and/or squamous cell carcinoma.
 Histology: Collagen hyalinized smooth sheet, extensive fibrosis,
obliterated the mucosal blood vessels, eliminated melanocytes, absent
fibroblasts within the hyalinized zones, total loss of epithelial rete pegs,
presence of mild to moderate atypia and extensive degeneration of
muscle fibers.

 Pindborg JJ (1989) separated OSMF into three stages based on
clinical features:
 Stage 1: Stomatitis includes erythematous mucousa, vesicles,
mucosal ulcers, melanotic mucosal pigmentation and mucosal
patechiae.
 Stage 2: Fibrosis occurs in healing vesicles and ulcer, which is the
hallmark of this stage. Early lesions demonstrate blanching of oral
mucosa. Older lesion include vertical and circular palpable fibrous
bands in the buccal mucosa and around the mouth opening or lips,
resulting in a mottled marble like appearance of the mucosa
because of the vertical thick, fibrous bands associated with
balanced mucosa.

 Stage 3: Sequelae of OSMF
 Leukoplakia is found in more than 25% of individuals with OSMF.
 Speech and hearing deficits may occur because of involvement of
the Eustachian tubes

 Nagesh and Bailoor (1993) Classified OSMF into three stages as
follows:
 Stage I Early OSMF: Mild blanching, no restriction in mouth
opening (normal distance between central incisor tips.Burnig
sensation on taking spicy food or hot beverages.
 Stage II Moderate OSMF: Moderate to severe blanching, mouth
opening reduced by 33%, cheek flexibility alsodemonstrably
reduced, burning sensation also in absence of stimuli, palpable
bands felt. Lymphadenopathy, either unilateral or bilateral and
demonstrable anemia on hematological examination.

 Stage III Severe OSMF: Burning sensation is very severe patient
unable to do day-to-day work, more than 66% reduction in the
mouth opening, cheek flexibility and tongue protrusion. Tongue may
appear fixed.Ulcerative lesions may appear on the cheek, thick
palpable band sand lymphadenopathy is bilaterally evident.

 Haider et al (2011) divided it based on severity of the disease with
functional staging and objective measures inter-incisal opening:
 Clinical Staging:
 • Stage 1: facial bands only
 • Stage 2: facial and buccal bands
 • Stage 3: facial and labial bands

 Functional Staging
 Stage A: Mouth opening 13 to 20 mm
 Stage B:Mouth opening 10 to 11mm
 Stage C:Mouth opening <10mm

Clinical features
 Site Distribution:- Most Common areas for oral submucous fibrosis is
buccal mucosa, soft palate, tongue, uvula, palatal fauces, labial mucosa
and retromolar area.
 Prodromal Symptoms:- Burning sensation in mouth
Dryness of mouth
Vesiculation and ulceration
 Late Symptoms:- Trismus
Difficulty in tongue protrusion
Difficulty in swallowing

 Signs:- Blanching of mucosa or marble like appearance of mucosa.
 Circumoral fibrous bands around the orbicularis oris muscle,
causing labial mucosa to become rubbery.
 Vertical fibrous bands can be palpated in the region of buccal
mucosa. The buccal mucosa becomes coarse, blanched, tough
and leathery.
 The movement of Soft Palate becomes restricted. Uvula becomes
shrunken and in some cases it gives a hockey stick appearance.

 The fibrous bands radiate from pterygomandibular raphe to anterior
faucial pillar.
 Tounge becomes depapillated and its mobility is restricted.
 Gingiva when affected, becomes fibrotic, blanched and inelastic.

Blanching of mucosa giving it a
marble like appearance
Depapillated tongue
Shrunken uvula

HISTOPATHOLOGIC FEATURES
 Atrophic Oral epithelium.
 Loss of rete pegs .
 Epithelial atypia may be observed.
 Hyalinization of collagen bundles.
 Fibroblasts decreased and blood vessels obliterated.

