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Tiffany Chen, MD, FRCPC

Tiffany Chen is a board-certified dermatologist in Canada and the United States. She received her Honours B.Arts Sc. and MD from McMaster University. She completed her dermatology residency at the University of Toronto and served as chief resident in her final year. Dr. Chen practices in Toronto and is a clinical associate in the Division of Dermatology at Sunnybrook Health Sciences Centre.

Canadian Dermatology Today, Volume 2, Issue 2, May 2021

An Update on Treatments for Lichen Planopilaris

Lichen planopilaris (LPP) is an immune-mediated cicatricial alopecia that is often challenging to treat. In LPP, hair follicles are selectively destroyed by a chronic lymphocytic inflammatory process, leading to irreversible scarring and permanent hair loss (Figure 1 and 2). Several variants of LPP have been described in the literature including the classic form, the Graham-Little-Piccardi-Lassueur syndrome, frontal fibrosing alopecia, and recently, a new clinical variant, lichen planopilaris diffuse pattern.1

Figure 1. Lichen planopilaris of the scalp characterized by perifollicular scale, perifollicular erythema, and scarring

Figure 2. A case of lichen planopilaris in a female patient

LPP is associated with a high burden of disease and causes significant psychological distress to patients. In addition to visible hair loss, many patients experience burning, itching, and scalp tenderness which contribute to the quality of life impairment associated with the condition. The understanding that it is an incurable disease and that there are no consistently effective treatment options can also make coping with LPP difficult for patients. A recent retrospective review of 215 women with LPP with a mean age of 59.8 years found a high incidence of depression (45.7%), anxiety (41.8%), and sleep disturbance (29.2%).2

When approaching the management of LPP, patient selection and clear communication around treatment expectations are essential. Patients most likely to benefit from treatment are those with active disease—the presence of perifollicular scale and erythema, progressive hair loss, symptoms, and an inflammatory process on scalp biopsy compatible with LPP indicate that the condition is active. Conversely, end-stage lesions of LPP are unlikely to respond to treatment. With respect to treatment expectations, patients should understand that the goal of therapy is to stop disease progression and alleviate symptoms. Due the scarring nature of LPP, hair regrowth in areas of existing alopecia is not expected.

Treatment of LPP remains difficult. Due to a lack of high-quality evidence on therapies and the unpredictable clinical course of the disease, the best approach to the treatment of LPP is currently unclear. The absence of consistent methods to assess the response to treatment in the literature has also contributed to uncertainty about treatment efficacy. As a result, treatment varies widely. 

Traditional first-line therapy for limited disease involves the use of topical and intralesional corticosteroids. Common systemic therapies include hydroxychloroquine and systemic antibiotics such as doxycycline. Despite the initial effectiveness of these treatments, relapses are common.2,3 As a result, a range of other therapeutic options has been investigated. In addition to the treatments discussed in this article, data suggest that methotrexate, cyclosporine, oral retinoids, pioglitazone, and 5-alpha reductase inhibitors such as finasteride and dutasteride could be helpful in the treatment of LPP. 

The objective of this article is to review recent data published in the literature on therapeutic modalities for LPP. 

Oral Minoxidil

Oral minoxidil is a systemic vasodilatory agent which has demonstrated efficacy in the treatment of androgenetic alopecia and chronic telogen effluvium. A recent retrospective review evaluated the role of low dose oral minoxidil (LDOM) in increasing hair thickness in patients with LPP.4 LDOM was started at a dose of 0.25 to 1 mg and gradually uptitrated over a minimum treatment duration of 6 months. Subjects’ change in global hair thickness was assessed before and after LDOM treatment. The study found that hair thickness improved in 39% of patients, remained stable in 53% of patients, and worsened in only 8% of patients. LDOM was generally well-tolerated, with mild adverse events such as hypertrichosis, postural hypertension, tachycardia, and weight gain being reported in a minority of patients.

