Lichen Planus

Are You Confident of the Diagnosis?

Lichen planus (LP) is a papulosquamous disorder of the skin, mucous membranes, hair, and nails. Depending on subtype and area of involvement, lesions may range from asymptomatic to pruritic and erosive. Patients may have involvement of one or more of the areas listed above. Lesions of the glabrous skin are most commonly pruritic papules, but many subtypes have been described (see Table I).

Table I.
LP Subtype  Clinical Features
Typical LP Pruritic, polygonal, purple, flat-topped papules on extensor surfaces
Actinic LP More common in darkly pigmented individuals. Thought to be caused by UV light. Found in sun-exposed areas of the body. Hyperpigmented, atrophic lesions with a rolled border.
Annular LP Most common in men. Small papules in an annular configuration. May have a central region of atrophy and hypopigmentation. Often asymptomatic. Commonly involves the penis, scrotum and axilla.
Erosive LP Rare cutaneous form involving feet and toes most commonly. May require skin grafting. Commonly found in oral forms of LP.
Follicular LP Small hyperkeratotic papules centered on hair follicles
Hypertrophic LP Verrucous, hypertrophic plaques most common over the anterior lower extremities, particularly the shins.
Nodular LP Variant of hypertrophic LP whereby individul lesions become nodular
Inverse LP Papules and plaques without scale due to location in intertriginous areas
Invisible LP Pruritic lesions only visible with a Woods lamp examination or histologic evaluation
Linear LP  Papules and plaques in a linear pattern. May be caused by koebnerization.
Localized LP Limited number of papules and plaques. Chronic. Shin most commonly involved.
Blashkoid LP  Papules and plaques following the lines of Blashko
Bullous LP This is not related to LP pemphigoides. Vesicles or bulla develop at sites of chronic lesions of LP. Most frequently seen on the legs.
LP Pemphigoides Vesicular and bullous lesions overlying areas of typical or classical LP. Autoantibodies to the 180kd bullous pemphigus antigen have been demonstrated.
LP Pigmentosus  Hyperpigmented, lichenified lesions. More common in dark skin types.
Palmar – Plantar Papules and plaques on the palms and soles. Painful. Difficult to treat.
Erosive LP Fairly common in oral LP. New areas should be evaluated for conversion to squamous cell carcinoma (SCC). Lesional biopsies should be performed with any non-healing erosion.
Erythematous LP  Red patches predominate in association with Wickham’s striae.
Reticular LP By far the most common form of oral LP. Reticulated white patches and/or plaques most commonly on the buccal mucosa but can occur anywhere along the oral mucosa including the gingiva, lip, palate, and esophagous.
Genital and Anal LP Glans penis most commmon site in genital LP. Anal LP can cause intense itching.
   Lichen Planopilaris A form of cicatrical alopecia with follicular hyperkeratosis. Diagnosis is made with clinical and histologic findings.
LP of the nail Multiple abnormalities have been described. They include the dorsal pterygium, onycholysis, onychodystrophy, trachyonychia, erythronychia, onychorrhexis, thinning, splitting, and longitudinal nail ridging or grooving.Subungual hyperkeratosis may be prominent in chronic cases involving the toe nails. The lunula may appear red secondary to underlying inflammation. Only the dorsal pterygium is specific for LP. In dorsal pterygium the proximal nail fold scars down on the nail matrix and nail bed
Characteristic findings on physical examination

Mucosal lesions can be oral or genital. Inquire specifically if the patient has genital involvement, as this is not uncommon but can easily be overlooked if not specifically addressed. Genital involvement may be asymptomatic or symptoms may include pruritus, burning, hyperalgesia, dyspareunia, vaginal discharge, or bleeding. Remodeling of vulval and vaginal architecture may prevent sexual intercourse.

Oral lesions may be asymptomatic if reticular, but other patients with erythematous or ulcerative disease may complain of pain, difficulty eating, odynophagia, or bleeding gums (Figure 1). Involvement of the hair ranges from scarring alopecia of the scalp to nonscarring alopecia of the axilla and pubic hair (Figure 2). LP of the nails can cause formation of pterygium, onychorrhexis, and trachyonychia. It may also, rarely, be the cause of 20-nail dystrophy in children (Figure 3).

Figure 1.

Oral LP with the characteristic white patches

Figure 2.

