RED ANDWHITE LESIONS

OF THE ORAL MUCOSA

The normal colour of the oral
mucosa
“PINK”===➔ passage of light through the
translucent superficial layer of soft
tissue.

“light strikes the capillary

bed and reflects back resulting in the
pink colour of the oral mucosa.”
White colour of the oral mucosa is
due to:
• Increase Keratin or
parakeratin
(hyperkeratosis or
hyperparakeratosis).
• Increae Prickle cell layer
(acanthosis).
• Intracellular edema
(spongiosis).
• Intercellular edema.
• Increase Collagen fibers
(fibrosis).
• 6. Pseudomembrane over
the oral mucosa.
Red colour of the oral mucosa is
due to
• Thinning of the
epithelium (atrophy).
• Increase Vascularity: as
in inflammation due to
vasodilatation
Leukolakia (Idiopathic
true leukoplakia)
Definitions
• Precancerous lesion: “morphologically altered
tissue in which cancer is more likely to occur than
in its apparently normal counterpart…(WHO,1972)
• Leukoplakia: “a white patch or plaque that cannot
be characterized clinically or pathologically as any
other disease” (WHO, 1978)
Leukolakia (Idiopathic true
leukoplakia)
Etiological factors
• Tobacco,
• Alcohol,
• Candidiasis,
• Sunlight exposer
• Electrogalvanic reactions,
• Herpes simplex and papillomaviruses,
Leukolakia (Idiopathic true
leukoplakia)
Epidemiology
• Age; adults older than 50 years of age. 8% of men older than
70 years of age are affected.
• Sex; Men>> Female,
• Site:
a. Buccal mucosa, vermilion border of the lower lip, and
gingiva. (70%)
b. Palate, maxillary mucosa, retromolar area, floor of the
mouth, and tongue. (Less common)

**lesions of the tongue and the floor of the mouth account for
more than 90% of cases that show dysplasia or carcinoma.**
 Leukolakia (Idiopathic true
leukoplakia)
Classification

1. “Homogeneous Leukoplakia” (or “Thick Leukoplakia”)

2. Nodular (Speckled) Leukoplakia

3. “Verrucous Leukoplakia” or “Verruciform Leukoplakia”

4. Proliferative Verrucous Leukoplakia (PVL)

Leukolakia (Idiopathic true
leukoplakia)
1. “Homogeneous
leukoplakia”
• Well-defined white patch
• Localized or extensive
• Slightly elevated
• Has a fissured, wrinkled,
or corrugated surface
• On palpation, these
lesions may feel leathery
to “dry, or cracked mud-
like.”
Leukolakia (Idiopathic true
leukoplakia)
Nodular (speckled)
leukoplakia
• granular or
nonhomogeneous
• mixed red-and-white
lesion in which keratotic
white nodules or patches
are distributed over an
atrophic erythematous
background
• higher malignant
transformation rate (2/3rd
case)
Leukolakia (Idiopathic true
leukoplakia)
“Verrucous leukoplakia” or
“Verruciform leukoplakia”
• Thick white lesions with
papillary surfaces in the
oral cavity
• Heavily keratinized
• May exhibit an exophytic
growth pattern.
• Seen in older adults in
the sixth to eighth
decades of life
Leukolakia (Idiopathic true
leukoplakia)
Proliferative verrucous
leukoplakia (PVL)
• First described in 1985.
• Extensive papillary or
verrucoid white plaques
• Tend to slowly involve
multiple mucosal sites
• Inexorably transform into
squamous cell
carcinomas over a period
of many years
Leukolakia (Idiopathic true
leukoplakia)
Differential diagnosis
• Lichen planus,
• Lesions caused by cheek biting,
• Frictional keratosis,
• Smokeless tobacco–induced keratosis,
• Nicotinic stomatitis,
• Leukoedema,
• White sponge nevus.
Leukolakia (Idiopathic true
leukoplakia)
Laboratory investigations;
• Toluidine blue staining
• The cytobrushtechnique (brush biopsy)
Treatment
• Behavior modification
• Excision of the lesion/ cryosurgery/ laser ablation
HEREDITARY WHITE
LESIONS
1- Leukoedema
2- White Sponge Nevus
3- Hereditary Benign Intraepithelial Dyskeratosis
4- Dyskeratosis Congenita
Leukoedema
• Mucosal alteration that represents a variation of
the normal condition-→ not a true pathology
• Epidemiology:
a. Ethnicity: Black (90% Black Adult, 50% Black
Teenagers)
b. Site: buccal mucosa**and it may be seen rarely
on the labial mucosa, soft palate, and floor of the
mouth.
Leukoedema
• Clinical presentation:
• Faint, white, diffuse,
and filmy appearance,
with numerous surface
folds resulting in
wrinkling of the mucosa
• Cannot be scraped off
• Disappears or fades
upon stretching the
mucosa.
Leukoedema
Histopathological features
• Thickening of the
epithelium
• Significant intracellular
edema of the stratum
spinosum.
• The surface of the
epithelium may
demonstrate a thickened
layer of parakeratin.
Leukoedema
• TREATMENT
a. No treatment is indicated for leukoedema since it
is a variation of the normal condition.
b. No malignant change has been reported.
White Sponge Nevus

