Indian Journal of Paediatric Dermatology

: 2021  |  Volume : 22  |  Issue : 4  |  Page : 306--315

Childhood lichen planus

Arun Joshi, Sanjay Kumar Rathi, Yashpal Manchanda 
 Department of Dermatology, Farwaniya Hospital, Sabah Al Nasser, Kuwait

Correspondence Address:
Sanjay Kumar Rathi
Address: 51 Gulmohar Cross Road No. 4, JVPD Scheme, Mumbai - 400 049, Maharashtra


Lichen planus (LP) is a relatively uncommon chronic skin condition with varied clinical presentations seen mostly in adults. It is rarely encountered in children, although increasingly more pediatric cases are being recognized and reported. LP can affect skin, mucosae, hair and nails, alone or in various combinations. All forms of LP seen in adults also occur in children. Certain types (eruptive, generalized) are observed more commonly in children than adults whereas appendageal (follicular and nail), mucosal (oral, genital, esophageal), hypertrophic and bullous variants have also rarely been reported in pediatric population. The exact etiopathogenesis of LP is not known. Immune dysregulation, infections, environmental, and genetic factors have been studied extensively and speculated to play some roles. A wide variety of treatment modalities for LP have been used in adults, and the same are employed in children. There is dearth of randomized controlled trials of evidence based treatments in LP, especially in children probably because of the rarity of the condition, heterogeneity of presentations, and gaps in understanding the exact etiology. This review attempts to present the up to date current information on the epidemiology, etiopathogenesis, clinical features and therapeutic options for lichen planus in children.

How to cite this article:
Joshi A, Rathi SK, Manchanda Y. Childhood lichen planus.Indian J Paediatr Dermatol 2021;22:306-315

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Joshi A, Rathi SK, Manchanda Y. Childhood lichen planus. Indian J Paediatr Dermatol [serial online] 2021 [cited 2021 Nov 28 ];22:306-315
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Lichen planus (LP) is a chronic immune mediated inflammatory papulosquamous dermatological condition affecting skin, hair, nails, and mucosae. The disease derives its name from the Greek word λειχήν (lichen) for “tree moss” and the Latin word planus for “planar.” LP is a heterogeneous clinical entity with diverse morphologic, topographic, and configurational manifestations, all showing similar and consistent histopathological features of a lichenoid interface dermatitis.[1] The onset is usually gradual but uncommonly can be sudden and generalized too. Classic LP is characterized by 6 ps (purple, plane, polygonal, pruritic, papules, and plaques). There are many distinct clinical variants described in LP, each having different natural history, sequelae, and outcomes.[1]


LP is a relatively uncommon dermatosis affecting mostly adults (middle-aged persons of both sexes, females more often than males). It is reported to affect <1% of the population (0.4 to 1.2% of all dermatology and hospital referrals).[1] LP in children (commonly referred to as childhood or pediatric LP) is rare, constituting 1%–4% of all LP cases.[2] Childhood LP is reported to be more common in South Asia and Middle East,[2],[3],[4],[5],[6],[7] compared to Europe,[8],[9],[10] North America,[11],[12] or Africa.[13]

The global pooled prevalence of oral LP (OLP) among adults is reported to be 1.01%, being lowest in India (0.49%) and highest in Europe (1.43%). The prevalence is higher in non-Asian countries, and among females, more than 40 years of age.[14] OLP can present alone (15%–25%) or as a component of classic cutaneous LP (60-70%),[15] and rarely as part of plurimucosal orogenital LP syndromes.[16] Both OLP[17] and genital LP[2],[18] are extremely rare in children.


