LEUKOPLAKIA
SYNOPSIS
●   INTRODUCTION
●   ETIOLOGY
●   CLASSIFICATION
●   PATHOPHYSIOLO
    GY
●   CLINICAL
    FEATURES
●   DIAGNOSIS
●   TREATMENT
●   PROGNOSIS K
      INTRODUCTION :
      ( LEUKO - WHITE ; PLAKIA -
      PATCH )
● Oral leukoplakia is defined by the WHO as “ a
  white patch or plaque that cannot be
  characterised clinically or pathologically as any
  other disease”.
● As with most oral white lesions,the clinical colour
  results from a thickened surface keratin layer ,
  which appears white when wet or a thickened
  spinous layer,which makes the normal
  vascularity ( redness ) of the underlying connective
     INCIDENCE AND
     PREVALENCE :
● Affects 1.5 % - 12 % of total population.
● The onset usually takes place after 30
  years : resulting in peak incidence above
  the age of 50 years.
● Prevalence is usually higher in males.
● 4 % of malignant transformation.
                ETIOLOGY
● Chemical : Alcohol,Tobacco.
● Mechanical : Sharp tooth or crown margins ,
  irritating denture clasps.
● Premalignant epithelial changes.
● Candida Albicans.
● Ultra-violet radiation.
● Trauma.
● Toothpaste or mouth rinses ( sanguinaria )
              SITES OF PREDILECTION
●   Lateral and ventral tongue.
●   Floor of the mouth.
●   Alveolar ridge mucosa.
●   Corner of the mouth.
●   Less frequently ; soft palate
    and lip
                CLINICAL FORMS
1. Homogeneous           - lesions that are uniformly white.
2. Non - homogeneous - lesions in which part is white
   and part is red.
3. Proliferative verrucous leukoplakia.
4. Erythroleukoplakia.
5. Sublingual keratosis.
6. Oral hairy leukoplakia.
7. Syphilitic leukoplakia.
             HOMOGENOUS
• Uniform flat appearance that may exhibit shallow
  cracks and has a small , plaque like , wrinkled or
  corrugated surface with a consistent texture
  throughout.
• IMAGE : A diffuse , corrugated white patch on the
  right ventral surface of the tongue and floor of the
                NON - HOMOGENOUS
• Non – homogenous leukoplakia is a lesion of non – uniform
  appearance. The colour may be predominantly white or a
  mixed white and red. The surface is irregular and may be
  flat ( popular ) , nodular or exophytic.
• IMAGE : Exophytic leukoplakia on the buccal mucosa.
                 GRANULAR LEUKOPLAKIA
• Most thick , smooth lesions remain indefinitely at this
  stage. Some perhaps as many as one third , regress or
  disappear ; a few become even more severe , develop
  increased surface irregularities.
• IMAGE : Focal leukoplakic lesion with a rough granular
  surface on the posterior lateral border of the tongue .
    PROLIFERATIVE VERRUCOUS LEUKOPLAKIA
• A special high risk form of leukoplakia and is characterised
  by the development of multiple keratotic plaque with
  roughened surface projections.
• It is usually uncommon and involves the buccal mucosa
  and the gingiva.
             ERYTHROLEUKOPLAKIA
• Erythroleukoplakia is a non homogenous lesion of mixed
   white
 ( keratotic ) and red ( atrophic ) colour .
• Erythroplakia is an entirely red patch that cannot be
   attributed to any other cause.
• Erythroplakia can therefore be considered a variant of
   either leukoplakia or erythroplakia since its appearance is
   midway between.
             ORAL HAIRY LEUKOPLAKIA
• Oral hairy leukoplakia is a corrugated white lesion on the
  other side of the tongue caused by opportunistic infection
  with EBV on a systemic background of immunodeficiency
  almost always HIV.
• The condition is not considered to be a true idiopathic
  leukolplakia since the causative agent has been identified.
                  HISTOLOGIC APPEARANCE
• Leukoplakia has a wide range of possible appearance.
• The degree of hyperkeratosis,epithelial
  thickness,dysplasia and inflammatory cell infiltration in the
  underlying lamina propria are variable.
• The following are commonly cited are being possible
  features of epithelial dysplasia in leukoplakia specimens ;
   1. Cellular pleomorphism.
   2. Nuclear atypia.
   3. Increased number of cells seen undergoing mitosis , including both normal and
      abnormal mitoses.
   4. Abnormal keratinization.
                     DIAGNOSIS
•   The clinician should first try to rule out any of the defin