lichen planus white lesion in the mouth

1. Lichen planus
Dr. Amitha
Dept of Oral pathology

2. Content
1. Introduction
2. History
3. Epidemiology
4. Definition
5. Etiology
6. Predisposing factor
7. Clinical features
8. Clinical variants of lichen planus
9. Histopathology

3. Oral Lichen Planus
Introduction
• Lichen planus is derived from the Greek word "leichen" means
tree moss and Latin word "planus" means flat.
• It’s a immunologically mediated mucocutaneous disease.
• First described by Wilson in 1869
• Affect 0.5–1% of the world’s population.
• This condition can affect either the skin or mucosa or both.
• Its cause bilateral white striations, papules, or plaques on the
buccal mucosa, tongue, and gingivae.

4. History
• Erasmus Wilson first described LP in 1869, as a chronic disease affecting the
skin, scalp, nails, and mucosa, with possible rare malignant degeneration.
• Francois Henri reported the first oral lichen planus (OLP)–related carcinoma in
1910.
• Thibierge first described the oral lesions symmetrically in 1893
• WICKHAM 1895 described the characteristic appearance of whitish striae and
punctuations that developed a flat surfaced papules

5. Epidemiology
• The overall prevalence of oral lichen planus among Indians was 1.5%
• Its 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.

6. Definition
Oral lichen planus (OLP) is as a common chronic immunological mucocutaneous disorder
of the stratified squamous epithelia.
• It’s a mucocutaneous disease. Which was first described by Wilson in 1869.
• Lichen planus (LP) is a relatively common disorder of the stratified squamous epithelia .
(Duske and Frick, 1982; Scully and El-Kom, 1985; Conklin and Blasberg, 1987; Jungell, 1991).
• Lichen planus (LP) is a common disorder in which auto-cytotoxic T lymphocytes trigger
apoptosis of epithelial cells leading to chronic inflammation. Oral LP (OLP) can be a
source of severe morbidity and has a small potential to be malignant. - Crispian Scully 2007

7. Etiology
• Inspite of extensive research ,exact etiology is still unknown.
• The most accepted and current data suggests that OLP is a T cell mediated
inflammatory disease,in which there is a production of cytokines which leads to
apoptosis. (Regezi et al., 1978) (Gilhar et al., 1989), (Porter et al., 1997) (Sugerman et al., 2002)
• Auto cytotoxic CD8 and T cells trigger apoptosis of oral epithelial cells.(Eversole
1997 porter et al 1997)
• Abnormal recognition and expression of basal keratinocytes of epithelium as
foreign antigens by langerhans cells.

8. • Other possible theories include the genetic background ,where the weak
association between HLA antigen and lichen planus (POWELL et al 1986 and roston 1994 )
• Strong association of psychological factors like higher level of anxiety, greater
depression and psychic disorders in patients with erosive lichen planus. (Vincent et al
1990 ,soto araya et al 2004)

9. Predisposing factor
Genetic background
An association has been observed with HLA-A3, A11, A26, B3, B5, B7, B8, DR1, and DRW9
Infectious agents
OLP has been suggested to be related to bacteria such as a Gram-negative anaerobic bacillus
and spirochetes but this has not been confirmed.
Viral agents such as human papilloma virus (HPV), Epstein Barr virus (EBV), human herpes
virus 6 (HHV-6) and human immunodeficiency virus (HIV).
HCV replication has been reported in LP lesions by reverse transcription/polymerase chain
reaction or in-situ hybridization.
HCV-specific CD4 and CD8 lymphocytes were reported in the subepithelial band.
These probably suggest that HCV-specific T lymphocytes may play a role in the pathogenesis
of OLP.

10. Predisposing factor
Habits
patients with habit of cigarette smoking, Betel nut chewing is more prevalent with OLP than
in those without the habit.
Diabetes and hypertension
Studies have revealed that both diabetes mellitus (DM) and high blood pressure are
associated with OLP.
Dental materials
Materials commonly used in restoration treatments in the oral cavity have been identified
as triggering elements for OLP (lichenoid drug reaction)
Drugs
Oral lichenoid drug reactions may be triggered by systemic drugs including NSAIDs, beta
blockers, sulfonylureas. (lichenoid drug reaction)

11. Clinical features
Race: Oral lichen planus affects all racial groups.
Gender: The female-to-male ratio is 1.4:1
Site : Affects the oral cavity bilaterally.
Oral lesions usually involve the posterior buccal mucosa, or less commonly the tongue and
although any site can be involved palatal and sublingual lesions are not common.
Age- middle aged or elderly people , Mean age of onset- 5th decade of life rarely in young
adults and children
Lichen planus commonly affects 1-2% of the general population ,prevalance rate being 0.5 to
2.2% , 40% lesions occur on both oral and cutaneous surfaces, 35% occur on cutaneous
surfaces alone, and 25% occur on oral mucosa alone

12. • The skin lesions of lichen planus appear as small, angular,
flat-topped papules only a few millimeter in diameter.
These may be discrete or gradually coalesce into larger
plaques, each of which is covered by a fine, glistening scale.
• The papules are sharply demarcated from the surrounding
skin.
• Early in the course of the disease the lesions appear red,
but they soon take on a reddish, purple or violaceous hue.
Later, a dirty brownish color develops.
• The center of the papule may be slightly umbilicated. Its
surface is covered by characteristic, very fine grayish-white
lines, called Wickham’s striae.

