2. DEFINITION It was defined by WHO as the “ a morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart. ex: leukoplakia, erythroplakia carcinoma in situ

3. LEUKOPLAKIA Originates from two Greek words leuko (white) and plakia(patch) WHO defined it as whitish patch or plaque that can not be characterized clinically or pathologically as any other disease and which is not associated with any other physical or chemical causative agent except the use of tobacco.

4. CLINICAL FEATURES Older age group 50 yrs and above Males are affected more than females Common sites are buccal mucosa, commisures and lips. Commonly involves central zone of buccal mucosa in molar region and along occlusal line Site depends upon type of tobacco habits Sublingual keratosis refers to leukoplakia occurring in floor of mouth and ventral surface of tongue Patches of leukoplakia varies from well localized irregular to diffused and non palpable, faintly translucent white area to thick papillomatous

5. ETIOLOGY Tobacco smoking Alcohol Candidiasis Diet deficiency Electromagnetic reaction Syphillis

6. CLASSIFICATION Homogeneous - uniformly white Non-homogeneous - white and red lesions ( erythroleukoplakia, speckled leukoplakia)  Verrucous leukoplakia (PVL)  Nodular leukoplakia  Ulcerated leukoplakia

7. STAGING L1- size of leukoplakia<2cm L2- size of leukoplakia 2-4cm L3- size of leukoplakia >4cm Lx- size of leukoplakia not specified P - pathology P0- no epithelial dysplasia P1 - distinct epithelial dysplasia Px - dysplasia not specified

8. OLEP(Oral leukoplakia)staging Stage I –L1P0 Stage II–L2P0 Stage III–L3P0 or L1L2P1 Stage IV-L3P1

9. ERYTHROPLAKIA Also called as “Erythroplasia” It is bright red velvety or eroded plaques which can not be characterized clinically or pathologically as due to another condition

10. ETIOLOGY Idiopathic Smoking Alcohol …

11. CLASSIFICATION A) homogeneous erythroplakia B) erythroplakia interspersed with patches of leukoplakia C)granular or speckled erythroplakia

12. DIAGNOSIS

13. HISTOPATHOLOGICAL FEATURES of LEUKOPLAKIA Keratinisation of epithelium of mucosa is increased Epithelial dysplasia and surface hyperkeratosis are hallmark of leukoplakia Loss of polarity of basal cell layer Presence of more than one layer of cells having basaloid appearance Increased nuclear cytoplasmic ratio Drop shaped rete process Irregular epithelial stratification Increased no. of mitosis Cellular pleomorphism Nuclear hyperchromatism Enlarged nucleoli Keratinisation of single cell or group cells

14. Moderate epithelial displasia Severe epithelial displasia

15. HISTOPATHOLOGICAL FEATURES of ERYTHROPLAKIA Epithelium shows lack of keratin production & often atrophic. This epithelium thinness allows underlying microvasculature to show through causing the red color. Connective tissue retepegs extends very high into epithelium.

16. TREATMENT of LEUKOPLAKIA Surgical excision Cryosurgery,CO2 laser surgery, retinoids and other drugs and recently photodynamic therapy.

17. TREATMENT of ERYTHROPLAKIA Surgical excision. Elimination of suspected irritant. Prompt biopsy is indicated for persisting lesion.

18. CARCINOMA IN SITU It is also called as “intraepithelial carcinoma” Commonly occurring on skin but also occurs on mucous membrane. Bowen’s disease is special form of intraepithelial carcinoma particularly in patients who had arsenical therapy.

19. CLINICAL FEATURES Male predilection & elderly persons are commonly affected Common sites are floor of mouth, tongue & lips. Clinically appears as -leukoplakia in 45% of lesion -erythroplakia in 16% of lesion -combination of both in 9% of lesion -ulcerated in 13% of lesion -white & ulcerated in 5% of lesion -red & ulcerated in 1% of lesion -unstated in 11% of lesion

20. HISTOPATHOLOGICAL FEATURES Keratin may or may not be present but if present is more apt to be parakeratin than orthokeratin. Loss of orientation of cells and their polarity Sharp line of division between normal & altered epithelium from surface down to connective tissue. Increase in nuclear/ cytoplasmic ratio and nuclear hyperchromatism.

21. TREATMENT No uniformly accepted treatment. Surgical excision of lesions, irradiation, cauterized & expose to solid carbon dioxide.

22. THANKS FOR YOUR ATTENTION