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Lichen Planus

Hyperkeratosis, hypergranulosis, irregular acanthosis

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Definition

Common, intensely pruritic, symmetrical, papulosquamous dermatosis.

Clinical Features

Relatively common
Rare in children1–6
Appearance:
- violaceous papules:
  - usually pruritic 7,8
  - may be network of fine white lines (Wickham's striae) on surface
Location:
- palmoplantar lesions more common than once thought 9
- commonly oral lesions:
  - may be only manifestation10
- rarely esophageal involvement11,12
- may be:
  - localized to:
    - lip 13
    - vulva14,15
    - eyelid 16
  - nail changes:17,18
    - may be only manifestation 10
Usually spontaneous resolution within 12 months:
- postinflammatory pigmentation may persist for some time afterwards19
Associations:
- HLA-DR1 in non-familial cases20
- immunodeficiency states21
- internal malignancy22,23
- primary biliary cirrhosis 24,25
- peptic ulcer (but not Helicobacter pylori infection)26
- chronic hepatitis C infection27–35
- hepatitis B vaccination 36–41
- pemphigus 42
- porphyria cutanea tarda43
- ulcerative colitis44
- Becker's nevus45
- lichen sclerosus et atrophicus with coexisting morphea46
Increased frequency of HLA-DR6 in Italian patients with hepatitis C virus-associated oral lichen planus47
Familial cases:
- uncommon
- rarely associated with HLA-D748–50
Squamous cell carcinoma:
- rare complication of:
  - hypertrophic and ulcerative variants 51–54

Clinical Variants

Clinical variants:
- zosteriform 55
- erosive
- actinic
- follicular
- erythematous
- bullous

Atrophic Lichen Planus

May resemble porokeratosis
Usually typical papules of lichen planus at margins
Rare form composed of annular lesions56–58

Hypertrophic Lichen Planus

Usually confined to shins
Single or multiple pruritic plaques:
- may be verrucous appearance 59
- usually persists many years
Rarely may lead to:
- squamous cell carcinoma if longstanding60
- cutaneous horns
- keratoacanthoma
- verrucous carcinoma61–63
Occasional association with HIV infection 64

Linear Lichen Planus

Rare
Distinguish from linear nevi and other dermatoses with linear variants65,66
Usually involves limbs
May follow lines of Blaschko 67

Ulcerative Lichen Planus

Ulcerated and bullous lesions on feet68
Sometimes:
- mucosal lesions
- alopecia
- more typical lesions of lichen planus
May be squamous cell carcinoma in longstanding lesions
Reported variants involve:
- perineal region69
- penis70
- mouth71
- vulva, vagina and mouth:
  - vulvovaginal-gingival syndrome72–74
- flexures 75
Rare associations:
- Castleman's tumor
- malignant lymphoma76,77
- long-term therapy with hydroxyurea
- hepatitis C infection 78

Lichen Planus Erythematosus

Challenged as an entity
Non-pruritic, red papules, with predilection forearms59

Erythema Dyschromicum Perstans79

Slowly progressive
Asymptomatic
Ash-colored or brown macular hyperpigmentation80–82
Most parts of world:
- most prevalent in Latin America
Lesions:
- may be:
  - unilateral 83
  - linear84
Disease activity may cease after several years

Lichen Planus Actinicus

Sun-exposed areas of body85,86
Predilection for certain populations 87 particularly young individuals of Oriental origin
Some variability in clinical expression in different countries resulting in proliferation of terms such as:
- lichen planus tropicus88
- lichen planus subtropicus89
- lichenoid melanodermatitis90
Lesions have been induced by repeated exposure to UV radiation91

Lichen Planopilaris

Clinically heterogeneous
Keratotic follicular lesions
Lichen planus present or develops subsequently in ≈50% of cases92–95
Scarring alopecia of scalp:
- keratotic follicular lesions and associated erythema best seen at margins 92
Graham Little–Piccardi–Lassueur syndrome:
- rare but closely related
- cicatricial alopecia of scalp
- follicular keratotic lesions of glabrous skin
- variable alopecia of axillae and groins95–97
Two other clinical groups:94
- 1:
  - follicular papules
  - no scarring
  - usually on trunk and extremities
- 2:
  - quite rare
  - plaques with follicular papules
  - usually retroauricular region94
  - called ‘lichen planus follicularis tumidus'98
Rare variants include:
- linear form99–101
- lesions confined to vulva 102

