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 Table of Contents  
Year : 2021  |  Volume : 22  |  Issue : 4  |  Page : 316-325

Current perspectives in the treatment of childhood lichen planus

1 Department of Dermatology, Maharashtra Medical Foundation's Joshi Hospital, Pune, Maharashtra, India
2 Department of Dermatology, BJ Government Medical College and Sassoon Hospital, Pune, Maharashtra, India

Date of Submission01-Nov-2020
Date of Decision02-Mar-2021
Date of Acceptance16-Apr-2021
Date of Web Publication01-Oct-2021

Correspondence Address:
Sharad D Mutalik
Department of Dermatology, Maharashtra Medical Foundation's Joshi Hospital, 778, Deccan Gymkhana, Pune - 411 004, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijpd.ijpd_165_20

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Childhood lichen planus (CLP) is relatively common in India. With a mean age of onset at 7–8 years, CLP poses a therapeutic challenge as most guidelines for treatment cater to adult lichen planus (LP) with no defined evidence-based recommendations for CLP. Each case of CLP needs customized therapy with a step-wise approach. Topical corticosteroids are ably supported by topical calcineurin inhibitors, while oral retinoids, immunosuppressants like cyclosporine, and immunomodulators such as dapsone and narrowband ultraviolet B phototherapy are taking center stage in place of oral corticosteroids as systemic treatment modalities. However, the management of mucosal and appendageal LP requires systemic steroids more often than not. For the present review, we extracted the available data published in the English literature (Google Scholar databases, PubMed, and Medline) using search terms “lichen planus,” “treatment,” “children,” “pediatric,” and synthesized documented evidence regarding the risk–benefit profile of each therapeutic modality used in CLP. Undoubtedly, reporting of anecdotal successes, case studies, and conducting randomized controlled trials will help to structure consensus guidelines for the therapeutic conundrum of CLP.

Keywords: Adolescent, children, lichen planus, pediatric, treatment

How to cite this article:
Mutalik SD, Belgaumkar VA, Rasal YD. Current perspectives in the treatment of childhood lichen planus. Indian J Paediatr Dermatol 2021;22:316-25

How to cite this URL:
Mutalik SD, Belgaumkar VA, Rasal YD. Current perspectives in the treatment of childhood lichen planus. Indian J Paediatr Dermatol [serial online] 2021 [cited 2021 Nov 28];22:316-25. Available from: https://www.ijpd.in/text.asp?2021/22/4/316/327447

  Introduction Top

Lichen planus (LP) is a multifactorial, inflammatory disease of the skin, hair follicles, nails, and mucous membranes with diverse presentations and varying natural course. With an incidence of 2%–3% of total cases of LP, most childhood LP (CLP) cases are sporadic, with familial cases accounting for only 1%–2%.[1],[2] Children from the Indian subcontinent appear to have LP more frequently (prevalence up to 11%–19%), probably due to undefined genetic factors, environmental triggers, and possibly the Fitzpatrick skin type.[3] The mean age of onset is 7.1–8.4 years with the earliest reported age at 2 weeks.[4]

CLP is often asymptomatic yet deserves judicious treatment in view of probable chronicity and postinflammatory hyperpigmentation. Classical LP (42%–76%) is the most common morphology, followed by eruptive LP (13%), lichen planus hypertrophicus (LPH) (12%), and actinic LP (11.5%). The Koebner's phenomenon occurs more frequently in children (24%–28%); however, both scalp (0%–9%) and nail involvement (8.7%) are uncommon.[2],[5] Nail LP in childhood presents mostly as longitudinal ridging, with twenty-nail dystrophy and idiopathic atrophy being peculiar presentations. The mucous membrane involvement in CLP is largely asymptomatic with significantly lower prevalence (0.03%) and better prognosis as compared to adults.[2],[5]

