Oral Lichen Planus
Oral Medicine: Week 1
Edvin Agadzhanov #100,
Ryan Plewe #168, Dave Tajima #181
Introduction
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Oral Lichen Planus
 A chronic
inflammatory disease that causes bilateral
papules, striations or plaques
 May cause erythema, erosions and blisters
 Found on buccal mucosa, tongue and gingiva
 Female:Male ratio: 1.4:1
 Predominantly seen in adults over 40 years.
 0.5% to 2% of general population
 Affects all ethnicities
Picture 1: Plaque-like OLP
Picture 2: Reticular OLP
Picture 3: Erosive OLP
Picture 4: Reticular OLP
Pathogenesis of Reticular LP
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Oral Lichen planus is a purely T cell mediated
inflammatory response.There are no B cells, plasma
cells and no deposits of immunoglobulin or complement.
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The trigger for keratinocyte apoptosis in OLP is, for the
most part, unknown. However, the lymphocytic infiltrate
in OLP is composed almost exclusively of T cells, and
the majority of T cells within the epithelium and adjacent
to damaged basal keratinocytes are activated CD8+
lymphocytes. Therefore, it is very probable that cytotoxic
T cells trigger keratinocyte apoptosis in OLP.
Proposed Immunopathogenesis
of OLP
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A lichen planus-specific antigen is expressed in
conjunction with MHC class 1 molecules on keratiocytes
at the OLP lesion site.
Antigen specific CD8+ T cells are activated in the area.
Activated antigen-specific CD8+ cytotoxic T lymphocytes
trigger keratinocyte apoptosis, possibly by secreted
TNF-α.
The activated T lymphocytes undergo intra-lesional
clonal expansion and release soluble mediators
(cytokines and chemokines), which recruit lymphocytes
from the local microvasculature and cause migration
toward the epithelium.
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This hypothesis predicts that the majority of lymphocytes
recruited to the OLP lesion site are not specific for the
lichen planus-specific antigen. However, they may
contribute to the pathogenesis of OLP by secreting
MMP-9, which leads to epithelial basement membrane
disruption.
Epithelial basement membrane disruption allows for the
passage of lymphocytes into the epithelium and denies
keratinocytes a cell survival signal, resulting in further
keratinocyte apoptosis.
This hypothesis predicts that the earliest events in OLP
lesion formation are confined to the epithelium and that
basement membrane and connective tissue changes
occur secondarily.
Clinical Presentation

Oral lesions-more persistant and resistant
to treatment than skin lesions
 30-50%
of pts also have cutaneous lesions
 Three common types
Reticular
 Erosive
 Plaque
Variants of Plaque and Erosive types
Atrophic
Bullous
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Clinical Presentation
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Reticular lesions
 Most
common type
 Interlacing white kerototic lines w/
erythematous borders (Wickham’s striae)
 Typically bilaterally on buccal mucosa,
mucobuccal fold and gingiva
 Less common on tongue, palate and lips
 Assymptomatic
Clinical Presentation
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Erosive lesions
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2nd most common type
Mix of erythematous and ulcerated areas sorrounded by
radiating keratotic striae
Similar appearance to candidiasis, pemphigus and lupus
Lesions tend to migrate and often multifocal
Mostly buccal mucosa and vestibule
Symptomatic:
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Sore mouth sensitive to heat, cold, spices, and alcohol
Pain and bleeding on touch
Plaque lesions
-
Resemble focal leukoplakias
Vary from smooth flat areas to raised irregular plaques
Often multifocal
Dorsum of tongue and buccal mucosa
Clinical Presentation
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Variants of Erosive and Plaque lesions
 Atrophic
Diffuse, erythematous patches
 Causes significant discomfort
 Gingiva and buccal mucosa
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 Bullous
Intraoral bullae on buccal mucosa and lateral
surface of tongue
 Rupture soon after appearance resulting in classic
appearance of erosive lesions
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Diagnostic tests
Clinical exam: for reticular LP with
characteristic appearance of Wickham’s
striae or annular pattern on erythematous
background
 Histological and Direct Immunofluorescent
examinations: for plaque and erosive LP
because they can resemble other mucosal
lesions including malignancy
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Diagnostic tests
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Histological exam
 Requires biopsy
 Varies based on the type of lesion
 Typically: epithelial hyperplasia, orto
and para
keratosis, acanthosis, atrophic areas w/ loss of rete
pegs, dense accumulation of T-lymphocytes in the
basilar cell layer
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Direct Immunofluorescent examination
 Requires
biopsy
 Differentiates between other autoimmune conditions
 Detects shaggy deposition of fibrinogen along the
basement membrane
Histology: Reticular Lichen Planus
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Consists of local areas of epithelial hyperplasia in which
the surface contains a thick layer of orthokeratin or
parakeratin.
