Lichenoid Dermatoses, Characteristics of Lichenoid Dermatoses, What are the Major Lichenoid Dermatoses, Lichen planus (LP), Introduction of LP, Epidemiology of LP, Etiology of LP, Pathogenesis of LP, Clinical Features & Clinical variants of LP, Histopathology of LP, Immunohistochemistry of LP, Differential Diagnosis of LP, Treatment of LP

1. Lichenoid Dermatoses

3. Lichenoid Dermatoses
They represent a heterogeneous
inflammatory group of
conditions that resemble
idiopathic LP in terms of their
clinical appearance and
histological appearance
demonstrating lichenoid tissue
reaction characterized by;
• Liquefaction degeneration of epidermal basal cells
• Band-like infiltrate primarily lymphocytes in the papillary dermis.

4. Major Lichenoid Dermatoses
1. Lichen planus
2. Lichen striatus
3. Lichen nitidus
4. Graft-versus-host disease
5. Erythema dyschromicum
perstans
6. Lichenoid drug eruption
7. Fixed drug eruption
8. Keratosis lichenoides
chronica
9. Pityriasis Lichenoides
10. Erythema multiforme
11. Lupus erythematosus
12. Dermatomyositis
13. Paraneoplastic pemphigus
14. Mycosis fungoides
15. Lichenoid pigmented
purpura
16. Secondary syphilis
17. Lichen sclerosus (Lichen
sclerosus et atrophicus)

6. Lichen planus

7. Lichen planus (LP)
• Introduction
• Epidemiology
• Etiology
• Pathogenesis
• Clinical Features & Clinical variants
• Histopathology
• Immunohistochemistry
• Differential Diagnosis
• Treatment

8. Introduction
• LP is an idiopathic inflammatory
papulosquamous disease of the skin and
mucous membranes with varying clinical
presentation.
• Where the trigger is known, a lesion is known
as a lichenoid lesion.
• Lichen planus lesions are so called because of
their "lichen-like" appearance.

10. Epidemiology
• PREVALENCE:
– Cutaneous LP 0.2% to 1% of the adult population.
– Oral LP have been observed in up to 1–4% of the population.
• AGE:
– Onset of LP occurs most commonly during the fifth or sixth
decade.
– LP is rare in both infants and the elderly but it is more common
in children in Arab populations.
• SEX: Females>males.

11. Etiology
• Exact etiology is unknown

12. Etiology
• Autoimmune reaction against epitopes on lesional keratinocytes that may have been modified by
any of the following factors;
1. VIRAL INFECTION: hepatitis C virus infection (oral LP is most commonly viewed as a
manifestation of HCV infection), HHV6, HHV7.
2. MEDICATIONS: Cutaneous eruptions similar or even identical to LP (both clinically and
histologically) have been linked to a variety of drugs. The terms “lichen planus-like” and
“lichenoid” are often used to describe this phenomenon.
3. CONTACT ALLERGEN: metallic dental restorations or constructions (amalgam, copper and
gold), positive patch test results, and then regression or complete clearing after removal
of the sensitizing metal and replacement with other materials.
4. Others; Stress, diabetes, trauma, vaccinations (HBV vaccines), chronic active hepatitis, and
primary biliary cirrhosis. It may be found with other diseases of altered immunity, such as
ulcerative colitis, lichen sclerosis, myasthenia gravis, chronic graft-versus-host disease of
the skin etc.

13. DRUGS IMPLICATED IN LICHENOID DRUG ERUPTIONS
CLASS AGENTS
ANTIMICROBIALS • Griseofulvin
• Isoniazid
• Ketoconazole
• Tetracyclines
• Streptomycin
• Sulfamethoxazole
ANTIHYPERTENSIVES • Captopril
• Enalapril
• Labetalol
• Doxazosin
• Methyldopa
• Propranolol
ANTIARRHYTHMICS • Quinidine
ANTIMALARIALS • Chloroquine • Quinacrine • Hydroxychloroquine
Anti-TNF-α • Etanercept • Infliximab
ANTIPSYCHOTICS • Chlorpromazine
ANTICONVULSANTS • Phenytoin
ANTIDEPRESSANTS • Amitriptyline • Imipramine
ANTIDIABETICS • Glyburide • Tolbutamide
METALS • Gold salts
• Arsenic
• Bismuth
• Mercury

