olp

1. Oral Lichen Planus
Dr . Gaurav S. Salunkhe
2ND
MDS

2. Introduction
 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

3. Picture 1: Plaque-like OLP Picture 2: Reticular OLP
Picture 3: Erosive OLP Picture 4: Reticular OLP

4. Pathogenesis of Reticular LP
 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.
 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.

5. Proposed Immunopathogenesis
of OLP
 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.

6.  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.

7. 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

8. Clinical Presentation
 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

9. Clinical Presentation
 Erosive lesions
 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:
 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

10. Clinical Presentation
 Variants of Erosive and Plaque lesions
Atrophic
 Diffuse, erythematous patches
 Causes significant discomfort
 Gingiva and buccal mucosa
Bullous
 Intraoral bullae on buccal mucosa and lateral
surface of tongue
 Rupture soon after appearance resulting in classic
appearance of erosive lesions

11. 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

12. Diagnostic tests
 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
 Direct Immunofluorescent examination
 Requires biopsy
 Differentiates between other autoimmune conditions
 Detects shaggy deposition of fibrinogen along the
basement membrane

13. Histology: Reticular Lichen Planus
 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.

14. Histology: Erosive Lichen Planus
 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.

15. Histology: Plaque Lichen Planus
 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.

18. Treatment of OLP
 No treatment for OLP is curative
 Goal:
 Reduce painful symptoms
 Resolution of oral mucosal lesions
 Reduce risk of oral squamous cell carcinoma
 Improve oral hygiene
 Eliminate exacerbating factors
 Repair defective restorations or prosthesis
 Remove offending material causing allergy
 Diet
 Eliminate smoking and alcohol consumption
 Eat fresh fruit and vegetables (but avoid tomatoes and nuts)
 Reduce Stress

19. Treatment of OLP
 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
Can be applied directly or mixed with Orabase

20. Treatment of OLP
 Medication
 Systemic Steroid Therapy
 Prednisone (for 70kg adult)
 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
 1mg/kg/d for 6-8 weeks
 Methylprednisolone (Medrol Dosepak)
 to reduce pain and inflammation
 Prophylactic use of 0.12% dhlorhexidine gluconate may help
reduce fungal infection during corticosteroid therapy

21. Alternative Treatment of OLP
 0.1% topical tacrolimus ointment 2x/day
 Tacrolimus: immunosuppresive macrolide
Suppresses T-cell activation
 Intraoral ulceration resolved after 3
months of daily application
 Remission for 1 year without maintenance