The exact etiology of LP is unknown, and its pathogenesis complex and multifactorial. Four major areas in the pathobiology of LP pertains to immune dysregulation, infections, environmental, and genetic factors.[1] The current level of knowledge favors it to be a T-cell (Th1)-mediated condition targeting basal keratinocytes. In a genetically susceptible individual, environmental factors (drugs, infections, vaccines, contact allergens, stress, or unknown agents) may trigger the immune patho-mechanisms involved, initiating the inflammatory processes resulting in LP and its perpetuation. Plasmacytoid dendritic cells (pDCs), various populations of T-cells, and mast cells participate in a complex interplay to bring about the initial step of damage to the epidermal basal keratinocytes.[19],[20],[21] Self-antigens thus exposed may induce the inflammatory cascade through molecular mimicry resulting in the pathologic changes and lesions of LP.[22],[23]

In the induction phase, pDCs and keratinocytes stimulated by external pathogens through toll like receptors (TLR), or endogenous ligands release type-1 interferons (IFN) leading to activated CD8+ cytotoxic T-cell damage to the epidermal cells with the help of CD4 T-helper.[1],[19],[20] The damaged basal keratinocytes attract more CD8+ T-cells perpetuating a vicious cycle resulting in chronicity.[1],[19] Pro-inflammatory myeloid dendritic cells, T-regulatory cells (Tregs), polyfunctional T-cells, and TLRs mediate innate immune response involved. Cytokines such as interleukins,[4],[6],[8],[9],[17] IFN-α, IFN-γ, tumor necrosis factor (TNF)-α, vascular endothelial growth factor, transforming growth factor-β (activin-A) 1, caspase 3, bcl 2, and transcription factor Brn2 are up-regulated.[1],[19],[20] Various chemokine and chemokine receptor pairs act to directionally attract antigen presenting CD1a+ Langerhans dendritic cells and Factor XIII-a-positive cells,[1],[19],[20] and T-lymphocytes to the site of the lesions.[24],[25],[26],[27],[28] Th17[29] and Th9/IL9[30] pathways are also implicated. Matrix metalloproteinase 9 (MMP9) secreted from activated T-effector cells, and degranulation products from mast cells disrupt the basement membrane zone (BMZ).[19],[20],[21],[24] Micro-RNAs involved in regulating the expression of pro-inflammatory and pro-apoptotic protein coding genes are also up-regulated.[31]

Shao et al.[32] demonstrated that LP is characterized by a type II interferon inflammatory response also that is dependent on Janus Kinase 2 (JAK2) and signal transducer and activator of transcription 1 (STAT1), but not on JAK1 or STAT2 signaling. It provides evidence for the therapeutic use of JAK inhibitors in LP.

In a first study of its kind, increased number of B-cells in the vicinity of the BMZ points to a possible role of these cells in the pathogenesis of LP.[33] Humoral immune response contribution in LP is hinted by elevated levels of anti-keratinocyte, antinuclear, anti-desmoglein 1 and 3, anti-mitochondrial, and anti-thyroglobulin antibodies.[34]

Among environmental factors, infections especially HCV[35],[36] and others (HBV, HHV 6, HHV 7, VZV),[1] drugs,[1] dental amalgam,[1] other chemicals,[1] and vaccines[37],[38],[39] are well-documented triggers for LP. HCV is associated significantly with cutaneous and OLP both, in certain geographical areas (Japan, Middle East, Southern Europe but not in France, UK and India). Patients with LP have higher prevalence of HCV and vice versa. There is a 6-fold higher risk of HCV infection in OLP patients. Patients with HCV have a 2 to 4 fold increased risk of developing LP especially OLP.[35] Exact mechanism about how HCV induces LP in some is beginning to be understood.[36]

Hepatitis B, influenza, and herpes zoster vaccines are the three most common vaccines reported to have caused LP in some patients.[37] Most cases of hepatitis B vaccine induced LP occur after the 2nd dose. The median time of onset of LP following vaccination is fourteen days. Rosengard et al.[38] described an HCV-infected African American male patient who developed LP after receiving tetanus-diphtheria-acellular pertussis (tDAP) vaccine. An et al.[39] reported the second only known case of LP after rabies vaccination.