14. Pathogenesis
LP represents T-cell-mediated
autoimmune damage to basal
keratinocytes that express
altered self antigens
(epitopes) on their surface

15. Pathogenesis
PHASES OF LP
A. INDUCTION PHASE
B. EVOLUTION PHASE
C. RESOLUTION PHASE

16. Pathogenesis
A. INDUCTION PHASE
Self-peptides modified by exogenous antigens [viruses, medications
and contact allergens])  stimulation of keratinocytes and
plasmacytoid dendritic cells (pDCs),  release IFN-α  activation and
migration of DCs  Ag presentation to naïve T-cells in lymph node 
differentiation into CD8+ effector memory T cells  attracted by
chemokines (released locally by pDCs) migrate into the inflammatory
site.

17. Pathogenesis
B. EVOLUTION PHASE
Effector T cells (Te) expressing skin-homing receptors
(E-selectin ligands)  recognition of antigens  activated and
release proinflammatory cytokines and cytotoxic granules 
epidermal injury.

18. Pathogenesis
TWO DIFFERENT MECHANISMS OF T-CELL CYTOTOXICITY:
1. Perforin which forms pores in the target cell's plasma membrane this
causes ions and water to flow into the target cell, making it expand and
eventually lyse then Granzyme B that can enter target cells via the
perforin-formed pore and induce apoptosis. IFN-γ and TNF-α, released by
both CD4+ T cells and CD8+ T cells, can induce keratinocyte expression of
ICAM-1, thereby rendering these T-cells more adhesive to the
keratinocytes and thus facilitating exocytosis of granules containing
perforin and granzymes.
2. Activation of the death receptor Fas on the target cell by expressing the
cognate death ligand Fas L. The activated Fas also triggers apoptosis.

19. Pathogenesis
C. RESOLUTION PHASE
• “Inflammatory” and “ ‘homeostatic” chemokines produced by keratinocytes
direct the traffic of not only “pathogenic” T cells (Te) but also “immune
surveillance” T cells (Ts) or regulatory T cells (Treg) into the sites; the relative
balance of chemokines produced may determine the outcome of the T-cell-
mediated immune responses .
• Because keratinocytes are not only targets but also produce granzyme B,
perforin and Fas L to protect themselves from immune-mediated damage, Fas L-
bearing keratinocytes can induce Fas/Fas L-mediated death in neighboring Fas-
bearing T cells, contributing to the resolution of the lichenoid tissue reaction.
This pathway serves to eliminate potentially harmful auto-aggressive T-cells.
Recovery from the inflammation is associated with the migration of regulatory T
(Treg) cells into the site which have the capacity to suppress activated T-cells.

22. Clinical Features
• Cutaneous LP resolves approximately in 12-18 months
while Oral LP resolves approximately in 5 years.
• Mucosal involvement, particularly oral lesions, may be
observed in up to 75% of patients with cutaneous LP, but
the oral LP can be the only manifestation of the disease.
• Only 10–20% of patients whose initial presentation is oral
LP will eventually develop cutaneous LP.
• 15% to 20% of cases follow a relapsing course for years.

23. Clinical Features
THE TYPICAL OR CLASSICAL LP RASH;
1. Papules may be discrete or
gradually coalesce into plaques.
2. Bilaterally symmetrical.
3. Sharply demarcated.
4. Increase in size if subjected to any
irritation.
5. Surface: shiny or scaly looking.
6. Initially red  purple or violaceous
hue  a dirty brownish color.
7. Periods of regression and
recurrence.
8. Pruritus; rubbing than scratching.
9. Koebner’s phenomenon.
10. Most often on flexural wrist,
forearms, knees, flanks. trunk,
medial thighs, shins of tibia,
genitals especially glans penis, nails,
scalp & oral mucosa.
11. Face remains uninvolved.
12. May be covered with thin white
streaks (called Wickham's striae).
13. After lesions subside, post lichen
hyperpigmentation occurs.

