Oral Lichen Planus

Dr . Gaurav S. Salunkhe 2ND MDS

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

Picture 1: Plaque-like OLP Picture 2: Reticular OLP

Picture 3: Erosive OLP Picture 4: Reticular OLP

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.

Proposed Immunopathogenesisof 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.

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 lesions30-50% of pts also have cutaneous lesionsThree common types

Reticular Erosive PlaqueVariants of Plaque and Erosive types

AtrophicBullous

Clinical Presentation

Reticular lesionsMost common type Interlacing white kerototic lines w/

erythematous borders (Wickham’s striae)Typically bilaterally on buccal mucosa,

mucobuccal fold and gingivaLess common on tongue, palate and lipsAssymptomatic

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

Clinical Presentation

Variants of Erosive and Plaque lesionsAtrophic

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

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

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

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.

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.

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.

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

Treatment of OLP

MedicationTopical 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

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

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