The list of drugs causing LP (also known as drug induced LP or lichenoid drug eruption [LDE]) is long and ever increasing.[1],[19],[20] Antimalarials, antibiotics, NSAIDs, antidiabetics, antiepileptics, diuretics, and anecdotally various biologics, are the drugs that have caused LP, mostly in adults. Drugs can induce lesions resembling cutaneous LP, OLP, and LP in a photo-distributed areas.[1] Generalized, eruptive, micropapular, and eczematous lesions are seen in LDE. They lack Wickham's striae and show eosinophils in the infiltrate near the BMZ. However, drug-induced LP has not been reported to occur in children so far. A recent meta-analysis has found that circumcision increases the risk of developing genital LP.[40]

The incidence of mercury amalgam-induced OLP has reduced significantly coinciding with its decreased use. Similarly, with the advent of automated color photo printing technology replacing manual one, color photo developers caused LP is now rare.[19]

The occurrence of familial cases and discovery of various HLA genetic loci in different populations points to genetic factors imparting susceptibility for LP (HLA A3, A5, A 7, B7, DR 1 in different parts of the world, HLA DR10 in Arabs, DsR BI*01:01 in Sardinia and Mexico, and HLA-a28 in Israeli patients).[1] A 308G/A single nucleotide polymorphism in TNF-α is associated with OLP but not CLP.[41] A phenome-wide association study has found new genetic associations located on HLA complex with eight diseases including LP.[42]

Psychological factors (stress, anxiety, and depression) could trigger, exacerbate, precipitate and perpetuate LP through neuroendocrine and neuroimmunologic mechanisms.[43] The association of stress with LP is indicated by changes in immune and endocrine functions shown by elevated levels of IL2r, sFasL, neopterin, sIL6R, and IL 8.[1] Stress hormones levels are elevated in OLP patients, during activity, and reduced after treatment.[44]

 Pathogenesis of Special Variants of Lichen Planus

Pathogenesis of lichen planopilaris is speculated to be due to collapse of immune privilege at the level of the hair follicle bulge and destruction of hair follicle stem cell site.[1],[45],[46]

A recent study found significantly reduced expression of IL-17A, IL-22, IL-23A/R, IFN-γ and Foxp3 (mRNA skin and IHC skin) in LP pigmentosus (LPPig) patients in comparison to LP, indicating the role of Th17 pathway in the pathogenesis.[47]

 Clinical Features

LP is not as commonly reported in children as it is in adults.[7] Most of the published data on childhood LP, has shown the age of onset to vary from 5 months to 13 years, with occurrence in infancy being very rare. The youngest age of onset described is at 2 weeks of life.[3] Clinical presentation of LP in childhood [Figure 1], [Figure 2], [Figure 3], [Figure 4] is not significantly different from the adult variant.{Figure 1}{Figure 2}{Figure 3}{Figure 4}

Numerous clinical types of LP have been described in children based on the morphology, pattern, and site of lesions. The classical papular type is the most common clinical type seen in children as also in adults.[2],[3],[4],[5],[6],[7],[8] It is characterized by pruritic, shiny, flat topped, violaceous, polygonal papules, typically around 3–6 mm in size Lower limbs are the most commonly affected body sites, and flexural surfaces of the ankles, wrist, and genitalia are often involved. The lesions typically demonstrate isomorphic phenomenon or koebnerization [Figure 5] at the sites of trauma.[6] The nail and mucosal involvement is reported to be less common in children (approximately 40% of cases, compared to 50%–70% reported in adults).[2] At times, due to close proximity of the lesions, a characteristic small grayish punch or even streaks can be seen forming a network on the surface of contiguously lined papules and plaques. These delicate white lines, termed as “Wickham's striae” [Figure 6] are the best visualized under magnification after applying oil on the surface of the lesions.[5] Eruptive LP is characterized by recurrent generalized classical morphological lesions occurring in crops.[12]{Figure 5}{Figure 6}

