White lesions oral medicine in dentistry..

Oral medicine

1. White lesions

2. Causes of white lesions White epithelial lesions result from: A thickened layer of keratin. Epithelial hyperplasia. Intracellular epithelial edema. Decreased vascularity . White non-epithelial lesions due to: fibrinous exudate covering an ulcer. submucosal deposits. surface debris. fungal colonies.

3. Lipoma Gingival Cysts Ectopic Lymphoid Tissue Fordyce's Granules Submucous Fibrosis Mucosal Burns candidasis Nonepithelial White-Yellow Lesions

4. Leukoedema White Sponge Nevus Hereditary Benign Intraepithelial Dyskeratosis Darier's disease Hereditary Conditions

5. snuff dipper keratosis Nicotine Stomatitis Frictional Hyperkeratosis Hairy Leukoplakia Reactive Lesions

6. Focal (Frictional) Hyperkeratosis

7. Is a white lesion that is related to chronic rubbing or friction against an oral mucosal surface. occur in areas that are commonly traumatized.

8. Focal (Frictional) Hyperkeratosis cheek chewing .

9. Focal (Frictional) Hyperkeratosis chronic rubbing of the lip against teeth

10. Focal (Frictional) Hyperkeratosis ill-fitting lower denture.

11. Histopathology Hyperkeratosis. A few chronic inflammatory cells may be seen in the subjacent connective tissue

12. Focal (Frictional) Hyperkeratosis Normal epithelium with hyper- parakeratosis

13. Treatment Depending on the cause of the keartosis if related to habit control the habit causing the lesion

14. White Lesions Associated with Smokeless Tobacco snuff pouch snuff dipper's lesion tobacco pouch keratosis spit tobacco keratosis Smokeless tobacco keratosis

15. Etiology The development of this lesion is most strongly influenced by: habit duration the brand of tobacco used total hours of daily use amount of tobacco consumed daily.

16. Clinical features a thin gray or gray- white, almost translucent plaque with a border that blends gradually into the surrounding mucosa usually takes 1-5 years to develop. Once it occurs, however, the keratosis typically remains unchanged indefinitely unless the daily tobacco contact time is altered.

17. Histopathology The squamous epithelium is hyperkeratinized and acanthotic . Parakeratin chevrons may be seen as pointed projections. Increased subepithelial vascularity and vessel engorgement

18. Smokeless tobacco keratosis acanthosis and parakeratosis

19. hyperkeratosis with "chevron" formation.

20. Treatment Without microscopic evidence of dysplasia or malignancy, keratoses are not treated. habit cessation leads to a normal mucosal appearance (usually within 2 - 6 weeks). A lesion that remains after 6 weeks without smokeless tobacco contact should be considered to be a true leukoplakia.

21. NICOTINE PALATINUS SMOKER'S PALATE NICOTINE STOMATITIS

22. Clinical features associated most often with pipe smoking. it develops in response to heat rather than the chemicals in tobacco smoke. men >45 years of age. palatal mucosa becomes diffusely gray or white; numerous slightly elevated papules are noted, usually with punctate red centers

23. NICOTINE STOMATITIS

24. NICOTINE STOMATITIS

25. Histopathology hyperkeratosis and acanthosis . chronic inflammation of subepithelial connective tissue. hyperplastic ductal epithelium may be seen near the orifice

26. NICOTINE STOMATITIS hyperplastic ductal epithelium

27. Treatment completely reversible. The palate returns to normal usually within 1 - 2 weeks of smoking cessation.

28. Hairy Leukoplakia

29. Caused by Epstein-Barr virus ( EBV ). Associated with immunosuppression (esp. AIDS and organ transplantation). lateral border of the tongue. well-demarcated white lesion that varies from a flat and plaque-like to papillary/ filiform or corrugated lesion.

30. Hairy Leukoplakia Vertical streaks along the lateral border of the tongue

31. Hairy Leukoplakia

32. Hairy Leukoplakia lateral and ventral tongue.

33. Histopathology hyperkeratosis, which demonstrates surface corrugations or thin projections. The epithelium is hyperplastic and contains a patchy band of lightly stained "balloon cells“. Scattered cells with nuclear clearing and a peripheral margination of chromatin termed nuclear beading. Heavy candidal infestation of the parakeratin layer

34. Hairy Leukoplakia hyper- parakeratosis with surface corrugations.

35. Hairy Leukoplakia layer of "balloon cells" in the upper spinous layer. Inset demonstrate nuclear beading.

36. Treatment Surgical removal for cosmetic reasons. Lesions may respond to antiretroviral drugs with a return of lesions on discontinuation of therapy.

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