Lichenplanopilaris, a scarring form of alopecia

Figure 3.

Longitudinal nail ridging in LP

On physical examination there are multiple variants of LP, which may demonstrate overlapping features. For descriptive purposes it is helpful to divide these variants by anatomic location, although in practice, many patients will have involvement of multiple areas.


Classically described as small, violaceous, polygonal, flat-topped papules and plaques on glabrous skin (Figure 4). A fine white, reticulated scale or punctae (Wickham’s striae) may be appreciated with dermoscopy. Commonly affected areas include the flexural surface of arms, legs, and wrists. The face and scalp are typically spared.

Figure 4.

Classic cutaneous LP

Multiple subtypes of LP have been described:

Actinic LP is more common in dark-pigmented individuals. It is thought to be caused by UV light and is found in sun-exposed areas. Physical findings include hyperpigmented, atrophic lesions with a rolled border (Figure 5).

Figure 5.

Actinic LP

Annular LP is most common in men. It consists of small papules in an annular configuration. There may be a central region of atrophy and hypopigmentation. These lesions are often asymptomatic and commonly involve the penis, scrotum, or axilla.

The erosive form of LP can rarely occur on the feet and toes. Treatment may require skin grafting. Erosive subtype is very common in mucosal LP.

Hypertrophic LP is most commonly found in the anterior legs. The lesions are hypertrophic, verrucous, and scaly (Figure 6).

Figure 6.

Hypertrophic LP with post-inflammatory hypopigmentation

Inverse LP is found in the intertriginous areas. Scale is commonly absent.

Invisible LP demonstrates pruritic skin with no obvious lesions. Wood lamp or histologic biopsy may be demonstrative.

The papules and plaques of linear LP follow lines of Blaschko.

LP pemphigoides occurs when vesicles and bullae (clinically and histologically consistent with bullous pemphigoid) appear in conjunction with typical lesions of LP.

LP pigmentosus occurs more commonly in dark skin types. The typical lesions are hyperpigmented and lichenified.


Most commonly involves the oral cavity or vulvar mucosa. Rarely the esophagus, eyes, bladder, and ostomy stomas sites can be affected. Mucosal LP is divided into three subtypes: reticular, erythematous, and erosive.

The reticular form is often asymptomatic. Lesions are fine, reticulated, white patches and plaques most commonly overlying the buccal mucosa. This is the most common form of oral LP. The erythematous subtype also includes atrophic lesions.

Erosive LP causes painful erosions. In the oral cavity, these most frequently occur on the buccal mucosa, gingiva, and tongue. The most common type of genital involvement is erosive.

LP of the hair, also known as lichen planopilaris causes cicatricial alopecia with follicular hyperkeratosis. Graham-Little-Piccardi-Lassueur syndrome is the triad of cicatricial alopecia of the scalp, nonscarring alopecia of the axilla, groin, or eyebrows, and perifollicular hyperkeratotic papules.

Nail involvement by LP can range from a single nail to 20-nail dystrophy. The findings are nonspecific and include pterygium formation, longitudinal ridging, grooves, and striae, nail plate thinning, and anonychia.

Subtypes of LP are summarized in Table I.

Expected results of diagnostic studies

Laboratory studies are usually not necessary. Plasma eosinophilia may be present in drug-induced LP. LP can be difficult to distinguish from systemic lupus erythematosus and thus an ANA or anti-Smith antibody may be helpful in differentiation. LP pemphigoides may have anti-BP180 antigen antibodies.

The association between hepatitis C (HCV) and LP is well established but has considerable geographic variability. There may be an association with HCV-induced OLP in patients with the HLA-DR6 allele. Egypt has been reported to have the highest seropositivity rate for HCV. Southeast Asia and the Middle East have high rates as well, followed by the United States. Thus, screening for HCV may be indicated in high prevalence areas and of high-risk populations. High-risk individuals include IV drug users, patients with a history of multiple blood transfusions (especially before 1990), needle stick injuries in the health care setting, multiple sexual partners, and sharing of contaminated objects (razor, toothbrush, tattoo needles).