Management of CLP begins with a search for the causative trigger including history about familial LP (autosomal dominant with variable penetrance) which presents with earlier onset, and/or recalcitrant course, auto-immune diseases (such as systemic lupus erythematosus, Sjogren's syndrome, dermatomyositis, vitiligo, and alopecia areata), and immunization (uncommonly after hepatitis B, influenza, and herpes zoster vaccine). The association of LP with hepatitis C virus infections has not been noted in children, but the association with human herpes virus-7 infections has been documented.[1],[2] While antihypertensives (captopril, enalapril, labetalol, and propranolol), diuretics (hydrochlorothiazide), antimalarials (hydroxychloroquine and quinidine), penicillamine, and gold salts are known to trigger LP, drugs frequently used in children and adolescents such as griseofulvin, tetracycline, carbamazepine, phenytoin, and nonsteroidal anti-inflammatory medications have also been occasionally implicated. Attention also needs to be paid to the presence of mercury compounds in dental amalgam or gold dental restorations which have been causally related to mucosal LP.[1]

Overall, CLP has a favorable response to treatment with two-third of cases showing resolution within 1 year. About 10%–20% of cases show intermittent recurrences for years with disfiguring residual pigmentation.[2] Malignant transformation in pediatric oral LP, though rarely reported (0.4%–12.5% in adults), is a possibility, particularly in erosive and atrophic types, owing to the longer duration of lesions and high renewal rate of oral epithelial cells in children. Therefore, regular meticulous follow-up is warranted.[6],[7]

  Treatment of Childhood Lichen Planus Top


Related English literature published until June 2021 was obtained from the following electronic database searches: Google Scholar, Medline, and PubMed. The following search terms were transcribed to yield articles of relevance: “lichen planus,” “treatment,” “children,” and “pediatric” in combination with “cutaneous,” “mucosal,” “appendageal,” and “nail.” Screening of the literature (25 articles from Google Scholar, 10 each from Pubmed and Medline) was performed independently by all the authors to validate the reliability of the information and obviate author bias. Reference lists of included papers were scanned, and further relevant publications were retrieved and categorized as case reports, case series, and review articles. We were unable to retrieve any randomized case–control trials specific for CLP. The documented evidence was synthesized to summarize and highlight the risk–benefit profile of each therapeutic modality for specific presentations of CLP.

The literature about CLP and its treatment is chiefly anecdotal with most of the data drawn from adult nonprospective observational randomized trials or recommendations based on the personal experience of experts.[8] The reasonable approach in the management of CLP remains removal of triggers (where identified) with control of the severity of lesions, suppression of the pruritus, and curtailing the cosmetically debilitating postinflammatory hyperpigmentation.

  Topical Therapies in Pediatric Cutaneous Lichen Planus Top

Emollients and antipruritic agents

Water-based moisturizers provide a cooling effect from water evaporation on the skin surface providing antipruritic effect and minimizing koebnerization.[9] Antipruritic lotions containing menthol, camphor, and calamine are particularly beneficial in patients with infrequent but violent paroxysm of pruritus.[10] In addition, harsh soaps are best avoided and children are advised to wear full sleeve cotton clothes, shoes, and socks (instead of playing barefoot) which can help reduce friction-related Koebner phenomenon.

  Topical Glucocorticosteroids Top

Class II–IV topical glucocorticosteroids (TCs) in a cream base with or without occlusion applied carefully and sparingly as a very thin film once daily has been used for the treatment of localized classic cutaneous CLP. The pruritus usually reduces by 3–4 weeks, while flattening of lesions is achieved at around 6 weeks. Most cases of localized cutaneous LP show remission by the 20–24th week of therapy.[11],[12] However, TCs do little to change the chronic course of disease and cannot prevent emergence of new lesions or hasten the resolution of the postinflammatory hyperpigmentation. Once the lesions have changed color from erythematous–violaceous to gray-brown with flattening, there is no further response to the TCs. TCs are quite safe only if used for few weeks, not more than 2–4 months, to avoid local side effects.

The use of Class I super-potent TCs in ointment base under hydrocolloid occlusive dressing is reserved with caution for localized discrete hypertrophic, erosive, and palmoplantar LP.[2],[11] It has to be borne in mind that employing occlusion has a very real risk of accelerated local toxicity and percutaneous absorption (e.g., tachyphylaxis, suppression of hypothalamic-pituitary-adrenal axis, Cushing's syndrome, and growth retardation) and is not routinely recommended in children.

