2. WHITE LESIONS of Oral Cavity
Presented by
Mohammad Abdel-Hamid Mohey-Eldin
BDS, MSc. Oral and Maxillofacial Surgery - Mansoura Univ.
Assistant Lecturer - Department of Oral surgery and Anaesthesia – Delta Univ.
4. WHITE LESIONS
• A lesion is any
abnormality in the
tissue of an organism,
usually caused by
disease or trauma.
Lesion is derived from
the Latin word laesio
meaning injury.
Thickened layer of keratin
Epithelial hyperplasia
Intracellular epithelial
edema
Reduced vascularity of subjacent
connective
tissue
8. Leukoedema Hereditary
1- Leukoedema
2- White Spongy
Nevus
3- HBID ( Witkop’s )
4- Follicular Keratosis
( Darier’s)
ETIOLOGY and PATHOGENESIS
to date, cause has not
been established
smoking
chewing tobacco
alcohol ingestion
bacterial infection
salivary condition
electrochemical interactions
have been implicated
Generalized opacification of buccal mucosa that is
regarded as a variation of normal
9. Leukoedema Hereditary
1- Leukoedema
2- White Spongy
Nevus
3- HBID ( Witkop’s )
4- Follicular Keratosis
( Darier’s)
Appears as gray-white, diffuse, filmy or milky
surface
More exaggerated cases, whitish cast with surface
textural changes
With stretching of buccal mucosa, opaque changes fade
More apparent in non-whites especially African-American
Clinical Features
Usually discovered as incidental finding
Asymptomatic
Symmetrically distributed in buccal
mucosa
10. Leukoedema
-Acanthotic epithelium
-Flattened and show pyknotic nuclei
-Cells of stratum spinosum are enlarged showing intracellular edema
,not infiltrated with inflammatory cells.
Hereditary
1- Leukoedema
2- White Spongy
Nevus
3- HBID ( Witkop’s )
4- Follicular Keratosis
( Darier’s)
Histopathology
11. LeukoedemaLeukoedema
Leukoedema Hereditary
1- Leukoedema
2- White Spongy
Nevus
3- HBID ( Witkop’s )
4- Follicular Keratosis
( Darier’s)
Differential Diagnosis
Leukoplakia, Hereditary Benign Inraepithelial Dyskeratosis
, White Spongy nevus
Treatment
NO treatment is necessary since there is no malignant
potential
if there is any doubt about
diagnosis, a biopsy can
be performed
12. White Spongy Nevus Hereditary
1- Leukoedema
2- White Spongy
Nevus
3- HBID ( Witkop’s )
4- Follicular Keratosis
( Darier’s)
Autosomal Dominant Condition
Clinical Features
asymptomatic bilateral and symmetrical
• folded white lesions
• may affect several mucosal sites such as buccal mucosa ,
tongue, vestibular mucosa , conjunctiva, and esophageal
mucosa may be involved
• lesions tend to be thickened and spongy in consitency
•usually appears early in life, typically before puberty
16. White Spongy Nevus Hereditary
1- Leukoedema
2- White Spongy
Nevus
3- HBID ( Witkop’s )
4- Follicular Keratosis
( Darier’s)
Treatment
•NO treatment necessary since it is asymptomatic
and benign
Differential Diagnosis
HBID , Hypertrophic lichen planus , frictional
keratosis
17. Hereditary Benign Intraepithelial Dyskeratosis Hereditary
1- Leukoedema
2- White Spongy
Nevus
3- HBID ( Witkop’s )
4- Follicular Keratosis
( Darier’s)
Also called “ Witkop’s disease “
a benign disease of the conjunctiva,
cornea, and oral mucosa
Clinical Features
- Asymptomatic
-White, spongy plaques of the buccal
mucosa, tongue, or lips
- Arises early in life
-Bilateral or unilateral whitish-gray, elevated,
gelatinous corneal or conjuctival plaques
18.
