White lessons about oral desires

1. WHITE LESIONS
Dr Huzaifa Saeed ul Khair
Department of oral medicine

2. Color of oral
mucosa
depends on
• Concentration and dilation of
blood vessels in the
underlying connective tissue
• Degree of keratinization
• Amount of melanin pigment
in epithelium
• Thickness of epithelium

3. Classification
• Hereditary
• Oral epithelial naevus
• Leukoedema
• Dyskeratosis congenita
• Traumatic
• Mechanical
• Thermal
• Chemical
• Infective
• Candidosis
• Syphilitic leukoplakia
• Hairy leukoplakia

4. • Leukoplakia
Idiopathic
• Lichan planus
• Lupus erythematosus
dermatological
• Carcinoma in situ
• Squamous cell carcinoma
Neoplastic

5. White
Sponge
Nevus:
• It is a developmental
anomaly inherited as
an autosomal
dominant trait
caused by mutation
in keratin gene (4 and
13)
• Buccal mucosa is
usually affected.

6. CLINICAL
FEATURES
• The affected mucosa is white,
soft and irregularly thickened.
• The abnormality is
usually bilateral.
• There are no defined borders
and the
edges fade imperceptibly into
normal tissue.
• The condition is usually
asymptomatic and mainly affect
buccal mucosa, ventral
surface of tongue, floor of
the mouth and soft palate.

8. HISTOPATHOLOGY
• The epithelium is hyperplastic,
with uniform acanthosis and the
rete ridges have a smooth lower
border.
• Shaggy hyper parakeratosis and
intracellular oedema with
abnormally prominent epithelial c
ell membrane produce so called
basket weave appearance.

9. MANAGEMENT
• The appearance is readily
recognized, particularly when
there is widespread mucosal
involvement.
• A positive family history is
confirmatory.
• Biopsy confirms the diagnosis.
• The main requirement is to
reassure the patient of the
benign nature of the condition

10. LEUKOEDEMA
• Leukoedema is a
bilateral, diffuse,
translucent greyish
thickening particularly
of the buccal mucosa.
• Leukoedema lesions
disappear when the
mucosa is stretched

11. Histopathology
• increased epithelial thickness,
• broadening and elongation of the rete ridges,
• parakeratosis
• intracellular edema of the spinous layer.
• The cells of the spinous later are vacuolated,
large and possess pyknotic nuclei.
• The superficial squamous cells have a
clear cytoplasm

13. TREATMENT • Reassurance may be required

14. TRAUMATIC
Mechanical
Frictional keratosis
Chemical
Thermal

15. FRICTIONAL
KERATOSIS

16. CLINICAL FEATURES
• At first, the patches are pale and translucent
but later become dense and white.
• Habitual cheek biting causes an area of buccal
mucosa to appear patchily red and white with
a rough surface.
• Histologically epithelium is moderately
hyperplastic with a prominent granular cell
layer.

18. MANAGEMENT
• Removal of the irritant causes
the patch quickly to disappear.
• Biopsy is necessary only if patch
persists.

19. Pipe smoker's keratosis
(STOMATITIS NICOTINA)
It is seen among heavy, long term pipe smokers and
some cigar smokers.
The appearance are distinctive in that the
palate is affected by any part protected by a denture is
spared.
Changes are only seen on the soft palate.

20. CLINICAL
FEATURES
• The lesion has two
compartments:
Hyperkeratosis
and inflammatory swelling
of minor mucous glands.
• White thickening of the palatal
mucosa is associated with small
umbilicated swellings with red
centers.
• The white plaque is sometimes
distinctly tessellated (pavement
like)

21. MICROSCOPY
• White areas show hyper orthokeratosis and
acanthosis with a variable inflammatory
infiltrate beneath.
• The diagnostic feature is the swollen,
inflamed mucous glands with
hyperkeratosis extending up to the duct
orifice

22. MANAGEMENT
• The clinical appearance, history and ease of
management are so distinctive that biopsy
should not be necessary.
• If patient is persuaded to stop smoking the
lesion resolves within weeks.

23. Lichen Planus
• Lichen planus is a chronic
autoimmune, mucocutaneous
disease which affect the skin and/or
mucous membrane.
• It is thought be the result of an
autoimmune process with
an unknown initial trigger.

24. EPIDEMIOLOGY
• Prevalence is 0.5-
2.2%
• Commonly seen in
women than men.
• Mean age at
the time of diagnosis is
approximately 55 years.

25. ETIOLOGY
• Etiology is unknown
• Immune system has a primary role supported by
the subepithelial band formed infiltrate dominated
by T lymphocytes and macrophages and the
degeneration of basal cells known as liquefaction
generation.
• Autoreactive T lymphocytes may be of
primary importance for the development of oral
lichen planus

26. Pathophysiolgy
• Keratinocyte antigen expression or unmasking of
an antigen.
• T cells (mostly CD8+,CD4+ cells) migrate into the
epithelium .
• Activation of these cells….bind to MHC 1 on
keratinocyte.
• Langerhans cells increased along with up
regulation of MHC-II.
• antigen presentation to CD4+ cells and Interleukin
(IL)-12 activates CD8+ T cells.
• The activated CD8+ T cells in turn kill the basal
keratinocytes through tumor necrosis factor (TNF)-
α, Fas–FasL mediated or granzyme.