24. The P's to Describe LP Lesions
1. Papulosquamous disorder (Papules/Plaques)
2. Planar (flat-topped)
3. Purple (violaceous)
4. Polygonal
5. Pruritic
6. Post-inflammatory hyperpigmentation

30. Clinical variants
1. Mucosal lichen planus
(oral &
genital/vulvovaginal)
2. Lichen planus of the nails
3. Follicular LP (LPP)
4. Hypertrophic lichen
planus
5. Annular lichen planus
6. Atrophic lichen planus
7. Ulcerative lichen planus
8. Bullous lichen planus
9. LP pemphigoides
10.LP pigmentosus
11.Inverse lichen planus
12.Linear lichen planus
13.Zosteriform LP
14.Actinic lichen planus
15.Acute (exanthematous) LP
16.Drug-induced LP
(Lichenoid drug eruption)

31. Mucosal LP
• The most common location of mucosal lichen planus is the
oral mucosa.
• Predominantly women are affected.

32. TYPE DESCRIPTION
1.RETICULAR
• Most common presentation.
• Commonly on buccal mucosa and buccal vestibule. Sometimes on tongue, gingiva, lips and floor
of the mouth.
• The lesions tend to be bilateral and are asymptomatic:
(a) Slightly elevated fine grey-white lines (Wickham’s striae) lacelike pattern or a pattern of fine
radiating lines or;
(b) Annular lesions- lesions, develop gradually from single small pigmented spots into circular groups
of papules with clear, central unaffected mucosa.
2.EROSIVE/
ULCERATIVE
• Commonly on buccal mucosa and vestibule.
• Complication of the atrophic process after trauma or ulceration .
• May be covered with Pseudomembrane.
• Asymptomatic- uncomfortable -mild burning to severe pain provoked by sour, spicy or hot foods
• Central area of erosion with yellowish fibrinous exudate surrounded by erythema. Bleeding may
occur.
• Wickham's striae may also be seen near these ulcerated areas. This form may undergo malignant
transformation.
3.ATROPHIC
• Inflamed areas of oral mucosa covered by thinned red-appearing epithelium.
• Smooth, poorly defined erythematous areas with or without peripheral striae.
• Usually associated with desquamative gingivitis.
• Pain and burning sensation.

33. TYPE DESCRIPTION
4.BULLOUS
• Rare form characterized by large vesicles or bullae (4mm to 2cm).
• Combined with reticular or erosive pattern.
• Lesions usually develop within an erythematous base, rupture
immediately leaving painful ulcers.
• Usually have peripheral radiating striae and seen on posterior part of
buccal mucosa.
5.PAPULAR
• Form minute white papules which gradually enlarge and coalesce to form
either a reticular, annular, or plaque pattern.
6.PLAQUE-LIKE • Flattened white areas favors dorsal surface of tongue.
7.HYPERTROPHIC
• Well circumscribed, elevated white lesion resembling leukoplakia
• Biopsy needed for diagnosis
8.PIGMENTED
• Rare type shows flanked brown macular foci.
• Can be associated with other types particularly erosive.

47. Vulvovaginal LP
• Most common appears to be erosive disease.
• Vaginal involvement occurs in up to 70% of women with
erosive vulvar LP, and if there is oral mucosal involvement 
“vulvovaginal–gingival syndrome”.
• Scarring may be a sequel.

49. LP of the nails
• Nail lesions can precede the appearance of LP on the rest of the skin or on the mucous membranes or develop in a
delayed fashion.
• 10% of patients with LP.
• These changes are manifestations of matrix damage, which can lead to scarring and dorsal pterygium formation if
left untreated.
• Nail changes include;
1. Thinning of the nail plates
2. Longitudinal ridging
3. Pterygium unguis
4. Trachyonychia: marked roughness of the nail plate, loss of transparency and often by a gray discoloration
when widespread trachyonychia involving all 20 nails  Twenty-nail dystrophy (more common in children).
5. Onycholysis
6. Onychorrhexis
7. Koilonychia
8. Subungual hyperkeratoses

