2. – ORAL LICHEN PLANUS is a mucocutaneous disease
described by ERASMUS WILSON In 1869
– The condition can affect either skin or mucosa or both
– It can cause bilateral white striations, papules or
plaques on the buccal mucosa, tongue, and gingiva
– Erythema, erosions and blisters may or may not be
present
INTRODUCTION
3. PREVALENCE
– It is predominantly a disease of the middle aged or older,
and has a prevalence of 0.5% to 2% in adults.
– It is more common in females than in males ratio of
approximately 2:1
– It is also seen in children, although it is rare, and they
may be present with atypical findings. Familial LP occurs in
1-2% of all childhood cases.
– The prevalence of oral lichen planus in children is about
0.03%
4. ETIOLOGY
– OLP has been associated with multiple disease
processes and agents such as Viral And Bacterial
Infections, Autoimmune Diseases (such as ulcerative
colitis, myasthenia gravis, lupus erythematosus)
Medications, Vaccinations and Allergy to Dental
Restorative Materials (such as gold and amalgam),
Local trauma (Koebner phenomenon) and Systemic
diseases (such as diabetes mellitus and hypertension)
5. – Childhood lichen planus has been documented as a
complication of Hepatitis B Vaccinations (HBV) where
the recombinant proteins of the HBV vaccine may
trigger a cell mediated autoimmune response targeted
at keratinocytes giving rise to a lichenoid reactions.
– It is also found in association with predisposing
conditions, such as graft vs host disease and chronic
Hepatitis C
6. PATHOGENESIS
CD8+ T CELLS TRIGGER
APOPTOSIS OF BASAL
CELLS
T CELLS MIGRATE INTO
EPITHELIUM TOWARDS
THE BASAL
KERATINOCYTES
T CELLS ARE ACTIVATED
BY ANTIGEN ON
KERATINOCYTE OR
THROUGH ACTIVATED
CD4+ LYMPHOCYTES
THE ACTIVATED T CELLS
KILL THE BASAL
KERATINOCYTES
THROUGH TNF-α
ACTIVATED APOPTOSIS
7.
8. • The histopathology include the existence of a band of lymphocytic
inflammatory infiltrate in the subepithelial connective tissue,
hydropic degeneration of the basal layer and the absence of
epithelial dysplasia.
• If the above three criteria are met, the lesion is considered a
typical lichen planus from a histological perspective; and as for
those that do not meet one of the histological criteria, they are
considered to be lesions that are histologically compatible with
lichen planus.
HISTOPATHOLOGY
9.
10. CLINICAL FEATURES
– OLP in childhood was first described in 1920.
– The family history of lichen planus is more commonly
positive in patients with lichen planus in childhood than
in adulthood.
11. – No malignant transformation of Oral Lichen Planus has been
reported
– Bilateral and symmetrical white striations are seen
commonly called the “WICKHAMS STRIAE”.
12. – Oral lichen planus is chronic and usually persists for several
years with periods of exacerbation and quiescence.
– During exacerbation areas of erythema or erosion increases
with slight increase in pain and sensitivity and vice versa in
period of quiescence.
– Usually exacerbations are associated with psychological
stress, anxiety and mechanical trauma (Koebner’s
Phenomenon)
13. – Andreason described six types :
Reticular
Papular
Plaque
Atrophic
Erosive
Bullous
TYPES
14. – Reticular lesions are often asymptomatic, and may appear as
symmetrical white lace like pattern on buccal mucosa, affects
tongue or gum.