Intralesional corticosteroids

Intra- and sublesional injections with triamcinolone acetonide (TAC) in strength of 5–20 mg/ml injected in the center of lesion (0.5–1 ml per 2-cm2 lesion) is an effective therapy for recalcitrant thicker lesions of LPH, palmoplantar LP, and other unresponsive lesions is an effective therapy for recalcitrant thicker lesions of LPH, palmoplantar LP, and other unresponsive lesions. Given once in 3–6 weeks, they provide immediate short-term benefits with symptomatic relief within 72 hours.[11]

  Topical Calcineurin Inhibitors Top

Topical calcineurin inhibitors (TCIs) like tacrolimus 0.03% ointment and pimecrolimus 1% cream are valid alternatives to TCs and are of undeniable value in maintaining remission. Topical tacrolimus has been found to be most effective in scaly papuloplaque lesions. There are no documented reports of use of 0.1% tacrolimus for CLP. Pimecrolimus has been used in generalized and palmoplantar LP. Barring LPH, they are good step-down agents or steroid-sparing adjuncts, particularly in children with steroid-induced side effects. Due to the potential risk of malignancies, they are not recommended below 2 years of age.[13],[14],[15] Usually, TCIs are safe and well tolerated. The most common side effects are burning sensation, transient pruritus, and erythema at the site of the application which can be reduced by pre refrigerating the medication.

Miscellaneous agents

Topical tazarotene with keratolytic agents (6%–12% salicylic acid) is of value in the treatment of palmoplantar LP.[16] Topical calcipotriol has limited benefit and is not used routinely.[17]

[Table 1] details studies documenting topical therapies for LP.[18],[19],[20]
Table 1: Studies depicting use of topical therapeutics in childhood lichen planus

Click here to view

  Systemic Therapies in Pediatric Cutaneous Lichen Planus Top


First-generation H (1) antihistamines at bedtime are vital in controlling pruritus with a desirable sedative effect. However, they may cause disruption of sleep patterns and affect learning when taken for a prolonged duration. Nonsedative second-generation H (1) antihistamines are useful for daytime control of pruritus. They are well tolerated with fewer adverse effects on cognition in children.[21]

  Systemic Glucocorticosteroids Top

Glucocorticoids (GC) are widely used for CLP as they score well in view of efficacy, availability, and cost. Their drawback includes the systemic side effects and the risk of relapse when doses are tapered.

  Oral Glucocorticosteroids Top

A short course of systemic GC over 2–3 weeks with gradual tapering over 4–6 weeks is justified as first-line therapy in very early presentation of classic eruptive LP, severe extensive recalcitrant LP, severe LPH, eczematized, atrophic, or bullous LP.[2],[8],[22] LP pemphigoides (LPP) and bullous LP require high doses of systemic steroids along with dapsone or azathioprine.[2]

Widespread cutaneous lesions respond well to short-course therapy with systemic steroids but tend to relapse as the dose is reduced. Prednisolone at a dose of 0.5–2 mg/kg/day is tapered slowly at the rate of 2.5 mg/week over 2–6 weeks to minimize the occurrence of relapse.

Oral GC needs to be administered only as short courses in children. Long courses, especially during two major growth spurts of childhood: before age 2 and at puberty, may cause loss of height.[23] Betamethasone in an early morning dose of 0.1 mg/kg dose on 2 consecutive days per week over 3 months as oral mini-pulse therapy has been used in CLP with good response and minimal adverse effects.[24]

Intramuscular corticosteroids

Intramuscular (i/m) injections of TAC, 10–20 mg every 6–8 weeks for a maximum of 3 doses, can be used in unresponsive cases of generalized cutaneous CLP although there is no corroborative published evidence. Hypothalamo-pituitary-adrenal suppression and myopathy due to longer-acting TAC entail cautious use restricted to children >6 years of age.[5],[25]

  Retinoids Top

The anti-inflammatory retinoids have shown a good level of evidence of efficacy for cutaneous LP. Acitretin (<0.5–1 mg/kg/day) is safe, effective, well tolerated in children with LPH and acute severe generalized or exanthematous mucocutaneous LP. Due to a longer half-life, it induces sustained remission. For dose titration according to weight, the capsule contents can be opened and dissolved in a liquid dietary medium or frozen and cut in the required fraction and dispensed in a liquid, namely honey, milk, or infant formula before administration. Since acitretin is sensitive to light, the remaining fraction should be discarded.[26]