However, few variants such as linear, annular, and hypertrophic LP are more commonly seen in children. Actinic variant of LP [Figure 4] has also been reported more often in children especially from tropical countries.[48] Some variants have different prognosis in comparison to their adult counterparts. Cutaneous LP is mostly a self-limiting disease, and usually resolves completely leaving behind hyperpigmentation. The time for complete resolution is variable, ranging from a few weeks to up to couple of years. Mucosal and follicular LP are resistant and recalcitrant to treatment and can leave behind irreversible sequelae. Hamade et al. described a 5-year-old boy with hepatitis, who subsequently developed three different morphological variants of LP (follicular papules, hypertrophic plaques, and linear lesions), all showing characteristic histopathology of LP. The child did not have any mucosal or nail involvement.[49]

Oral lichen planus

It is less commonly seen in pediatric age group and the exact incidence is not yet known.[17] The oral lesions demonstrate a greater degree of clinical variability than the cutaneous lesions of LP. Commonly reported clinical variants of OLP are: reticular, papular, plaque like, atrophic, erosive, or bullous.[50] The lesions are most commonly reported on tongue, followed by buccal mucosa. The most common pattern seen in children is reticular form, reported in two thirds of all cases. The hypertrophic variants are largely asymptomatic and are often detected during routine mucosal examination in a case of cutaneous LP. Atrophic variant, on the other hand, is consistently more often associated with symptoms, which can be in the form of pain or burning sensation aggravated during eating or drinking.[51] Unlike cutaneous lesions, the diagnosis of the oral lesions can sometimes be extremely difficult to make, and require a biopsy for histopathological and immunofluorescence examination. Depending on the age of the patient, the differential diagnosis can vary from lupus erythematous, candidiasis, leukoplakia, graft versus host disease, lichenoid drug reaction, frictional keratosis, erythema multiform, allergic contact dermatitis, auto-immune bullous diseases, and so on.[52]

Nail lichen planus

It is seen in less than 10% of the cases, and the changes seen do not differ significantly from those typically seen in adults. The nail change seen in children [Figure 7] include thinning of nail plate, brittle nail plate, longitudinal ridges or striations, nicking or splitting of nail plate, pterygium formation, partial or complete loss of nail plate, and rarely subungual hyperkeratosis and distal separation of the nail plate from nail bed.[53] Pandhi et al. reported nail involvement in 13.9% of 316 childhood LP cases. Some children may rarely present with only nail changes suggestive of LP in the absence of skin lesions, including cases with characteristic twenty-nail dystrophy (trachyonychia). Unlike nail matrix LP, twenty-nail dystrophy never leads to permanent destruction of the nail. Another unique form described in children with nail LP is idiopathic atrophy of nails. It is characterized by the progressive asymptomatic nail atrophy in the absence of any skin and/or mucous membrane lesion. The diagnosis in twenty-nail dystrophy and idiopathic atrophy of the nails can only be confirmed by nail biopsy.{Figure 7}

Linear lichen planus

It is a rare variant of LP seen more commonly in children, presenting mostly as lesions that are morphologically typical of LP but are arranged along the lines of Blaschko. These are arranged in 'S' shaped pattern on abdomen; 'V-' shaped near the midline on trunk posteriorly; linear pattern on the limbs; and whorls on the scalp. It was initially described in 1976.[54] Other terms used synonymously for this entity include Blaschkoid LP and Blaschkolinear LP.[55] It is usually unilateral, although it can involve multiple areas in a single patient. Rarely, the morphology of the lesions in linear LP can be annular, vesicular, or hypertrophic. It also has benign and self-limiting course and often heals leaving behind hyperpigmentation. Its differential diagnosis includes inflammatory linear verrucous epidermal nevus, lichen striatus, linear graft versus host disease, and linear LP pigmentosus (especially in burnt out stage). It also needs to be differentiated from zosteriform LP, which is basically post herpetic LP occurring as an isomorphic response at the site of herpes zoster.

Familial lichen planus

It has been seen in about 1%–4% of childhood LP cases reported in the literature. It has an earlier age of onset, presents as widespread disease, and the mucosal surfaces are commonly involved. Its mode of inheritance is thought to be autosomal dominant with variable penetration.[56] Some researchers have also reported an association with human leukocyte antigen (HLA)-B7 and HLA-DR10.[57]

Apart from the common clinical variants described above, there are few reports of other rarer clinical variants seen in children.