DIAGNOSIS
 Clinically appreciable blanching and pallor.
Palpable bands and restriction-of mouth opening.
 Severe burning sensation of mouth, aggravated by use of even
moderate spicy food.
 Biopsy report
Khan S, Sinha A, Kumar S, Iqbal H Oral submucous fibrosis: Current concepts on
aetiology and management – A review.. J. Indian Acad Oral Med Radiol. 2018; 30(4):
407-11

 Scleroderma
 Generlized Fibromatosis
 Amylodosis

NON SURGICAL THERAPY
 Steriod therapy:-
 Dexamethasone(4mg/ml) + hyaluronidase( 1500 I.U) given for 8 weeks.
 Triamcinalone 40 mg given biweekly for 12 weeks
 Topical Triamicinalone 0.1% and Betamethasone 0.5%
 Methyl prednisolone 40 mg given at monthly intervals given for 6
months
 Hydocortisone(12.5mg)+ hyaluronidase( 1500 I.U) given for 1 week
407-11

 Interferon Gamma (0.25ml) given twice a week over 8weeks
 Levamisole (50mg) given at 3 times daily for 3 consecutive days in
a week for 3 alternate weeks.
 Lycopene 2000 mcg for 3 months
 Placental extract(2ml)+ Dexamethasone(4mg/ml) for 8 weeks.
 Pentoxifylline 400 mg twice daily for 3 months.
407-11

Intralesional steroid injection
 Dexamethasone1.5 ml, hyaluronidase 1500 IU with 0.5 ml
lignocaine HCL injected intralesionally biweekly for 4 weeks.
 Hyaluronidase by breaking down hyaluronic acid (the ground
substance in connective tissue) lowers the viscosity of intercellular
cement substance.
 Dexamethasone acts as an immune suppressive agent by its
antagonistic activity on the soluble factors released by the
sensitized lymphocytes succeeding the activation by nonspecific
antigens. Thus, fibrosis is prevented by a decrease in fibroblastic
proliferation and deposition of collagen.

 Procedure:-
 An insulin syringe needle is employed for this purpose.
 The Buccal mucosa is divided into 9 imaginary planes.
 The Syringe is filled with Dexamethasone1.5 ml, hyaluronidase 1500 IU with
0.5 ml lignocaine HCL.
 The fibrous bands are palpated in buccal mucosa and retromolar region.
 The needle( thin bore needle) is directed towards the band areas of mucosa
 This procedure is done twice a week for about 4 weeks
James L, Shetty A, Rishi D, Abraham M. Management of Oral Submucous Fibrosis
with Injection of Hyaluronidase and Dexamethasone in Grade III Oral Submucous
Fibrosis: A Retrospective Study. J Int Oral Health. 2015;7(8):82-85.

Surgical management
 Excision of the fibrous bands followed by reconstruction using:-
 Bilateral full thickness nasolabial flaps
 Bilateral temporalis myotomy and coronidectomy
407-11

ORAL PHYSIOTHERAPY
 Oral Excercises are also adviced
 Mouth opening using ice cream sticks and balloning of the mouth
 Forceful opening of mouth using mouth gags and acrylic surgical
screw.
407-11

Discoid Lupus Erythematosus
 Discoid lupus erythematosus (DLE) is a chronic, scarring, atrophy
producing, photosensitive dermatosis.
 It occurs in in patients with systemic lupus erythematosus (SLE),
and some patients (<5%) with discoid lupus erythematosus
progress to systemic lupus erythematosus .
 Patients with Discoid lupus erythematosus rarely have clinically
significant systemic disease. Lesions may produce scarring or
atrophy.

Etiopathogenesis
 DLE probably occurs in genetically predisposed individuals, but the
exact genetic connection has not been determined.
 Genes associated with DLE are TYK2, IRF5, and CTLA4
 Some of the contributing environmental factors include ultraviolet
radiation (UVR) and cigarette smoking
 It has been suggested that a heat shock protein is induced in the
keratinocyte following ultraviolet (UV) light exposure or stress, and
this protein may act as a target for T-cell-mediated epidermal cell
cytotoxicity.

