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Oral Lichen Planus Overview

1. Oral lichen planus is a chronic inflammatory disease that affects around 0.5-1% of the population. It is characterized by relapses and remission and is caused by an immune response against an unknown antigen. 2. Clinically, it presents as white striations or plaques on the oral mucosa in reticular, plaque, erosive, or atrophic forms. Histopathology shows hyperorthokeratosis, sawtooth rete pegs, a subepithelial lymphocytic infiltrate, Civatte bodies, and degeneration of basal keratinocytes. 3. The pathogenesis involves migration of cytotoxic CD8 T cells into the epithelium where they are activated
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0% found this document useful (0 votes)
195 views29 pages

Oral Lichen Planus Overview

1. Oral lichen planus is a chronic inflammatory disease that affects around 0.5-1% of the population. It is characterized by relapses and remission and is caused by an immune response against an unknown antigen. 2. Clinically, it presents as white striations or plaques on the oral mucosa in reticular, plaque, erosive, or atrophic forms. Histopathology shows hyperorthokeratosis, sawtooth rete pegs, a subepithelial lymphocytic infiltrate, Civatte bodies, and degeneration of basal keratinocytes. 3. The pathogenesis involves migration of cytotoxic CD8 T cells into the epithelium where they are activated
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Dr Meenakshi

MDS Oral Pathology


CONTENTS

Introduction

Epidemiology of Oral Lichen Planus

Aetiopathogenesis of Oral Lichen Planus

Clinical Features

Histopathology

Summary
Oral Lichen Planus: (Lichen ruber planus)
 Lichen planus is a relatively common, chronic dermatologic
disease that often affects the oral mucosa.

 Oral lichen planus (OLP) is a common mucocutaneous disease.


It was first described by Wilson in 1869 and is thought to affect
0.5–1% of the world's population.

 Lichens are primitive plants composed of symbiotic algae and


fungi. The term planus is Latin for flat. Wilson probably
thought that the skin lesions looked similar enough to the
lichens growing on rocks to merit this designation.

 Even though the term lichen planus suggests a flat, fungal


condition, current evidence indicates that this is an
immunologically mediated muco-cutaneous disorder.
The condition can affect either the skin or
mucosa or both. It can cause bilateral white
striations, papules, or plaques on the buccal
mucosa, tongue, and gingivae.

Erythema, erosions, and blisters may or may


not be present.

The involvement of the oral mucous membrane


is so frequent and accompanies or precedes the
appearance of lesions on the skin and genital
mucous membrane.
INTRODUCTION
 Oral lichen planus is a chronic inflammatory disease
characterized by relapses and remission.

 It is a cell-mediated immune condition.

T lymphocytes accumulate beneath the epithelium of the oral


mucosa.

 Increased rate of differentiation of the stratified squamous


epithelium, resulting in hyperkeratosis and erythema with or
without ulceration.
Epidemiology
The overall prevalence of oral lichen planus among Indians
was 1.5%; it was highest (3.7%) in those people with mixed
oral habits and lowest (0.3%) in nonusers of tobacco.

The annual age-adjusted incidence rate was 2.1 and 2.5 per
1,000 among men and women, respectively (Bhonsle et al,
1979).

The relative risk for oral lichen planus was highest (13.7)
among those who smoked and chewed tobacco.
Etiology

An interesting association of Lichen planus, Diabetes Mellitus and Vascular


Hypertension has been described by Grinspan, the triad being described as
Grinspan's syndrome by Grupper.
Etiopathogenesis
AETIOPATHOGENESIS

Majority of T- cells adjacent to


damaged basal keratinocytes are
CD8+ T cells
AETIOPATHOGENESIS
Specific immune response to the unidentified antigen involves
following steps

1. Migration of T lymphocytes in to the


epithelium

2. Activation of T lymphocyte

3. Killing of keratinocytes
AETIOPATHOGENESIS
1. Migration of T lymphocytes in to the epithelium
a. Chance encounter hypothesis
b. Directed migration hypothesis

2. Activation of T lymphocyte

The lymphocytic infiltrate in OLP


is composed almost exclusively of
T cells and majority of T cells
within the epithelium and adjacent
to damaged basal keratinocytes are
activated CD8 lymphocytes
AETIOPATHOGENESIS
3. Killing of keratinocytes
 Activated cytotoxic T cells kill the basal keratinocytes.