– Atrophic OLP may appear as mixture of clinical subtypes (like
white and grey streaks in linear or reticular pattern on
erythematous background) red lesions often with a whitish
border. May cause erosions (superficial ulceration). Most often
affects the gums (gingiva) and lips. Can be very painful
16. – Plaque type OLP appears as homogenous white patch resembling
leukoplakia. Usually seen in Smokers
– Erosive OLP can be present as irregular erosion covered with
pseudomembrane. Symptoms range from episodic pain to severe
discomfort that interferes with normal masticatory function
– Bullous type OLP which is the least common usually present with
bullae (diameters about few mm to cm) tends to rupture leaving
ulcerated and painful surfaces
18. – It is an uncommon medication-induced chronic change inside the
mouth. It appears the same as idiopathic oral lichen planus
clinically and under the microscope, but an oral lichenoid drug
eruption resolves if the triggering drug is ceased
– An oral lichenoid drug eruption is predominantly a problem seen
in adults, probably because adults are the most frequent users
of the majority of medications associated with this reaction.
However it has also been reported rarely in children.
ORAL LICHENOID
DRUG REACTION
20. – Medications associated with this reaction include:
– • Penicillamine
– • Antimalarials such as hydroxychloroquine
– • Antihypertensives including beta-blockers, angiotensin
converting enzyme (ACE) inhibitors and diuretics
– • Non steroidal anti-inflammatory drugs (NSAID)
– • Oral hypoglycaemic agents for type 2 diabetes
– • Antiretroviral medications to treat HIV infection
21. Grinspans syndrome
– Characterised by the presence of the triad DIABETES
MELLITUS ,HYPERTENSION and ORAL LICHEN
PLANUS
– ORAL LICHEN PLANUS is thought to be a result of
the drugs used for treatment of hypertension and
diabetes mellitus, but this is not confirmed.
– Rarely seen in children than adults
22. DIAGNOSIS
– Complete history
– Physical examination by a multidisciplinary group of
health care providers
– Biopsy to differentiate between OLP and other white
chronic lesions
– Direct immunofluorescence to distinguish
erosive,ulcerative or bullous forms of OLP
24. management
CORTICOSTEROIDS :
TOPICAL CORTICOSTEROIDS such as 0.05% Clobetasol
proprionate gel, 0.1 or 0.05% Betamethasone valerate gel, 0.05%
Fluocinonide gel, 0.1% Triamcinolone acetonide ointment. Patients
are instructed to apply a thin layer up to 3times a day after
meals and at bedtime
Side effects are fewer. Adverse effects include Candidiasis,
Thinning of Oral Mucosa and Discomfort on application
Potent corticosteroids can cause adrenal suppression if used in
large amounts for longer period of time
25. SYSTEMIC CORTICOSTEROIDS is indicated in patients who are
unresponsive to topical steroids or mucocutaneous disease in a
dosage of 0.5-1mg/kg as a tapering dose over 3-6weeks
Systemic PREDNISONE is used to control ulcers and erythema in
OLP
26.
27. – IMMUNOSUPPRESANTS Tacrolimus Ointment (given two or three
times daily for three months with chlorhexidine mouthwash) had
better penetration into mucosal surface and tends to be 100
times more potent than cyclosporine
– Topical Tacrolimus 0.1% ointment induced better therapeutic
response than Triamcinolone Acetonide 0.1% in patients with
symptomatic OLP
28. RETINOIDS are metabolites of Vitamin A. they have anti-
keratinising and immunomodulating effects
Retinaldehyde 0.1%, Isotretinoin gel 0.1% shows good clinical
efficacy
Fenretinide and Tazarotene gel 0.1% has been used successfully
29.
30. – ULTRAVIOLET IRRADIATION
Photochemotherapy with 8-methoxypsolarine and Long wave UV
light (PUVA) is used
To avoid side effects photosensitisation with topical 0.01%
Trioxsalen is used
Side effects nausea, headache, eye symptoms, dizziness,
paraesthesia
It is also shown to have oncogenic potential
31. LASER THERAPY
308nm excimer laser, 980nm diode laser, CO2 laser evaporation
are used in treating OLP
CO2 laser evaporation showed no problem with wound healing and
there was complete epithelisation within 3 weeks
It is a good treatment option for OLP when there is no further
improvement with steroids
32. conclusion
OLP is rare in children and the clinical
presentations resembles those of adult OLP.
However, the prognosis of OLP in childhood
seems to be more favourable