Lichen planus pemphigoides

It is a rare autoimmune bullous disorder characterized by occurrence of bulla on LP lesions as well as normal appearing skin. The lesions are histologically characterized by typical features of LP but also have subepidermal split. Immunofluorescence staining reveals linear deposition of IgG and C3 along the basement membrane zone.[58]

Actinic lichen planus

It is a rare variant of LP characterized by lesions on the photo exposed parts, most often reported in Asian countries with dark skin people. The lesions typically appear or become severe in summer months and disappear or significantly clear up in winters. Four distinct clinical variants of actinic LP are described: annular; dyschromic; classic plaque type; and pigmented. It is usually seen in adults, but few reported cases in children are also available.[59]

Lichen planopilaris

It is an entity usually reported in middle aged women and presents characteristically as cicatricial alopecia on scalp. Few patients also complain of pruritus, burning sensation on scalp. Moreover, on examination under magnification perifollicular scaling and erythema can be seen in early stages. There are very few case reports of lichen plano pilaris reported in children,[60] one of the case had associated ocular LP also.[61]

Graham-Little-Piccardi-Lassueur syndrome

It is a rare clinical variant of lichen planopilaris initially described by Piccardi in 1914, who reported a case with progressive cicatricial alopecia of scalp associated with non-cicatricial alopecia of axillary and pubic areas and a follicular lichenoid papular lesion on the trunk and extremities. A year later, Ernst Graham-Little also published a similar case, which he described as “folliculitis decalvans et atrophicans.”[62] It is commonly seen in middle-aged Caucasian women, with only one pediatric case reported so far.[63]

Palmoplantar lesions in LP are uncommon even in adult patients occurring as yellow hyperkeratotic papules and plaques present on the palms or soles or with contiguous typical violaceus lesions on the adjacent wrists.[1],[19],[20] There are very few case reports of palmoplantar LP in children.[64] Joshi et al. reported diffuse palmoplantar involvement in a 4 year-old boy having generalized LP.[65] Handa and Sahoo[4] were the first to report eyelid involvement (3/87) cases of childhood LP. Genital lesions were described for the first time by Pandhi et al.[2] in 14/316 pediatric patients of LP. Genital LP could be a underreported in children, emphasizing the need for thorough history and complete physical examination.

Management of lichen planus

The diagnosis of LP is most of the times made by clinical examination only. However, in some cases dermoscopy and histopathological examination of the biopsy specimen along with DIF may be helpful.



Characteristic dermoscopic features of LP elucidated in various studies have been broadly classified into three main areas as follows: (1) Wickham's striae-pearly white colored structures arranged in round, linear, annular, reticular, or arboriform pattern; (2) Vascular features-If present they appear as red dots and lines; (3) Pigmentary changes-granular and/or structureless appearance with brown to bluish gray dots/clods.[66],[67]


Histopathology of LP is quite typical and diagnostic. The characteristic features include basal cell layer hydropic degeneration and band-like chronic lymphocytic inflammatory infiltrate in the upper dermis. The presence of large number of plasma cells in the band-like infiltrate of lymphocytes is more a feature of OLP. Other characteristic findings include hyperkeratosis without parakeratosis, acanthosis, “wedge shaped” hypergranulosis, “sawtooth” appearance of rete ridges, apoptotic keratinocytes in the epidermis as Civatte bodies and eosinophilic colloid bodies in the papillary dermis and small clefts (Max Joseph spaces) at the dermoepidermal junction, pigment incontinence, and melanophages in the upper dermis.[1],[19],[20]

Direct immunofluorescence

Shows a “shaggy” band of fibrinogen along the dermoepidermal junction and colloid bodies in the papillary dermis, which can be stained by using any of the autoantibodies such as IgM, IgG, IgA, and C3.[1]


Since exact etiopathogenesis of LP is still not known, there is lack of evidence based targeted therapies for LP, especially in children. Most of the studies on efficacy and safety of various treatment modalities in LP have been in adult patients, and there are no prospective case control or randomized controlled studies in pediatric cases of LP. Majority of them are anecdotal case reports or short case series with small number of patients.

