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Oral Pathology I

Oral Pathology I
Third Year

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Oral White lesions Oral White lesions Presentation Transcript

  • Oral White lesions Aiman A. Ali, DDS, PhD.
  • Classification of oral white lesions Hereditary Reactive Preneoplastic Other white lesions Non-epithelial White-yellow lesions Aiman A. Ali, DDS, PhD.
  • Oral White Lesions  Hereditary: Leukoedema  White sponge nevus.  Hereditary benign intraepithelial dyskeratosis.   Follicular keratosis. Aiman A. Ali, DDS, PhD.
  • 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.
  • Oral white lesions Preneoplastic  Actinic cheilitis  Idiopathic leukoplakia Aiman A. Ali, DDS, PhD.
  • Oral white lesions  Others:    Geographic tongue Lichen planus Lupus erythematosus Aiman A. Ali, DDS, PhD.
  • 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.
  • Definitions  Acanthosis Aiman A. Ali, DDS, PhD.
  • Definitions  Hyperorthokeratosis Aiman A. Ali, DDS, PhD.
  • Definitions  Hyperparakeratosis & epithelial dysplasia Aiman A. Ali, DDS, PhD.
  • Definitions  Intercellular & Intracellular edema Aiman A. Ali, DDS, PhD.
  • Definitions  Atrophic epithelium Aiman A. Ali, DDS, PhD.
  • Dyskeratosis US EU Aiman A. Ali, DDS, PhD.
  • Why we see these lesions clinically as white ? Aiman A. Ali, DDS, PhD.
  • Aiman A. Ali, DDS, PhD.
  • Increase amount of collagen fibers Aiman A. Ali, DDS, PhD.
  • 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.
  • 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.
  • 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.
  • Hereditary benign intraepithelial dyskeratosis [Witkop’s disease]
  • 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.
  • 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.
  • 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
  • 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.
  • Aiman A. Ali, DDS, PhD.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • Aiman A. Ali, DDS, PhD.
  • Aiman A. Ali, DDS, PhD.
  • 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.
  • Idiopathic leukoplakia Treatment: - conservative: remove the cause, vitamins A & E. - Surgery: resection, Laser. Prognosis and classification . Aiman A. Ali, DDS, PhD.
  • 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.
  • 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.
  • Aiman A. Ali, DDS, PhD.
  • 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.
  • 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.
  • Candidiasis Clinical features: - Acute: - Thrush - Erythematous - Chronic: - Erythematous - Hyperplastic - Mucocutaneous: - Localized - Familial - Syndrome associated Aiman A. Ali, DDS, PhD.
  • 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.
  • Mucosal burns Aiman A. Ali, DDS, PhD.
  • Submucous fibrosis Aiman A. Ali, DDS, PhD.
  • Fordyce’s granules Aiman A. Ali, DDS, PhD.
  • Ectopic lymphoid tissue Aiman A. Ali, DDS, PhD.
  • Gingival cyst Aiman A. Ali, DDS, PhD.
  • Parulis Gingival abscess, puss or fistula. Aiman A. Ali, DDS, PhD.
  • Lipoma Tumor of adipose tissue Aiman A. Ali, DDS, PhD.
  • Main Points for Differential Diagnosis  Keratotic or non-keratotic  Symmetrical or asymmetrical  Biopsy and microbiology Aiman A. Ali, DDS, PhD.