Lichen planus (LP) is a chronic mucocutaneous disorder of the stratified squamous epithelium that affects oral and genital mucous membranes, skin, nails, and scalp

1. Oral Lichen Planus
Presented by
Dr. Rahul Srivastava
Professor
Rama Dental College Hospital
& Research Centre Kanpur

2. Lichen planus (LP) is a chronic mucocutaneous
disorder of the stratified squamous epithelium that
affects oral and genital mucous membranes, skin,
nails and scalp.
Word lichen planus derived from the Greek word
“leichen” means tree moss and Latin word “planus”
means flat.

3. The designation and description of the pathology
were first presented by the English physician
Erasmus Wilson in 1866.
He considered this to be the same disease as “lichen
ruber,” previously described by Hebra and
characterized the disease as “an eruption of
pimples remarkable for their color, their figure,
their structure, their habits of isolated and
aggregated development.”

4. In 1892, Kaposi reported the first clinical variant
of the disease, lichen ruber pemphigoides.
In 1895, Wickham noted the characteristic
reticulate white lines on the surface of LP papules,
today recognized as Wickham striae.
Darier is credited with the first formal description
of the histopathological changes associated with
LP.

5. Etiology of oral lichen planus
Exact etiology is still unknown, but some factors
are associated with it. These are as follows:
1- Genetic background
Familial cases are rare. An association observed
with HLA-A3, A11, A26, A28, B3, B5, B7, B8, DR1,
and DRW9.

6. 2- Dental materials
Silver amalgam, gold, cobalt, palladium, chromium
and even non-metals such as epoxy resins
(composite) and prolonged use of denture wear.

7. 3- Drugs
Oral lichenoid drug reactions triggered by systemic
drugs like: NSAIDs, beta blockers, sulfonylureas,
some angiotensin-converting enzyme (ACE)
inhibitors, antimalarials, contact allergens
including toothpaste flavorings, especially
cinnamates.

8. 4- Infectious agents
A- Hepatitis C virus (HCV)
B- Epstein Barr virus (EBV).
C- Human herpes virus 6 (HHV-6).
D- Human immunodeficiency virus (HIV).
5- Autoimmunity.
6- Stress.
7- Diabetes and hypertension.

9. Pathophysiology
Cellular-mediated immunity, initiated by
predisposing factors results in the production of
Tumor Necrosis Factor-alpha (TNF-a), Interferon-
cytokine (IFN-c), and keratinocyte, T cell or antigen-
presenting cell associations.

10. The increased production of T-helper 1 (Th1)
cytokines occurs in the early event in OLP, genetic
polymorphism of cytokines and IFN-gamma will
lead to the development of oral mucosal lesions,
increase in the frequency of 308A TNF-alpha allele
will lead to the development of skin lesions.

11. A hypothesis of the pathogenesis of OLP was
introduced by Sugerman et al. and is based on a
theoretical interaction between CD8+ T cells and
CD4+ T cells through a “request cytotoxic
activity” (RCA) cell surface molecule.
The activated CD8+T cells can trigger
keratinocytes apoptosis through TNF-alpha or a
Fas–Fas Ligand mechanism.

12. The role of metalloproteinases(MMPs) and tissue
inhibitors of metalloproteinases(TIMPs) are proven to
initiate pro-inflammatory cytokines which will lead
to inflammation.

13. RANTES (regulated on activation, normal T cell
expressed and secreted) a chemokine family also
plays a role in pathogenesis by activating the
number of cells like lymphocytes, monocytes,
natural killer cells, eosinophils, basophils, and
mast cells in oral lichen planus and the cell surface
receptors are also increased.

15. Clinical features of lichen planus:
The lesions show white striations, which are
slightly elevated, fine, whitish lines known as
Wickham’s striae (Honiton lace).
Usually affect buccal mucosa, ventral and lateral
borders of tongue, gingiva and floor of the mouth.
Lingual papillae become atrophied in the areas of
involvement and the resulting smooth surface
accentuates the white striae.