19. Hereditary Benign Intraepithelial Dyskeratosis Hereditary
1- Leukoedema
2- White Spongy
Nevus
3- HBID ( Witkop’s )
4- Follicular Keratosis
( Darier’s)
Histopathology
-Acanthosis
-Hydropic degeneration of spinous
cells
-Enlarged, hyaline, waxy,
eosinophilic cells ( dyskeratotic
elements )
-Dyskeratotic cells may be
surrounded by adjacent cells
producing “ Cell within cell”
-Inflammatory cell infiltrate is
minimal
20. Follicular Keratosis Hereditary
1- Leukoedema
2- White Spongy
Nevus
3- HBID ( Witkop’s )
4- Follicular Keratosis
( Darier’s)
- Also known as “ Darier’s disease “
-It’s an autosomal dominant disorder discovered by
French dermatologist Ferdinand-Jean Darier
-Oral + Epidermal lesions
-Childhood or adolescence
Clinical Picture
-Thickening of skin of palms and soles
-Papular lesions on skin
-May follow snburns
-Intraorally it affects attached gingiva , hard
palate in form of papule and may extend to -
oropharynx and pharynx
23. Frictional Hyperkeratosis Reactive
1- Frictional
Hyperkeratosis
2- with Smokeless
Tobacco
3- Nicotine Stomatitis
4-Hairy Leukoplakia
5- Hairy Tongue
6- Dentrifice
associated slough
Etiology:-
1-chronic rubbing of friction against an oral mucosa.
2-It represents a protective action against low grade, long term
trauma as habitual lip or cheek biting.
Clinically:-
Age: 5-6 decades.
Sex: male>female.
Site: mandibular mucosa, cheek, palate, floor of
the mouth, maxillary mucosa, tongue, buccal
mucosa along occlusal line, edentulous ridges.
Shape: focal keratosis clinically show outlined
white patches, not indurated ,have no red
margin, painless.
24. Frictional Hyperkeratosis Reactive
1- Frictional
Hyperkeratosis
2- Nicotine Stomatitis
3-Hairy Leukoplakia
4- Hairy Tongue
5- Dentrifice
associated slough
Histopathology
1-hyperkeratosis (hyperparakeratosis) .
2-thickening of granular cell layer.
3-acanthosis but the individual cells are
normal.
4-a few chronic inflammatory cells in
adjacent connective tissue.
25. Frictional Hyperkeratosis Reactive
1- Frictional
Hyperkeratosis
2- Nicotine Stomatitis
3-Hairy Leukoplakia
4- Hairy Tongue
5- Dentrifice
associated slough
Diagnosis:-
1. Careful history taking.
2. Careful examination.
3. Biopsy must be taken if no exact cause
is known.
Treatment:-
Removal of the cause, the lesion may
disappear in 2-3 weeks.
26. Nicotine Stomatitis Reactive
1- Frictional
Hyperkeratosis
2- Nicotine Stomatitis
3-Hairy Leukoplakia
4- Hairy Tongue
5- Dentrifice
associated slough
Def.
It is the most frequently leukoplakic lesion of the palate.
Etiology:-
1-pipe and cigar smoking.
2-long term use of extremely hot beverges.
3-reverse smoking.
27. Nicotine Stomatitis Reactive
1- Frictional
Hyperkeratosis
2- Nicotine Stomatitis
3-Hairy Leukoplakia
4- Hairy Tongue
5- Dentrifice
associated slough
Clinically:-
Age: more than 45 years.
Sex: male > female.
Site: palatal mucosa.
Shape:-
Erythematous patches over time increase in
keratinization ,opacification.
Red dots are seen in posterior portion of hard palate.
These dots are surrounded by white keratotic ring ,
these dots represent inflammation of ductal
elements of underlying minor salivary gland.
28. Nicotine Stomatitis Reactive
1- Frictional
Hyperkeratosis
2- Nicotine Stomatitis
3-Hairy Leukoplakia
4- Hairy Tongue
5- Dentrifice
associated slough
Histopathology:-
1-epithelial hyperplasia.
2-acanthosis.
3-hyperkeratinization.
4-chronic inflammatory cell
infiltration of sub epithelial
connective tissue.
5-minor salivary gland show
moderate degrees of
inflammation.
6-excretory ducts show squamous
metaplasia.
29. Nicotine Stomatitis Reactive
1- Frictional
Hyperkeratosis
2- Nicotine Stomatitis
3-Hairy Leukoplakia
4- Hairy Tongue
5- Dentrifice
associated slough
Treatment:-
1-Stop smoking.
2-It is a completely reversible habit, the palate return
to normal within 1-2 weeks of smoking cessation.
30. Hairy Leukoplakia Reactive
1- Frictional
Hyperkeratosis
2- Nicotine Stomatitis
3-Hairy Leukoplakia
4- Hairy Tongue
5- Dentrifice
associated slough
Def.:-
It is an unusual white lesion with a hairy appearance or corrugated
surface that occurred on the lateral border or dorsum of tongue.
