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Summary

  1. Top of page
  2. Summary
  3. Introduction
  4. Epidemiology
  5. Clinical findings
  6. Variants of lichen planus
  7. Histopathology
  8. Differential diagnostic considerations
  9. Therapy
  10. Acknowledgments
  11. References

Lichen planus is characterized by lichenoid, polygonal papules with fine white lines, called Wickham striae. Lesions most commonly occur on the limbs and on the dorsal aspect of the trunk. At the same time often leukoplakia of mucous membranes as well as nail disorders are seen.

There are numerous variants of lichen planus which can be distinguished from the classical form on the basis of morphology and distribution of the lesions. The typical primary lesion of lichen planus may be replaced by other forms, such as patches, hyperkeratoses, ulcerations, or bullous lesions. Moreover, distribution patterns of these lesions may vary and include erythrodermic, inverse or linear arrangements. In contrast to these numerous clinical features, histologic findings remain characteristic in the variants, so that the diagnosis can be made securely. Differential diagnoses of lichen planus include diverse dermatoses such as bullous pemphigoid or paronychia.


Introduction

  1. Top of page
  2. Summary
  3. Introduction
  4. Epidemiology
  5. Clinical findings
  6. Variants of lichen planus
  7. Histopathology
  8. Differential diagnostic considerations
  9. Therapy
  10. Acknowledgments
  11. References

Lichen planus (LP) is an acutely occurring inflammatory skin disease frequently with a chronic course with characteristic clinical and histopathologic features. Besides the skin and adjoining mucous membranes, hair and nails are also involved. The etiology and pathogenesis of LP remain unclear. An autoimmune reaction in which CD8+-T lymphocytes attack basal keratinocytes leading to apoptosis of the cells has been favored. Various potential triggers, e.g. viral or bacterial antigens, metal ions, drugs or physical factors, could initiate the autoimmune process [1, 2]. Nonetheless, the role of the individual trigger factors is controversial. This is particularly true for hepatitis viruses, whose significance in the etiology of LP has not been determined conclusively. Nonetheless, associations between hepatitis C infection and LP have been reported [3, 4].

The diagnosis of LP in its classical form is usually not difficult. The appearance of unmistakable polygonal papules at sites of predilection frequently in association with characteristic mucous membrane lesions allows for a secure clinical diagnosis. The clinical-morphological diversity of its variants is all the more surprising. Here the typical clinical findings of LP can be lost to a large extent, as the following examples will demonstrate. When in doubt, the diagnosis can be made on the basis of histopathologic features that may vary to some degree but retain the basic pattern.

Epidemiology

  1. Top of page
  2. Summary
  3. Introduction
  4. Epidemiology
  5. Clinical findings
  6. Variants of lichen planus
  7. Histopathology
  8. Differential diagnostic considerations
  9. Therapy
  10. Acknowledgments
  11. References

The prevalence of LP in the total population is unknown. The frequency is estimated at between 0.5 and 1.0 % [1, 2, 5, 6]. In epidemiologic studies on selected patient or population groups (Table 1) prevalence rates between 0.07 and 0.84 % were found, so that the frequency of LP in the total population is probably lower than the estimated 0.5–1.0 %. Special manifestations such as mucosal lichen planus can often be observed disproportionately within individual, e.g. gynecological or dental, patient groups [7, 8]. The gender distribution of LP is balanced. In occasional studies, a slight female predominance of perhaps 1.2: 1 has been observed [9]. An exception to the rule of equal gender distribution is once again oral mucosal lichen planus, where a female predominance of 1.4: 1 or 2: 1 has been found [10, 11]. LP can manifest at any age, preferentially between 30 and 60 years of age [12]. LP is uncommon in childhood, as only 1–3 % of patients are children [9, 13, 14]. LP can occur in its diverse cutaneous manifestations alone or in combination with mucosal lichen planus or in the event of subungual location with lichen planus of the nails. The frequency of mucosal involvement in LP patients is 30–70 % [1, 15, 16]. The subungual manifestations of LP take a special position. On the one hand, the clinical morphology of LP cannot be recognized in this location; on the other hand, LP of the nails is by no means rare with about 3–15 % [17, 18]. For the individual cutaneous variants of LP no epidemiologic data exist in the literature. The corresponding reports are usually case reports or small case series.