58. Lichen planopilaris (LPP/Follicular LP)
• Involvement of the hair follicle is observed, both clinically & histologically.
• Multiple, keratotic plugs surrounded by a narrow violaceous rim are
observed primarily on the scalp, although other hair bearing areas can
also be affected.
• The inflammatory process may result in scarring and loss of follicular
structure, i.e. a permanent alopecia. Over time, the areas of involvement
often “burn out” centrally and are indistinguishable from other causes of
“end stage” cicatricial alopecia.).
• Women are more frequently affected than men, and this form may occur
alone or with typical LP lesions elsewhere.
• Variants of lichen planopilaris:
I. Graham–Little–Piccardi–Lassueur syndrome: is characterized by
the triad of (need not be present simultaneously ):
1. Non-cicatricial loss of pubic and axillary hairs and disseminated spinous or
acuminated follicular papules.
2. Typical cutaneous or mucosal LP.
3. Scarring alopecia of the scalp with or without atrophy .
II. Frontal fibrosing alopecia: progressive frontotemporal hair loss
occurs primarily in elderly women.

64. Hypertrophic LP (LP Verrucosus)
• Extremely pruritic, thick hyperkeratotic reddish-brown plaques are seen
primarily on the shins or dorsal aspect of the foot and may be covered by a
fine adherent scale.
• The lesions are usually symmetric and tend to be chronic because of
repetitive scratching.
• The average duration of hypertrophic LP in patients whose lesions had
cleared was reported to be 6 years.
• Chronic venous stasis frequently contributes to the development of this
condition.
• Squamous cell carcinoma may develop within a background of
longstanding hypertrophic LP.

67. Annular LP
• This form is thought to occur when papules spread peripherally and the
central area resolves.
• The annular edge is slightly raised and typically purple to white in color,
while the central portion is hyperpigmented or skin-colored.
• Annular lesions occur in about 10% of patients with LP and are usually
scattered among more typical lesions, but may represent the
predominant finding.
• The most common site of involvement is the axilla, followed by the penis,
extremities and groin.
• Most patients are asymptomatic, while some have pruritus.

71. Atrophic LP
• Atrophic LP may represent a resolving phase of LP, given the history of the
lesions: papules coalesce to form larger plaques that often, over time,
become centrally depressed and atrophic with residual
hyperpigmentation.
• The clinical appearance of atrophic LP is likely a result of thinning of the
epidermis rather than degeneration of elastic fibers, and the epidermal
atrophy may be accentuated by the use of potent topical corticosteroids.
The most common site of involvement is the lower extremity.
• Occasionally, morphea of the trunk has been reported in association with
oral LP, as has the simultaneous occurrence of LP and/or lichen sclerosus.

74. Ulcerative LP
• Can occur at the nails or palmoplantar lesions of LP,
particularly those on the soles.
• Typical LP lesions may be present in additional sites of the
body.
• More common in female patients.
• The ulcers are intensely painful and often recalcitrant to
conventional therapy. Chronic ulcerative lesions are at risk of
developing SCC.

76. Bullous LP & LP pemphigoides
BULLOUS LP LP PEMPHIGOIDES
CLINICAL
• Occur in longstanding preexisting lesions blisters
arise only on or near the lesions of LP.
• Lesions last for short duration.
• LP acute and generalized and is followed by the
sudden appearance of large bullae mainly on
uninvolved skin.
• May evolve into pemphigoid nodularis.
PATHOGENESIS
• Intense lichenoid infiltration of lymphocytes =>
severe liquefaction degeneration of the basal cell
layer => exaggerated Max-Joseph spaces.
• Lichenoid infiltrate => damage to the basal layer=>
expose hidden antigens to the autoreactive T-cell =>
formation of circulating IgG autoantibodies directed
against the 180 kDa BP antigen (BPAG2, type XVII
collagen), => subepidermal bulla.
HISTOLOGICAL
• Subepidermal bulla formation with typical changes of
LP.
• Subepidermal bulla with no evidence of associated LP
with an abundance of eosinophils.
IMF
• Direct and indirect.
• IMF is negative.
• Direct IMF shows linear basement-membrane-zone
deposition of IgG and C3 in perilesional skin.
IMMUNOELECTRON-
MICROSCOPY
• Negative.
• Deposition of IgG and C3 in the base of the bulla and
not in the roof as found in bullous pemphigoid.