Histopathology of LP is distinctive and can aid in diagnosis. Mature lesions classically display destruction of the basal layer, irregular acanthosis in a “sawtooth” pattern, lichenoid lymphocytic infiltrate, and Civatte bodies, which represent collections of necrotic keratinocytes (Figure 7). Wickham’s striae are thought to represent an increased granular cell layer. Direct immunofluorescence (DIF) shows shaggy fibrinogen and IgM deposits along the basement membrane zone and Civatte bodies, respectively. DIF may be particularly helpful in distinguishing LP from lupus or immunobullous disorders.

Figure 7.

Histologic view of cutaneous lichen planus demonstrating a “saw-toothed” appearance of the epidermis, a lichenoid infiltrate, and pigment incontinence.

Diagnosis confirmation

The differential diagnosis of cutaneous LP includes the following entities: 1) lichenoid drug eruptions (tissue or serum eosinophilia, photo-exposed areas, confluent or widespread, greater degree of parakeratosis, exposure to ACE inhibitors, antimalarials, ß-blockers, methyldopa, NSAIDs, or penicillamine); 2) Lupus erythematosus (+ANA, IgM and IgG deposits in Civatte bodies, deep nodular perivascular lymphoplasmacytic infiltrates, fat lobule necrosis); 3) lichen nitidus (small, pin-point sized, flesh colored, nonpruritic papules); 4) guttate psoriasis (prominent extensor surface involvement, no oral lesions, white silvery scale).

The differential diagnosis of oral LP includes the following entities 1) lichen sclerosus et atrophicus (waxy or cigarette paper appearance, vaginal involvement extremely rare); 2) bullous disease: mucous membrane pemphigoid, pemphigus vulgaris, or linear IgA bullous disease (distinguished by presence of bullae and biopsy with DIF); 3) vulvar intraepithelial neoplasm (distinguished by biopsy); 4) lichenoid contact stomatitis. (Identical clinical findings. Typically lesions are adjacent to a dental amalgam filling, and patch testing with a dental tray can help with diagnosis).

The differential diagnosis of hair and nail LP include the following entities: 1) discoid lupus erythematosus (distinguished by scarring discoid plaques, sun-exposed rash and biopsy); 2) onychomycosis (positive potassium hydroxide test or fungal culture); 3) psoriasis (nail pitting, oil staining, onycholysis, skin involvement).

Who is at Risk for Developing this Disease?

The prevalence of LP in the general population is estimated to be less than or equal to 1%. Children represent only 4% of LP cases. LP may be familial in less than 1% of cases. Women and men are equally affected. Incidence in men increases around 20 years of age and then plateaus, remaining relatively constant through life. Incidence in women, in contrast, increases steadily until peaking around 60 years of age.

Isolated oral involvement occurs in 15% to 35% of cases, but 65% of all patients have some oral involvement; 25% of women with oral LP will also have vulvovaginal involvement, thus the need to specifically inquire about genital involvement. Nail involvement is reported in 1% to 10% of cases; 80% of lichen planopilaris occurs in women. Trauma (Koebner phenomenon) is a known risk factor for development of LP.

What is the Cause of the Disease?

The etiology of LP is unknown. It is believed to be an autoimmune disorder involving the activation of T-lymphocytes against basal keratinocytes. Both CD4- and CD8-positive lymphocytes have been implicated. Increased keratinocyte expression of ICAM-4, an adhesion molecule, may play a role in the interaction between T-lymphocytes and basal keratinocytes. This interaction leads to apoptosis of basal keratinocytes. The bullous forms of LP have been shown to have anti-BP180 antigen antibodies. Mechanical factors such as previous trauma and repetitive friction due to dentures or biting may contribute to the pathogenesis of LP.

Systemic Implications and Complications

The reciprocal association between LP and HCV has been well documented and debated. Globally, there is a statistically significant association between HCV and LP. This association is not statistically significant in South Asia, Africa, or North America. Japan and the Mediterranean region have the highest association.

Thus screening for HCV in LP patients is not routinely performed in the United States, although screening for HCV in high-risk populations or those from high-prevalence areas may be reasonable. HCV-related oral lichen planus may be seen in patients with HLA-DR6, a HLA class II allele; this may account for the geographic differences seen. LP has also been associated with HBV immunization and primary biliary cirrhosis. Routine screeing for HLA-DR6 is not done.

