Oral lichen planus (OLP) is a chronic inflammatory disease that affects the oral mucosa. It is characterized by white striations or plaques on the buccal mucosa, tongue, and gingiva. The precise cause is unknown, but it is considered a T-cell mediated autoimmune reaction where cytotoxic CD8+ T-cells trigger apoptosis of oral epithelial cells. OLP has several clinical variants including reticular, papular, plaque-like, atrophic/erythematous, erosive/ulcerative, and rare bullous forms. It predominantly affects middle-aged women and can cause pain.

1. CONTENTS
Introduction
Aetiology
Pathogenesis
Clinical variants
Oral Lichen Planus

2. Is a chronic systemic mucocutaneous disease
affecting either the skin or mucosa
OLP has been classified as an OPMD i.e oral
potentially malignant disorder by WHO
OLP is characterised by bilateral interlacing
white striations, papules or plaques on the buccal
mucosa, tongue and gingiva.
• Oral mucous membrane is frequently involved
• Other sites involve skin and genital mucous
membrane.
LICHEN PLANUS

3. • Sir Erasmus Wilson coined the term Lichen planus
in 1869
• Lichen Planus is a Greek word:
i. Lichen meaning tree moss and
ii. Planus meaning white
 It obtained its name because of the lacy white lines that bear a
close resemblance to the symbiont, lichen, a composite
organism consisting of
1. a fungus (the mycobiont) and
2. a photosynthetic partner (the phycobiont, usually, a green
algae) living together in a symbiotic relationship, seen growing
on rocks.

4. • The precise cause of OLP is unknown
• However the data available suggests that OLP is a T
cell mediated autoimmune disease in which cytotoxic
CD 8+cells trigger the apoptosis of oral epithelial
cells.
TRIGGERING / ETIOLOGICAL FACTORS:
Aetiology

5. Lichenoid Reaction (LR)
 Represent a group of lesions similar to
LICHEN PLANUS clinically and
histologically .
 May involve skin or mucosa
 Unlike Lichen Planus, the underlying cause
is identifiable and withdrawal of the same
leads to remission of the lesion.

6. Pathogenesis
 Initiating factor: antigenic stimulation
(endogenous/exogenous)that serves as the
trigger and/or driver of the immune responses .
 It is likely, in the majority of cases, to be an
endogenous peptide, a protein sequence innate
to the basal keratinocyte; therefore, OLP can be
characterised as an auto-immune condition.
 Supposed exogenous triggers for OLP serve to
expose such self-antigens or alter the normal
innate peptide sequences so that they are
perceived by the immune-surveillance cells and
system as being “non-self, that is “foreign”.

7. The immune responses to this
unidentified antigen develops in three
stages:
(1) T-cell migration into the epithelium
(2) T-cell activation followed by
(3) Induction of basal keratinocyte
apoptosis

8. T cell migration into Epithelium
The “chance
encounter” hypothesis
suggests that normally
circulating, antigen-
specific CD8+ cytotoxic
T-cells enter the
epithelium for routine
surveillance and by
chance encounter the
antigen when it is
present in the
epithelium.
The “Directed
migration” hypothesis
suggests that the
keratinocytes direct the
CD8+ cytotoxic T-cells
to migrate into the
epithelium by the
release of keratinocyte
- derived chemokines
that allow the
lymphocytes to “home-
in” on the antigen-
bearing basal

9. T cell activation
 Cytotoxic CD8+ T-cells binding of antigen on the MHC
Class I site of keratinocytes releases cytokines that attract
other lymphocytes and immune-cells into the site of the
developing OLP lesion.
Basal Keratinocyte Apoptosis
 After antigen recognition and T- cell activation ,
CD8+ T cells may trigger keratinocyte apoptosis.

11.  Grinspan’s syndrome :
Association of
a) lichen planus
b) Diabetes
c) Hypertension
Is said to occur due to the unmasking of LP antigen by :
Anti -hypersensitive drugs
Anti -diabetic drugs
 Koebners phenomenon :
 Isomorphic phenomenon
 appearance of lesions on previously healthy skin or oral
mucosa
 occurs due to mechanical irritation or micro trauma usually.

12. C/F of Lichen Planus
 Shows a female predilection
 Majorly affects adults over 40 years of age
 Skin lesions show 6 P features i.e
1. PLANAR ( flat topped)
2. PRURITIC
3. PURPLE
4. POLYGONAL
5. PAPULE
6. PLAQUE - like

13. C/f of OLP
 Sites involved
1. Buccal mucosa 80%
2. Tongue 65%
3. Lips 20%
4. Gingiva , floor of the mouth, palate < 10%
 WICKHAM’S STRIAE
tiny white elevated intersecting lines or dots usually
present at the periphery of the lesion
 Appears similar to Honiton lace

14. Various clinical patterns OLP seen in
oral cavity
a. Reticular (most common)
b. Papular form
c. Plaque like
d. Atrophic/Erythematous
e. Erosive/Ulcerative
f. Bullous/ Vesicular form (rare forms)

15. Reticular type of OLP
 Most common form
 Characterised by radiating white , grey ,
velvety thread like papules in a linear ,
retiform/ annular arrangement forming
typical lacy white patches , rings or streaks

16. Papular form of OLP
Elevated , pinhead sized white dots which
intermingle with the reticular form

17. Plaque type of OLP
• Closely resembles
Leukoplakia
• However can be
differentiated from
Leukoplakia by the
presence of
peripherally white
interlacing strands
• Common in tobacco
smokers

18. Erosive form of OLP
• Eroded, raw ,
ulcerated and
irregular lesions
• Occurs due to
epithelial
destruction as
result of
degeneration in
the basal layer
• Often painful
• Peripheral white
striations can be

19. Atrophic form of LP
Appears as
smooth ,
Red , poorly
defined areas
May or may not
show the
presence of
peripheral straie.

20. Bullous/Vesicular form of OLP
Rare form – Short lived
On rupturing leave an ulcerated
surface and appear similar to
erosive form
erosive type of OLP – if severe
may lead to epithelial
separation causing in a bulla
formation.

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