16. Gingival lesions present as fiery red areas
affecting the entire width of attached gingiva called
desquamative gingivitis.
It is associated with intense sensitivity of gums to
hot or spicy food or brushing of teeth with intense
burning sensation to pain.
Skin lesions described by the six p's:
Planar, plaque, pruritic, purple, polygonal, and
papular.

17. They may be discrete and gradually coalesce in to
large plaques each covered with fine glistening
scale.
Early in onset of disease they appear red, soon
they take on reddish purple or violaceous colour.
Skin lesions commonly involve flexor surface of
legs and arms, especially the wrists, forearms,
inner aspect of thighs, trunk especially in sacral
areas.

18. Nail beds may also be affected with resultant
ridging, thinning and subungual hyperkeratosis.
Scalp involvement, if untreated can lead to
scarring and permanent hair loss.
Patients are often unaware of quiescent OLP,
which may be present only with faint white
striations, papules or plaques.

19. Exacerbations of OLP have been linked to periods
of psychological stress, anxiety or mechanical
trauma. This phenomenon is referred as Koebner’s
phenomenon.

20. Vulvovaginal-gingival syndrome
Association of LP of vulva, vagina and gingiva is
recognized as vulvovaginal-gingival syndrome.
Graham-Little syndrome
The combination of follicular LP with scarring
alopecia of scalp and non-scarring alopecia of
axilla and pubis or other areas is known as
Graham-Little syndrome.

21. Greenspan syndrome
Triad of Diabetes mellitus, hypertension and oral
lichen planus.

22. Clinical Presentation of Oral
Lichen Planus

23. Reticular
It is the most common clinical form of this disease
and presents with fine, asymptomatic intertwined
lace-like pattern called “Wickham striae” in a
bilateral symmetrical form and involves the
posterior mucosa of the cheek in most cases.

24. Erosive
This is the most significant form of the disease
because it shows symptomatic lesions often
surrounded by fine radiant keratinized striae with
a network appearance.

25. Atrophic
It exhibits diffuse red lesions and it may resemble
the combination of two clinical forms, such as the
presence of white striae characteristic of the
reticular type surrounded by an erythematous area.
Atrophic type lichen planus−sometimes representing as desquamative
gingivitis

26. Plaque-like
This type shows whitish homogeneous irregularities
similar to leukoplakia; it mainly involves the
dorsum of the tongue and the mucosa of the cheek.

27. Papular
This form is rarely observed and is normally
followed by some other type of variant described. It
presents with small white papules with fine striae
in its periphery.

28. Bullous
It is the most unusual clinical form, exhibiting
blisters that increase in size and tend to rupture,
leaving the surface ulcerated and painful.
Nikolsky’s sign may be positive.

29. Gingival Involvement
The gingival lesions in LP fall into one or more of
the following categories:
Keratotic lesions are usually present on the
attached gingiva as small raised round white
papules of pinhead size with a flattened surface.

30. Vesiculo-bullous lesions are other mucocutaneous
disorders especially pemphigoid, dermatitis
herpetiformis or linear IgA disease.
Atrophic and Erosive: Produce the desquamative
gingivitis.

31. Pigmentation is frequently associated with OLP?
Degenerative changes in basal keratinocytes
frequently led to pigmentary incontinence.
Gamma-aminobutyric acid (GABA) imbalance occurs
in anxiety disorders and might be passed through
the cranial nerve, stimulating production of
melanocytes, resulting in excessive deposition in
OLP.

32. Investigations for lichen planus
Direct Immunofluorescence
Fibrinogen and fibrin are deposited in a linear
pattern in the BM zone. Colloid bodies contain
fibrin, IgM, C3, C4 and keratin. Laminin and
fibronectin staining may be absent in areas of heavy
fibrin deposition and colloid body formation. This
finding suggests BM damage in these areas.

33. Immunohistochemical (Ihc) Studies
Immunohistochemical staining using the antibody to
the S-100 protein indicates an increase in
langerhan cells in mid layer of the epithelium.
Serology
There are no consistent serological changes
associated with OLP but some patients do present
an elevated antinuclear antibody (ANA) titer.

