LECTURE ON ORAL LEUKOPLAKIA

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LECTURE ON ORAL LEUKOPLAKIA: 

LECTURE ON ORAL LEUKOPLAKIA DR KHIN SOE B.D.S, M.D.Sc DEPARTMENT OF ORAL MEDICINE UNIVERSITY OF DENTAL MEDICINE MANDALAY

Precancerous Lesion: 

A benign lesion with morphologically altered clinical or histopathological tissue which has greater than normal risk of containing microscopic focus of cancer or of transforming into malignant lesion after diagnosis at a later date. Precancerous Lesion

Precancerous lesions: 

Leukoplakia Erythroplakia Palatal changes associated with reverse smoking (leukokeratosis nicotina palatinae) Chronic hyperplastic candidiasis (candida leukoplakia) Carcinoma in situ Precancerous lesions

Precancerous Condition: 

A disease or patient habit which does not necessarily alter the clinical appearance of local tissue but is known to have a greater than normal risk of precancerous lesion or cancer development. Precancerous Condition

Precancerous conditions: 

Syphilis Sideropenic dysphagia Oral submucous fibrosis Oral lichen planus Actinic keratosis Discoid lupus erythematosus Precancerous conditions

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Confusion prevailed between these two terminologies, and many opinioned that the prefix ‘pre ’ quotes that all precancerous lesions will eventually become cancer, whereas studies found this to be untrue. Hence it was recommended in WHO workshop of 2005 to abandon the distinctions between precancerous lesions and conditions and to use instead the term “Potentially Malignant Disorders” incorporating both the terminologies.

Potentially malignant disorders (WHO 2005): 

The risk of malignancy being present in a lesion or condition either at the time of initial diagnosis or at a future date. Potentially malignant disorders (WHO 2005)

Leukoplakia- Definitions: 

A predominantly white lesion of oral mucosa that cannot be characterized as any other definable lesion clinically or pathologically, often associated with tobacco products, some of which will transform into cancer (WHO 1994) A white plaque of questionable risk having excluded other known diseases or disorders that carry no increased risk of cancer (WHO 2005) Leukoplakia- Definitions

Leukoplakia: 

Leukoplakia

Leukoplakia: 

Leukoplakia

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Does NOT wipe off.

Leukoplakia: 

Leuko means white . Plakia means plaque . The term is strictly a clinical one and does not imply a specific histopathologic tissue alteration . It makes the diagnosis dependent not so much on definable appearances as on the exclusion of other entities that appear as oral white plaques. Leukoplakia

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Such lesions as lichen planus , morsicatio (chronic cheek nibbling ), frictional keratosis, tobacco pouch keratosis, nicotine stomatitis , leukoedema, and white sponge nevus must be ruled out before a clinical diagnosis of leukoplakia can be made.

AETIOLOGY: 

The etiology of idiopathic and leukoplakia is by definition unknown. But some predisposing factors can be identified that are associated with the development of other white lesion (as in the etiology of squamous cell carcinoma that they are causative. AETIOLOGY

1. TOBACCO: 

A. SMOKING B. CHEWING 1. TOBACCO

A. TOBACCO SMOKING: 

Higher prevalence of leukoplakia Smoker > non smoker e.g. Cigarette smoker Cheek, lip + Tongue (less in the floor of the mouth) A. TOBACCO SMOKING

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e.g Bidi smoking Labial commissure Reverse smoking White patch, Redness + Ulcerative Smokeless tobacco Associated with oral ulceration

B. TOBACCO CHEWING: 

Coal miners (++) (i) Many of chemical constituents in tobacco are irritating substances which are capable of producing leukoplakia of oral mucosa. B. TOBACCO CHEWING

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(ii) Sources of irritation of mucous membrane are not only the combustion products brought about by buring tobacco and heat but also the materials which leach out of the tobacco, when it is chewed.