 Apoptosis has been proposed as mechanism of keratinocytes


death

 Possible mechanisms of keratinocytes apoptosis are

Pathogenesis of oral lichen planus- a review. J oral pathol med (2010) 39: 729-734
Lichen planus antigen is unknown, although it
may be self peptide.

The expression or unmasking of the lichen planus


antigen may be induced by drugs, contact
allergen, mechanical trauma, viral infects or
unidentified agents.
CLINICAL FEATURES
OLP affects all racial groups with female-to-male ratio of
1.4:1.

Predominantly occur in adults older than 40 yrs, although


younger adults and children can be affected.

Skin lesions of Lichen planus appear as small, angular, flat


topped papules only a few milimeter in diameter.

May be discrete or gradually coalesce in to larger papules

Sharply demarcated

Red to reddish purple or violaceous hue to dirty brownish


CLINICAL FEATURES
CLINICAL MANIFESTATIONS

PLAQUE FORM
RETICULAR
FORM EROSIVE FORM
LICHEN
PLANUS
BULLOUS FORM
Oral Manifestations

Lesions consisting of radiating white or gray, velvety,


thread-like papules in a linear, annular or retiform
arrangement

A tiny white elevated dot is frequently present at the


intersection of the white lines, known here also as the
Striae of Wickham.
RETICULAR FORM
Papule surface is covered by characteristic,
WICKHAM’S very fine grayish white line
STRIAE

Bilaterally
symmetrical
PLAQUE FORM

Plaque –like form


Clinically resembles leukoplakia
Range from smooth, flat areas to
irregular, elevated areas
EROSIVE FORM
 Second most common type.

Patients with this form of


OLP often present with
symptoms ranging from
episodic pain to severe
discomfort that can interfere
with normal mastication

Desquamative gingivitis
ATROPHIC AND BULLOUS FORM
 Both are considered variants of the erosive type.

Atrophic form Bullous form

Diffuse erythematous
patches surrounded
by fine white striae
HISTOPATHOLOGY
Hyperorthokeratosis with thickening of the granular layer,
acanthosis with intracellular edema of the spinous cells

The development of a ‘saw tooth’ appearance of the rete


pegs.

Band-like subepithelial mononuclear infiltrate consisting of


T-cells and histiocytes;

Increased numbers of intraepithelial T-cells; and degenerating


basal keratinocytes that form colloid (Civatte, hyaline,
cytoid) bodies, which appear as homogenous eosinophilic
globules
Degeneration of the basal keratinocytes and disruption of the
anchoring elements of the epithelial basement membrane and
basal keratinocytes (e.g. hemidesmosomes, filaments, fibrils)
weakens the epithelial-connective tissue interface. As a result,
histologic clefts (i.e. Max-Joseph spaces) may form.
HISTOPATHOLOGY
SUMMARY

PLAQUE FORM
RETICULAR
FORM EROSIVE FORM

ERYTHEMATOUS
OR ATROPHIC
FORM BULLOUS
FORM

1. Migration of T lymphocytes in to the epithelium


2. Activation of T lymphocyte
3. Killing of keratinocytes
MCQs
Q 1. Lichen types include all except
 ulcerative
 reticular
 erosive
 atrophic

Q 2. Compy’s sign (white patches due to degenerated squamous


epithelium occurring on buccal Mucosae and gums) is seen in
 Moniliasis
 Pemphigus
 Lichen planus
 Measles
Q 4. Civatte bodies are found in
  Lichen planus
  Psoriasis
  Dermatophytosis
  Vitiligo

Q 5. Wickham`s striae are found in


  reticular form of lichen planus
  erosive form of lichen planus
  popular lichen planus
  bullous lichen planus

Q 3. Pterygium of nail is characteristically seen in:


  Lichen planus
  Psoriasis
  Tinea unguium
  Alopecia areata

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