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POTENTIALLY CONDITIONS

MALIGNANT

LESIONS

AND

PRESENTED BY NALEENA JOSEPH CTAHBDS029 KMCT DENTAL COLLEGE

POTENTIALLY MALIGNANT LESION Definition: A morphologically altered tissue in which cancer is more likely to occur than its normal counterpart - Shafer 1) 2) 3) 4) Leukoplakia Erythroplakia Palatal Keratosis associated with reverse smoking Actinic Keratosis, Cheilitis, & Elastosis

POTENTIALLY MALIGNANT CONDITION Definition: A generalized state or condition associated with significantly increased risk of cancer development - Shafer 1) 2) 3) 4) 5) 6) 7) 8) Oral Submucous Fibrosis Oral Lichen Planus Discoid Lupus Erythematosus Dyskeratosis Congenita Sideropenic Dysphagia Syphilitic Glossitis Xeroderma Pigmentosum Epidermolysis Bullosa

LEUKOPLAKIA DEFINITION: A white patch or plaque that cannot be characterized clinically or pathologically as any other lesion -WHO A predominantly white lesion of the oral mucosa that cannot be characterized as any other definable lesion. Some oral leukoplakia will transform into cancer. -Axell 1996 A predominant white lesion of oral mucosa that cannot be characterized as any other definable lesion - Pindborg 1997

EPIDEMIOLOGY Risk of malignant transformation is 4-6% Global prevalence of 2.6% Common in patients above 50 yrs of age Common in men

ETIOLOGY TOBACCO - Smoking form - Smokeless form ALCOHOL CHRONIC IRRITATION SANGUINERIA CANDIDIASIS VIRAL INFECTION NUTRITIONAL DEFICIENCY DRUGS IDIOPATHIC CLASSIFICATION LEUKOPLAKIA 1) Mild / Thin Leukoplakia 2) Homogenous Leukoplakia 3) Non homogenous Leukoplakia HOMOGENOUS LEUKOPLAKIA Well-defined white patch, localized or extensive, that is slightly elevated and that has a fissured, wrinkled, or corrugated surface on palpation, these lesions may feel leathery to dry, or cracked mud-like NON HOMOGENOUS LEUKOPLAKIA White patches or plaque intermixed with red tissue elements. Also called Erythroleukoplakia and speckled leukoplakia NODULAR VERRUCOUS PROLIFERATIVE VERRUCOUS ULCERATED ERYTHROLEUKOPLAKIA 6

NODULAR LEUKOPLAKIA Keratotic white nodules or patches are distributed over an Erythematous background. Associated with higher rate of malignant transformation

VERRUCIFORM LEUKOPLAKIA Presence of thick white lesions with papillary surfaces in the oral cavity. These lesions are usually heavily keratinized and are most often seen in older adults in the sixth to eighth decades of life. Some of these lesions may exhibit an exophytic growth pattern. PROLIFERATIVE VERRUCOUS LEUKOPLAKIA (PVL) Extensive papillary or Verrucoid white plaques that tend to slowly involve multiple mucosal sites in the oral cavity and to inexorably transform into Squamous cell carcinomas over a period of many years. PVL has a very high risk for transformation to dysplasia, Squamous cell carcinoma or verrucous carcinoma .Verrucous Carcinomas is a slow growing and well-differentiated lesion that seldom metastasizes. CLINICAL FEATURES Asymptomatic Common sites buccal mucosa, lower lip, Gingiva Less common sites palate, retro molar area Lesions on the floor of mouth and lateral borders of tongue are high risk sites for malignant transformation

HISTOPATHOLOGY

Epithelial hyperplasia and surface hyperkeratosis Mild to moderate epithelial dysplasia Chronic inflammatory changes

DIAGNOSIS 1) 2) 3) 4) Elimination of possible causes Biopsy (gold standard test) Toluidine blue staining Exfoliative cytology (Limited value)

MANAGEMENT 1) MEDICAL topical vitamin A / Retinoid (single and combination dosages of vitamins A, C, and E; beta carotene; analogues of vitamin A; and diets that are high in antioxidants and cell growth suppressor proteins (fruits and vegetables). 2) SURGICAL Cold knife surgical excision Laser ablation & cryosurgery - preferred because of their Precision and rapid healing MANAGEMENT OF LEUKOPLAKIA PROVISIONAL CLINICAL DIAGNOSIS Elimination of possible causes No possible causes (2-4 weeks observation) (Definitive clinical diagnosis) -------------------------------- Biopsy Good response No response (Definitive clinical diagnosis) ___________________________ Definable lesion 8

