Definition: White patch or plaque of squamous epithelium that cannot be characterized clinically or pathologically as any other disease.

Most common sites:

  1. Buccal mucosa.
  2. Oral commissure.
  3. Ventral surface of tongue.
  4. Floor of mouth.
  5. Rarely, larynx.


  1. Predisposing factors:

    a) Sharp tooth.

    b) Smoking.

    c) Sepsis.

    d) Spirits (Alcohol).

    e) Spices.

    d) Syphilis.

    g) Ill-fitting dentures.

    h) Plummer Vinson syndrome.

    i) Oral submucous fibrosis.

    j) Chronic hyperplastic candidiasis.

  2. Age: Can occur in any age but middle aged (fourth decade) or elderly are more commonly affected.
  3. Sex: Males more frequently affected than females due to smoking and alcohol habits.

Types of leukoplakia:

Homogenous leukoplakia

Characterized by white patch – surface may be smooth or wrinkled.

Speckled or nodular leukoplakia

White patches or nodules or nodules on erythematous base.

Erosive or erythroleukoplakia

Leukoplakia is interspersed with erythroplakia and has erosions and fissures.

The latter two varieties have higher incidence of malignant transformation.


Macroscopic: Affected area of mucous membrane appears as a thickened grey-white plaque with cracks or fissures.

Microscopically: Hyperplasia of superficial layer of squamous epithelium with hyperkeratosis, swelling, vacuolation of cells of middle layer with hyperplasia and hyperchromasia of basal layers of cells. Dyskeratosis is a serious complication associated with malignancy. About 25% of leukoplakias may show some form of epithelial dysplasia from mild to severe. Higher the grade of dysplasia more are the chances of its going into malignant changes.

Signs of neoplastic changes in the leukoplakia:

  1. Usually within tissue.
  2. Suspected if there is thickening, bleeding, area of erythema and pain.

The chances of leukoplakia becoming malignant are cited from 1 to 17.5%. On an average about 5% become malignant.

Clinical Stages of Leukoplakia:

Stage I: Appearance of thin grey transparent patch on the tongue which may be localized or wide spread.
Stage II: Thin patch gradually turns white and opaque. This is leukoplakia.
Stage III: Gradually, hyperplasia leads to small nodule or warty desquamation leaving areas of smooth red and shiny patches.
Stage IV: Stage of appearance of carcinoma. All characteristic features of carcinoma seen. The carcinomatous change usually occurs within the fissures and should be suspected if there is local thickening, pain or bleeding.

ENT Specialist Doctor In Mumbai Screenshot 2020 12 02 ORAL CAVITY AND PHARYNX SEMIFINAL BS

Treatment of leukoplakia:

  1. Removal of predisposing cause.
  2. Oral antioxidants are useful.
  3. Excision Biopsy of the suspicious white patch.
  4. Small superficial patches of leucoplakia may be satisfactorily treated by CO2 laser excision, laser vaporization, photodynamic therapy and cryosurgery.
  5. Patients should be examined at regular three-month intervals to note appearance of warty excrescence. Any doubtful lesions if present must be removed and examined histologically.
  6. Radiotherapy: Not commonly given as it may increase the chances of malignancy.

Differential diagnosis:

  1. Lichen planus.
  2. Discoid lupus erythematosus.
  3. White spongy nevus.
  4. Candidiasis.


  • Erythroplakia is a red patch or plaque on the mucosal surface. Red color is due to decreased keratinization with red vascular connective tissue of the submucosa.
  • Most common sites are lower alveolar mucosa, gingivobuccal sulcus and the floor of the mouth. 
  • Most of lesions of erythroplakia show severe dysplasia, carcinoma in situ or a frank invasive carcinoma when first seen. Malignant potential is 17 times higher than in leukoplakia. 
  • Grossly, the lesion may be of three varieties— homogenous, speckled or granular, and erythroplakia, interspersed with areas of leukoplakia (often indistinguishable from erythroleukoplakia, type of leukoplakia). 
  • Treatment is excision biopsy and follow-up.


  • It is a brown-black oral mucosal pigmentation seen in Africans. It is frequent in yellow and brown races, and relatively frequent in white persons with “dark” complexion.
  • It also has been associated with
    • Local factors like exposure to heavy metals, foods, dental abnormalities, foreign bodies, dyes, acids, gases, radiant energy, especially in the ultraviolet range.
    • Malignant growths, including Hutchinson’s lentigo maligna of malignant melanomas arise from an initial lesion in the oral mucosa.
    • Systemic diseases including Addison’s disease, cachexia, carcinomatosis, diabetes, hemochromatosis, hyperthyroidism, tuberculosis, malaria, Niemann Pick disease, hepatic diseases, pancreatic diseases, gynecologic diseases, and rarely pernicious anemia, pellagra, sprue, and Gaucher’s disease.
    • Dermatologic diseases, especially those with marked cutaneous pigmentation.
    • Melanoplakia is also seen white adults with acromegaly, Addison’s disease, erythroderma, neurofibromatosis, systemic lupus erythematosus and porphyria.
  • Treatment includes excision biopsy. The lesion should be excised with a small, curved scissors. Electrocautery can be used to stop the hemorrhage and to diminish the possibility of recurrence.

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