 Smoking smoking provokes DNA damage, resulting in the
formation of DNA adducts and the production of ds-DNA antibodies.
 Keratinocytes may also participate in lupus skin damage by
increasing the apoptotic rate and the production of proinflammatory
cytokines such as IFN-lambda.
Ranginwala AM, Chalishazar MM, Panja P, Buddhdev KP, Kale HM. Oral discoid
lupus erythematosus: A study of twentyone cases. J Oral Maxillofac Pathol
2012;16:368-73

ClINICAL FEATURES
 DLE occurs more frequently in women in their fourth and fifth
decades of life.
 It is more common in women than in men.
 Although any skin area may be involved by the discoid form of
lupus erythematosus, the most common sites are the face oral
mucous membranes, chest, back and extremities.
Burrows NP, Lovel CR. Disorders of connective tissue. In: Burns T, Breathnach S, Cox N, Griffiths
C, editors. Rook’s Textbook of Dermatology. Sussex: Wiley-Blackwell; 2010. p. 4532.

 The typical cutaneous lesions are slightly elevated red or purple
macules that are often covered by gray or yellow adherent scales.
 Forceful removal of the scale reveals numerous ‘carpet tack’
extensions.
 The lesions increase in size by peripheral growth, this feature
partially characterizing the disease.

 The periphery of the lesion appears pink or red, while the center
exhibits an atrophic, scarred appearance indicative of the long-
standing nature of the disease with characteristic central healing.
 The discoid form of the disease may also assume a typical
‘butterfly’ distribution on the malar regions and across the bridge of
the nose.

Oral MANIFESTATIONS
 Oral mucous membrane involvement is reported in 20–50% of
cases of discoid lupus erythematosus.
 The oral mucosa reportedly may be involved either prior to or
following the development of skin lesions or even in the absence of
skin manifestations.
 Lesions begin as erythematous areas, sometimes slightly elevated
but more often depressed, usually without induration and typically
with white spots.
Schiödt M, Halberg P, Hentzer B. A clinical study of 32 patients with oral
discoid lupus erythematosus. Int J Oral Surg 1978;7:85-94.

 Occasionally, superficial, painful ulceration may occur with crusting or bleeding
but no scale formation.
 The margins of the lesions are not sharply demarcated .Often, fine white striae
radiate out from the margins. Central healing may result in depressed scarring.
 The vermilion border of the lower lips is a very common site for these lesions.
The erythematous, atrophic plaques, surrounded by a keratotic border, may
involve the entire lip and extend onto the skin surface.

INVESTIGATIONS
 Histopathology:-
 Hyperkeratosis with keratotic plugging,
 Atrophy of the rete pegs, liquefaction, degeneration of the basal
layer of cells, perivascular infiltration of lymphocytes and their
collection about dermal appendages, and basophilic
 Degeneration of collagen and elastic fibers, with hyalinization,
 Edema and fibrinoid change, particularly prominent immediately
beneath the epithelium
Karjalainen TK, Tomich CE. A histopathologic study of oral mucosal lupus
erythematosus. Oral Surg Oral Med Oral Pathol 1989;67:547-54.

 Direct immunoflouresence:- The most characteristic DIF finding is
antibody deposition at the dermal-epidermal junction .These
deposits are typically granular, and they are composed primarily of
IgG and/or IgM.
 Serological investigation for detecting the autoantibody against
annexin 1. Higher level of anti-annexin 1 antibodies are found in
DLE patients,
Chhabra S, Minz RW, Saikia B. Immunofluorescence in dermatology. Indian J
Dermatol Venereol Leprol 2012;78:677-91

MANAGEMENT
 Corticosteroids:-
 0.05% fluocinonide cream to be applied 2-4 times a day
 Intralesional therapy with 2.5 to 10mg/mL triamcinolone
solution once in a month for a time period of 6 months.
 0.03% of tacrolimus to be applied 2 times daily for 4 weeks
 Systemic therapy with mycophenolate mofetil 1 to 3 g once daily for
2 months
Winkelmann RR, Kim GK, Del Rosso JQ. Treatment of Cutaneous Lupus
Erythematosus: Review and Assessment of Treatment Benefits Based on Oxford Centre
for Evidence-based Medicine Criteria. J Clin Aesthet Dermatol. 2013;6(1):27-38.