Spontaneous resolution or remission seen in most cases of cutaneous LP over 1-2 years could possibly be one of the reasons for the difficulty in evaluating the various therapeutic modalities in children. In general, oral, genital and follicular LP needs aggressive early treatment. The aim of the treatment is to arrest disease activity, stop progression in rapidly progressive eruption or generalized LP, and control symptoms.

Topical and systemic corticosteroids, topical calcineurin inhibitors (TCIs), phototherapy, retinoids, and systemic immunosuppressants are the agents available for the treatment of LP The main consideration in childhood LP has to be age of the child, the extent, numbers, location, and type of lesions and the duration of disease.[65]

 Cutaneous and Oral Lichen Planus

Topical treatment

Topical corticosteroids

The limited and localized lesions can be managed with topical corticosteroid (TCS), which remains the first line treatment of LP. Mid to high potency corticosteroids (TCSs) are usually sufficient to control localized disease (<10%–15% BSA) in cutaneous LP.[2] Hypertrophic LP may require intralesional triamcinolone (10 mg/ml), or potent TCS under occlusion.[68] In one case series, TCS was given for 1–14 months, with varying response.[2] Postinflammatory hyperpigmentation was distressing to most patients and parents.[2],[6] TCS should preferably be given for shorter durations (2–3 weeks), combined with other modalities to prevent TCS induced side effects.[6]

Most of the clinical trials for TCS for OLP have been in adults. For localized lesions, triamcinolone acetonide 0.1% oral-base or gel form is more effective.[69] Fluticasone propionate spray and betamethasone sodium mouth rinse, both were effective in reducing pain. Similarly, fluocinolone acetonide 0.1% orabase was found to be better than triamcinolone acetonide 0.1% orabase after 4 weeks of treatment. A new delivery system containing 0.025% of clobetasol in lipid microsphere found to be equally effective as ointment base.[69] These topical applications may be useful in symptomatic oral lesions in childhood LP also, more specific trials in this age group are needed.

Topical calcineurin inhibitors

Topical tacrolimus (0.03%) is a good second line alternative for recalcitrant LP to TCS especially if used over long periods.[2],[70] Earlier recommended as a second line therapy for OLP in adults, TCIs (tacrolimus and pimecrolimus) are now regarded to be at par with TCS as first line modalities, despite the frequent side effects of burning sensation.[69] There are no comparative trials reported in childhood OLP, but topical tacrolimus was found to be effective in adult OLP.[71] There is difference of opinion in literature regarding superiority of tacrolimus or pimecrolimus.[72],[73] Local irritation and burning sensation is of concern if lesions are eroded.

Miscellaneous agents

Topical calcipotriol[74] and cyclosporin[75] were tried and reported beneficial in isolated case reports in adult LP. There are no reports of its use in childhood LP. Recently in various case, reports and trials topical curcumin has been tried found effective in reducing pain in some studies; can be a safe adjunct in the treatment of OLP even in childhood LP.[76]

Systemic agents

Oral corticosteroids

Systemic corticosteroids are considered if area of involvement is more, and lesions not responding to topical treatments. They can be given in conventional oral daily doses or in weekly pulse therapy form.[77],[78] For extensive and recalcitrant cases, the addition of oral corticosteroids (0.5-1 mg/kg per day) for 2-6 weeks is helpful in arresting the progress and helps in clearance of lesions.[2],[3],[6] However, they should be given for short periods, being watchful for the adverse effects.[79],[80]


This modality has primarily been used for extensive LP, and found to have superior efficacy over even oral corticosteroids in RCTs.[80],[81] Narrow band UVB (NBUVB), UVA1, topical and oral PUVA all have been tried. One RCT data suggest NBUVB and PUVA have comparable efficacy in adult LP.[82] NBUVB is a better choice in childhood LP for safety reasons.[12] UVB phototherapy was found to be safe and effective in few cases of childhood from Kuwait by Nanda et al.[5]

Oral retinoids

Oral retinoids (isotretinoin, alitretinoin, and acitretin) in lower doses may be effective and useful in LP.[83],[84] There are mostly case reports and one RCT of use of oral retinoids in adult LP.[1],[85] Appropriate precautions and investigations before prescribing this drug in pediatric age group must be followed. Acitretin has also been effective in hypertrophic LP.[86] Acitretin was tried by Pandhi et al.[2] in two children having nail LP with no response.