The study concluded that LDOM can help to maintain or improve hair thickness in most patients with LPP, with an acceptable safety profile. The increase in background hair thickness generated by LDOM might provide better concealment of adjacent areas of hair loss, thus reducing patient disease burden. Although there were limitations of the study, including its small sample size (n = 51) and retrospective design, LDOM may be a promising therapeutic option to add to the treatment armamentarium for patients with LPP.

Mycophenolate mofetil

While the pathophysiology of LPP remains poorly understood, the disease is thought to result from a T-lymphocyte-mediated cytotoxic immune reaction to follicular antigens. Mycophenolate mofetil (MMF) is an antimetabolite that blocks de novo guanine nucleotide synthesis by inhibiting inosine monophosphate dehydrogenase. Both T and B lymphocytes lack purine scavenger mechanisms and consequently, their DNA replication pathways are inactivated by MMF. Recently, a systematic review and meta-analysis was published regarding the outcomes of MMF in LPP.5  Based on a total of six studies comprising 94 LPP patients, the pooled proportion of any good response (either partial or complete) was 69.2%
(95% CI 47.8 – 77.0). Side effects occurred in 16.9% of cases, which included elevated liver function tests, edema, hyperlipidemia, anaemia, herpes zoster infection, photosensitivity, and urinary tract infection. Based on these findings, it was concluded that MMF is reasonably effective and well-tolerated in the treatment of LPP, with fewer associated adverse events than other immunosuppressive medications such as cyclosporine. Although the current evidence for MMF remains limited, it appears to be a potential therapeutic option for patients with severe or recalcitrant LPP who have failed hydroxychloroquine and other immunosuppressants.

Platelet-rich plasma

Platelet-rich plasma (PRP) has emerged as a popular treatment option for non-scarring alopecias such as androgenetic alopecia. Until recently, its effectiveness in treating cicatricial alopecias including lichen planopilaris was largely unknown. Over the last two years, there has been increasing evidence to support its clinical benefits in the treatment of LPP.6,7 A recent retrospective analysis examined the effect of PRP in 10 patients with LPP.6 After an average of four treatments, four out of ten patients demonstrated improvement in LPP, defined by disease stabilization and/or attenuated symptoms, and three out of ten patients demonstrated neither improvement nor worsening. While the exact mechanism of action of PRP remains unclear, it is thought to promote hair growth via its effects on platelets, growth factors, and anti-inflammatory mediators. There have been concerns regarding the potential for PRP to cause new areas of disease (i.e., koebnerization) in patients with LPP. However, this retrospective review concluded that PRP need not necessarily be avoided for LPP patients and that it may result in clinical improvement without koebnerization. Future studies are needed to better understand the role of PRP in the treatment of LPP.


Tofacitinib is a pan-Janus kinase (JAK) inhibitor approved for the treatment of moderate-to-severe rheumatoid arthritis, psoriatic arthritis, and ulcerative colitis. It has been used off-label in its topical and systemic forms for the treatment of various dermatologic conditions including psoriasis and vitiligo, as well as in the non-scarring alopecia, alopecia areata.8 Two recent retrospective review studies found that tofacitinib was an effective therapeutic option for patients with LPP. Responses in both studies were evaluated based on patient-reported symptoms and physical examination findings. The first retrospective case series, published in 2018, included six females and four males and the average age at presentation was 55 years (range 33–68 years). The diagnosis of LPP was biopsy proven in five patients and was a clinical diagnosis in the remaining five patients. This study reported that eight out of ten patients treated with oral tofacitinib 5 mg twice daily or three times daily for 2-19 months as either monotherapy or adjunctive therapy had clinical improvement as measured by lichen planopilaris activity index (improvement ranged from 30% to 94%). Adjunctive therapies were used in five patients and included intralesional triamcinolone (two patients), hydroxychloroquine (one patient), intralesional triamcinolone and hydroxychloroquine (one patient), and intralesional triamcinolone and tacrolimus ointment (one patient).9 Tofacitinib was well tolerated by all patients.