The risk of developing malignancy in LP lesions has been debated. Current data indicates that risk of cutaneous malignancy is not elevated in cutaneous LP. There may be an elevated risk of developing SCC in erosive LP involving mucosal surfaces. The physician should be alert for other risk factors that would additionally elevate this risk such as cigarette and alcohol use. There is no association between LP and internal malignancies. Case studies of LP occurring in conjunction with thymoma, lupus erythematosus, lichen sclerosis, alopecia areata, and vitiligo have been reported.

Treatment Options

Table II. Treatment Ladder for Cutaneous Lichen Planus

Table II.
Medical Treatment Surgical Treatment Physical Modalities
Topical corticosteroidsTriamcinolone 0.1% twice dailyFluocinonide 0.05% twice dailyClobetasol 0.05% twice dailyOcclusion can be used as well Surgical  excision with skin grafting— rarely done  Narrow-band UVB and broadband UVB
Oral AntihistaminesHydroxyzine 10 to 25mg orally every 6 to 8 hours, increase as tolerated to maximum of 100mg orally every 6 hoursDiphenydramine 25mg orally every 6 to 8 hoursCertirizine 10mg orally once daily Biopsy should be considered in cases or oral disease that ulcerate or erode to rule out transformation to SCC UVA1  or  PUVA
Intralesional corticosteroid (triamcinolone)10 to 40mg/cc concentration. Never more than 1cc of 40mg/cc in a 2-month period    Photodynamic therapy with delta amino levulinic acid
Topical calcineurin inhibitorsTacrolimus 0.03% or 0.1% ointment twice dailyPimecrolimus cream 1.0% twice daily    
Systemic corticosteroid: prednisone 1mg/kg tapering over 3 weeks    
Retinoids: Acitretin 10 to 25mg daily, isotretinoin rarely used because of iPledge regulations, but up to 40mg daily of isotretinoin can be used ( lower doses can control oral disease)    
Griseofulvin 500mg orally daily for 1 to 2 months    
Metronidazole 500mg orally twice daily for 1 to 2 months    
Sulfasalazine: Start with 500mg orally twice daily and increase to a maximum of 1.5g twice daily if tolerated. Enteric coated version is easier to tolerate.    
Mycophenolate mofetil 500mg orally twice daily increasing to a maximum of 1.5g orally twice daily    
Azathioprine: Start at 0.5 to 1.0mg/kg and increase every 6 to 8 weeks to a maximum of 2.5mg/kg divided twice daily    
Cyclosporine: Start at 1mg/kg and increase to a max of 4.5mg/kg divided twice daily.  Should not be used more than 12 months due to renal toxicity.    
Enoxaparin 3mg subcutaneously once a week    
Thalidomide for severe refractory cases. Start with 50mg orally daily and increase to a maximum of 150mg orally daily    
Efaluzimab: Off the market, once a promising therapy    

Optimal Therapeutic Approach for this Disease

The optimal therapeutic approach to cutaneous lichen planus depends on the surface area of involvement, symptoms, and the effect on patients’ activities of daily living.

Those with mild scattered asymptomatic disease may be best left untreated as many cases will spontaneously resolve. It is always a good idea to ask about new medications as many may induce LP.

Those with mild symptomatic disease are typically best treated with a combination of a topical medium-to-high strength topical corticosteroid (such as triamcinalone 0.1% or clobetasol 0.05%) in conjunction with an oral sedating antihistamine (hydroxyzine or diphenydramine). Those who can not tolerate the antihistamine due to drowsiness can be treated with a less sedating antihistamine such as cetirizine. Intralesional kenalog can be very successful in treating localized disease.

Patients with widespread severely symptomatic disease are by far the most difficult to control therapeutically. Oral prednisone 1mg/kg and tapering over 3 weeks can give some quick symptomatic relief, but the disease invariably recurs once a certain threshold of oral steroids is crossed. Steroid-sparing agents are a must as the use of long-term oral steroids is not a good long-term solution.

Very little evidence in the form of randomized placebo-controlled prospective trials exists for the treatment of severe LP. Phototherapy can be effective and has fewer side effects than oral immunosuppressives, starting with narrow band (nb) UVB or broadband UVB. UVA1 is an option but is not widely accessible. PUVA should be reserved for those that fail nbUVB or broadband UVB. We will typically start the phototherapy at the same time as the patient is on the oral corticosteroid and overlap the two for 3 weeks. Therapies can be 2 to 3 times weekly.