Palatal Lesions Associated with reverse smoking
 Stomatitis Nicotina:-
 It is also called as ‘smoker’s palate’, ‘stomatitis nicotina palati’.
 It refers to a specific white lesion that develops on the hard and soft
palate in heavy cigarette, pipe, and cigar smokers.
 Here, hand rolled cigarettes and cigars are smoked with the
burning end held within the mouth. This habit is called as ‘reverse
smoking’ and the lesion associated

 This habit is prevalent in Columbia, Panama, Venezuela, Asia
(South India), and Europe (Sardinia).
 In Seemandhra Pradesh, it is prevalent in the coastal areas of
Godavari, Visakhapatnam, Vizianagaram, and Srikakulam districts.
 In Andhra this is reffered to as chutta smoking and habit is called as
adda poga.
 In Goa dhumti is smoked, in which rolled leaf is kept inside the leaf
of jackfruit tree.
Harini G, Krishnam Raju KV, Raju DV, Chakravarthy KK, Kavya SN.
Psychosocial factors associated with reverse smoking: A qualitative
research. J Int Soc Prev Community Dent. 2016;6(6):529-534

 The Chutta is cured tobacco wrappped in a dried tobacco leaf.
 It is derived from Tamil word Shruttu, which means to roll.
 About 9% of the total tobacco production in India is used to
prepare 300 million pieces of these forms of tobacco.
 Reverse smoking produces palatal patches which are reported to
exhibit a malignant change of 12 per 1000 cases.
 This habit is called as ‘reverse smoking’ and the lesion associated
with it is called as ‘reverse smoker palate’.

 Changes occuring in palate:-
 Keratosis:- diffuse whitening of the entire palatal mucosa.
 Excrescences:- 1-3 mm elevated nodules, often with central red
dots corresponding to the opening of palatal mucous glands.
 Patches:- well defined, elevated white plaques, which could qualify
for the clinical term leukoplakia.

Clinical Features
 It is usually seen in men who are pipe smokers. It is common in
middle age and elderly adults.
 Site—most commonly affected site is palate. The lesion is well
developed and prominent on hard palate.
 It is restricted to the area which is exposed to heavy cigarette
smoke.
 In the early stages, mucosa is reddened. It subsequently becomes
grayish white, thickened and fissured. Fissures and cracks may
appear producing a wrinkled, irregular surface.

 The discoloration is homogenous with the exceptions of numerous
erythematous spot .
 It represent focal thickening surrounding the orifice of the salivary
gland which appears as white umblicated nodule with red center.
 This area is often stained black to brown because of continous
smoking.

Differential Diagnosis
 Denture induced hyperplasia
 Discoid lupus erythematosus,
 Oral candidiasis,
 Darier's disease
Kumari S, Mishra SK. Diagnosis of smokers' palate in a denture wearer
patient. BLDE Univ J Health Sci 2017;2(2):125-6

Investigations
 Histopathology:-
 In biopsy epithelium shows acanthosis and hyperkeratosis.
 Epithelium lining of minor salivary gland often shows squamous cell
metaplasia and hyperplasia.

Management
 Habit Cessation counselling should be given to the patient.
 This lesion is completely reversible and disappears within few
weeks of discontinuing the habit.

REFERNCES
 Burket, Lester W., Martin S. Greenberg, and Michael Glick. 2015. Burket's oral
medicine:. Hamilton, 12th Edition. Ont: BC Decke.
 Wood N., Goaz P, Red and White lesions: Differential diagnosis of Oral &
Maxillofacial Lesions 5th Edition
 Shafer, William G., Maynard K. Hine, and Barnet M. Levy. 2016. A textbook of
oral pathology. 8th Edition.Philadelphia: Saunders.
 Somasundaram E, Gera R, Peethambaran HB. Actinic cheilitis: A review. J
Indian Acad Oral Med Radiol 2015;27(4):569-71
 Cawson, R. A., and E. W. Odell. 2017. . Cawson's essentials of oral pathology
and oral medicine . 9th Edition,Edinburgh: Churchill Livingstone
 Warnakulasuriya S. Clinical features and presentation of oral potentially
malignant disorders. Oral Surg Oral Med Oral Pathol Oral Radiol.
2018;125(6):582‐590