A therapy of 8 weeks is usually sufficient. It can be safely combined with topical drugs and narrowband ultraviolet B (NBUVB) phototherapy. However, the duration of post-treatment remission in children remains undocumented.[2],[27]

Long-term use of high-dose acitretin (generally not required for CLP) may be associated with premature closure of the epiphyses.[28] Cheilitis, xerosis, pruritus, epistaxis, and transient elevation in serum lipids and hepatic enzymes can be managed symptomatically and do not warrant discontinuation.[22] Oral isotretinoin (0.5 mg/kg/day) too has been found to be useful in severe cases of mucocutaneous LP.[29]

  Oral Immunosuppressants Top


There are no specific guidelines or consensus yet on cyclosporine (CsA) use in pediatric dermatosis, and all the data available are experience-based retrospective analysis, mostly in cases of atopic dermatitis and psoriasis.[30] Anecdotal reports in adults suggest efficacy in severe disseminated treatment-resistant CLP. It has a rapid onset of action and provides long-term remission in cutaneous CLP.

In children, the oral absorption may be lower, the clearance more rapid, and the volume distribution greater at a steady state, necessitating somewhat higher dosages and more frequent administration than adults. Both low (1–2 mg/kg) and high doses (3–6 mg/kg) have been found to offer control or cure lesions by 6 weeks, with relapses controlled with topical steroids.[12] Pruritus disappears by 1–2 weeks of treatment with sustained remission for up to 10 months. Phototherapy is contraindicated with this regimen as there is a high risk of epithelial skin cancer.

Availability as an oral solution (100 mg/ml, 50 ml) allows accurate weight-based dose titration with the help of a calibrated syringe. Administered in milk or orange juice (not grapefruit juice) to conceal the taste, it should preferably be given in glass or ceramic cups since CsA binds to plastics. Although fairly well tolerated, regular serum creatinine and blood pressure monitoring is recommended and it is prudent to keep daily doses <5 mg/kg to avoid renal toxicity.[28],[31],[32] Used judiciously, CsA is a safe and effective option for extensive CLP, particularly as a fast-acting rescue drug offering longer periods of remissions.

  Methotrexate Top

Methotrexate (MTX) with folic acid co-administration is safe and effective in CLP in doses as low as 0.2–0.5 mg/kg/week with a reduction in pruritus by 4 weeks and response by 14–24 weeks. This dosing can be used for short periods in acute generalized recalcitrant or severe mucocutaneous CLP including LPP.[33],[34]

MTX offers the advantage of convenient weekly oral or subcutaneous doses. Orally, it can be given as crushed tablets mixed in nonmilk food as milk may interfere with absorption.[35] Nausea and vomiting are commonly reported adverse effects with transient elevation in liver enzymes. In acute LP after achieving therapeutic control, it is recommended to taper the dose to reduce side effects. In cases where LP has been chronic or recurrent, MTX is not the preferred therapy.

Mycophenolate mofetil and Azathioprine

There are no documented reports of the use of mycophenolate mofetil (MMF) or azathioprine (AZA) in CLP.

MMF should be reserved for severe, recalcitrant, erosive mucocutaneous LP in a dose range of 600 mg/m2 daily, for children above 6 months.[36],[37] Complete blood counts are to be monitored weekly during the 1st month of therapy, followed by, twice monthly for 2 months, and then monthly for the remainder of therapy. Side effects include mild gastrointestinal symptoms and cytopenia.