Table 1. Prevalence of lichen planus.
AuthorsSample sizeCohortPrevalence [%]
  1. N. s.: No statement

Oberste-Lehn [19]N. s.Outpatients, Department of Dermatology, University of Kiel, Germany0.84
Hornstein et al. [17]N. s.Out-/inpatients, Department of Dermatology, University of ≠Erlangen, Germany0.83
Hard, Holmberg [84]40,450Dermatologic patients, Sweden0.78
Omal et al [86]18,306Patient of a clinic for ìoral medicine and radiologyî, India0.64
Arndt [12]676,376Patient group, USA0.442
Bhattacharya et al. [9]60,312Dermatologic outpatients, India0.38
Arndt [12]131,111Outpatients, Palestine0.14
Augustin et al. [87]90,880Coworkers of 312 German companies0.07

Clinical findings

  1. Top of page
  2. Summary
  3. Introduction
  4. Epidemiology
  5. Clinical findings
  6. Variants of lichen planus
  7. Histopathology
  8. Differential diagnostic considerations
  9. Therapy
  10. Acknowledgments
  11. References

Lichen planus

The typical primary lesion of LP in its classical form is a polygonal, violaceous papule of a few millimeters in diameter with sharp borders. Its surface possesses streaky or net-like pattern, i.e. Wickham striae (Figure 1). The papules can be distributed individually in a grouped or in an exanthematous fashion. Through confluence bizarre, 1–2 cm large, round or oval plaques with or without keratoses develop. Te isomorphic response or Koebner phenomenon can be observed in LP, just as in psoriasis. One to two weeks after mechanical irritation, usually due to scratching, linear lesions develop [19, 20]. In a similar manner physical factors such as thermal irritation or UV irradiation can result in an acute exacerbation of LP [20]. The isomorphic response is frequent and can be observed in the acute phase of the disease in about 50 % of LP patients [9]. The predilection sites of LP include the upper and lower limbs, particularly the extensor surfaces of the lower legs and the volar aspect of the wrists and forearms as well as on the trunk and the lumbar region [9, 17]. Commonly, the face is not affected. On the scalp lichen planus follicularis is a frequent manifestation. As a rarity LP can develop at intertriginous sites, where it can completely lose its classical morphology (Figure 2). In analogy to psoriasis, the intertriginous presentation of LP is termed inverse lichen planus [1, 16, 21]. Subjectively, LP is characterized by a frequently agonizing pruritus that can affect up to 80 % of patients [9, 16]. LP is considered a self-limited dermatosis; the mean duration is reported to be 1–2 years [2]. Nevertheless, longer and chronically recurrent courses are possible, so that the prognosis in the individual case cannot be predicted [16, 22]. After the remission of the papules and plaques of LP, postinflammatory hyperpigmentation, leuko- or pseudoleukoderma as well as atrophy may remain.

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Figure 1. Lichen planus (detail).

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Figure 2. Inverse lichen planus.