Lichen Planus Pemphigoides

Rare
Coexistence of lichen planus and heterogenous group of subepidermal blistering diseases resembling bullous pemphigoid103–105
Tense bullae:
- may develop in:
  - lesions of lichen planus 106–109
- do not necessarily recur with subsequent exacerbations of lichen planus 110,111
Oral lesions exceedingly rare 112
Reported in children110,111
Rarely:
- onset following PUVA therapy 113,114
Similar lesions induced by:
- ACE inhibitor ramipril 115,116
Lichenoid erythrodermic bullous pemphigoid:
- unlike lichen planus pemphigoides, presence of:
  - frequent mucosal lesions 117

Pathogenesis

Unknown etiology:
- contact allergy to metals, flavorings and plastics may be important in oral lichen planus118
Cell-mediated immune reactions:
- appear important119
- suggested that they are precipitated by alteration in antigenicity of epidermal keratinocytes, possibly caused by:
  - virus
  - drug
  - allogeneic cell120
Keratinocytes express:
- HLA-DR on their surface:
  - may be antigen with inductive or perpetuating role121–123
- fetal cytokeratins (K13 and K8/18):
  - speculative whether responsible for triggering T-cell response 124
CD4+ lymphocytes:
- comprise initial cellular response125
- increased in peripheral blood126
- traditional ‘helper’ role
Cytotoxic CD8+ lymphocytes:
- appear to:
  - play significant role as effector cell
  - recognize antigen associated with MHC class I on lesional keratinocytes, resulting in their death by apoptosis127
Recruitment of lymphocytes to interface region may be result of chemokine MIG (monokine induced by interferon-γ)128
Lymphokines produced by T lymphocytes may have effector role in producing apoptosis of keratinocytes129,130
and include:
- interferon-γ
- interleukins-1β, -4 and -6
- tumor necrosis factor
A unique subclass of cytotoxic T lymphocyte (γδ) found in established lesions 131
Langerhans cells:
- increased
- suggested that they initially process the foreign antigen122
In dermis:
- factor XIIIa-positive cells
- macrophages expressing lysozyme125
Matrix metalloproteinases may play concurrent role by destroying basement membrane:
- cell survival signals derived from basement membrane may be required to prevent keratinocyte apoptosis132

Clinical Variants

Atrophic Lichen Planus

Impaired capacity of atrophic epithelium to maintain regenerative steady state

Ulcerative Lichen Planus

Antibodies directed against nuclear antigen of epithelial cells reported when involves oral mucosa133

Erythema Dyschromicum Perstans

Has been regarded as macular variant of lichen planus134 due to:
- simultaneous occurrence of both in several patients82,135,136
- similar immunopathological findings 137,138
Paraphenylenediamine incriminated in etiology 134
Association with HIV infection139

Lichen Planus Pemphigoides

Appears to be due to epitope spreading
Suggested that damage to basal layer in lichen planus may expose or release a basement membrane zone antigen, which leads to:
- formation of circulating antibodies
- consequent blister formation140–142
Target antigen is novel epitope (MCW-4) within C-terminal NC16A domain of 180Kd bullous pemphigoid antigen (BP180, type XVII collagen)143–145