Etiology:-
1-In male homosexuals.
2-An opportunistic infection relates to Epstein-Barr virus.
3-It is related to AIDS patients.
N.B. Viral particles are present and replicated within the epithelial
cells of tongue. Human papilloma virus present in co-existence
with EBV.
31. Hairy Leukoplakia Reactive
1- Frictional
Hyperkeratosis
2- Nicotine Stomatitis
3-Hairy Leukoplakia
4- Hairy Tongue
5- Dentrifice
associated slough
Clinically:-
Site: lateral surface of tongue,
dorsum of tongue, floor of
mouth, palate.
Shape: unilateral or bilateral
surface which is folded or
corrugated or papillary(
hairy).
No associated symptoms
unless it is superimposed by
candidal infection.
32. Hairy Leukoplakia Reactive
1- Frictional
Hyperkeratosis
2- Nicotine Stomatitis
3-Hairy Leukoplakia
4- Hairy Tongue
5- Dentrifice
associated slough
Histopathology:-
1-Epithelial hyperplasia.
2-Marked hyperparakeratosis.
3- Formation of keratotic surface
irregularities and ridges.
4-Spinous cell layers show koilocytosis.
5-Alterationas of nuclear chromatin in
form of viral inclusions.
6-Candidal albicans hyphae extend into
superficial epithelial layers.
7- No inflammatory cell infiltration in C.T.
33. • Koilocytosis is a form of cellular changes which is
characterized by perinuclear
vacuolation .
35. Hairy Tongue Reactive
1- Frictional
Hyperkeratosis
2- Nicotine Stomatitis
3-Hairy Leukoplakia
4- Hairy Tongue
5- Dentrifice
associated slough
Clinical term referring to a
condition of filiform papillae
overgrowth on dorsal surface
of tongue
There are numerous initiating
or predisposing factors for
hairy tongue
- Self limiting condition , tongue scrubbing is effective
36. Hairy Tongue Reactive
1- Frictional
Hyperkeratosis
2- Nicotine Stomatitis
3-Hairy Leukoplakia
4- Hairy Tongue
5- Dentrifice
associated slough
Broad spectrum antibiotics such as penicillin + systemic
cortiocosteroids are often identified in clinical history of patients with
this condition
oxygenating mouthrinses
containing:
hydrogen peroxide
sodium perborate
carbamide peroxide
have been cited as
possible etiologic agents
37. Hairy Tongue
Clinical Features
clinical alteration translates to hyperplasia of filiform
papillae; result is
• thick matted surface(serves to trap bacteria, fungi,
foreign materials )
extensive elongation of papillae occurs,
• gagging may be felt
color may range from white to tan to deep brown depending on:
• diet
• oral hygiene
• composition of bacteria
inhabiting papillary surface
38. Dentrifice associated slough Reactive
1- Frictional
Hyperkeratosis
2- Nicotine Stomatitis
3-Hairy Leukoplakia
4- Hairy Tongue
5- Dentrifice
associated slough
It’s a relatively common phenonmenon that has been associated
with different brands of tooth pastes
Etiology
Mucosal Reaction to a component such as detergent or flavouring
compounds
Clinical Feeatures
Asymptomatic
Superficial Whitish slough of buccal mucosa
Treatment
Shift to another brand of tooth paste
39. Actinic Chelitis Preneoplastic
1- Actinic chelitis
2- Idiopathic
Leukoplakia
It represents accelerated tissue degeneration of the lips especially the
lower lip, secondary to regular and prolonged exposure to sunlight
Clinical features
Affects Vermilion portion of the lips
Atrophic pale glossy appearance often with fissuring and wrinklings
Histopathological features
Atrophic and hyperkeratotic overlying epithelium
Hyperchromatic basal cells
Telangiectasia ( Small Dilated Blood Vessels )
Basophilic changes of submucosa
Treatment
No treatment ( only decrease sun exposure )
Strong relation between development of Carcinoma at this site
40. Idiopathic Leukoplakia Preneoplastic
1- Actinic chelitis
2- Idiopathic
Leukoplakia
A white patch or plaque that cannot be characterised clinically or
pathologically by any other disease
Clinical Features
Site : Buccal/Vestibular mucosa
Borders of the tongue
Floor of the mouth etc
Symptoms : Mostly asymptomatic
Discovered on routine examination
Sometimes patient may aware of a white lesion/
roughness.