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Mucosal lichen planus

The most common location of mucosal lichen planus (MLP) is the oral mucosa (Figure 3). About half the patients have solitary lesions; an equal number have multiple changes [11]. The topographic distribution of oral lesions is not uniform. In studies by Shen et al. buccal mucosa was involved most frequently with 14.9 % [11]. The clinical morphology of MLP is diverse. According to Andreasen on the oral mucosa six different morphological forms can be differentiated: reticular, plaque-like, atrophic, papular, erosive and bullous manifestations [23]. The reticular and erosive forms are the most common variants [16, 22]. A special association of the individual morphological forms with particular locations on the oral mucosa has not been described, except that plaque type MLP favors the top or side of the tongue. Erosive or atrophic MLP are often accompanied by burning pain that can be provoked by sour, spicy or hot foods. In the other forms subjective symptoms do not occur or are less intense. Oral MLP is a facultative precancerous lesion. In individual studies malignant transformation was observed in 0.4–3.7 or 5.3 % of cases [11, 15, 24]. A recent review article documented esophageal involvement by LP [25]. The authors demonstrated that predominantly women were affected and the majority complained of dysphagia or odynophagia. Occasionally esophagus involvement by LP has been reported without typical oral lesions [25].

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Figure 3. Mucosal lichen planus.

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MLP of genital skin is preferentially located on the glans penis. Often lesions with an annular configuration are seen here (Figure 5). In women the vulva and less commonly the vagina are involved. Erosive MLP is particularly frequent on the vulva (Figure 5). In a group of 125 women Micheletti et al. found erosive lesions in 33.6 %. On the basis of a literature search the same authors were able to calculate a frequency of 70 % [7]. The risk of development of squamous cell carcinoma on vulvar MLP cannot be definitively estimated due to the scarce data. The estimates range from a “low risk” up to a frequency of 2.4 % [26, 27]. Malignant transformation of penile MLP is limited to individual case reports [28, 29]. The simultaneous occurrence of MLP on the oral and female genital mucosa is termed vulvo-vaginal-gingival syndrome [30]. There exists a marked tendency for scarring and the development of strictures. Involvement of the urethral, nasopharyngeal or esophageal mucosa is possible [31-33]. 80 % of women with vulvo-vaginal-gingival syndrome have the HLA DQB1*0201 gene, suggesting a genetic predisposition for the syndrome [32].

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Figure 4. Annular lichen planus.

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Figure 5. Erosive lichen planus.

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Lichen planus of the nails

LP of the nail organ, particularly in the matrix [34], can result in very diverse morphological alterations of the nail plate that are, nevertheless, not pathognomonic (Table 2). A first hint of isolated involvement of the nails is thinning of the nail plate and longitudinal ridging [35]. Characteristic nail lesions of LP include dorsal pterygium and trachyonychia [36]. A pterygium develops through adhesion of eponychium and matrix leading first to a split nail and later to possible complete loss of the nail plate. Trachyonychia is characterized by marked roughness of the nail plate, loss of transparency and often by a gray discoloration (Figure 6). The nail alterations of LP typically develop simultaneously on several nails. It is not uncommon for all 20 nails to be affected. In the studies of Tosti et al., 10 0f 24 patients had 20-nail dystrophy, in 7 further patients all fingernails were affected [18]. 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. With isolated nail involvement the diagnosis of should be confirmed histopathologically when in doubt.

Table 2. Clinical findings of lichen planus of the nails.
▸ Thinning of the nail plates
▸ Longitudinal ridging
▸ Pterygium unguis
▸ Trachyonychia
▸ Onycholysis
▸ Onychorrhexis
▸ Koilonychia
▸ Subungual hyperkeratoses
▸ Chromonychia
▸ Onychomadesis
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Figure 6. Lichen planus of the nails.

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Variants of lichen planus

  1. Top of page
  2. Summary
  3. Introduction
  4. Epidemiology
  5. Clinical findings
  6. Variants of lichen planus
  7. Histopathology
  8. Differential diagnostic considerations
  9. Therapy
  10. Acknowledgments
  11. References

The classification of the clinical variants of LP (Table 3) is based both on peculiarities of the morphology as well as on the topographic distribution of the lesions on the skin. In some variants the etiology is also taken into consideration. Combinations of morphological peculiarities are possible in the individual case.

Table 3. Clinical variants of lichen planus.
  1. The classification presented takes morphology of the lesions, peculiarities of the topographic distribution and in individual cases the etiology into consideration.