AZA is reserved for children with recalcitrant LP or as steroid-sparing agents in LPP. The concern of immunosuppression and the potential development of malignancy has limited its use. AZA has a slow onset of action. Pediatric patients with normal thiopurine methyltransferase (TPMT) activity levels (≥15.4 U/mL) should receive AZA at 2.5 mg/kg/day, possible carriers of a mutant allele (11.9-15.3 U/mL) 2.0 or 2.5 mg/kg/day, while definite carriers with intermediate enzyme levels (6.0–11.8 U/mL) begin at 1.0 mg/kg/day. Individuals with low TPMT levels (≤5.9 U/mL) should not be prescribed AZA.[38],[39]

Guidelines for vaccination in children on immunosuppressants

Immunization of the child should preferably be updated for age before commencing immunosuppressive therapy. Systemic steroid dose higher than prednisolone 2 mg/kg, (or 20 mg/day or its equivalent for those weighing more than 10 kg) for a period longer than 14 days causes immunosuppression. Live vaccines should not be administered to these children until at least 1 month after steroid discontinuation. Live vaccinations are not contraindications with lower doses or shorter duration of oral treatment or with topical or intralesional steroid therapy.

Live vaccines should be avoided for at least 3 months after other immunosuppressive drugs (CsA, MTX, AZA, and MMF) and 6 months after biologic agents.

Killed vaccines are safe but may be less efficacious. There are no specific recommendations about when to restart immunosuppressives after vaccination. However, immunosuppressive therapy initiation should be deferred for 4 weeks after live vaccine and 2 weeks after inactivated vaccines.[40]

  Oral Immunomodulators Top


Dapsone is an effective, safe therapy with a remarkable antipruritic effect.[11] Used for acute generalized LP, it reduces itching within 2–4 weeks with flattening of lesions in 8–10 weeks with complete remission achieved in 14–16 weeks. Localized LP may take longer to respond, usually up to 20–22 weeks. It has been found to be ineffective in LPH. It has value as a steroid-sparing agent in the management of LPP.[2]

However, dapsone (1.5–2 mg/kg/day as a single bedtime dose) can be given only when the hemoglobin is >10 gm% with age-appropriate G6PD levels, with monthly monitoring of hemogram and liver function tests.


Metronidazole has been used at a dose of 10 mg/kg dose, three times a day leading to a reduction in pruritus within 3–6 weeks in cases of acute generalized, classic CLP and LPH. Complete remission has been achieved by 20 weeks.[2],[11]


Narrow-band ultraviolet B phototherapy (NB-UVB) is safe and effective, particularly in acute eruptive or generalized LP or as maintenance therapy while tapering systemic drugs. Given thrice a week on nonconsecutive days (average 40–50 sittings, at a starting UVB dose of 150 mJ/cm2, with weekly increments of 20%, according to the clinical response and tolerance), it leads to control of pruritus and complete flattening of lesions.[41] Oral photochemotherapy with psoralens and ultraviolet A is contraindicated in children aged below 11 years because of psoralen toxicity (e.g. gastric and ocular damage).


Hydroxychloroquine (4–6 mg/kg/day as a short tapered course over 6–8 weeks) has promising efficacy in actinic LP due to its immunomodulatory, anti-inflammatory, and photoprotective effect.[42] Adverse effects include gastrointestinal disturbance and headache.


It is postulated that apremilast could be effective in the treatment of lichenoid dermatitis; however safety, efficacy, and posology in children remain to be evaluated. A study in pediatric patients with psoriasis reports the use of 20–30 mg apremilast in ages 12–17 with weight >35 kg and 20 mg in ages 6–11 years with weight >15 kg.[43],[44]


Oral erythromycin (30 mg/kg in four divided doses) and nicotinamide (150 mg three times a day) have been shown to be useful in LPP or bullous LP.[2],[45]

Biologics (like adalimumab) and Janus kinase inhibitors (tofacitinib) have been used in therapy of LP in adults; however, there is no evidence of their use in pediatric subjects.[46],[47] Other drugs such as griseofulvin, pulsed itraconazole, and subcutaneous enoxaparin have been tried with variable success.[32],[48]

[Table 2] enumerates studies reporting systemic therapies in CLP. [Table 3], [Table 4], [Table 5] summarize therapeutic options for the management of cutaneous CLP.[2],[12],[49],[50],[51]
Table 2: Studies documenting systemic therapies for childhood lichen planus

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Table 3: Interventions (as monotherapy or in combination) suggested for localized pediatric cutaneous lichen planus

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Table 4: Interventions suggested for acute eruptive generalized pediatric cutaneous lichen planus (in addition to topical therapy as detailed in Table 3)