Systemic medications are useful, and our first-line agent is an oral retinoid, acitretin being the easier of the two to prescribe. Starting at a dose of 10 to 25mg daily of acitretin and increasing as tolerated to a maximum of 30 to 50mg. Very few patients can tolerate 50mg daily. As always, women of child-bearing potential should not use this medicine. Accutane can be used as well at doses of 40 to 80mg daily.

Oral immunosuppresants are the next line of therapy. Azathioprine starting at 0.5 to 1.0mg/kg and increasing to 2.5mg/kg slowly, and mycophenolate mofetil starting at 500mg orally twice daily and increasing as tolerated to 1.5g orally twice daily are my favorites. If no response is seen after 3 to 4 months, one should discontinue the agent and try another.

If you have a patient that continues to fail the above therapeutic approaches, the next steps in therapy are all anecdotal in nature. The many possibilities are listed in table form for your review (Table II, Table III, Table IV, Table V, and Table VI). My approach is to always start with the medication that has the best risk-to-benefit ratio. As an example, I would try metronidazole well before ever considering using thalidomide.

Table III.
 Medical Treatment  Surgical Procedures  Physical Modalities Psychological Measures
Topical corticosteroids: Clobetasol gel 0.05% applied once to twice dailyFluocinonide gel 0.05% compounded in orabase applied once or twice dailyCompounding in orabase may help with adhesion to the oral mucosaDental trays can be used to apply topical steroids to gingival lesions Biopsy should be considered in cases of oral disease that ulcerates or erodes to rule out transformation to SCC  PUVA This disease can cause psychosocial dysfunction. Assessment and referral to a psychologist or psychiatrist can be very helpful
Topical retinoids: tretinoin gel 0.025% daily; can be irritating Surgical excision — rarely performed  Cryotherapy  
Topical calcineurin inhibitor (tacrolimus 0.03% or 0.1% ointment). Must counsel patients not to overapply CO2 laser ablation  Low-dose excimer laser  
Intralesional corticosteroidinjections (ILK 5 to 10mg/cc) Cryosurgery  CO2 laser  
Hydroxychloroquine 50 to 100mg orally twice daily    Nd:YAG laser  
Systemic corticosteroids (short-term therapy) 1mg/kg tapered over 3 weeks   Avoidance of acidic and or spicy foods  
Methotrexate 2.5mg tabs. Start with test dose of 2.5mg once, and if labs 1 week later (CBC differential and platelet count, and LFTs) are okay, increase to 10mg orally once weekly. After a month increase by 2.5mg to 5mg per week. Max dose of 20mg orally a week. Liver biopsies recommended after 1g total dose and therafter by recommendations of Hepatology. Use in conjunction with oral folate 1mg daily. Methotrexate has many contraindications including HCV, pregnancy, and renal disease.      
Azathioprine: Start at 0.5 to 1.0mg/kg and increase every 6 to 8 weeks to a maximum of 2.5mg/kg divided twice daily      
Mycophenolate mofetil: Start at 500mg orally twice daily and increase as tolerated to 1.5g orally twice daily      
Aloe vera gel applied once to twice daily      
Thalidomide: Start with 50mg orally daily and increase to a maximum of 150mg orally daily      
Etanercept 50mg subcutaneously once weekly; can increase to twice weekly      
Acitretin 10 to 25mg orally daily. Avoid in females of childbearing age      
Dapsone 25 to 100mg daily      
Efalizumab: Off the market; once a promising therapy      
Table IV.
 Medical Treatment  Surgical Treatment  Physical Modalities Psychological Measures
Topical corticosteroidsClobetasol 0.05% ointment twice dailyHalobetosol 0.05% ointment twice dailyFluocinonide 0.05% ointment twice dailyBefore application, soaking in a warm bath will help decrease some scale and allow for better penetration into the skinSitz bath and bland topical emollients such as plain petrolatum can help with symptoms. Consider topical lidocaine but be vigilant for the development of allergic contact dermatitisConsider hydrocortisone  1% suppositories for vaginal LP Surgical dilation may be required for scarring of the vaginal or uretheral openings. Referral to a urologist is preferred. Photodynamic therapy This disease can cause psychosocial and sexual dysfunction. Assessment and referral to a psychologist or psychiatrist can be very helpful
Topical calcineurin inhibitorsTacrolimus 0.03% or 0.1% ointment twice dailyPimicrolimus 1.0% cream once or twice daily Biopsy any suspicious lesions (ulcers, morphologically unique areas) to rule out malignant transformation    
High-dose oral corticosteroids Prednisone 1mg/kg and tapering over 3 weeks. Not a long-term solution but acutely can help abort or minimize flaresThe oral medications used to treat cutaneous LP can be used      
Table V.
 Medical Treatment  Surgical Treatment  Physical Modalities  Psychological Measures
Topical corticosteroidsClobetasol cream/ointment/gel/solution once to twice dailyHalobetasol cream/ointment/solution once or twice dailyTriamcinalone 0.1% cream/ointment/gel/solution once to twice dailyTopical retinoidsTretinoin 0.1% daily  Hair transplantation can be consideredEvaluation by an expert after the disease has been in remisson for 1 to 2 years is the best time to get a consultation  None This disease can cause psychosocial dysfunction.  Assessment and referral to a psychologist or psychiatrist can be very helpful
Intralesional corticosteroids (triamcinolone) 10 to 40mg/cc      
Oral corticosteroidsPrednisone 1mg/kg tapering over 3 weeks      
Hydroxychloroquine 50 to 100 mg twice once to twice daily      
Retinoids: Acitretin 10 to 25mg orally daily. Limited by drug-induced hair loss and mucocutaneous side effects      
Pioglitazone 15mg orally daily for 6 to 8 months; 1 case report showing efficacy      
Table VI.
 Medical Treatment Surgical Treatment Physical Modalities 
Topical AgentsTopical CorticosteroidsClobetasol 0.05% ointment or cream twice daily or another medium-to-high potency topical corticosteroidTopical RetinoidsTretinoin gel (0.025%, 0.05% or 0.1%) once to twice dailyTopical immunomodulatorsTacrolimus (0.03% or 0.1%) ointment once to twice dailyPimicrolimus 1% cream once to twice dailyTopical cyclosporin once to twice dailyTazarotene gel 0.025% daily to twice daily Surgical avulsion in severe cases  None
Intralesional corticosteroidsILK 10 to 40mg/cc injected into the region of the nail matrix    
Oral agentsCorticosteroidsPrednisone 1mg/kg tapering over 3 weeksImmunosuppresantsAll of the oral immunosuppressive agents listed in the treatment of cutaneous and oral LP can be used    