79. LP pigmentosus
• LP pigmentosus typically presents in individuals with skin types III
and IV as brown to gray–brown macules or patches in sun-exposed
areas of the face and neck, usually with no preceding erythema
and often evolving into diffuse or reticulated pigmentation.
• Involvement of intertriginous sites is occasionally observed, and a
linear distribution following Blaschko’s lines has also been
described.
• Histologically; marked pigment incontinence and epidermal
atrophy.
• Coexistence of classic LP lesions in approximately 20% of patients.

82. Inverse LP
• Pink to violaceous papules and plaques appear in
intertriginous zones (axillae >inguinal and inframammary
folds) and less often in the popliteal and antecubital fossae.
Occasionally, LP lesions occur elsewhere on the body.
• Hyperpigmentation is usually present as well and it may be
the sole manifestation, leading to overlap with LP
pigmentosus.

85. Linear LP
• Lesions that appear spontaneously within the lines of
Blaschko.
• Usually seen in patients in their late 20s or early 30s.
• Presumably this pattern reflects somatic mosaicism, but how
the involved and uninvolved skin differ is not known.

88. Zosteriform LP
• Koebnerization of LP into the site of a previous herpes zoster
infection.
• When LP has a strictly dermatomal pattern, this represents
an isotopic phenomenon following “zoster sine herpete”.

91. Actinic LP (LP actinicus)
• Most patients are young adults or children with a dark skin type.
• The onset of this variant is during the spring and summer, and the
lesions primarily involve sun-exposed skin of the forehead and
face, followed by the dorsal surfaces of the arms and hands and
the neck.
• The lesions usually consist of red–brown plaques with an annular
configuration, but melasma-like hyperpigmented patches may
occur.

99. Acute (exanthematous/eruptive) LP
• Because lesions are usually widely distributed and
disseminate rapidly.
• The commonly affected areas include the trunk, the inner
aspects of the wrists and the dorsal aspect of the feet.
• Probably due to lichenoid drug eruptions.
• The clinical course is usually self-limited and, in general,
lesions resolve with hyperpigmentation within 3 to 9 months.

101. Drug-induced LP (Lichenoid drug eruption)
• Despite the significant overlap between LP and lichenoid drug
eruption there are both clinical and histologic clues that favor one
diagnosis over the other.
• There is usually a latent period of several months from drug
introduction to the appearance of the cutaneous eruption.
• The latent period varies depending not only on the offending drug,
but also on other factors such as the frequency of drug
administration, the dosage, and the intensity of the patient’s
individual reaction to the offending drug.

106. Complications
1. Squamous cell carcinoma may develop in oral ulcers (rare <
0.4-5.3%), cutaneous ulcers or hypertrophic LP that are
present for a long time.
2. Cicatricial alopecia in scalp LP.
3. Postinflammatory hyperpigmentation.
4. Atrophy and scarring are seen following hypertrophic lesions.
5. Erythroderma. Rare.

107. Histopathology
LAYER FINDINGS
HORNY CELL LAYER
1. Hyperkeratosis w/o parakeratosis
2. Oral LP  parakeratosis rather than hyperkeratosis
GRANULAR CELL LAYER • Focal hypergranulosis  grey white puncta
PRICKLE CELL LAYER
1. Irregular acanthosis with saw-toothed rete ridges (older lesions)
2. Intercellular edema
BASAL CELL LAYER
1. Vacuolar alteration )Liquefaction degeneration( of the basal cells
2. Colloid (Civatte, hyaline or cytoid) bodies
3. Max Joseph spaces (Clefts between the epidermis & dermis)
PAPILLARY DERMIS
1. Lichenoid lymphohistiocytic infiltrate  dense, band-like infiltrate (interface dermatitis)
2. Colloid (Civatte, hyaline or cytoid) bodies
3. Melanin incontinence  Melanophages
4. LPP  lymphohistiocytic infiltrate around hair follicle  its destruction

117. Immunohistochemistry
• In a nonspecific “sponge-like”
manner, colloid bodies often stain
with fibrin, IgM, IgA, IgG or C3,
and this is the characteristic
finding by DIF.
• In LPP lesions, IgM, IgG and IgA
are found in varying combinations
along the follicle–dermal
interface.