Speckle variety may cause burning sensation.
42. Signs of Dysplasia
– 1- Bulbous or teardrop-shaped rete ridges
– 2- Keratin pearls (focal round collections of keratinized cells)
– 3- Loss of typical epithelial cell cohesiveness
– 4- Crowding and disorganization
– 5- Enlarged nuclei and cells
– 6- Large and prominent nucleoli
– 7- Increased nuclear-to-cytoplasmic ratio
– 8- Hyperchromatic nuclei
– 9- Pleomorphic nuclei and cells
– 10- Dyskeratosis (premature keratinization of individual cells)
– 11- Loss of basal cell polarity
– 12- Abnormal mitotic figures
43. Classification of Epithelial Dysplasia
• Mild: Alterations limited to the basal and parabasal layers
• Moderate: Alterations extending from the basal layer to the
midportion of the spinous layer
• Severe: Alterations from the basal layer to a level above the
midpoint of the epithelium
• Carcinoma in situ: Alterations involve the entire thickness of
the epithelium – NO INVASION
48. Candidiasis Non-Epithelial
1- Candidiasis
2- Mucosal Burns
3- Submucous
Fibrosis
4- Fordyce’s Granules
5- Ectopic Lymphoid
tissue
This is a term that encompasses a group of
mucosal and cutaneous conditions with a common
etiological agent from the Candida genus of fungi.
Etiology:-
The causative organism is Candida Albicans.
The predisposing factors are:-
1-topical corticosteroids.
2-malabsorption , malnutrition.
3-poor oral hygiene.
4-xerostomia.
5-systemic antibiotic therapy.
6-Cancer chemotherapy.
7- AIDS.
50. Laboratory findings:-
- Part of the candidal plaque is
smeared on a microscopic
slide,.
-Then examination for typical
hyphae.
Candidiasis Non-Epithelial
1- Candidiasis
2- Mucosal Burns
3- Submucous
Fibrosis
4- Fordyce’s Granules
5- Ectopic Lymphoid
tissueHistopathology:-
1-hyperparakeratosis.
2- chronic inflammatory cell infiltration
in CT
3-collections of neutrophils (micro-
abscess) in parakeratin layer.
4-The candidal hyphae embedded in
parakeratin layer.
51. Mucosal Burn Non-Epithelial
1- Candidiasis
2- Mucosal Burns
3- Submucous
Fibrosis
4- Fordyce’s Granules
5- Ectopic Lymphoid
tissue
Chemical Burns:-
Topical applications of
chemicals as aspirin tablets
which is used in self
medication and held locally
against a painful tooth and
allowed to dissolve slowly.
Thermal Burns:-
Common in hard palatal
mucosa caused by hot,
sticky food.
52. Oral submucous fibrosis Non-Epithelial
1- Candidiasis
2- Mucosal Burns
3- Submucous
Fibrosis
4- Fordyce’s Granules
5- Ectopic Lymphoid
tissue
Def.
It is a chronic , progressive, scarring high precancerous
condition of oral mucosa.
Etiology:-
1-chronic chewing of areca and betel nut.
2-general nutritional deficiency.
3-hypersensitivity to various dietary constituents as
spicy.
Clinical Features
Site: buccal mucosa, retro molar area, soft palate may
extend into pharynx, esophagus.
Shape: White yellowish lesion, the oral mucosa loses
its resilience and elasticity, the process progresses from
lamina propria to underlying musculature.
53. Oral submucous fibrosis Non-Epithelial
1- Candidiasis
2- Mucosal Burns
3- Submucous
Fibrosis
4- Fordyce’s Granules
5- Ectopic Lymphoid
tissue
Histopathological Features
1- Hyperkeratosis with epithelial atrophy.
2- Variable degrees of dysplastic changes.
3- Superficial portions of lamina propria
are poorly vascularized and hyalinized.
4- Submucosal deposition of extremely dense
and a vascular collagenous C.T. with variable
numbers of chronic inflammatory.
54. Represents ectopic sebaceous
glands or sebaceous
choristomas
normal tissue in abnormal
location
regarded as developmental
considered a variation of normal
Asymptomatic , only slight roughness may be felt.