In the second retrospective review, published in 2020, topical and oral tofacitinib were used adjunctively in nine patients with LPP.10 Three of four patients receiving topical therapy (2% cream twice daily) achieved a positive response, and all patients receiving systemic therapy (5 mg twice daily or three times daily) demonstrated a favourable response. Minor laboratory abnormalities were noted in patients on systemic therapy and included mild, transient hemoglobin and creatinine abnormalities, and mildly elevated triglyceride and cholesterol levels, but none required treatment. No other adverse events were reported. Despite these promising results, further investigation of tofacitinib in the setting of LPP is warranted.


Naltrexone is a long-acting opioid antagonist. At a low daily dose of between 1 and 5 mg, naltrexone exhibits both analgesic and anti-inflammatory effects and has been used successfully in treating a variety of inflammatory conditions. In the context of dermatology, low-dose naltrexone (LDN) has demonstrated benefit in the treatment of pruritus, Hailey-Hailey disease, Grover disease, and Darier disease.11 In a case series of 4 patients with LPP treated with 3 mg of naltrexone daily, a reduction in pruritus, clinically evident scalp inflammation, and disease progression was seen in all patients. Improvements were noted within 1 to 2 months of starting therapy and no adverse events were reported.12 LDN is an interesting treatment option for LPP as it is relatively inexpensive, well-tolerated, and does not require laboratory monitoring. Further studies are required to better understand its potential role in the treatment of LPP.


In conclusion, new data continues to emerge on therapeutic options for LPP. As with other challenging and refractory dermatologic conditions, LPP will likely require a multimodal treatment approach involving the combination of therapeutic agents to achieve optimal outcomes. Although there is still a need for high quality data, the promising therapies reported in the literature in recent years will likely be a useful addition to our clinical repertoire.


1. Goldstein AT, Marinoff SC, Christopher K, Srodon M. Prevalence of vulvar lichen sclerosus in a general gynecology practice. J Reprod Med. 2005;50(7):477-480.

2. Bleeker MC, Visser PJ, Overbeek LI, van Beurden M, Berkhof J. Lichen Sclerosus: Incidence and Risk of Vulvar Squamous Cell Carcinoma. Cancer Epidemiol Biomarkers Prev. 2016;25(8):1224-1230. doi:10.1158/1055-9965.EPI-16-0019

3. Fistarol SK, Itin PH. Diagnosis and treatment of lichen sclerosus: an update. Am J Clin Dermatol. 2013;14(1):27-47. doi:10.1007/s40257-012-0006-4

4. Gao XH, Barnardo MC, Winsey S, et al. The association between HLA DR, DQ antigens, and vulval lichen sclerosus in the UK: HLA DRB112 and its associated DRB112/DQB10301/04/09/010 haplotype confers susceptibility to vulval lichen sclerosus, and HLA DRB10301/04 and its associated DRB10301/04/DQB10201/02/03 haplotype protects from vulval lichen sclerosus. J Invest Dermatol. 2005;125(5):895-899. doi:10.1111/j.0022-202X.2005.23905.x

5. Marren P, Yell J, Charnock FM, Bunce M, Welsh K, Wojnarowska F. The association between lichen sclerosus and antigens of the HLA system. Br J Dermatol. 1995;132(2):197-203. doi:10.1111/j.1365-2133.1995.tb05013.x

6. Powell J, Wojnarowska F, Winsey S, Marren P, Welsh K. Lichen sclerosus premenarche: autoimmunity and immunogenetics. Br J Dermatol. 2000;142(3):481-484. doi:10.1046/j.1365-2133.2000.03360.x

7. Meyrick Thomas RH, Ridley CM, McGibbon DH, Black MM. Lichen sclerosus et atrophicus and autoimmunity–a study of 350 women. Br J Dermatol. 1988 Jan;118(1):41-6. doi: 10.1111/j.1365-2133.1988.tb01748.x. Erratum in: Br J Dermatol 1988 May;118(5):736. PMID: 3342175.