Histopathology 146

Basal cell damage:
- multiple, scattered Civatte bodies (Fig. 1
  Fig. 1: Lichen planus. Two apoptotic keratinocytes (Civatte bodies) are present in the basal layer of the epidermis. An infiltrate of lymphocytes touches the undersurface of the epidermis. (H & E)
  ):
Band-like dermal infiltrate of lymphocytes and some macrophages:
- press against undersurface of epidermis (Fig. 2
  Fig. 2: Lichen planus. A band-like infiltrate of lymphocytes fills the papillary dermis and touches the undersurface of the epidermis. (H & E)
  )
- occasional lymphocytes extend into basal layer:
  - may be close contact with:
    - basal cells
    - sometimes Civatte bodies
- does not obscure interface or extend into mid-epidermis:
  - unlike erythema multiforme and fixed drug eruptions
- sometimes karyorrhexis147
Plasma cells:
- rarely prominent in cutaneous lesions148–150
- invariably in lesions adjacent to or on mucous membranes
Variable melanin incontinence:
- most conspicuous if long duration and dark-skinned
Eosinophilic colloid bodies:
- diastase resistant (Fig. 3
  Fig. 3: Lichen planus. There are numerous colloid bodies in the papillary dermis. (H & E)
  )
- ≈20μm diameter
Other characteristic epidermal changes include:
- hyperkeratosis
- wedge-shaped areas of hypergranulosis related to:
  - acrosyringia
  - achromotrichia
  - variable acanthosis
Sometimes:
- rete ridges become pointed:
  - give ‘saw tooth’ appearance to lower epidermis
- mild hypereosinophilia of keratinocytes in malpighian layer
- small clefts151 at dermoepidermal junction secondary to basal damage:
  - Caspary–Joseph spaces
- eccrine duct adjacent to acrosyringium involvement:152
  - reported variant with lichenoid changes localized entirely to acrosyringium153
Rarely:
- transepidermal elimination with perforation154
Milia:
- late complication155
Evolution of lesions:146
- very early:
  - increased number of Langerhans cells in epidermis before any significant dermal inflammatory infiltrate
- resolving:
  - infiltrate:
    - less dense
  - may be minimal extension into reticular dermis

Electron Microscopy

Lymphocytes attach to basal keratinocytes resulting in:
- basal keratinocyte apoptosis156–158
many cell fragments:
- phagocytosed by adjacent keratinocytes and macrophages 159
- large tonofilament-rich bodies:
  - result from redistribution of tonofilaments during cell fragmentation
  - appear to resist phagocytosis
  - extruded into upper dermis
  - recognized on light microscopy as colloid bodies160–162

Clinical Variants

Atrophic Lichen Planus

Epidermis:
- thin
- loss of normal rete ridge pattern
Infiltrate:
- usually less dense than in typical lichen planus

Hypertrophic Lichen Planus

Epidermis:
- overlying orthokeratosis (Fig. 4
  Fig. 4: Hypertrophic lichen planus. The epidermis shows irregular hyperplasia. The dermal infiltrate is concentrated near the tips of the rete ridges. (H & E)
  )
- at margins usually psoriasiform hyperplasia representing lichen simplex chronicus secondary to the rubbing and scratching:
  - if severe may mimic squamous cell carcinoma on shave biopsy163
  - associated with vertically oriented collagen (‘vertical-streaked collagen') in papillary dermis
- basal cell damage:
  - usually confined to tips of rete ridges (Fig. 5
    Fig. 5: Hypertrophic lichen planus. There are a number of Civatte bodies near the tips of the rete ridges.
    )
  - may be missed on casual observation
Infiltrate not as dense or as band-like as in usual lichen planus:
- may be a few eosinophils and plasma cells:
  - sometimes beta blockers incriminated

Ulcerative Lichen Planus

Epidermal ulceration:
- more typical changes of lichen planus at margins of ulcer
Invariably plasma cells if involves mucosal surfaces
Eosinophils prominent in oral lesions of case associated with methyldopa therapy

Lichen Planus Erythematosus

May be proliferation of blood vessels in upper dermis in addition to usual features of lichen planus

Erythema Dyschromicum Perstans149

Active phase:
- a lichenoid tissue reaction with:
  - basal vacuolar change
  - occasional Civatte bodies
  - infiltrate in comparison to lichen planus:
    - usually quite mild
    - may be deeper extension
Prominent melanin incontinence (Fig. 6
Fig. 6: Erythema dyschromicum perstans. There is patchy basal cell damage and some pigment incontinence. (H & E)
):
- only significant feature in older lesions
- pigment usually extends deeper in dermis than in postinflammatory pigmentation of other causes164
- similar features in cases reported as lichen planus pigmentosus
Immunofluorescence:
- IgM, IgG and complement-containing colloid bodies in dermis
Electron microscopy:
- apoptosis and residual filamentous bodies80

