Oral White lesions


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Oral Pathology I
Third Year

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Oral White lesions

  1. 1. Oral White lesions Aiman A. Ali, DDS, PhD.
  2. 2. Classification of oral white lesions Hereditary Reactive Preneoplastic Other white lesions Non-epithelial White-yellow lesions Aiman A. Ali, DDS, PhD.
  3. 3. Oral White Lesions  Hereditary: Leukoedema  White sponge nevus.  Hereditary benign intraepithelial dyskeratosis.   Follicular keratosis. Aiman A. Ali, DDS, PhD.
  4. 4. Oral white lesions  Reactive: Frictional hyperkeratosis.  WL associated with smokeless tobacco  Nicotine stomatitis.  Hairy leukoplakia  Hairy tongue  Dentifrice-associated slough  Aiman A. Ali, DDS, PhD.
  5. 5. Oral white lesions Preneoplastic  Actinic cheilitis  Idiopathic leukoplakia Aiman A. Ali, DDS, PhD.
  6. 6. Oral white lesions  Others:    Geographic tongue Lichen planus Lupus erythematosus Aiman A. Ali, DDS, PhD.
  7. 7. Non-epithelial white-yellow lesions Candidiasis  Mucosal burns  Submucous fibrosis  Fordyce’s granules  Ectopic lymphoid tissue  Gingival cyst  Parulis  Lipoma  Aiman A. Ali, DDS, PhD.
  8. 8. Definitions  Acanthosis Aiman A. Ali, DDS, PhD.
  9. 9. Definitions  Hyperorthokeratosis Aiman A. Ali, DDS, PhD.
  10. 10. Definitions  Hyperparakeratosis & epithelial dysplasia Aiman A. Ali, DDS, PhD.
  11. 11. Definitions  Intercellular & Intracellular edema Aiman A. Ali, DDS, PhD.
  12. 12. Definitions  Atrophic epithelium Aiman A. Ali, DDS, PhD.
  13. 13. Dyskeratosis US EU Aiman A. Ali, DDS, PhD.
  14. 14. Why we see these lesions clinically as white ? Aiman A. Ali, DDS, PhD.
  15. 15. Aiman A. Ali, DDS, PhD.
  16. 16. Increase amount of collagen fibers Aiman A. Ali, DDS, PhD.
  17. 17. Leukoedema Etiology: Unknown Clinically: Symmetrical, gray-white or milky buccal mucosa, dissipate with stretching Histopathologically: Acanthosis, parakeratosis and intracellular edema. No treatment is necessary Aiman A. Ali, DDS, PhD.
  18. 18. White sponge nevus Etiology: hereditary Clinically: asymptomatic, symmetrical, folded and spongy white lesion usually appears early in life. Histopathologically: severe acanthosis, parakeratosis, characteristic perinuclear eosinophilic condensation of prickle cell cytoplasm. No treatment is necessary Aiman A. Ali, DDS, PhD.
  19. 19. Hereditary benign intraepithelial dyskeratosis [Witkop’s disease] Etiology: hereditary Clinically: Oral WL with conjunctivitis appear in the 1st year and increase with age. Occur anywhere of the oral mucosa. Blindness were reported in some cases. Histopathologically: Epithelial hyperplasia, intracellular edema, and dyskeratotic elements in the superficial half of the epithelium. No treatment is necessary Aiman A. Ali, DDS, PhD.
  20. 20. Hereditary benign intraepithelial dyskeratosis [Witkop’s disease]
  21. 21. Follicular keratosis [Darier’s disease] Etiology: hereditary Clinically: occur between 6 and 20 years. In 13% of cases it affects the oral cavity. Skin lesions are small symmetrical papules over the face, and trunk which become greasy due to keratin production; fingernail changes. Keratinized mucosa is favored oral sites where it appears as small whitish papules which may extend to the oropharynx. Aiman A. Ali, DDS, PhD.
  22. 22. Follicular keratosis [Darier’s disease] Histopathologically: - proliferation of the basal layer. - formation of suprabasal clefts containing acantholytic cells. - corps nods, which are dyskeratotic cells. Treatment : administration of vitamin A Aiman A. Ali, DDS, PhD.
  23. 23. Frictional hyperkeratosis Etiology: chronic friction Clinically: adjacent to the etiologic factor (cheek and lip mucosa, lateral borders the tongue, alveolar ridges). Histopathologically: Hyperkeratosis, acanthosis and mild II. Treatment remove the cause. Aiman A. Ali, DDS, PhD. of
  24. 24. WL associated with smokeless tobacco Etiology: mechanical/chemical irritation induced by smokeless tobacco Clinically: asymptomatic lesion localized in the area where tobacco is placed, lesion appears granular, wrinkled or folded, less often erythroleukoplakic. Histopathologically: parakeratosis, mild II superficial intracellular edema. ED may develop in long-time users. Treatment remove the cause, biopsy in persistent lesions. Aiman A. Ali, DDS, PhD.
  25. 25. Aiman A. Ali, DDS, PhD.
  26. 26. Nicotine stomatitis Etiology: Pipe and cigar or reverse smoking Clinically: palatal white plaques with red dots, which represent inflammation of the salivary gland duct. Histopathologically: epithelial hyperplasia and hyperkeratosis, inflammatory changes of the minor salivary glands, squamous metaplasia of the ducts. Treatment is remove the cause Aiman A. Ali, DDS, PhD.
  27. 27. Hairy leukoplakia Etiology: - HIV, EBV, medically induced suppression, corticosteroids, few cases in healthy persons. Clinically: papillary or filiform white plaque, the vast majority occur bilaterally on the borders of the tongue. Histopathologically: acanthosis, parakeratosis edematous S. cells, nuclear viral inclusion in the upper layers. Treatment no specific treatment, antiviral drugs may improve the case. Aiman A. Ali, DDS, PhD.