 Cavalcante AS, Anbinder AL, Carvalho YR. Actinic cheilitis: Clinical
and histological features. J Oral Maxillofac Surg 2008;66(3):498-503.
 Picascia DD, Robinson JK. Actinic cheilitis: A review of etiology,
differential diagnosis, and treatment. J Am Acad Dermatol
1987;17(2):255-64
 Parlatescu I, Gheorghe C, Coculescu E, Tovaru S. Oral leukoplakia -
an update. Maedica (Buchar). 2014;9(1):88–93.
 Awadallah M, Idle M, Patel K, et al. Management update of potentially
premalignant oral epithelial lesions. Oral Surg Oral Med Oral Pathol
Oral Radiol. 2018;125(6):628‐63
 Clydesdale GJ, Dandie GW, Muller HK. Ultraviolet light induced injury:
Immunological and inflammatory effects. Immunol Cell Biol
2001;79(6):547-68

 Patait M, Nikate U, Saraf K, Singh P, Jadhav V . Oral erythroplakia – A case
report. Int. J. Appl. Den. Sci. 2016; 2(4): 79-82
 Khan S, Sinha A, Kumar S, Iqbal H Oral submucous fibrosis: Current
concepts on aetiology and management – A review.. J. Indian Acad Oral Med
Radiol. 2018; 30(4): 407-11
 Wollina U, Verma SB, Ali FM, Patil K. Oral submucous fibrosis: an
update. J.Clin Cosmet Investig Dermatol. 2015;8:193–204
 James L, Shetty A, Rishi D, Abraham M. Management of Oral Submucous
Fibrosis with Injection of Hyaluronidase and Dexamethasone in Grade III Oral
Submucous Fibrosis: A Retrospective Study. J Int Oral Health. 2015;7(8):82-
85.
 Mortazavi H, Baharvand M, Mehdipour M. Oral potentially malignant
disorders: an overview of more than 20 entities. J Dent Res Dent Clin Dent
Prospects. 2014;8(1):6–14.

 Mollaoglu N. Oral lichen planus: a review. Br J Oral Maxillofac Surg .2000;
38(4): 370-77
 Nosratzehi T. Oral Lichen Planus: an Overview of Potential Risk Factors,
Biomarkers and Treatments. Asian Pac J Cancer Prev. 2018;19(5):1161–
1167.
 Ranginwala AM, Chalishazar MM, Panja P, Buddhdev KP, Kale HM. Oral
discoid lupus erythematosus: A study of twentyone cases. J Oral Maxillofac
Pathol 2012;16(3):368-73
 Burrows NP, Lovel CR. Disorders of connective tissue. In: Burns T,
Breathnach S, Cox N, Griffiths C, editors. Rook’s Textbook of Dermatology.
Sussex: Wiley-Blackwell; 2010. p. 4532.
 Schiödt M, Halberg P, Hentzer B. A clinical study of 32 patients with oral
discoid lupus erythematosus. Int J Oral Surg 1978;7(2):85-94.

 Chhabra S, Minz RW, Saikia B. Immunofluorescence in dermatology.
Indian J Dermatol Venereol Leprol 2012;78:677-91
 Winkelmann RR, Kim GK, Del Rosso JQ. Treatment of Cutaneous Lupus
Erythematosus: Review and Assessment of Treatment Benefits Based
on Oxford Centre for Evidence-based Medicine Criteria. J Clin Aesthet
Dermatol. 2013;6(1):27-38.
 Harini G, Krishnam Raju KV, Raju DV, Chakravarthy KK, Kavya SN.
Psychosocial factors associated with reverse smoking: A qualitative
research. J Int Soc Prev Community Dent. 2016;6(6):529-534.
 Kumari S, Mishra SK. Diagnosis of smokers' palate in a denture wearer
patient. BLDE Univ J Health Sci 2017;2(2):125-6

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