Oral disease can also be broken down into mild disease and severe disease. All patients should avoid acidic and spicy foods. Patch testing should be considered if an oral lichenoid contact dermatitis is suspected. Asymptomatic disease may be observed without therapy. Ulcerations and erosions or any suspicious areas should be biopsied to rule out transformation to SCC. If SCC is diagnosed, a prompt referral to a head and neck surgical oncologist is a must, and one should discontinue any immunosuppressive agents you may be using for treatment of the patient’s LP.

Symptomatic oral LP can be treated initially with fluocinonide compounded in orabase or clobetasol gel. I found many patients will respond to this therapy nicely. It is easy and well tolerated. The use of dental trays for 15 minutes to help apply the medication to the involved gingival surfaces can be very useful. My next choice is the use of tacrolimus 0.03% ointment; if after 6 weeks of twice daily treatment does not help, I will increase to 0.1%. One must educate patients on the use of this medicine so that they are not taking what amounts to systemic doses.

After attempting these topical agents I will typically try hydroxychloroquine or azathioprine or mycophenolate mofetil, based on patient preference, comorbidities and side-effect profile.

Nail LP can be very difficult to treat, and you should not be bashful in telling this to the patient. Often no therapy is the best therapy. If a patient wishes treatment for the nails only, I often start with a combination of a topical high potency steroid in conjunction with a topical retinoid. I will give patients 3 months to tell me if they notice any difference. I use an alternating 2 weeks on, 1 week off approach with the topical steroids to minimize atrophy. The retinoids can be used continuously.

ILK to the proximal nail fold above the nail matrix is my next approach. If this does not work, oral medications can be attempted. I have personally not found an oral medication that uniformly works for all patients with nail LP.