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( iii) Tobacco (smoke, chewing) Tobacco smoking – (I) Polycyclic aromatic hydrocarbon (main precarcinogen in tobacco) PAH stimulated by Hydrocarbon hydrolase carcinogen (microsomal complex enzyme)

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Tobacco chewing – (ii) N- nitrosonornicotine which is produced by bacteria and enzymatic nitrosation of nicotine formed by salivary nitrates with nornicotine . Betel quid – Lime causes constant aberration of oral mucosa allowing direct assess to carcinogen.(The area of the lower buccal sulcus close to the molar)

2. ALCOHOL: 

Heavy consumption of alcohol is second most important risk factor, it acts synergistically with tobacco. 3.CANDIDA INFECTION Candida albicans infection (chronic hyperplastic candidiasis) may play a role in the etiology of leukoplakia. 2. ALCOHOL

4. VIRUSES: 

HSV1, HPV, HHV6, HHV8 (HHV = Human Herpes Viruses) (HSV = Herpes Simplex Viruses) (HPV = Human Papilloma Virus) (Type 16,18) 4. VIRUSES

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High risk type Associated with CA of uterine cervix Hairy Leukoplakia associated with Ebstein – barr virus. 5. CHRONIC IRRITATION Sharp edges, crown fracture, ill fitting prosthesis, malocclusion.

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6. Oral sepsis 7. Vitamin deficiencies (A,B complex and Iron) 8. Idiopathic 9. Endocrine disturbances 10. Chronic syphilitic lesion associated with leukoplakia (tertiary syphilis)

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11. Galvanism 12. Actinic Radiation 13. Oral submucous fibrosis 14. Tumor suppressor genes(p53, pRb etc.)

CLINICAL FEATURES: 

Approximately 7O% of oral leukoplakias are found on the lip vermilion, buccal mucosa, and gingiva. Lesions on the tongue, lip vermilion, and oral floor account for more than 90% of those that show dysplasia or carcinoma. CLINICAL FEATURES

CLINICAL FEATURES: 

TYPES Homogenous Non-homogenous May vary from a quite small and circumscribed plaque to an extensive lesion involving a large area of mucosa. Color may be white, whitish yellow or gray CLINICAL FEATURES

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HOMOGENOUS - Uniform white patch lesion with smooth or corrugatd surface sometimes, slightly raise mucosa. - Usually plaque like. - Some are smooth, may be wrinkled (or) criss-crossed by small crack (or) fissure.(Producing tessellated appearance.) - Malignant transformation – 1% to 7%

Homogenous Leukoplakia: 

Homogenous Leukoplakia

Contd.: 

2. NON-HOMOGENOUS Redness, ulcerative Verrucous (proliferative verrucous leukoplakia) or Granular (4% - 15%) Nodular Speckled (High malignant transformation) (Erythroleukoplakia – 28%) Contd.

Contd.: 

Verrucous Warty surface (white lesion with hyperplastic surface) Nodular Heaping up of the surface (or) Like a nodule on an erythematous background.(white lesion with a granular surface) associated with candida. Contd.

Non-homogenous Leukoplakia: 

Non-homogenous Leukoplakia

Non-homogenous Leukoplakia: 

Non-homogenous Leukoplakia

Contd.: 

Speckled Mixture of red and white area in plaque. (Erythroleukoplakia) Hairy leukoplakia found in HIV/ AIDS patients caused by EBV (Epstein- Barr Virus). Age Over 40 are most common, (Recent studies shows increase in young adults ) Contd.

Hairy leukoplakia on lateral border of tongue in patient with AIDS: 

Hairy leukoplakia on lateral border of tongue in patient with AIDS

Candida leukoplakia: 

Candida leukoplakia

Candida leukoplakia: 

Candida leukoplakia

leukoplakia: 

leukoplakia Homogenous Verrucous Speckled

Contd.: 

Sex Male > Female (Recent studies Female > Male in West Europe and North America) Site Anywhere of oral mucosa. - Most common site floor of the mouth + Buccal Mucosa) - High risk of malignant transformation – Ventral tongue + floor of the mouth (sublingual keratosis) Contd.