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Table 5: Interventions for generalized chronic/recurrent pediatric cutaneous Lichen planus (in addition to topicaltherapy detailed in Table 3)

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  Treatment of Pediatric Mucosal Lichen Planus Top

Pediatric oral lichen planus

Majority of cases tend to be asymptomatic and can be left untreated with careful semiannual follow-up; however, erosive or ulcerated oral lichen planus (OLP) often has a refractory course and demands quick symptomatic therapy ensuring compliance and palliation.[2],[22] Reduced intake of spicy, acidic food with avoidance of oral hygiene products like minty toothpastes and trauma (lip/cheek chewing) are to be advised.[52] Local anesthetic sprays or soothing gels containing aloe barbadensis during meal times offer symptomatic relief.[53]

The first-line therapy is high-potency topical corticosteroids in orabase applied as a thin film on dried oral mucosa twice a day with the child refraining from eating, drinking, or speaking for 30 min post application. It is then tapered as required over several months. Prolonged use may cause secondary candidiasis, a smarting sensation in the mouth, gingival tenderness, adrenal insufficiency, and potential tachyphylaxis. Concomitant antimycotic treatment along with alcohol-free oral rinse with plaque control regimen is advised.[52]

Intra- and sublesional injections in fractional amounts circumferentially just below the edge of ulcers at various points with TAC (0.5 ml of 10 mg/ml to avoid mucosal atrophy) repeated at an interval of 3–6 weeks are used with rapid relief of pain and ulceration at the end of 2 weeks. Additional injections are given in the floor in case of large ulcers. Lip lesions tend to respond less favorably. In severe cases, 0.3–0.5 mg/kg of oral steroid with tapering over 3–6 weeks is helpful.[2],[54]

In children between 2 and 15 years, tacrolimus 0.03% ointment is used. A common side effect is local burning which improves with time or can be minimized by refrigerating the ointment prior to application. Comparatively pimecrolimus 1% cream causes less local burning and effectively treats erosive OLP with long-lasting therapeutic effects. They are to be applied twice a day for 4–6 weeks.[55]

Topical isotretinoin gel 0.1% for buccal mucosal lesions was found to be effective in providing symptomatic relief as well as achieving early response (within 6 weeks). Topical tretinoin 0.05% gel used twice a day for 2 weeks has resulted in remission by 4 weeks.[56] Recombinant bovine basic fibroblast growth factor gel, a pleiotropic cytokine that promotes angiogenesis, neurotrophy, and mucosal integrity, has been reported to induce remission in childhood OLP by 2 months.[7]

In diffuse/multisite recalcitrant erosive OLP, systemic steroids can be given either in intermediate doses (0.3–0.5 mg/kg) as short bursts to induce remission or as a mini-pulse with betamethasone on 2 consecutive days a week.[24]

Oral acitretin (0.5–1 mg/kg) provides satisfactory response at 8–12 weeks with longer remissions.[57] Oral immunosuppressants, particularly CsA, can be considered in severe OLP recalcitrant to first-line therapies (others being MTX, MMF, and AZA).[12] Apremilast, griseofulvin, dapsone, hydroxychloroquine, zinc supplementation, curcuminoids, NBUVB phototherapy, cryotherapy, and interferons among others have been used on a very limited basis with varied success. Lasers (Excimer, diode, CO2) give gratifying results in OLP and have shown to yield long-term remission of symptoms, and may be promising as first-line therapy in painful OLP.[52],[58],[59] Excision with free tissue grafts is alternative in localized lesions of erosive LP.

  Pediatric Genital Lichen Planus Top

Few studies have reported genital involvement in children. It should however be actively looked for, in patients with oral LP, where the lesions may go unnoticed by the patient.[60]

Plain warm water washes, avoidance of soap and tight underwear, with the application of liberal nonirritating emollient like petrolatum or chilled aqueous cream pre and post micturition with icepacks are important supportive measures. Mid to ultrapotent corticosteroids in ointment base are applied once a day as a thin smear in mild cases till relief is obtained, followed by slow tapering. The cream may be preferred but is more likely to sting on application. Hydrocortisone foam can be used inside the vagina or anus. TCI once or twice daily have been used in erosive disease with limited success. High-dose systemic corticosteroids in combination with steroid-sparing agents have been used, with steroids tapered over 3–6 weeks after the effect of steroid-sparing agent sets in. In severe refractory cases, stronger immunesuppressants may be needed such as MTX, CsA, MMF, or AZA. Surgical release of LP-induced vulval and vaginal adhesions and scarring may occasionally be performed to reduce urination difficulties.[61]