13. • The lesions may occur anywhere on the skin surface, but
usually are distributed in a bilaterally symmetrical
pattern, most often on the flexor surfaces of the wrist
and forearms, the inner aspect of the knees and thighs,
and the trunk.
• In chronic cases, hypertrophic plaques may develop,
especially over the shins.
• The primary symptom of lichen planus is a severe
pruritus that may be intolerable.
• In patients with OLP, scalp involvement (lichen
planopilaris) and nail involvement is rare.

14. Oral Manifestations
• In the oral cavity, lesions consist of radiating white, gray, velvety,
thread-like papules in a linear, annular and retiform arrangement
forming typical lacy, reticular patches, rings and streakes.
• A tiny white elevated dot is present at the intersection of white
lines known here as Wickham striae .
• The lesions are asymptomatic, bilaterally/symmetrically anywhere
in the oral cavity,
• Its most common on buccal mucosa, tongue, lips, gingiva, floor of
mouth, palate and may appear weeks or months before the
appearance of cutaneous lesions.

15. Types of oral lichen planus
OLP has six classical clinical presentations described in the literature:
1. Reticular
2. Erosive
3. Atrophic
4. Plaque-like
5. Papular
6. Bullous.

16. Reticular type lichen planus− on
the lips and mucosa of the cheek
1. Reticular
• Most common form.
• Commonly seen on posterior buccal mucosa.
• May not be seen on tongue ,less commonly in gingiva &lips
and vermillion border.
• They are usually bilaterally seen.
• Characteristic pattern of interlacing white lines (Wickham’s
striae).
• The striae often displays a peripheral erythematous zone
,which reflects the subepithelial inflammation.
• Lines are wavy and parallel.

17. 2. Erosive
• The lesions are usually symptomatic.
• Atrophic areas with central ulceration of varying degree.
• Periphery of the atrophic regions is usually bordered by
fine ,white radiating striae.
• Symptoms include Pain, burning sensation, bleeding,
desquamative gingivitis.
• Pseudo membrane covered ulcerations with keratosis and
erythema
Erosive type lichen
planus− ulcerated lesion in
the buccal mucosa with
erythematous borders

18. 3. Atrophic
• It is characterized by a homogenous red area.
• Smooth, poorly defined erythematus areas with or without
peripheral striae.
• Symptoms include Pain and burning sensation
• Keratotic changes combined with mucosal erythema
• When this type of OLP is present in the buccal mucosa or in the
palate striae are frequently seen in the periphery
Atrophic type lichen
planus− sometimes representing
as desquamative gingivitis

19. Plaque type lichen
planus− lesion on tongue
4. Plaque
• Plaque type OLP shows a homogenous well demarcated white
plaque often, but not always surrounded by striae.
• Common in tobacco users
• Single / multi focal

20. 5. Papular
• The papular type of OLP is usually present in the initial
phase of the disease.
• It is clinically characterized by small white dots, which
in most occasions intermingle with the reticular form.
• Sometimes the papular elements merge with striae as
part of the natural course.
• SIZE 0.5MM
Papular type lichen planus− lateral
border of tongue

21. 6. Bullous
• Vesciculobullous presentation combined with reticular or
erosive pattern
• Rare form characterized by large vesicles or bullae (4mm to
2cm)
• Lesions usually develop within an erythematus base, rupture
immediately leaving painful ulcers.
• Usually have peripheral radiating striae and seen on posterior
part of buccal mucosa.
• Severe form with extensive degeneration and separation of
epithelium from connective tissue.
Bullous type lichen planus− lesion
on upper buccal mucosa

22. • Faint white zone resembling radiating striae seen at the junction
with normal epithelium.
• Commonly seen on buccal mucosa and vestibule.
• Chance of malignant transformation.

23. Histopathology
• FIRST DESCRIBED BY DUBRENILL 1906 later revised by Shklar in 1972
• Hyper orthokeratinisation or hyper parakeratinisation
• Thickening of granular layer
• Acanthosis of spinous layer
• Intercellular oedema in spinous layer
• “ Saw-tooth” rete pegs
• Liquefaction necrosis of basal layer- Max Joseph cleft space
• Civatte ( hyaline or cytoid) bodies
• Juxta epithelial band of inflammatory cells
• An eosinophilic band may be seen just beneath the basement membrane and
represent fibrin covering lamina propria

24. Histopathology

25. “ Saw-tooth” rete pegs Basal cell degeneration