Genital LP can be truly one of the most difficult areas to treat. High potency topicals and ILK are my first choice with topical tacrolimus and pimecrolimus my second-line agents. The physician should be aware that this is a condition with psycho-social-sexual connotations and referral to a gynecologist and psychiatric specialist may be helpful in certain cases. One should inquire, “How is this affecting your sex life? How does this affect you on a day-to-day basis?” Patients will not offer this information up without being asked.

Lichen planopilaris is a scarring alopecia in which my goal of therapy is to stabilize hair loss, with the understanding that what has been lost and scarred is unlikely to ever come back. Hair transplantation can be considered after the disease has been in remission for 2 to 3 years. I like to wait at least 3 years before referring a patient for hair restoration consultation.

The use of topical high potency drugs such as clobetasol with hydroxychloroquine are my first-line therapies. Oral retinoids have been used, but unfortunately in my experience they induce hair loss, which is not acceptable in these cases.

As seen, LP is a complex disease with many various manifestations and therapeutic options. One should take time on the first visit to educate patients on the disease and the lack of a curative agent. This will save you much time in the future. Handouts are a great resouce for your patients. I strongly suggest you make a personalized handout for your patients.

Patient Management

Explain the natural history of LP to the patient before beginning treatment. Isolated cutaneous LP is a self-limited disease that may resolve spontaneously between 1 month and 7 years, with a mean duration of 5 years. Two-thirds of cases resolve within 1 year. In contrast, mucosal LP is a chronic disease that rarely resolves spontaneously. Erosive LP does not spontaneously resolve. However, reticular LP can spontaneously resolve in about one third of patients.

Treatment can result in substantial improvement, but recurrence is common when discontinued. Follow-up is based on patient symptomatology and clinical examination as to response and extent of disease. Repeat laboratory studies and imaging is unnecessary in follow-up.

The long-term side effects of treatment such as atrophy, adrenal suppression, and immunosuppression must be taken into consideration when initiating treatment. For mild disease requiring only topical treatment, patients should follow up every 3 to 6 months. For those requiring systemic treatments, follow-up should be scheduled according to appropriate monitoring for that drug. Those treated with surgical or physical modalities will also need monitoring based on disease severity and potential for treatment complications.

Unusual Clinical Scenarios to Consider in Patient Management

Because LP may be difficult to differentiate from lupus, lichenoid drug reaction, lichen sclerosis, and cutaneous malignancy, a biopsy may be warranted to confirm the diagnosis and ensure proper prognostication and treatment.

Patients with diabetes and OLP have a higher rate of erosive OLP. Patients with LP do not have a higher risk of developing diabetes.

Graham- Little – Picard- Lasseur syndrome” to “Graham-Little-Piccardi-Lassueur syndrome is a combination of scarring alopecia (lichen planopilaris), follicular-centered LP, and a non-scarring alopecia of the groin and axilla. This is an exceedingly rare syndrome.

Oral lichen planus and oral lichenoid contact stomatitis can appear clinically and histologically identical. Clinically, oral lichenoid contact dermatitis is most frequently caused by dental amalgams. Mercury and palladium are the two most frequently implicated metals to cause this type of reaction. On clinical examination, the physician may suspect oral lichenoid contact dermatitis over oral lichen planus based on the location of the areas involved. The most reliable clinical manner to separate the two is when oral lesions are juxtaposed to the dental amalgams and nowhere else in the mouth. This is most prevelant in oral lichenoid stomatitis.

Oral lichenoid stomatitis can occur within a few months or many years after amalgam placement. The therapy for this form of contact dermatitis is to remove the amalgam and replace with a ceramic or other type of nonmetal dental restoration. This is best diagnosed by conventional patch testing. Histopathologic evaluation may show some subtle differences, although this is still debated by expert dermatopathologists.

Chronic Graft vs Host Disease (GVHD) is more commonly seen these days due to the increasing number of bone marrow transplants. One subtype of chronic GVHD is a lichenoid variant. The appearance is typically more widespread. Therapy with oral prednisone in conjunction with an immunosuppressive medication is usually the first therapeutic option. PUVA is also helpful.

What is the Evidence?

Lehman, JS, Tollefson, MM, Gibson, LE. ” Lichen Planus”. Int J Dermatol. vol. 48. 2009. pp. 682-94. (A thorough review of LP including subtypes and treatment. Briefly covers hair and nail involvement.)