Fordyce’s Granules Non-Epithelial
1- Candidiasis
2- Mucosal Burns
3- Submucous
Fibrosis
4- Fordyce’s Granules
5- Ectopic Lymphoid
tissue
55. Ectopic Lymphoid tissue Non-Epithelial
1- Candidiasis
2- Mucosal Burns
3- Submucous
Fibrosis
4- Fordyce’s Granules
5- Ectopic Lymphoid
tissue
-Also known as “ Lingual Tonsils “
Clinically :
They are located on the dorsal surface at the
base of the tongue. Their lymphatic tissue are
dense and nodular,
Histopathologically
their surface is covered with stratified squamous epithelium which
invaginates as a single crypt into each lingual tonsil.
They are partially surrounded by connective tissue placing them in
the group of Partially Encapsulated Lymphatic Organs, tonsils, the
only one of its kind. They have associated mucous glands which are
drained by ducts directly into the single tonsillar crypt.
56. Geographic Tongue Others
1- Geographic tongue
2- Lichen Planus
3- Lupus
Erythromatosis
also known as erythema migrans,
benign migratory glossitis
strongly associated with fissure
tongue
emotional stress may enhance
the process
Clinical Features
characterized initially by
presence of atrophic patches
surrounded by elevated
keratotic margins , Asymptomatic , Migrating
57. Lichen Planus Others
1- Geographic tongue
2- Lichen Planus
3- Lupus
Erythromatosis
Lichen = Tree moss
Planus = Flat
Clinical Features
variable and present as white striations (Wickham striae), white papules,
white plaques, erythema (mucosal atrophy), erosions (shallow ulcers), or
blisters.
( Reticular, Plaque, atrophic and erosive forms + bullous variants)
The lesions predominantly affect the buccal mucosa, tongue, and gingivae,
although other oral sites are occasionally involved.
Etiology
a T-cell–mediated autoimmune disease in which autocytotoxic CD8 + T cells
trigger the apoptosis of oral epithelial cells
59. Lichen Planus Others
1- Geographic tongue
2- Lichen Planus
3- Lupus
Erythromatosis
Ulcerative oral lichen planus on the
dorsum of the tongue
Plaque form on buccal mucosa
60. Lichen Planus Others
1- Geographic tongue
2- Lichen Planus
3- Lupus
Erythromatosis
• Civatte bodies (arrows),
• keratinocyte enlargement, and
coarse collagen bundles are
illustrated.
• Hyperpara(or ortho)keratosis
• Eosniophilic band above basal
layer
• Lymphocytic band in lamina
propria
• Destruction of Epith-C.T interface
Histopathologic features
61. Lupus Erythematosus Others
1- Geographic tongue
2- Lichen Planus
3- Lupus
Erythematosus
Lupus erythematosus is an autoimmune connective tissue disease
which has two main forms namely systemic and discoid.
Clinical Features
Skin lesions ( Butterfly rash, Facial Odema ,
Chronic uricaria … )
Oral lesions :
-Vesicles, ulcerations, mucosal stiffening,
decreased mouth opening ,
xerostomia, burning sensation , blanched fibrotic
mucosa
-Usually involves the buccal mucosa, soft palate,
posterior pharynx, lips, and tongue.
62. Lupus Erythematosus Others
1- Geographic tongue
2- Lichen Planus
3- Lupus
Erythematosus
Histopathologic Features:
• Liquefaction degeneration of basal cell layer.
• Degenerative changes in the connective tissue
(hyalinization, oedema,..).
• Lupus erythematosus shows more irregular
patterns of acanthosis and lacks the band-like
distribution of lymphocytes in the
lamina propria of
lichen planus.
• The inflammatory infiltrate may have
a perivascular distribution.
63. Lupus Erythematosus Others
1- Geographic tongue
2- Lichen Planus
3- Lupus
Erythematosus
Microphotograph of a histological
section of human skin prepared for
direct immunofluorescence using an
anti-IgG antibody. The skin is from a
person with systemic lupus
erythematosus and shows IgG deposits
at two different places:
The first is a bandlike deposit along the
epidermal basement membrane
("lupus band test" is positive); the
second is within the nuclei of the
epidermal cells (antinuclear antibodies
are present).
65. Conclusion
• White lesions are always of suspections
• Know normalities before looking for abnormalities
• Science is in a rush, so update your sources
• Seek for biopsies for your undoubts before your doubts !
• Keep in touch with your microscope