For the severe and resistant cases of LP immunosuppressive drugs that have been used anecdotally in adult recalcitrant LP cases such as cyclosporin,[87] methotrexate,[88] azathioprine,[89],[90] MMF[1], may be indicated in selective cases, taking care of all proper evaluations and investigations and risk benefit ratio. Systemic methotrexate alone or in combination with topical triamcinolone is useful in management of moderate to severe OLP.[91] These agents are now being used routinely in many pediatric cases of severe psoriasis, alopecia areata, and debilitating morphea but their safety profile has not been confirmed in childhood LP.

Miscellaneous agents

Drugs such as sulfasalazine, griseofulvin, hydroxychloroquine, itraconazole, terbinafine, and various biologics[84],[92] have been tried with varying degree of success in adult LP cases, however there have been no follow-up larger randomized controlled trials. More studies are needed to assess the risk-benefit ratio in refractory cases. Oral dapsone was observed to be safe and effective in controlling chronic and recurrent disease in children with LP.[2],[12],[93] Dapsone is an inexpensive, easily available agent that avoids systemic side effects of oral or injectable steroids.[2],[79] More trials are needed to to assess the risk – benefit ratio in refractory cases of childhood LP.

 Nail Lichen Planus

There is scarcity of evidence-based treatments for nail LP. The main aim of treatment is to minimize scarring. Potent TCS, topical retinoids, and topical tacrolimus have been proposed as first line therapy.[94],[95] There are no definite treatment guidelines or significant evidence-based studies. Oral alitretinoin, oral steroids, etanercept, antimalarials, and dapsone are all tried in few cases only with variable results. Nail LP may respond to topical steroid under occlusion. Systemic steroids are the only evidence based treatment available supported by a single retrospective study.[96] Intralesional steroids have been recommended as first line therapy for isolated nail LP for adults followed by retinoids and immunosuppressive agents (methotrexate, azathioprine, cyclosporine) as second and third line modalities respectively in recent recommendations by an expert group.[97] Although prescribed frequently, even potent TCS under occlusion are not very effective for nail LP in half the cases. Intralesional steroids are painful, therefore a course of oral prednisolone in tapering dose for 6 to 12 weeks is justified early in the course for nail matrix LP to prevent permanent disfiguring scarring.[79]

 Future Therapies in Childhood Lichen Planus

The only guidelines published very recently for treating LP refer to adult population only.[98] Topical and oral steroids, retinoids, and immunosuppressives used for prolonged durations in extensive, fast spreading or recalcitrant LP can have significant side effects in children. Hence newer agents such as various biologics,[84],[92] oral apremilast,[99] and oral JAK inhibitor tofacitinib,[100] are used in some recalcitrant cases of LP in adults. They may be the future treatment options in childhood LP with extensive and recalcitrant varieties. However, good quality randomized controlled trials to establish their efficacy and adverse effect profile in this age group are warranted.


Childhood LP is a rare condition. Clinical presentations and treatment responses are similar to adults however some variants are more commonly encountered whereas appendageal and mucosal types are exceedingly rare in children. There have been no prospective clinical controlled trials for various treatments in childhood LP because of rarity and ethical reasons. Majority of the large series of childhood LP reported mostly from India, are retrospective in nature and only few have documented various treatment outcomes. There is a great need to have dedicated trials and guidelines for treating LP in pediatric age group. Studies to understand the exact etiopathogenesis of LP at cellular, molecular, and genetic level are needed to have safer targeted therapies for various clinical types of LP in children.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


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