Boyd, AS, Neldner, KH. “Lichen planus”. J Am Acad Dermatol. vol. 25. 1991. pp. 593-619. (Review of LP, including a historical perspective. Also has a section on miscellaneous lichenoid dermatoses. Treatment section does not include newest modalities.)

Torti, DC, Jorizzo, JL, McCarty, MA. ” Oral lichen planus: a case series with emphasis on therapy”. Arch Dermatol. vol. 143. 2007. pp. 511-5. (A case series with focus on oral LP. Contains a concise treatment ladder. Also mentions new findings of thalidomide and methotrexate for refractory disease.)

Zakrewska, JM, Chan, ES, Thornhill, MH. ” A systemic review of placebo-controlled randomized clinical trials used in oral lichen planus”. Br J Dermatol. . vol. 153. 2005. pp. 336-41. (A systematic review of treatment in oral LP. Shows general lack of randomized clinical trials (RCTs) for treatment of oral LP. The RCTs that have been published show a small but statistically significant treatment benefit.)

Goldstein, AT, Metz, A. ” Vulvar lichen planus”. Clin Obstet Gynecol . vol. 48. 2005. pp. 818-23. (Concise review of vulvar LP, including variants. Gives recommendations on treatment and preventive screening.)

Rogers, RS, Eisen, D. “Erosive oral lichen planus with genital lesions: the vulvovaginal-gingival syndrome and the peno-gingival syndrome”. Dermatol Clin . vol. 21. 2003. pp. 91-8. (A thorough review of all published cases of vulvovaginal-gingival syndrome and peno-gingival syndrome. Includes diagnostics, natural history, and potential therapeutic options.)

Piraccinni, BM, Saccani, E, Starace, M, Balestri, R, Tosti, A. ” Nail lichen planus: response to treatment and long term follow-up”. Eur J Dermatol. . vol. 20. 2010. pp. 489-96. (A clinical report of 105 cases of histologically confirmed LP of the nail. Most cases had almost exclusive involvement of the nail apparatus. Focuses on attempted treatments and outcomes; 66% of patients responded to intralesional or systemic corticosteroids with a 60% relapse rate.)

Eisen, D. ” The clinical features, malignant potential, and systemic associations of oral lichen planus: a study of 723 patients”. J Am Acad Dermatol . vol. 46. 2002. pp. 207-14. (Large case series of oral LP. Contains a concise review of the clinical presentation and systemic associations of oral LP. Documents 6 cases of oral SCC developing within lesions that were previously diagnosed clinically as LP.)

Shengyuan, L, Songpo, Y, wen, W, Wenjing, T, Haitao, Z, Binyou, W. ” Hepatitis C virus and lichen planus: a reciprocal association determined by a meta-analysis”. Arch Dermatol . vol. 145. 2009. pp. 1040-7. (Meta-analysis showing a statistically significant reciprocal association between HCV and LP globally. This association was not statistically significant when analyzed by geographic region in North America, Africa, and South Asia.)

Sigurgerisson, B, Lindelof, B. ” Lichen planus and malignancy”. An epidemiological study of 2071 patients and a review of the literature. Arch Dermatol . vol. 127. 1991. pp. 1684-8. (Thorough study of Swedish population demonstrating no increased risk of cutaneous or internal malignancy with LP. There was a statistically significant risk of oral SCC of the oral cavity in association with oral LP. The article investigates individual areas of LP involvement such as the oral cavity and the potential development of malignancy.)

Mirmarni, P, Karnik, P. ” Lichen planopilaris treated with a peroxisome proliferator-activated receptor gamma agonist”. Arch Dermatol. vol. 145. 2009. pp. 1363-6. (Research has discoverd that an abnormality of the PPAR-gamma receptor on sebaceous glands may lead to an accumulation of abnormal levels of lipids, setting off an inflammatory cascade and initiating LPP. The use of pioglitazone (Actos®) 15mg orally daily for 8 months and then discontinued, placed the patient in remission. After 1 year follow-up the patient was still in remission.)

Goldstein, AT, Metz, A. ” Vulvar lichen planus”. Clin Obstet Gynecol. vol. 48. 2005. pp. 818-23. (Wonderful review of vulvar and vaginal LP. Reviews etiology, epidemiology and goes through treatment options. Gives many suggestions on how to approach the patient and tips for treatment. Well written; I highly recommend reading this article when you are treating a patient with genital LP.)