Lichen Planus

malabar dental college
malabar academic city
mdc

1. LICHEN PLANUS
-Part 1
Dr Shabil Mohamed Mustafa
Associate Professor
Malabar Dental College and Research Centre

2. Contents
•Introduction
•Etiology
•Pathogenesis
•Clinical types
•Histopathology
•Immunopathology
•Management
§ Conclusion
•References

3. Introduction

• Lichen planus (LP) is defined as a subacute, chronic dermatosis
characterized by small, flat- topped, shiny, polygonal violaceous papules that may
coalesce into plaques.
•Inflammatory dermatologic disease of skin, mucous membrane, hair and nails –
0.5-1% of world population
Bernard criber ,Treatment of lichen planus,Dermatology 2008;6(3):217-232

4. ORAL LICHEN PLANUS : a chronic inflammatory autoimmune
mucocutaneous disease that affects the oral mucosa.
•Common disorder of the stratified squamous epithelium.
•White lesion – 9%
•Course is generally seilf limited to a period of several months to years, but may last
indefinitely.
•WHO categorized LP as a POTENTIALLY MALIGNANT DISORDERS
Indicators of risk of future malignancy

5. Historical aspect
• 1869 - Erasmus wilson.
•Previous term - Hebra
•Greek – leichen (algae and fungi)
•Latin – planum (flat).
•1885- Thiebiergi gave more detailed discription.
•1982 – Unna gave about whitelines and striae disciption.

6. Epidemiology
•World wide distribution – 1.9 -2%
•40- 50% both oral and cutaneous lesion
•15- 20% only oral lesion.
•Prevelance among Indians – 1.5%.

7. •Affect all racial group.
•F:M = 1.4:1
•Age>40
•1/3
rd
pts - asymptomatic

8. •Oral manifestation appears weeks or months before skin lesion,
relatively persistant over time. Corresponding skin lesion tends to
waxe and wane.
•Appear as small, angular, flat topped papules only few millimeter in
diameter. May be discrete or gradually coalesce in to larger plaques.
Each of which covered by glistening scale.
•Red- reddish purple or violaceous hue – dirty brown colour.
Covered by fine greyish white lines – wickhams striae.
•Untreated cases can perists for more than 10 years.
•Good response to corticosteroids.

9. •OLP – oral cavity – bilateral
•Buccal mucosa, tongue and gingiva
•Other mucosal inv- flexor surface of wrist & forearm, inner
aspect of knees , thighs & trunk . Scalp & nail- rare.
•Face – remain uninvolved

10. Shklar &McCarthy have reported the following distribution of oral
lesions
•Buccal mucosa- 80%
•Tongue - 65%
•Lips - 20%
•Gingiva,FOM &palate-10%

11. Etiology
•Unknown
•There is interplay of host factors, environmental factors &
life style
•Cell mediated immunity
•Other factors
Genetic background – HLA-B8
Emotional stress
Tobacco
Trauma
Microorganisms and infections

12. Psychological factors
ØPatients with OLP exhibit higher levels of anxiety,
greater depression and increased vulnerability to
psychic disorders .

ØThe level of anxiety and salivary cortisol of OLP
patients are high, supporting the relationship of OLP
with stress
12

13. Pathogenesis
vMechanisms Antigen specific cell
mediated immune response Non specific mechanisms
Autoimmune response Humoral
immunity

14. Antigen specific cell mediated immune response
•Antigen presentation by basal keratinocytes

15. •Migration of T lymphocytes
Chance encounter hypothesis
Directed migration hypothesis
•Antigen-specific keratinocyte killing by CD8
+
cytotoxic T-
cells

16. Non specific mechanism
Epithelial basement membrane

17. •Matrix metalloproteinases activation:
Zn containing endo proteinases with 20members
Function – proteolytic degradation of connective tissue matrix proteins
Gelatinases (2,9)- cleave collagen IV
Stomelysins (3,10) – cleave collagen IV & laminin
•Basement membrane – disruption

18. Chemokines – pro inflammatory cytokines
RANTES – produced by activated lymphocyte clonal
expansion- attract mast cells – stimulate degranulation- TNF
α, chymase, triptase.

19. •Accumulation of inflammatory cytokine ---
IL1 ---
Activation of several prostaglanding mediated events via COX 2
enzyme---

Carcinogen activation---
Tumor initiation.

20. Autoimmunity
•OLP – auto immune disease
•Role of autoimmunity – supporting features

21. Humoral immunity
•Circulating antibodies identified including autoantibodies against desmogleins 1
&3
•Exact role – unknown
(Pathogenesis of Oral lichen planus –a review,J Oral Pathol Med ,2010;39 :729-734)

22. Classification of lichen planus variants
Boyed AS, NeldnerKH, lichen planus J Am Acad Dermatol.1991;25:593-619
•Configeration- annular
linear.
•Morphology-classic
Hypertrophic
Atrophic
Vesiculobullous
Erossive & ulcerative
Follicular
Actinic
Lichen planus pigementosus
Exfoliative
Perforating
Guttate
Invisible
zosteriform
•Site of involvement- palms &soles
Mucousmembrane
Nails
Scalp
•Special forms- drug induced
Lichen planus- LE overlap
Lichen planus pemphigoides
Keratosis lichenoides chronica
Lichen planus & malignant transformation
Lichenoid reaction on GVHD
Lichenoid keratosis
Lichenoid dermatitis.

23. Clinical types
•Reticular
•Papular
•Plaque like
•Erosive
•Atrophic
•Bullous
Classification given by Andreson 1968.

24. Keratotic White &red
•Reticular
•Annular
•Papular
•Linear
•Floral
•Plaque like
•Atrophic
•Erosive
•Bullous

25. Eisen (2002) J Am Acad Dermatol 2002
•Reticular (white lines, plaque and papules)
•Atrophic or erythematous
•Erosive (ulcerations and bullae)
25

26. •Various clinical forms of oral lichen planus and
their incidence
26

27. THANK YOU