(Management accordingly)

No definable lesion (Treatment/ Observation/ Follow up)

Definable lesion (Management accordingly)

PROGNOSIS Long term follow up necessary Malignant changes occur 2-4 yrs after onset ERYTHROPLAKIA DEFINITION A fiery red patch that cannot be characterized clinically or pathologically as any other definable lesion - Pindborg 1997 Less common than Leukoplakia High frequency of pre-malignant & malignant changes Often associated with heavy smoking with or without concomitant alcohol use CLASSIFICATION ERYTHROPLAKIA - Homogenous Erythroplakia - Granular / Speckled Erythroplakia - Erythroleukoplakia CLINICAL FEATURES Seen in older men Irregular outline Common sites floor of mouth, Ventral aspect of tongue, soft palate Histopathology lack of Keratin production and Atrophic Epithelium Treatment same as Leukoplakia Recurrent rate less than 5%

PALATAL CHANGES ASSOCIATED WITH REVERSE SMOKING Peak incidence 55-64 yrs CLINICAL CHANGES Keratosis Diffuse whitening of entire Palate Patches Well defined, elevated white Plaques Excrescences 1-3mm elevated white Plaques Red areas Well defined reddening of the Palatal Mucosa Ulcerated areas Crater like areas covered by Fibrin Non pigmented areas Areas of Palatal Mucosa that are devoid of Pigmentation

HISTOLOGICAL FINDINGS Hyperorthokeratosis Epithelial Dysplasia Inflammatory cells in connective tissue Melanin deposits in Lamina Propria

Malignant changes were seen in 0.3% of the palatal lesions ACTINIC KERATOSIS Also called Solar Elastosis, Senile Elastosis or Actinic Elastosis It is Dermatological disease which is a degenerative condition of skin Also called Sailors or Farmers skin ETIOLOGY 1. Hereditary factors skin pigmentation or its absence 10

2. Exposure to elements sunlight and wind

CLINICAL FEATURES Common in elderly patients Site lips Affected skin appears wrinkled, dry, atrophic and flaccid On lips there is mild Keratosis and subtle blending of the lip vermillion with skin surface Increase in amount of elastic connective tissue fibers

HISTOPATHOLOGY TREATMENT No treatment

ORAL SUBMUCOUS FIBROSIS DEFINITION A insidious and chronic disease affecting mucosa of any part of oral cavity and occasionally extend into pharynx and esophagus ,although sometimes preceded by and / or associated with vesicle formation . It is always associated with a juxta epithelial inflammatory reaction followed by fibroelastic change of lamina propria with epithelial atrophy leading to stiffness of oral mucosa causing trismus and inability to eat. Also called Atrophica Idiopathica Mucosae Oris , idiopathic scleroderma of mouth, diffuse oral submucous fibrosis ETIOLOGY a) Areca nut chewing b) Chillies c) Genetic 11

d) Tobacco e) Autoimmune disorders

PATHOGENESIS Alkaloids like Arecolin modulate matrix metallo proteins, lysyl oxidases & collagenases which the affects collagen metabolism and leads to increased fibrosis Increased fibrosis results in decrease in water retaining proteoglycans which favor increased collagen type 1 production Polymorphism in gene coding for TNF Aberrations of TGF beta and Interferon gamma CLINICAL FEATURES Age group 4-75 yrs Common in middle & old age Female predilection 3.3% risk of malignant transformation

PRODROMAL SYMPTOMS/ EARLY OSF Burning sensation while consuming spicy food Blisters ,ulcerations ,altered salivary flow, defective gustatory sensation Appearance of vesicles, petechiae, pain ADVANCED OSF Blanching of mucosa and appearance of white fibrous vertical bands Buccal mucosa and lips are affected first Dense fibrosis of Pterygomandibular raphe results in trismus Restricted tongue movements and depappilation also seen

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OTHER SYMPTOMS Obstruction of Eustachian tube Nasal intonation of speech TMJ pain Inability to blow