▸ Annular lichen planus
▸ Hypertrophic lichen planus
▸ Atrophic lichen planus
▸ Ulcerative lichen planus
▸ Bullous lichen planus
▸ Lichen planus pemphigoides
▸ Lichen planus pigmentosus
▸ Erythrodermic lichen planus
▸ Inverse lichen planus
▸ Linear lichen planus
▸ Follicular lichen planus
▸ Lichen planus follicularis decalvans
▸ Actinic lichen planus

Annular lichen planus

Annular lichen planus is a frequent LP variant not only on the mucous membranes but also on the skin [12]. The sites of predilection include the trunk, the limbs and the scrotum [2]. Annular red to violet plaques develop through central clearing of usually larger LP lesions. In the event of simultaneous centrifugal growth the annular configuration of the lesions becomes even more distinct. Sometimes the regression of the original plaque leads to that central atrophy [37]. In other instances, the annular structure results from a ring-like arrangement of numerous solitary LP papules [2].

Hypertrophic lichen planus

This variant of LP, also known as lichen planus verrucosus or lichen planus hyperkeratosis, is predominantly found on the shins, less often on the arms or trunk [17]. The clinical morphology (Figure 7) is characterized by inflammation, red, yellow-gray or red-brown papules and plaques that can coalesce and possess a popular, verrucous or hyperkeratotic surface [6]. Upon palpation the lesions are firm or hard. Most are intensely pruritic. After years or decades of existence, the risk of development of squamous cell carcinoma appears elevated, possibly due to carcinogenic cofactors [38, 39].

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Figure 7. Hypertrophic lichen planus.

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Atrophic lichen planus

Atrophic lichen planus is a rare variant usually observed on the legs [17]. As clinical morphology round to oval, centrally atrophic depressed, brown or also violet papules and plaques are seen [2, 22]. If it is an independent variant or the regressive end stage of other LP forms cannot be concluded definitively, particularly as the combination of atrophic forms and other lesions of LP have been reported [12].

Ulcerative lichen planus

The most common locations of ulcerative or erosive lichen planus are the feet, particularly the soles and interdigital spaces [40-42]. Only a few cases have been reported on the trunk or perianal skin [2, 43]. The single or multiple lesions have sharp borders, bizarre configurations and are coin- to palm-size ulcers or erosions, sometimes with an elevated edge, or display rests of lattice-like leukoplakia. Typically marked pain is present that can severely impair walking or make it impossible.

Bullous lichen planus

Blistering of typical LP lesions characterizes bullous lichen planus. The blisters erupt during an acute flair. Again, the legs are affected (Figure 8). Numerous small grouped or sometimes even larger tense blisters are seen; some are multilocular. The intact bullae contain clear or pale yellow fluid [16, 44, 45].

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Figure 8. Bullous lichen planus.

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Lichen planus pemphigoides

Clinical features, histopathology and immunofluorescence of lichen planus pemphigoides display findings of LP as well as bullous pemphigoid [46]. In lichen planus pemphigoides the blisters develop not only on pre-existing LP lesions as is typical for bullous lichen planus, but also on unaltered skin [47]. Tense or flat blisters appearing multilocular at the edge are characteristic (Figure 9). The lesions are found predominantly on the limbs, more rarely on the trunk in grouped or disseminated distribution [5]. The exact pathophysiologic classification of this variant as LP or bullous pemphigoid has not yet been conclusively clarified.

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Figure 9. Lichen planus pemphigoides.

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Lichen planus pigmentosus

Clinically, pigmented macular or papular lesions in variable distribution are seen in lichen planus pigmentosus. Besides extensive, perifollicular, linear or zosteriform distribution, lichen planus pigmentosus may follow the lines of Blaschko (Figure 10) or the course of the saphenous varicose veins on the legs [48, 49]. Sites of predilection include intertriginous regions or the flexures of the limbs [49, 50]. We have repeatedly observed lichen planus pigmentosus in the lumbar region. The pigmentation encompasses shades of gray-brown, violet and dark brown. Patients with pale skin appear to be preferentially affected [50].