Rare autosomal dominant disorder

High degree of penetrance and variable expressivity;

Predominantly affects noncornified stratified squamous

epithelium.
White Sponge Nevus
• Epidemiology
a. Oral mucosa (buccal mucosa> ventral tongue, floor of
the mouth, labial mucosa, soft palate, and alveolar
mucosa. )
b. Mucous membranes of the nose, esophagus,
genitalia, and rectum (less commonly)
• Etiopathogenesis
a. Missense mutation in one allele of keratin 13 that
leads to proline substitution for leucine within the
keratin gene cluster on chromosome 17.
b. A glutamine insertion localized in the helix initiation
motif of the 1a alpha helical domain of keratin 4
gene.
White Sponge Nevus
• Clinical presentation:
a. Bilateral symmetric
white, soft, “spongy,”
or velvety thick
plaques
b. Usually asymptomatic
c. Does not exhibit
tendencies toward
malignant change.
White Sponge Nevus
White Sponge Nevus
• Differential diagnosis
I. Hereditary benign intraepithelial dyskeratosis or
pachyonychia congenita,
II. Traumatic lesions seen in cheek chewing
III. Chemical burns
IV. pre-neoplastic/neoplastic conditions
White Sponge Nevus
Histopathological features;
a. Epithelial thickening,
b. Parakeratosis,
c. A peculiar perinuclear condensation of the
cytoplasm, and
d. Vacuolization of the supra-basal layer of
keratinocytes.
e. Electron microscopy of exfoliated cells shows
numerous cellular granules composed of
disordered aggregates of tonofilaments.
White Sponge Nevus
TREATMENT
• No treatment
• Palliative treatment if the condition is symptomatic
(tetracycline rinse).
Hereditary Benign Intraepithelial
Dyskeratosis; “Witkop’s disease”
rare autosomal dominant disorder → oral lesions
and bilateral limbal conjunctival plaques.
Ethnicity: Native American, and African American
people and their descendants in Halifax county,
North Carolina.
Hereditary Benign Intraepithelial
Dyskeratosis; “Witkop’s disease”
• Oral manifestation
a. Site: Buccal Mucosa, floor of the mouth, the
lateral tongue, the gingiva, and the palate.
b. Thick, corrugated, asymptomatic, white “spongy”
plaques involving the buccal and labial mucosa.
Hereditary Benign Intraepithelial
Dyskeratosis; “Witkop’s disease”
• Eye features (red eye
disease):
a. Manifest very early in life
(usually within the first
year)
b. Bulbar conjunctiva presents
thick, gelatinous, foamy,
and opaque plaques form
adjacent to the cornea
c. Chronic relapsing ocular
irritation and photophobia
d. Blindness due to corneal
vascularization
Hereditary Benign Intraepithelial
Dyskeratosis; “Witkop’s disease”
• Treatment:
a. No treatment is required for the oral lesions.
b. For ocular lesions: refer to ophthalmologist.