White

• Focal Frictional Hyperkeratosis

  Reactive Lesions
• Focal Frictional Hyperkeratosis

  • Occurs in areas commonly traumatized, such as lips, lateral margins of tongue, buccal mucosa along occlusal line, edentulous alveolar ridges
  • Chronic cheek or lip chewing may result in opacification (keratinization) of affected area
  • Chewing on edentulous alveolar ridges produces same effect
• Smokeless tobacco can affect oral epithelium and alter its normal clinical and microscopical appearances
• Increased smokeless tobacco consumption related to peer pressure and increased media advertising
• Effects of long-term exposure to smokeless tobacco

  • Development of oral mucosal white patches with slightly increased malignant potential
  • Dependence
  • Alterations of taste
  • Acceleration of periodontal disease
  • Significant amounts of dental abrasion
• Duration of exposure to smokeless tobacco necessary to produce mucosal damage is measured in years
• Leukoplakia can be predicted with use of 3 tins of tobacco per week or duration of habit longer than 2 years
• Clinical features of smokeless tobacco-associated white lesions

  • Develop in immediate area where tobacco habitually placed, most commonly mucobuccal fold of mandible in incisor or molar region
  • Mucosa develops granular to wrinkled appearance, in advanced cases heavy, folded character
  • Less often, erythroplakic or red component may be admixed with white keratotic component
  • Lesions generally painless and asymptomatic, often incidental discovery on routine oral exam
• Nicotine Stomatitis


  Common tobacco-related form of keratosis, typically associated with pipe and cigar smoking
• Clinical features of Nicotine Stomatitis

  • Palatal mucosa initially responds with erythematous change followed by keratinization
  • Red dots surrounded by white keratotic rings appear, representing inflammation surrounding minor salivary gland excretory ducts
• Actinic Cheilitis


  Accelerated tissue degeneration of vermilion (dry mucous membrane) of lips, especially lower lip, due to chronic sun exposure; considered potentially premalignant condition
• Clinical features of Actinic Cheilitis

  • Affected vermilion of lips takes on atrophic, pale to silvery gray, glossy appearance, often with fissuring and wrinkling at right angles to cutaneous-vermilion junction
  • Slightly firm, bilateral swelling of lower lip common
  • In advanced cases, junction irregular or totally effaced, with degree of epidermization of vermilion
  • Mottled areas of hyperpigmentation and keratosis often noted, as well as superficial scaling, cracking, erosion, ulceration, and crusting
• Actinic keratoses of skin, cutaneous counterpart of actinic cheilitis, are epithelial changes noted typically in light-complexioned individuals with chronic sun exposure
• Sun-blocking agents


  Titanium dioxide or zinc oxide provide complete protection from both ultraviolet A (UVA) and UVB rays
• Chronic sun damage management

  1. Periodic examination

  2. Biopsy if ulceration persists or induration occurs

  3. If atypical changes, vermilionectomy with mucosal advancement

  4. Wedge excision for suspicious lesions

  5. Laser surgery or cryosurgery

  6. Topical 5-fluorouracil

  7. Topical imiquimod
• Actinic Keratoses (Solar Keratoses)

  Epithelial changes noted in light-complexioned individuals with long-term sun exposure<|>Small percentage develop into squamous cell carcinoma
• Actinic keratosis microscopic subtypes

  • Nuclear atypia
  • Increased nuclear-cytoplasmic ratio
  • Atypical proliferation of basal cells
  • Lymphocytic inflammatory cell infiltrate in dermis
  • Elastotic or basophilic changes in collagen
  • Irregular clumps of altered elastic fibers and regenerated collagen
• Actinic keratosis treatment

  1. Cryotherapy for individual lesions

  2. Topical 5-fluorouracil for confluent lesions

  3. Curettage and surgical excision

  4. Biopsy for indurated, nodular or inflamed lesions
• Oral Submucous Fibrosis


  High-risk, precancerous condition<|>Chronic, progressive scarring of oral mucosa
• Oral submucous fibrosis affects over 5 million people in India
• Pathogenesis of oral submucous fibrosis

  Disruption of collagen metabolism by areca nut components
• Leukoplakia


  White patch on oral mucosa that cannot be scraped off and is not another diagnosable disease<|>Small percentage are premalignant or invasive squamous cell carcinoma
• About 5% of oral squamous cell carcinoma appear clinically as white lesions (leukoplakia)
• Leukoplakia lesions associated with premalignancy

  • Sublingual keratosis
  • Speckled leukoplakia
• Leukoplakia etiological factors

  • Tobacco smoking
  • Alcohol
  • Chronic irritation
  • Galvanism from metal dental restorations
  • Syphilis
  • Vitamin deficiencies
  • Hormones
  • Candidiasis
• Leukoplakia subtypes

  • Frictional keratosis
  • Smokers keratosis
  • Galvanic lesion
  • Leukoplakia with candida
  • Idiopathic leukoplakia
• Non-homogenous types of leukoplakia are more likely to be associated with epithelial dysplasia
• WHO classification of oral leukoplakia

  • Homogenous type
  • Non-homogenous type (erythroleukoplakia, erosive leukoplakia, nodular leukoplakia, verrucous leukoplakia)
• Histopathological changes in leukoplakia

  • Hyperkeratosis with or without epithelial dysplasia
  • Carcinoma in situ
  • Squamous cell carcinoma
  • Enlarged nuclei and cells
  • Large, prominent nucleoli
  • Increased nuclear-cytoplasmic ratio
  • Hyperchromatic nuclei
  • Pleomorphic nuclei and cells
  • Dyskeratosis
  • Increased mitotic activity
  • Abnormal mitotic figures
  • Bulbous or teardrop-shaped rete ridges
  • Loss of polarity
  • Epithelial pearls
  • Loss of typical cellular cohesiveness
• Leukoplakia treatment

  1. Eliminate recognizable irritating factors

  2. Surgical removal by total excision if small

  3. Cryosurgery or laser treatment for large, diffuse lesions
• Leukoplakia prognosis

  Proportion undergo malignant transformation<|>Dysplastic lesions have increased risk of malignant transformation<|>Greater potential for malignant transformation in high-risk sites (sublingual)
• Erythroplakia


  Bright red, velvety plaque on oral mucosa<|>May represent severe epithelial dysplasia, carcinoma in situ, or invasive squamous cell carcinoma
• Chronic local physical irritants and tobacco smoke constituents can alter the normal clinical and microscopic appearance of the oral epithelium
• Precancerous lesions of the oral, pharyngeal, and laryngeal mucosa with malignant transformation potential


  • Proliferative verrucous leukoplakia (★★★★★★)
  • Nicotine palatinus in reverse smokers (★★★★★)
  • Erythroplakia (★★★★★)
  • Oral submucous fibrosis (★★★★★)
  • Erythroleukoplakia (★★★★)
  • Granular leukoplakia (★★★★)
  • Laryngeal keratosis (★★★)
  • Actinic cheilosis (★★★)
  • Smooth, thick leukoplakia (★★)
  • Smooth, red tongue of Plummer-Vinson syndrome (★★)
  • Smokeless tobacco keratosis (★)
  • Lichen planus (erosive forms) (★)
  • Smooth, thin leukoplakia