The spinous cell layer may be thickened (acanthosis)
with shortened and pointed rete pegs. The thickened
areas are seen clinically as Wickham’s striae.
Between these areas the epithelium is thinned
(atrophic), with loss of rete peg formation.
The adjacent underlying c.t. contains a thin, dense
accumulation of T lymphocytes that move through the
basement membrane and are observed in the basilar
and parabasilar cell layers of the epithelium.
Histology: Erosive Lichen Planus
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Exhibit an extensively thinned epithelium with areas of
complete loss of rete peg formation and a dense infiltrate
of T lymphocytes.
This T lymphocyte infiltrate obscures the basement
membrane and extends well into the middle and upper
levels of the epithelium.
Liquefaction of the basement membrane and destruction
of the basal cells is present in most areas.
Occasionally, subepithelial separation will be present.
Often, the epithelium is lost, exposing the underlying
connective tissue.
The lymphocytes are confined to a narrow zone in the
upper layers of the connective tissue.
Histology: Plaque Lichen Planus
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Plaque LP resembles the histology of reticular LP
because of the striae pattern but it lacks the intermittent
atrophic areas of the epithelium.
It consists of generalized hyperorthokeratosis or
hyperparakeratosis combined with acanthosis.
There may be loss of rete pegs at the epithelial and
connective tissue interface or alteration of their shape
into a “saw-tooth” pattern.
The basement membrane is noticeably thickened.
The band of T lymphocytes present in the superficial
connective tissue is more sparse than In reticular LP,
with only occasional cells found in the lower levels of the
epithelium.
Treatment of OLP
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No treatment for OLP is curative
Goal:
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Eliminate exacerbating factors
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Repair defective restorations or prosthesis
Remove offending material causing allergy
Diet
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Reduce painful symptoms
Resolution of oral mucosal lesions
Reduce risk of oral squamous cell carcinoma
Improve oral hygiene
Eliminate smoking and alcohol consumption
Eat fresh fruit and vegetables (but avoid tomatoes and nuts)
Reduce Stress
Treatment of OLP
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Medication
 Topical
corticosteroids
0.05% clobetasol proprionate gel
 0.1% or 0.05% betamethasone valerate gel
 0.05% fluocinonide gel
 0.05% clobetasol butyrate ointment
 0.1% triamcinolone acetonide ointment
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 Can
be applied directly or mixed with Orabase
Treatment of OLP
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Medication
 Systemic
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Prednisone (for 70kg adult)
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1mg/kg/d for 6-8 weeks
Methylprednisolone (Medrol Dosepak)
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10-20mg/day for moderately severe cases
As high as 35 mg/day for severe cases
Should be taken in the morning to avoid insomnia
Should be taken with food to avoid peptic ulceration
Azathioprine (Imuran) – Inhibits synthesis of DNA
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Steroid Therapy
to reduce pain and inflammation
Prophylactic use of 0.12% dhlorhexidine gluconate may help
reduce fungal infection during corticosteroid therapy
Alternative Treatment of OLP
0.1% topical tacrolimus ointment 2x/day
 Tacrolimus: immunosuppresive macrolide
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 Suppresses
T-cell activation
Intraoral ulceration resolved after 3
months of daily application
 Remission for 1 year without maintenance
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Questions
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What cells are responsible for mediating the Oral Lichen Planus reaction.
A. B cells
B. Plasma cells
C. T cells
D. Macrophages
Answer: C. T cells
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What type of skin/mucosal disease is Lichen Planus:
A.Hereditary
B.Infectious
C.Autoimmune
D.Neoplastic
Answer: C. Autoimmune