  28. 28. Hairy tongue Predisposing factors: use of antibiotics, systemic corticosteroids, mouth rinse, intense smoking, and radiotherapy. Clinically: elongation of the papillae, the color vary from white to deep brown or black depending on diet and other factors. Histopathologically: elongated filiform papillae, surface contamination, subjacent inflammation. Treatment remove the cause, brushing the tongue with sodium bicarbonate and water Aiman A. Ali, DDS, PhD.
  29. 29. Dentifrice-associated slough Etiology: chemical burn due to the use of different brands of toothpaste Clinically: painless superficial whitish slough of the buccal mucosa. Treatment change the toothpaste Aiman A. Ali, DDS, PhD.
  30. 30. Actinic cheilitis Etiology: Ultraviolet light waves (2900-3200 nm) Clinically: atrophic silvery gray glossy, fissured lesion commonly affect the lower lip, in some cases erosion or ulceration can be seen. Histopathologically: atrophic and hyperkeratotic epithelium, elastin replacement of collagen fibers and telangiectasia. Treatment: use of lip protectors (sunscreen agents), biopsy is mandated in aggressive cases. In cases with atypical changes vermilionectomy in combination with cryosurgery or chemotherapy Aiman A. Ali, DDS, PhD.
  31. 31. Idiopathic leukoplakia Definition: white patch that cannot be rubbed off and cannot be characterized clinically as any other disease. Risk factors: Tobacco, alcohol, nutrition, unknown. Clinical features: - Age and sex - Site - Clinical type Aiman A. Ali, DDS, PhD.
  32. 32. Aiman A. Ali, DDS, PhD.
  33. 33. Aiman A. Ali, DDS, PhD.
  34. 34. Idiopathic leukoplakia  Histopathologically: Non-dysplastic  Dysplastic   Epithelial dysplasia: Drop shaped rete ridges  Basal cell crowding  Increased mitotic figures  Nuclear pleomorphism & hyperchromatism  Individual cell keratinization  Cellular pleomorphism  Altered nuclear-cytoplasm ratio  Aiman A. Ali, DDS, PhD.
  35. 35. Idiopathic leukoplakia Treatment: - conservative: remove the cause, vitamins A & E. - Surgery: resection, Laser. Prognosis and classification . Aiman A. Ali, DDS, PhD.
  36. 36. Geographic tongue Etiology: unknown Clinically: asymptomatic red desquamated and white keratotic areas, this map change within few days. Histopathologically: red area: atrophic filiform papillae, white area: HK and acanthosis. No treatment is necessary Aiman A. Ali, DDS, PhD.
  37. 37. Lichen planus Etiology: Chronic, inflammatory, mucocutaneous, immunologically mediated process Clinically: - age and sex, - types Histopathologically: according to the type, dense band of inflammatory cell infiltration (T8 lymphocytes), liquefaction degeneration of basal cells, saw teeth rete ridges, hyperkeratosis, atrophic epithelium or fibrotic yellow pseudomembranous Treatment & prognosis: SAID, vit.A Aiman A. Ali, DDS, PhD.
  38. 38. Aiman A. Ali, DDS, PhD.
  39. 39. Lupus erythematosus Etiology: connective tissue, autoimmune, mucocutaneous disease. Systemic and Discoid. Clinically: DLE: Disk-shaped erythematous plaques common on the face and scalp, lip and oral cavity. SLE: involve multiple organs, erythematous rash of butterfly distribution, fever malaise loss of weight. Histopathologically: E atrophy, HK, BC destruction, subepithelial and perivascular II, dilatation of BV. IgG, IgA, IgM & C3 along the BM. Treatment is topical or systemic corticosteroids. Aiman A. Ali, DDS, PhD.
  40. 40. Candidiasis Etiology: mainly C. albicans, predisposing factors: - Immunodeficiency - Endocrine disturbances: - Diabetes mellitus - Pregnancy - Hypo pitutirism & parathyroidism - Corticosteroid therapy - Long-term antibiotic therapy - Malignancies and their therapy - Xerostomia and bad oral hygiene Aiman A. Ali, DDS, PhD.
  41. 41. Candidiasis Clinical features: - Acute: - Thrush - Erythematous - Chronic: - Erythematous - Hyperplastic - Mucocutaneous: - Localized - Familial - Syndrome associated Aiman A. Ali, DDS, PhD.
  42. 42. Candidiasis Histopathological features: fungal hyphae (PAS) penetrating the upper layers of the epithelium, Neutrophilic infiltration of the epithelium, and epithelial hyperplasia. Treatment: antifungal, nystatin, muconazole, clotrimazole, fluconazole and ketokonazole. Aiman A. Ali, DDS, PhD.
  43. 43. Mucosal burns Aiman A. Ali, DDS, PhD.
  44. 44. Submucous fibrosis Aiman A. Ali, DDS, PhD.
  45. 45. Fordyce’s granules Aiman A. Ali, DDS, PhD.
  46. 46. Ectopic lymphoid tissue Aiman A. Ali, DDS, PhD.
  47. 47. Gingival cyst Aiman A. Ali, DDS, PhD.
  48. 48. Parulis Gingival abscess, puss or fistula. Aiman A. Ali, DDS, PhD.
  49. 49. Lipoma Tumor of adipose tissue Aiman A. Ali, DDS, PhD.
  50. 50. Main Points for Differential Diagnosis  Keratotic or non-keratotic  Symmetrical or asymmetrical  Biopsy and microbiology Aiman A. Ali, DDS, PhD.