34. Biopsy
Histopathology
Liquefactive degeneration of the basal cell
accompanied by apoptosis of the keratinocytes, a
dense band-like lymphocytic infiltrate at the
interface between the epithelium and the connective
tissue.
Focal areas of hyperkeratinized epithelium (which
give rise to the clinically apparent Wickham’s
striae).

35. Occasional areas of atrophic epithelium where the
rete pegs may be shortened and pointed (saw tooth
rete pegs).
Eosinophilic colloid bodies (Civatte bodies).

36. Treatment of lichen planus
A- Topical agents
1- Corticosteroids
0.05% clobetasol propionate gel, 0.1% or 0.05%
betamethasone valerate gel, 0.05% flucinonide gel,
0.05% clobetasol butyrate ointment or cream and
0.1% triamcinolone acetonide ointment.

37. 2- Retinoids
Isotretinoin gel 0.1%, topically administered
Vitamin A, beta-all-trans retinoic acid all are
effective.
3- Topical Tacrolimus
Tacrolimus ointment is available in two strengths:
0.1% and 0.03%. The 0.1% formulation twice daily
is more effective in erosive lichen planus.

38. 4- Intralesional injection
Intralesional steroids such as triamcinolone
acetonide (10– 20 mg/ml) injections can be effective
and repeated every 2–4 weeks.
B- Systemic Steroid Therapy
The oral dose of prednisone for 70-kg adult ranges
from 10-20 mg/day for moderately severe cases to as
high as 35 mg/day (0.5 mg/kg daily) for severe
cases.

39. C- Griseofulvin
It is administered systemically in doses of
500mg/day to 1 gm/day.
D- Azathioprine
Azathioprine in doses of 50 to 100mg/day in
combination with systemic steroids shows positive
response.
E- Efalizumab
Efalizumab therapy with initial dose of 0.7mg/kg
followed by dose of 1.0 mg/kg per week for 5 week
provide good results.

40. F- Surgical excision, cryotherapy, CO2 laser, and
ND:YAG laser have all been used in the treatment of
OLP.
G- Photo chemotherapy, uses ultraviolet A (UVA) with
wavelengths ranging from the 320 to 400 nm, after
the injection of psoralen (8-Methoxypsoralen, 0.4-0.6
mg/kg) is also used.

41. References
1- Serrano-Sanchez P, Bagan JV, Jimenez-Soriano,
Sarrion G. Drug induced oral lichenoid reactions. A
literature review. J Clin Exp Dent 2010;2:e71-5.
2- Scully C, Carrozzo M. Oral mucosal disease:
Lichen planus. Br J Oral Maxillofac Surg
2008;46:15-21.
3- Scully C, Beyli M, Ferreiro MC, Ficarra G, Gill Y,
Griffiths M, et al. Update on oral lichen planus:
Etiopathogenesis and management. Crit Rev Oral
Biol Med 1998;9:86-122.

42. 4- Issa Y, Brunton PA, Glenny AM, Duxbury AJ.
Healing of oral lichenoid lesions after replacing
amalgam restorations: A systematic review. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod
2004;98:553-65.
5- Wray D, Rees SR, Gibson J, Forsyth A. The role of
allergy in oral mucosal leisons. QJM
2000;93:507-11.
6- Moravvej H, Hoseini H, Barikbin B, Malekzadeh R,
Razavi GM. Association of Helicobacter pylori with
lichen planus. Indian J Dermatol 2007;52:138-40.

43. 7- Vainio E, Huovinen S, Liutu M, Uksila J, Leino R.
Peptic ulcer and Helicobacter pylori in patients with
lichen planus. Acta Derm Venereol 2000;80:427-9.
8- Hulimavu SR, Mohanty L, V Tondikulam N, Shenoy
S, Jamadar S, Bhadranna A. No evidence for
Helicobacter pylori in oral lichen planus. J Oral
Pathol Med 2014;43:576-8.
9- Ertugrul AS, Arslan U, Dursun R, Hakki SS.
Periodontopathogen profile of healthy and oral
lichen planus patients with gingivitis or
periodontitis. Int J Oral Sci 2013;5:92-7.