Contd.: 

White patch with or without induration. Size > 1cm in diameter (highest risk). Histology Mild – moderate severe dysplasia Ca in situ invasive Ca Biopsy is essential. Contd.

Leukoplakia: 

Leukoplakia

leukoplakia: 

leukoplakia

Contd.: 

Contd. Erythroleukoplakia Leukoplakia

Leukoplakia: 

Leukoplakia Before toluidine blue staining After toluidine blue staining

Extensive leukoplakic patch affecting the floor of the mouth: 

Extensive leukoplakic patch affecting the floor of the mouth

HISTOLOGICAL FEATURES: 

( mild – moderate – severe dysplasia Ca in situ invasive Ca ) Hyperkeratosis - Hyperorthokeratosis - Hyperparakeratosis Prominent granular layer Acanthosis HISTOLOGICAL FEATURES

Epithelial dysplasia: 

Epithelial dysplasia

Malignant Transformation: 

Multiple studies over the years have shown a malignant transformation rate of 3.6-17.5%, while few Indian studies have shown a transformation rate as low as 0.3-0.5%. Malignant Transformation

WHO Classifications (1980): 

1 . Homogeneous leukoplakia – lesion that was uniformly white and unscrapable. 2 . Non Homogeneous leukoplakia – lesion predominantly white and speckled with red. WHO Classifications (1980)

WHO Classifications (1998): 

1 . Thin, smooth leukoplakia (preleukoplakia older terminology ) – translucent thin gray soft flat plaques usually with sharply demarcated borders. 2 . Thick, fissured leukoplakia – 2/3 of white plaques has distinctly white appearance (from thickening of keratin layer), fissured and are leathery to palpation . 3 . Granular, verruciform leukoplakia – lesions have surface irregularities of nodular or granular nature with verrucous appearance. 4 . Erythroleukoplakia – lesion showing intermixed red and white areas, because the epithelial cells are so immature that they no longer are able to produce keratin. WHO Classifications (1998)

WHO Classifications (2002): 

In 2002 WHO reclassified the above variants depending on the probability of a malignant change and prognosis of these lesions as 1 . Phase I : thin, smooth leukoplakia – better prognosis . 2 . Phase II : thick, fissured leukoplakia . 3. Phase III : proliferative verrucous leukoplakia (PVL ) – higher malignant transformation rate. 4. Phase IV : erythroleukoplakia – poor prognosis. WHO Classifications (2002)

Clinical Staging: 

A clinical staging system for oral leukoplakia ( OL-system) on the lines of TNM staging was recommended by WHO in 2005 taking into account the size (L) and the histopathological features (P) of the lesion. Clinical Staging

Clinical Staging: 

Lx : Size not specified. L1: Single or multiple lesions together <2 cm. L2 : Single or multiple lesions together 2-4 cm. L3 : Single or multiple lesions together >4 cm. Px : Epithelial dysplasia not specified. P0: No epithelial dysplasia. P1: Mild to moderate epithelial dysplasia. P2 : Severe epithelial dysplasia. Stage I : L1 P0. Stage II : L2 P0. Stage III : L3 P0 or L1/ L2 P1. Stage IV : L3 P1 or any L P2. Clinical Staging

Histopathology: 

Leukoplakia is purely a clinical terminology and histopathologically it is reported as epithelial dysplasia . WHO in 2005 proposed five grades of epithelial dysplasia based on architectural disturbances and cytological atypia. Histopathology

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1. Squamous Hyperplasia – benign lesion. 2. Mild Dysplasia – better prognosis. 3 . Moderate Dysplasia . 4. Severe Dysplasia . 5. Carcinoma In-situ – poor prognosis. It has been recently proposed to modify the above 5-tier system into a binary system of ‘high risk ’ and ‘ low risk ’ lesions to improve clinical management of these lesions .