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Figure 10. Lichen planus pigmentosus following the lines of Blaschko.

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Erythrodermic lichen planus

Erythrodermic LP has only very rarely been documented in the literature [17, 51, 52]. Morphologically, red or violet papules and extensive infiltrated erythematous plaques with or without scaling are seen. Amidst the erythroderma, typical LP lesions, blisters or erosions may appear in a localized fashion. Pruritus is severe and the general health is reduced.

Inverse lichen planus

Inverse LP typically affects axillae, inguinal creases, limb flexures and submammary region. Clinically, extensive erythematous lesions with poorly defined borders and in part with lichenification are seen. Additionally, keratotic papules and erosions with a bizarre configuration can occur (Figure 2). In the inverse locations, pigmentation of the individual lesions is also typical [1, 21].

Linear lichen planus

Linear lichen planus is a variant that possibly occurs more often in children and adolescents [53]. Clinical features are characterized by streak-like manifestations (Figure 11). The linear distribution can be limited to a few centimeters or be segmental, zosteriform or follow the lines of Blaschko. The individual lesions may be the typical flat-topped papules but purpuric papules, vesicular, hyperkeratotic and annular morphologies may be observed [54-56].

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Figure 11. Linear lichen planus (a), detail (b).

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Follicular lichen planus

Sites of predilection of follicular lichen planus or lichen planopilaris include the scalp, axilla, inguinal creases, sacrum and flexures of the limbs. Clinically, grouped or disseminated, follicular, flat, elevated or hemispherical erythematous papules with or without keratoses are observed [22, 55]. Follicular lichen planus on the scalp is likely to lead to scarring alopecia (Figure 12). The Graham-Little-Piccardi-Lasseur syndrome, seen predominantly in women and also in a familial pattern, is characterized by the joint appearance of follicular lichen planus on the trunk with lichen planus follicularis decalvans on the scalp. Further features such as onychodystrophy can manifest as variable minor criteria [58].

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Figure 12. Follicular lichen planus. The patient had his hair cut to facilitate treatment.

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Frontal fibrosing alopecia (Figure 13) was initially reported by Kossard et al. as a variant of lichen planopilaris [59]. It is observed predominantly in postmenopausal women as progressive frontotemporal hair loss [59]. Due to lack of typical LP criteria, some feel this is a separate form of scarring alopecia [60].

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Figure 13. Frontal fibrosing alopecia. Band of frontal hair recession.

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Actinic lichen planus

Typically in the spring and summer actinic lichen planus develops on sun-exposed areas of the face, hands and forearms. Children and young adults with a dark skin type in the tropics and subtropics are preferentially affected, which explains the synonyms tropical and subtropical lichen planus. Clinical features are variable. Besides lichenoid or annular papules macular hyperpigmentation and infiltrated erythematous plaques with variable borders and scaling are observed. Even in severe cases pruritus is not obligatory [16, 61-63].

Histopathology

  1. Top of page
  2. Summary
  3. Introduction
  4. Epidemiology
  5. Clinical findings
  6. Variants of lichen planus
  7. Histopathology
  8. Differential diagnostic considerations
  9. Therapy
  10. Acknowledgments
  11. References