8. Cooper SM, Ali I, Baldo M, Wojnarowska F. The association of lichen sclerosus and erosive lichen planus of the vulva with autoimmune disease: a case-control study. Arch Dermatol. 2008 Nov;144(11):1432-5. doi: 10.1001/archderm.144.11.1432. PMID: 19015417.

9. Eisendle K, Grabner T, Kutzner H, Zelger B. Possible role of Borrelia burgdorferi sensu lato infection in lichen sclerosus. Arch Dermatol. 2008;144(5):591-598. doi:10.1001/archderm.144.5.591

10. Requena López S, Hidalgo García Y, Gómez Díez S, Vivanco Allende B. Morphea and Extragenital Lichen Sclerosus et Atrophicus After Influenza Vaccination. Morfea y liquen escleroatrófico extragenital generalizados tras vacuna antigripal. Actas Dermosifiliogr. 2018;109(1):86-88. doi:10.1016/

11. Pass CJ. An unusual variant of lichen sclerosus et atrophicus: delayed appearance in a surgical scar. Cutis. 1984;33(4):405-408.

12. De Giorgi V, Scarfì F, Silvestri F, et al. Genital piercing: A warning for the risk of vulvar lichen sclerosus. Dermatol Ther. 2021;34(1):e14703. doi:10.1111/dth.14703

13. Fergus KB, Lee AW, Baradaran N, et al. Pathophysiology, Clinical Manifestations, and Treatment of Lichen Sclerosus: A Systematic Review. Urology. 2020;135:11-19. doi:10.1016/j.urology.2019.09.034

14. Bolognia JL, Schaffer JV,  Cerroni L. Dermatology. 4th edition. Elsevier; 2018

15. Patterson, J. Weedon’s Skin Pathology. 4th Edition. Elsevier; 2014

16. Rapini, R. Practical Dermatopathology. Elsevier, 2012. 

17. Kirtschig G, Becker K, Günthert A, et al. Evidence-based (S3) Guideline on (anogenital) Lichen sclerosus. J Eur Acad Dermatol Venereol. 2015;29(10):e1-e43. doi:10.1111/jdv.13136

18. Kim GW, Park HJ, Kim HS, et al. Topical tacrolimus ointment for the treatment of lichen sclerosus, comparing genital and extragenital involvement. J Dermatol. 2012;39(2):145-150. doi:10.1111/j.1346-8138.2011.01384.x

19. Cattaneo A, Carli P, De Marco A, et al. Testosterone maintenance therapy. Effects on vulvar lichen sclerosus treated with clobetasol propionate. J Reprod Med. 1996;41(2):99-102.

20. Bornstein J, Heifetz S, Kellner Y, Stolar Z, Abramovici H. Clobetasol dipropionate 0.05% versus testosterone propionate 2% topical application for severe vulvar lichen sclerosus. Am J Obstet Gynecol. 1998;178(1 Pt 1):80-84. doi:10.1016/s0002-9378(98)70631-3

21. Cuellar-Barboza A, Bashyam AM, Ghamrawi RI, Aickara D, Feldman SR, Pichardo RO. Methotrexate for the treatment of recalcitrant genital and extragenital lichen sclerosus: A retrospective series. Dermatol Ther. 2020;33(4):e13473. doi:10.1111/dth.13473

22. Bousema MT, Romppanen U, Geiger JM, et al. Acitretin in the treatment of severe lichen sclerosus et atrophicus of the vulva: a double-blind, placebo-controlled study. J Am Acad Dermatol. 1994;30(2 Pt 1):225-231. doi:10.1016/s0190-9622(94)70021-4

23. Ioannides D, Lazaridou E, Apalla Z, Sotiriou E, Gregoriou S, Rigopoulos D. Acitretin for severe lichen sclerosus of male genitalia: a randomized, placebo controlled study. J Urol. 2010;183(4):1395-1399. doi:10.1016/j.juro.2009.12.057