Epithelial Dysplasia: 

. Enlarged nuclei and cells . Large and prominent nucleoli . Increased nuclear-to-cytoplasmic ratio . Hyperchromatic (excessively dark-staining) nuclei . Pleomorphic (abnormally shaped) nuclei and cells Epithelial Dysplasia

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. Dyskeratosis (premature keratinization of individual cells ) . Increased mitotic activity (excessive numbers of mitoses ) . Abnormal mitotic figures (tripolar or star-shaped mitoses or mitotic figures above the basal layer)

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. Bulbous or teardrop-shaped rete ridges . Loss of polarity (lack of progressive maturation toward the surface) . Keratin or epithelial pearls (focal, round collections of concentrically layered keratinized cells) . Loss of typical epithelial cell cohesiveness

Severity and Intensity: 

Mild epithelial dysplasia refers to alterations limited principally to the basal and parabasal layers . Moderate epithelial dysplasia demonstrates involvement from the basal laver to the midportion of the spinous layer. Severe epithelial dysplasia demonstrates alterations from the basal layer to a level above the midpoint of the epithelium. Sometimes dysplasia will be seen to extend down the duct of a minor salivary gland , especially in lesions of the floor of the mouth Severity and Intensity

PowerPoint Presentation: 

When the entire thickness of the epithelium is involved , the term carcinoma in situ is used. Carcinoma in situ is defined as dysplastic epithelial cells that extend from the basal layer to the surface of the mucosa ('top-to bottom" change)

Hyperkeratosis: 

Hyperkeratosis

Hyperkeratosis: 

Hyperkeratosis

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Carcinoma-in-situ

Carcinoma-in-situ: 

Carcinoma-in-situ

TREATMENT AND PROGNOSIS: 

Because leukoplakia represents a clinical term only, the first step in treatment is to arrive at a definitive histopathologic diagnosis. Therefore , a biopsy is mandatory and will guide the course of treatment. Tissue obtained for biopsy, moreover, should be taken from the clinically most "severe" areas of involvement . Multiple biopsies of large or multiple lesions may be required . TREATMENT AND PROGNOSIS

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Leukoplakia exhibiting moderate epithelial dysplasia or worse warrants complete destruction or removal , if feasible . The management of leukoplakia exhibiting less severe change is guided by the size of the lesion and the response to more conservative measures, such as smoking cessation.

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Complete removal can be accomplished with equal effectiveness by surgical excision, electrocautery, cryosurgery, or laser ablation . Long-term follow-up after removal is extremely important because recurrences are frequent and because additional leuloplakias may develop . This is especially true for the verruciform or granular types , 83% of which recur and require additional removal or destruction . Leukoplakia not exhibiting dysplasia often is not excised, but clinical evaluation every 6 months is recommended because of the possibility of progression toward epithelial dysplasia. Additional biopsies are recommended if smoking continues or if the clinical changes increase in severity.

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The increased frequency of transformation of the different phases of leukoplakia is related closely to the degree of dysplasia present . The greater the clinical severity , the greater the chance of significant dysplasia and malignant transformation.

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Some smoking-related leukoplakias with no or minimal dysplasia may disappear or diminish in size within 3 months after the patient stops smoking. Thus habit cessation is recommended.

Chemoprevention: 

Chemoprevention also may be useful, but it remains primarily experimental. Isotretinoin (13-cis-retinoic acid, a form of vitamin A )-alone or in combination with betacarotene-has been reported to reduce or eliminate some leukoplakic lesions in short-term studies. Chemoprevention

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Agents such as bleomycin, lycopene, and cyclooxgenase-2 ( COX"2) inhibitors have been investigated as potential chemo preventive agents as well.

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However, to date there is insufficient evidence from well-designed clinical trials to support the effectiveness of such medical therapies in treating oral dysplasia or preventing the progression of oral dysplasia to squamous cell carcinoma.

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THANK YOU