The histopathological findings of LP are characteristic. The epidermis displays orthohyperkeratosis, circumscribed wedge-shaped hypergranulosis representing the histopathologic substrate of the Wickham striae as well as sawtooth-like acanthosis. In the upper dermis a band-like infiltrate consisting primarily of lymphocytes (Figure 14) is observed. It may include scattered histiocytes and neutrophils. Vacuolar degeneration is found along the dermoepidermal junction zone with apoptotic keratinocytes (colloid bodies). The vacuolar degeneration and possible cleft formation along the junction zone was first reported by Caspary in 1888, later also by Robinson and by Joseph (Caspary-Robinson or Max-Joseph cleft, respectively) [64, 65]. As a result of the apoptosis of basal keratinocytes, incontinence of pigment with uptake of the released melanin in dermal melanophages develops [66, 67]. The histopathologic pattern of LP undergoes diverse modifications in its variants. For example, acanthosis and hyperkeratosis are particularly marked in hypertrophic lichen planus, while atrophic lichen planus is characterized by distinct atrophy of the epidermis and an only slight lymphocytic infiltrate. Lichen planus pigmentosus features both striking incontinence of pigment with an accumulation of dermal melanophages as well as increased melanin in the basal layer [1, 16, 21]. In follicular lichen planus a peri-infundibular lymphocytic infiltrate and mucin-rich fibrosis are observed that lead to destruction and scarring of the follicle. Hypergranulosis is frequently observed at the follicle openings [22]. The bullous variants of LP exhibit subepidermal clefting that is probably secondary to the vacuolar degeneration. In contrast to bullous lichen planus, the infiltrate in lichen planus pemphigoides often contains eosinophilic and neutrophilic granulocytes. Further differences are observed in immunofluorescence microscopy. Here, band-like deposits of C3 along the basal membrane and of immunoglobulins along the junction zone can be observed in lichen planus pemphigoides. Almost always the autoantibodies are targeted against the NC16A-domain of the hemidesmosomal protein BP180 [46, 68].

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Figure 14. Histology: Orthohyperkeratosis with hypergranulosis and a superficial lymphocytic infiltrate at the dermoepidermal junction (hematoxylin & eosin stain).

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Differential diagnostic considerations

  1. Top of page
  2. Summary
  3. Introduction
  4. Epidemiology
  5. Clinical findings
  6. Variants of lichen planus
  7. Histopathology
  8. Differential diagnostic considerations
  9. Therapy
  10. Acknowledgments
  11. References

The clinical findings of LP in its classic form are unmistakable. In acute LP with exanthematous spread, guttate psoriasis, lichen nitidus, lichenoid drug eruptions and papular syphilid must be excluded. The others do not have Wickham striae or mucosal involvement; only guttate psoriasis shows the Koebner phenomenon. In addition guttate psoriasis usually has other signs of psoriasis that are not seen in LP [1, 16]. When mucosal changes are found, lichen sclerosus et atrophicus and other forms of leukoplakia must be considered [16]. Nail involvement by LP must be differentiated from psoriasis, Darier disease and onychotillomania [6, 18]. Considering the variants of LP, the differential diagnoses depend on varying clinical morphology (Table 4). Particular problems may develop in bullous, pigmented and ulcerative LP. Blistering over a LP lesion suggests bullous lichen planus. When blisters develop on unaltered skin in addition, lichen planus pemphigoides is present. In contrast to bullous pemphigoid, the blisters of lichen planus pemphigoides are found predominantly on the limbs and are not disseminated, the patients are usually younger and lichen planus pemphigoides typically has milder course than bullous pemphigoid [69]. Pigmented lesions are so unusual for LP that one tends not to think of an LP variant. Further, the Wickham striae are no longer detectable. The differential diagnoses of lichen planus pigmentosus include nodular sarcoidosis, urticaria pigmentosa, lichen amyloidosus and incontinentia pigmenti [19] as well as intertrigo for the inverse form [21, 50]. Erythema dyschromicum perstans (ashy dermatosis) must also be considered as a differential diagnosis and is characterized by ash-gray, sometime slightly pruritic macules mainly on the trunk [70].