118. Differential Diagnosis

119. DDx of Oral LP
1. Lichenoid reactions
2. Leukoplakia
3. Candidiasis
4. Chronic Ulcerative Stomatitis
5. Pemphigus Vulgaris
6. Cicatricial pemphigoid
7. Erythema multiforme
8. Syphilis
9. Recurrent aphthae
10. Lupus erythematosus
11. Squamous cell carcinoma
12. Frictional keratosis

120. Treatment
• Currently there is no definite cure for lichen planus but there
are certain types of medicines used to reduce the effects of
the inflammation.
• Lichen planus may go into a dormant state after treatment.
• Principal aims: resolution of painful symptoms, resolution of
mucosal lesions, reduction of risk of cancer & maintenance of
good oral hygiene.

121. Treatment
I. GENERAL MEASURES
II. LOCAL THERAPY
III. SYSTEMIC THERAPY
IV. PHOTO(CHEMO)THERAPY
V. SURGICAL TREATMENT

122. Treatment
I. GENERAL MEASURES “5”
1. Assurance
2. Avoidance of stress
3. Avoidance of sun in case of actinic LP
4. Stop offending drug
5. Rx of viral infection if present

123. Treatment
II. LOCAL THERAPY “5”
1. Topical steroid: Fluorinated e.g. clobetasol for cutaneous
LP or triamcinolone, fluticasone (nasal spray) for oral LP.
2. Topical retinoids
3. Topical calcineurin inhibitors: Tacrolimus or
pimecrolimus particularly for mucosal, ulcerative or
hypertrophic LP (under occlusion).
4. Mouth washes: for oral LP e.g. lidocaine to numb the
area and make eating more comfortable, steroids e.g.
Dexamethasone elixir & antiseptics.
5. Intralesional corticosteroids; particularly for
hypertrophic LP & LP of nails.

124. Treatment
III. SYSTEMICTHERAPY“10”
1. Oral corticosteroids: indicated for
short period when fail to respond
to topical steroids. Prednisone 40 to
80 mg daily for less than 10 days
without tapering & more prolonged
course in sever cases.
2. Oral retinoid: acitretin.
3. Immunosuppressant
medications
a) MTX (low dose/week for oral
LP) ,
b) Cyclosporine (in severe
recalcitrant cases particularly
LPP)
c) Sulfasalazine
d) Mycophenolate mofetil
4. Antimalarials: Hydroxychloroquin
200 mg b.i.d for actinic LP/LPP.
5. Dapsone: in resistant cases of
erosive OLP.
6. Antihistamines
7. Biologics: TNF alpha inhibitors,
basiliximab
8. Thalidomide
9. Metronidazole: 500 mg b.i.d for
20-40d.
10. Grizofulvin for long term 3-6 mo.

125. Treatment
IV. PHOTO(CHEMO)THERAPY “5”
1.Narrow-band or broadband UV-B.
2.Psoralen with UV-A (PUVA).
3.UVA1
4.Excimer laser for oral LP.
5.Extracorporeal Photopheresis.

126. V. SURGICAL TREATMENT
• To remove high-risk dysplastic areas in OLP
1. Surgical excision
2. Cryotherapy
3. CO2 laser
4. ND:YAG laser
Treatment

127. Rx of oral LP

128. References
• Dr shabeel pn Royal dental college
(Presentation).
• Aaron Sarwal (BDS 3rd Prof.) (Presentation).
• Raghavendra Kini, DV Nagaratna, Ankit Saha
• Jp journals, 2011, 2(3): 249- 253 (Presentation
By Dr. Priyadershini A. Rangari).
• Bolognia 3rd ed.