HISTOPATHOLOGY Early stage there is Epithelial Hyperplasia and later stage there is epithelial atrophy Sub-mucosal deposition of extremely dense and avascular collagenous tissue also seen Chronic inflammatory cells seen in connective tissue such as Lymphocytes and Plasma cells DIAGNOSIS Clinical examination and history of betel chewing habit At least one of the following should be present Palpable fibrous band Mucosa tough and leathery Blanching of mucosa and Histopathological features TREATMENT PREVENTION By stoppage of chewing habits EXERCISE In mouth opening MEDICAL Topical or systemic steroids - Vitamin and nutrient supplements - Placentrex - Fibrinolytic agents - Colloidal Iodine - Antioxidants SURGICAL Surgical excision of bands Surgical removal of affected followed by repair with grafts

mucosa

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ORAL LICHEN PLANUS Oral Lichen Planus (OLP) is a common chronic immunologic inflammatory mucocutaneous disorder that varies in appearance from Keratotic (reticular or plaque like) to Erythematous and ulcerative. The skin lesions are flat violaceous papules with a fine scaling on the surface. Unlike oral lesions, skin lesions are usually self-limiting, lasting only 1 year or less. ETIOLOGY Cell mediated immune response Autoimmune disease Stress Hepatitis C Virus CLINICAL FEATURES Radiating white or grey, velvety, thread like papules in a linear, annular or retiform arrangement with Wickhams striae 0.3-3% rate of malignant transformation. Common in erosive and atrophic form The Buccal mucosa is the most common site.

TYPES OF LICHEN PLANUS a) b) c) d) e) f) RETICULAR PLAQUE ERYTHEMATOUS BULLOUS PAPULAR EROSIVE

RETICULAR -Fine white striae or lines which form a network or annular pattern with peripheral Erythematous Zoneand usually seen bilaterally in buccal mucosa. 14

PLAQUE TYPE- Homogenous well demarcated white plaque. Common in smokers ERYTHEMATOUS FORM- Homogenous red area and striae seen in periphery BULLOUS FORM Appear as bullous structures surrounded by a reticular network PAPULAR FORM- seen in initial phase of disease, small white dots are seen which intermingle with reticular form EROSIVE FORM disabling form of OLP, fibrin coated ulcers surrounded by an Erythematous zone with radiating white striae HISTOPATHOLOGY Hyperparakeratosis Saw tooth rete pegs Subepithelial band of mononuclear infiltrate Civatte bodies degenerated basal Keratinocytes Max-Joseph space

TREATMENT Topical and systemic steroids Calcineurin inhibitors (Cyclosporine & Tacrolimus) Retinoid & UV phototherapy DYSKERATOSIS CONGENITA Also called Cole Engman Syndrome Rare Genodermatosis, inherited as x-linked characterized by Cutaneous reticulated hyper-pigmentation Nail dystrophy 15

recessive

trait

Pre-malignant leukoplakia of oral mucosa Progressive pancytopenia Striking male predilection is seen ETIOLOGY Mutations in DKC1 gene

CLINICAL FEATURES First manifestation is nail changes that is Dystrophic and shedding of nails at the age of 5yrs Grayish brown pigmentation appear at same time in trunk, neck and thighs Skin becomes atrophic & teleangiectactic. Face becomes red OTHER MINOR FEATURES Frail skeleton Mental retardation Small Sella Turcica Dysphagia Transparent tympanic membrane, deafness Eyelid infections

ORAL MANIFESTATIONS Mucosal Leukoplakia buccal mucosa, tongue & oropharynx Can become verrucous or ulcerative Dysphagia and Dysuria Increased incidence of malignant neoplasms,dental caries,and tooth loss

HISTOLOGICAL FINDINGS 16

Mild hyperkeratosis Epidermal atrophy Teleangiectasia of superficial BV TREATMENT Allogenic bone marrow transplant

DISCOID LUPUS ERYTHEMATOSUS Chronic, scarring, atrophy producing, Photosensitive Dermatosis ETOLOGY Genetic predisposition PATHOGENESIS- heat shock proteins is induced in Keratinocyte following UV exposure or stress and this protein act as target for T cell mediated epidermal cell cytotoxicity CLINICAL FEATURES Third and fourth decade of life and common in women Common sites are face, oral mucous membrane,chest,back and extremities Slightly elevated red or purple macules covered by grey or yellow scales Carpet tack lesions caused by forceful removal of scales Malar rash ORAL MANIFESTATIONS Begin as Erythematous raised or depressed area, without indurations and with white spots Superficial painful ulceration with crusting or bleeding is seen Central healing result in scar formation Common site are vermillion border of lower lips