28. Predisposing factors
Genetics
Tobacco
Stress
Diabetes
Graft vs host reaction
Dental materials
Hepatitis C virus
Drugs: antimalarials

29. Clinical Features
• It present with 2 types of lesions:
1. Cutaneous lesion
2. Oral manifestation

30. Skin lesions
• One-third of patients have skin lesions only, one-third
have oral lesions only and the remaining third have
both.
• Classic appearance of skin lesions consist of pruitic
erythematous to violaceous papules which are
flat topped, small, angular only a few millimeters
• Purplish papules, 2–3 mm across with a glistening
surface marked by minute fine ‘Wickham’s striae’*
• Typical sites are the flexor surface of the forearms and
especially the wrists and shins.

31. • Usually bilateral and very often
symmetrical.
• Posterior buccal mucous
membranes are most
commonly involved extending
up to commissures.
• Then lateral borders of tongue
and dorsum of tongue.
• The floor of the mouth and
palate are usually uninvolved
and apparent extension to
floor of mouth should raise
suspicion of either
misdiagnosis
Oral lesions

32. Oral lesions
• Any one patient may have several
presentations that change from one pattern
to another over time.
• Oral lesions are difficult to treat.
• When inflammation worsens or symptoms
become more severe, consider the possibility
of superinfection with Candida

33. Classification/Types
Reticular symptom free
Atrophic ulceration
Plaque like symptom free
Papular symptoms free
Erosive ulceration/painful
Bullous subepithelial vesicle/bulla

34. Reticular
• Most common and most readily recognized
form.
• Wickham's striae that produce an annular or
lacy pattern.
• The buccal mucosa is the site most
commonly involved- bilaterally.
• Minimal clinical symptoms and is often an
incidental discovery.
• Lateral border of tongue gingiva and the lips.
• Reticular lichen planus is likely to resolve in 4%
of cases.

36. Erosive
• The 2nd most common type.
• The lesion consist of mixture of
erythematous and ulcerated areas
surrounded by radiating keratotic
striae.
• Mostly affect the buccal mucosa
and vestibule
• symptomatic, characterized by:
• Sore mouth sensitive to heat,
cold, spices, and alcohol
• Pain and bleeding on touch
• More dysplasia and malignant
transformation

38. PLAQUE-LIKE
• The plaques generally range from
slightly elevated to smooth and flat.
• Dorsum of the tongue , buccal
mucosa.
• Resolves in only 7% of cases.
• More common among tobacco
smokers.

40. BULLOUS
TYPE
• Appear as small bullae or
vesicles that tend to rupture
easily.
• When ruptured leave an
ulcerated, painful surface.
• This form is rarer than the other
forms of oral lichen planus.
• Usually present in combination
with reticular or erosive
pattern.
• Commonly seen on the buccal
mucosa, lateral margin of the
tongue.

42. ATROPHIC
• The atrophic type is diffuse, red
and there are usually white
striae within the lesion.
• The attached gingiva is often
involved and the condition is
commonly referred to as
`chronic desquamative
gingivitis'.
• Burning sensation
• • About 12% of the atrophic
lesions will resolve spontaneously.

44. PAPULAR
• Usually present in initial phase of
disease.
• Characterized by small white dots
• Minute white papule
• These gradually enlarge to form
either a reticular, annular or plaque
pattern

45. Histopathology
• Ortho Para keratinization
• Atrophic/acanthotic.
• Sawtooth pattern of rete ridges.
• Well defined band of mononuclear T cell.
• Plasma cell are absent
• Liquefactive degeneration of basal cell.
• Civatte bodies.

48. Diagnosis
• Can be easily
diagnosed clinically
and confirmed by
biopsy.

49. Management
NO TREATMENT FOR THE UNDERLYING DISEASE PROCESS;
TREATMENT IS SYMPTOMATIC TO MANAGE ANY FLARE UP IN
SEVERITY AND COMPLICATIONS.
IT IS USUAL TO START WITH LOW-POTENCY TOPICAL
TREATMENTS. (FOR SYMPTOMATIC LESIONS AS IN ATROPHIC,
ULCERATED LESIONS)
PATIENTS NEED TO UNDERSTAND THAT LESIONS WILL PERSIST
FOR MANY YEARS, BUT THAT SYMPTOMS CAN BE MANAGED.
(COUNSEL AND REASSURE THE PATIENT)
SENSITIVITY PREVENTS TOOTH BRUSHING, BUT ACCUMULATION
OF PLAQUE WORSENS INFLAMMATION AND SYMPTOMS.
(CHLORHEXIDINE MOUTHWASH, ORAL HYGIENE
INSTRUCTIONS).

50. Management of Mild
to Moderate disease
• Beclomethasone inhalars, approximately
six puffs each day can be used to deliver
enough of the corticosteroid to an ulcer.
• 0.5 mg betamethasone dissolved in 5–10
mL water and used as a mouthwash for 1-2
minutes four times daily before spitting
out. (For gingival and mucous disease)
• Steroid gel with vacuum formed trays for
gingival disease.

51. Management of
Severe/Generalized Disease
• High-potency steroid mouth rinses like Fluocinonide or
clobetasol are required. Patients should not rinse, but hold
the preparation in the mouth for a minute over the affected
mucosa and then spit it out to avoid systemic effects.
• Systemic prednisolone is used for severe disease (1-2
weeks).
• Disease-Modifying Agents: Cyclosporine, tacrolimus and
Mycophenolate