Lichen Planus Actinicus89

Resemble lichen planus lesion, but:165
- usually more marked melanin incontinence86,91
- may be focal parakeratosis 85
- inflammatory cell infiltrate may be less marked
Direct immunofluorescence:
- usually numerous immunoglobulin-coated cytoid bodies166

Lichen Planopilaris92–94

Lichenoid reaction pattern involving basal layer of follicular epithelium
Dense perifollicular infiltrate:
- of lymphocytes and a few macrophages (Figs 7 and 8
  Fig. 7: Lichen planopilaris. The lichenoid infiltrate is confined to a perifollicular location. (H & E)
  Fig. 8: Lichen planopilaris. The lichenoid infiltrate is confined to a perifollicular location. (H & E)
  ):
  - changes involve infundibulum and isthmus of follicle
- unlike lupus erythematosus, does not extend around blood vessels of mid and deep plexus
- interfollicular epidermis involvement:
  - in up to 35% of cases with scalp involvement92,94,167 and in rare plaque type
  - not usually in variant with follicular papules on trunk and extremities 94
If scarring alopecia:
- variable perifollicular fibrosis
- hair follicle loss and replacement by linear tracts of fibrosis167
- papillary dermis may be fibrosed
- if advanced diagnostic features may no longer be present:
  - term ‘pseudopelade’ sometimes used for end-stage scarring alopecia
Direct immunofluorescence:
- colloid bodies containing IgG and IgM in dermis adjacent to upper portion of involved follicles95,168
- in one report of longstanding lesions (3–7 years):169
  - linear deposits of immunoglobulins along basement membrane of hair follicles of scalp in all cases
  - fibrin in one case
  - cytoid bodies not demonstrated169

Lichen Planus Pemphigoides

Typically:
- cell-poor subepidermal bulla
- mild, perivascular infiltrate of lymphocytes, neutrophils and eosinophils:170
  - neutrophils and eosinophils not mentioned in all reports
Sometimes lichenoid infiltrate at margins of blister171
Occasional degenerate keratinocytes in epidermis overlying blister106
Lesions arising in papules of lichen planus:
- predominant features of lichen planus:
  - usually a few eosinophils and neutrophils:
    - in contrast to bullous lichen planus in which they are absent106,172
Direct immunofluorescence of bullae:
- usually show IgG, C3 and C9 neoantigen in basement membrane zone
Often circulating antibody to basement membrane zone 173,174
Indirect split-skin immunofluorescence:
- has shown binding to roof of split 141
Electron microscopy:
- split in lamina lucida:
  - as in bullous pemphigoid141,175
Immunoelectron microscopy:
- localization of immune deposits may resemble that in:
  - epidermolysis bullosa acquisita 176

Special Stains and Immunohistochemistry

Usually:
- no autoantibodies
- no alteration in serum immunoglobulins177
Sometimes serum antibody to a lichen planus-specific antigen in epidermis of uncertain pathogenetic significance178
Keratin expression:
- resembles that in wound healing:
  - damaged basal cells replaced by increase in actively dividing keratinocytes in epidermis and skin appendages:
  - keratin 17 (K17) in suprabasal keratinocytes179
Direct immunofluorescence of involved skin:
- colloid bodies in papillary dermis:
  - stain for complement and immunoglobulins, particularly IgM
- usually irregular band of fibrin along basal layer:
  - often irregular extension into underlying papillary dermis (Fig. 9
    Fig. 9: Lichen planus. A band of fibrin involves the basement membrane zone and extends into the papillary dermis. (Direct immunofluorescence)
    )
Immunofluorescent analysis of basement membrane zone:
- suggests disruption in lamina lucida region180
Some studies show disturbance in epithelial anchoring system181

Differential Diagnosis

Select up to 2 differential diagnoses to compare with Lichen Planus

Clinical Variants

Lichen Planus Pemphigoides

Bullous lichen planus:182
- vesicles or bullae develop only in lichenoid papules, probably as a result of unusually severe basal damage and accompanying dermal edema171,183

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Last updated: 8 Jan 2007