Pediatric appendageal lichen planus

Lichen planopilaris is a rare, recalcitrant form of cicatricial alopecia occasionally reported in children.[61] First-line therapy for scalp involvement (<10% without cosmetically disfiguring alopecia) is ultra-potent topical corticosteroids or intralesional corticosteroids (ILS) in a tapering regimen. High-potency topical steroids are used twice daily for the initial 1 month and tapered to once daily for the subsequent 3 months and finally on alternate days for 3 months thereafter. ILS (TAC 3–5 mg/ml 3–4 weekly) is given circumferentially along the active edge of alopecic patch. TCIs (tacrolimus 0.03% ointment) are advised twice a day for at least 1 month. Oral corticosteroids are beneficial in rapidly progressive scarring disease (1 mg/kg tapered over 3–4 months). Retinoids are used as second-line therapy in extensive lesions. Acitretin (0.5–0.7 mg/kg) or isotretinoin (0.3–0.5 mg/kg) is used especially in cases with pronounced perifollicular hyperkeratosis. Oral immunosuppressants like MTX are an effective long-term alternative after initial corticosteroid therapy. CsA is used in refractory lichen planopilaris (3–5 mg/day for 3–5 months).[61],[62],[63]

Pediatric nail lichen planus

In most cases, nail LP (NLP) in children affects the nail matrix which if left untreated may lead to scarring. Systemic corticosteroids halt the disease process and preserve the existing nail. They may be administered orally (prednisolone, 0.5–0.75 mg/kg/day over 1–12 weeks/oral mini-pulse with dexamethasone 2.5 mg/day on 2 consecutive days a week) or as intramuscular injection (TAC 0.5–1 mg/kg every 30 days).[4] Intramuscular TAC has been reported to give a complete cure of fingernails at 6–8 months and toenails at 8–12 months while decreasing the risk for systemic side effects in comparison with oral corticosteroids. Adverse effects included lipoatrophy at the injection site and cushingoid facies.[5] Relapses might occur with both oral and intramuscular corticosteroids; however, these recurrences are always responsive to therapy.[64]

NLP presenting as twenty-nail dystrophy often improves without any treatment. Treatment is prescribed for cosmetic reasons with bland emollients and camouflage with nail polish. Nail plate dressings (ultra-thin adhesive bandage applied once a week with lactic acid, silicon dioxide, aluminum acetylacetonate, copolymer of vinyl acetate with acrylic acid, and azelaic acid) were found to improve symptoms after 3 months in a pediatric patient. Topical therapy includes corticosteroids, calcipotriol/betamethasone dipropionate ointment, tazarotene gel (0.05%), and 5% 5-fluorouracil application on periungual folds. Acitretin has been used in doses of 0.3–0.5 mg/kg/day in the treatment of trachyonychia secondary to LP.[65] Other systemic treatments include biotin 2.5 mg/day, CsA 2–3.5 mg/kg/day, systemic corticosteroids, and tofacitinib citrate.[66]

The scarring atrophic variant of NLP is found frequently in Indian children. Oral prednisolone as a tapering dose over 4–12 weeks may be tried to halt the acute and rapid course that may lead to diffuse painless nail destruction in a few months. Permanent damage to the nail matrix needs surgical correction after subsidence of disease activity and cessation of all oral medication.[2],[5]

[Table 6] summarizes published case series documenting therapeutic options for CLP.[67],[68]
Table 6: Case series illustrating treatment modalities of pediatric lichen planus

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  Conclusion Top

Most children with LP respond to treatment with full clearance over 1–6 months. Robust evidence of efficacy is lacking for most therapeutics and a more lucid consensus for the treatment of CLP is the need of the hour.

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Conflicts of interest

There are no conflicts of interest.

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  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]


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