24. Shelley WB, Shelley ED, Amurao CV. Treatment of lichen sclerosus with antibiotics. Int J Dermatol. 2006;45(9):1104-1106. doi:10.1111/j.1365-4632.2006.02978.x

25. Gardner AN, Aschkenazi SO. The short-term efficacy and safety of fractional CO2 laser therapy for vulvovaginal symptoms in menopause, breast cancer, and lichen sclerosus [published online ahead of print, 2021 Jan 4]. Menopause. 2021;Publish Ahead of Print:10.1097/GME.0000000000001727. doi:10.1097/GME.0000000000001727

26. Mendieta-Eckert M, Torrontegui Bilbao J, Zabalza Estévez I, Landa Gundin N. Treatment of Vulvar Lichen Sclerosus et Atrophicus With Fractional Carbon Dioxide Laser Therapy: A Report of 4 Cases. Tratamiento de liquen escleroso y atrófico vulvar con láser de dióxido de carbono fraccionado. Presentación de cuatro casos. Actas Dermosifiliogr. 2021;112(1):85-88. doi:10.1016/

27. Mendieta-Eckert M, Ocerin-Guerra I, Landa-Gundin N. Lichen sclerosus et atrophicus in a surgical scar treated with fractional laser. J Cosmet Laser Ther. 2017;19(2):106-108. doi:10.1080/14764172.2016.1262955

28. Lee A, Lim A, Fischer G. Fractional carbon dioxide laser in recalcitrant vulval lichen sclerosus. Australas J Dermatol. 2016;57(1):39-43. doi:10.1111/ajd.12305

29. Pagano, Tiziana, et al. “Effect of rescue fractional microablative CO2 laser on symptoms and sexual dysfunction in women affected by vulvar lichen sclerosus resistant to long-term use of topic corticosteroid: a prospective longitudinal study.” Menopause 27.4 (2020): 418-422.

30. Ferrara F, Messori S, Abbenante D, Patrizi A, Bardazzi F. Fractional CO2 laser therapy of lichen sclerosus in males: a new therapeutic opportunity? [published online ahead of print, 2020 Jul 20]. J Dermatolog Treat. 2020;1-5. doi:10.1080/09546634.2020.1793886

31. Tedesco M, Pranteda G, Chichierchia G, et al. The use of PRP (platelet-rich plasma) in patients affected by genital lichen sclerosus: clinical analysis and results. J Eur Acad Dermatol Venereol. 2019;33(2):e58-e59. doi:10.1111/jdv.15190

32. Behnia-Willison F, Pour NR, Mohamadi B, et al. Use of Platelet-rich Plasma for Vulvovaginal Autoimmune Conditions Like Lichen Sclerosus. Plast Reconstr Surg Glob Open. 2016;4(11):e1124. Published 2016 Nov 23. doi:10.1097/GOX.0000000000001124

33. Casabona F, Gambelli I, Casabona F, Santi P, Santori G, Baldelli I. Autologous platelet-rich plasma (PRP) in chronic penile lichen sclerosus: the impact on tissue repair and patient quality of life. Int Urol Nephrol. 2017;49(4):573-580. doi:10.1007/s11255-017-1523-0

34. Navarrete J, Echarte L, Sujanov A, et al. Platelet-rich plasma for male genital lichen sclerosus resistant to conventional therapy: First prospective study. Dermatol Ther. 2020;33(6):e14032. doi:10.1111/dth.14032

35. Tedesco M, Garelli V, Bellei B, et al. Platelet-rich plasma for genital lichen sclerosus: analysis and results of 94 patients. Are there gender-related differences in symptoms and therapeutic response to PRP? [published online ahead of print, 2020 Dec 6]. J Dermatolog Treat. 2020;1-5. doi:10.1080/09546634.2020.1854650