Table 4. Variants of lichen planus and their differential diagnoses.
LP variantClinical differential diagnoses
Annular lichen planusGranuloma annulare
Hypertrophic lichen planusLichen simplex chronicus
Atrophic lichen planusErythema dyschromicum perstans
Ulcerative lichen planusChronic paronychia, Gram-negative toe web infection, trophic ulcer
Lichen planus pemphigoidesBullous pemphigoid
Lichen planus pigmentosusIntertrigo, morphea
Erythrodermic lichen planusErythrodermas
Inverse lichen planusIntertrigo, inverse psoriasis
Linear lichen planusLichen striatus, ILVEN
Follicular lichen planus (decalvans)CDLE, Folliculitis decalvans
Actinic lichen planusChloasma, polymorphic light eruption

The macular pigmentation of actinic lichen planus is hard to distinguish from chloasma [49, 62]. A comparable situation exists in ulcerative lichen planus with its preference for the lower limbs. Here, the clinical morphology does not suggest LP, so that the diagnosis is often made only after years of ulceration; clues to the diagnosis are resistant to therapy and the presence of typical LP lesions elsewhere. The most important differentia diagnoses of ulcerative lichen planus include gram-negative toe web infection, chronic paronychia and neurotrophic ulcers [41]. When linear lichen planus develops in childhood, lichen striatus should be excluded as a differential diagnosis. This dermatitis lacks Wickham striae and can easily be differentiated from LP histopathologically [71].

Therapy

  1. Top of page
  2. Summary
  3. Introduction
  4. Epidemiology
  5. Clinical findings
  6. Variants of lichen planus
  7. Histopathology
  8. Differential diagnostic considerations
  9. Therapy
  10. Acknowledgments
  11. References

With few exceptions, all forms of LP are treated with the same measures. Depending on the severity of the findings, topical and systemic treatment options are available. Topical therapy encompasses primarily use of corticosteroids of class III and IV (in the German classification according to Niedner) with or without occlusion [72] (Table 5). There have also been reports of successful use of topical calcineurin inhibitors (e.g. tacrolimus or pimecrolimus [10, 72-78] (Table 5). In the event of exanthematous distribution, additional phototherapy with UVA, UVA1 or UVB can be helpful. The various forms of PUVA are also well-established [1]. In individual cases, photodynamic therapy has proven to be effective [79]. Cases refractory to topical therapy, as well as exanthematous and ulcerative forms, represent indications for systemic therapy. Corticosteroids and acitretin, alone or in combination (Table 5) as well as cyclosporine, dapsone and azathioprine are proven treatment methods [80-83]. Further, individual reports of successful use of biologics, low molecular weight heparins, metronidazole and thalidomide exist [1, 80]. Actinic LP obviously should not be treated with phototherapy; instead intensive sun protection and perhaps hydroxychloroquine employed [63]. Likewise, in lichen planus pigmentosus, phototherapy should also be avoided, as increased pigmentation appears possible. For hyperkeratotic lichen planus the injection of triamcinolone crystal suspension also in combination with cryotherapy is suitable. In ulcerative lichen planus there may be an indication for surgical measures. Recurrent ulcers or erosions on the soles have been removed by tangential excision with the resulting defects closed with free skin grafts [40-42]. Treatment of lichen planus pemphigoides is primarily systemic with corticosteroids as in bullous pemphigoid [5]. Erosive vaginal lichen planus often takes a frustrating course, so that in these cases systemic immunosuppressive therapy (cyclosporine, azathioprine) should be initiated early [84, 85].

Table 5. Treatment options of lichen planus.
Drug treatment optionsReferences
Topical 
Corticosteroids (classes III and IV of the German classification according to Niedner)[72, 81]
Alternative: 
▸ Tacrolimus[73-75]
▸ Pimecrolimus[78]
▸ Cyclosporine[72, 76, 77]
▸ Retinoid[10, 81]
Systemic 
Corticosteroids (e.g. prednisolone 0.5–1 mg/kg daily orally)[81]
Alternative, if indicated in combination with: 
▸ Acitretin (e.g. 30 mg daily orally)[81-83]

References

  1. Top of page
  2. Summary
  3. Introduction
  4. Epidemiology
  5. Clinical findings
  6. Variants of lichen planus
  7. Histopathology
  8. Differential diagnostic considerations
  9. Therapy
  10. Acknowledgments
  11. References