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Malignant transformation can occur TREATMENT Corticosteroid Therapy Pulse intravenous Cyclophosphamide regimen followed by quarterly infusion for maintenance is the mainstay of modern therapy

EPIDERMOLYSIS BULLOSA Heterogenous group of inherited mucocutaneous disorders 4 broad categories * Simplex * Junctional * Dystrophic * Hemidesmosomal ETIOLOGY Mutation of gene coding for keratins 5 and 14 causes simplex type Recurrent nonsensense mutation in the LAMB3 gene causes junctional type Mutation of gene encoding for type 4 collagen COL7A1 causes dystrophic type CLINICAL FEATURES EPIDERMOLYSIS BULLOSA SIMPLEX Occurs shortly after birth. Formation of vesicles and bullae on hands and feet at sites of friction or trauma. Heals in 2-10 days 18

without scarring or pigmentation (generalized form) Localized form occur in later childhood.Bullae also seen in oral cavity JUNCTIONAL EPIDERMOLYSIS BULLOSA Onset at birth with absence of scarring or pigmentation and death occurs within 3 months of age . Oral bullae are frequent, extremely fragile and produce feeding problems. Severe disturbance in enamel and dentin formation of deciduous teeth are also seen

DYSTROPHIC EPIDERMOLYSIS BULLOSA ( DOMINANT ) Blisters develop in ankles, knees, elbows, feet and head and it heals with scarring/ keloid. Dystrophic nails, palmar plantar keratosis with hyperhidrosis and hypertrichosis are also seen. Oral bullae also present DYSTROPHIC EPIDERMOLYSIS BULLOSA ( RECESSIVE ) Classical form of the disease withonset at birth and spontaneous bullae formation at sites of trauma, friction or pressure. It also exhibits Nikolskys sign and heals by scarring. Also dystrophic nails and sparse hair. Oral bullae initiated by nursing or any simple dental operative procedure. Scar formation can obliterate sulcus and restrict tongue movements. It can also result in hoarseness and Dysphagia and dental defects like congenitally absent teeth, hypoplastic teeth and rudimentary teeth seen TREATMENT Mild form- topical and intralesional steroids Tetracycline and doxycycline to control desquamative gingivitis Dapsone therapy 19

Long term systemic steroids and immunosuppresive therapy.

XERODERMA PIGMENTOSUM Genetically determined disorder Defective DNA repair mechanism due to excessive chronic UV damage leads to subsequent development of sun related skin tumors including melanoma

CLINICAL FEATURES Increased tendency to sunburn and skin changes like atrophy and freckled pigmentation Development of Actinic keratosis which progress to squamous cell or basal cell carcinoma. Melanoma also develops Oral manifestation squamous cell carcinoma of lower lip and tip of tongue TREATMENT Avoid sun exposure and use protective clothing Topical chemotherapeutic agents like 5 -Flurouracil to treat actinic keratosis Nonmelanoma skin cancers excised conservatively Genetic counselling SIDEROPENIC DYSPHAGIA Also called Plummer Vinson syndrome or Patterson Kelly syndrome Characterized by iron deficiency anemia, glossitis and dysphagia

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CLINICAL FEATURES Seen in Scandinavian women between 30-50 yrs of age Burning sensation of tongue and oral mucosa Severe angular chelitis Abnormal bands of tissue in esophagus- esophageal web Koilonychia

TREATMENT Dietary iron supplements Esophageal dilation

SYPHILLITIC GLOSSITIS Seen in tertiary stage Surface of tongue gets broken up by fissures due to atrophy and fibrosis of tongue musculature and hyperkeratosis Exclusively seen in males High rate malignant transformation Treatment by intensive antibiotic treatment using Penicillin or Erythromycin or Tetracycline

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REFERENCE

BURKETS ORAL MEDICINE 11TH EDITIONGREENBERG,GLICK,SHIP TEXTBOOK OF ORAL PATHOLOGY 6TH EDITION- SHAFER ORAL AND MAXILLOFACIAL PATHOLOGY 3RD EDITION NEVILLE, DAMM, ALLEN, BOUQUOT

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