A 25-year-old male who thought he had tinea pedis and corporis presented with red plaques extending from the medial aspect of his feet proximal into his lower extremities bilaterally. The patient had no pertinent past medical history, no medications and no history of dental work. The lesions were pruritic and he noticed when his cat scratched him, small marks remained on his legs that were also itchy. Due to this, he believed the skin disease was spreading and contagious.
He had been treating it with an over-the-counter topical antifungal for six months with no result. The patient also recently visited the dentist. At that time, he complained of canker sore-like lesions in his mouth. His dentist told him to stop chewing aspirin tablets but the patient denied ever doing so. He had a secondary complaint about his great toenails, noting that they were rough looking. The patient said he often wore closed-toe shoes to hide them.
During the physical exam, I noted small reddish plaques with a white scale that began at the medial ankle and continued up the leg into the thighs. The patient also had this distribution from the volar aspect of his wrists extending into his upper arm. No lesions were present on the trunk or the back. There were no vesicles, target lesions, purpura or ulcers. Bilateral hallux nails had trachyonychia at the proximal aspect of the nail plate. The patient’s fingernails were not affected at this time. There were no scalp lesions.
In the patient’s mouth, the left buccal mucosa had a small oval lesion, which was covered with white reticulated streaks.
The patient denied any further medical history and any current use of oral medications.
1. What are the characteristic skin lesions in this disease?
2. What is the most likely diagnosis?
3. What is your differential diagnosis?
4. What are the characteristic nail lesions in this disease?
5. What is the treatment?
1. The characteristics most associated with this skin condition are the P’s: plentiful, pruritic, polygonal, purple, planar, polished. Nails may appear rough and may have pterygium formation. Oral lesions with the characteristic Wickham’s striae may be present.
2. The most likely diagnosis is lichen planus, which has not only affected the skin but also the nails and the oral cavity.
3. Differential diagnoses include: psoriasis, tinea corporis, pityriasis rosea, lupus erythematosus, drug reaction, secondary syphilis and onychomycosis.
4. The characteristic nail deformity in this condition is the presence of nail plate thinning with longitudinal ridging, with or without pterygium.
5. Treatment varies and may include topical steroids, systemic steroids, systemic retinoids, or phototherapy depending on the severity of the presentation.
This patient most likely has both the cutaneous and oral manifestations of lichen planus. Lichen planus is an idiopathic, T-cell mediated inflammatory condition that affects the skin, hair, nails and mucous membranes. The cutaneous form of lichen planus may affect up to 1 percent of the population in their 40s and 50s.1
There are numerous variations of lichen planus: atrophic, bullous, hypertrophic and ulcerative. The most common cutaneous presentation begins as a violaceous pruritic papule on the flexor surface of the wrists that erupts into similar papules spreading up the extremity.2 It also affects anterior aspects of the legs, neck and dorsum of the hands.
After the initial crop of lesions, a more widespread eruption of the lesions occurs after a week and one can describe this eruption as having the characteristic “P’s”: plentiful, polygonal, pruritic, purple, planar, polished papules and plaques. These lesions also have a flat top. The fine white lacy network sometimes visible on the surface of both the skin and oral lesions is called Wickham’s striae.
It is also important to note the presence of Koebner’s phenomenon, which is the appearance of skin lesions in areas of skin trauma. This patient had the Koebner response after his cat scratched him. This manifested as linear versions of the polygonal violaceous lesions that followed the trauma of the scratch on his legs.
In addition to its impact on the skin, this condition affects the mucous membranes 50 percent of the time and may also affect the genitalia, the scalp and the nails.3 Be aware that the oral lesions of lichen planus can occur without the skin manifestation and appear as a white reticulated pattern against a violaceous plaque on the buccal mucosa or tongue. The oral form of lichen planus can be associated with the presence of hepatitis C virus.4 Oral lichen planus can also be induced or made worse by exposure to metallic dental implements, and has a higher incidence in tobacco smokers.3 The rate of malignant transformation of oral lichen planus is reportedly low at 3 percent. However, there has been some debate as to determining the extent of disease in the oropharyngeal cavity and screening for signs of transformation.5
It is been my clinical experience that the toenail disease is severe when present. Several nails are generally involved when it comes to lichen planus. Ten percent of the patients with lichen planus present with nail findings. The nails become thin, rough (trachyonychia), ridged (onychorrhexis), fissured and can develop a dorsal wing formation of the proximal nail fold (or pterygium formation) over the nail plate.6 If one does not address the matrix damage from the lichen planus, these nail findings become permanent scarred reminders of the skin disease that may never resolve.
Psoriasis and tinea corporis. When there is a characteristic red, scaly lesion that is bilateral and symmetrical, clinicians can easily confuse this with psoriasis and tinea corporis. Guttate psoriasis presents as small, salmon-pink colored droplets on the skin that are covered with a fine scale on the upper extremities and trunk. This skin eruption usually follows a Strep-based upper respiratory tract infection. Tinea corporis presents as an erythematous, scaly annular plaque, which eventually has central resolution of the lesion with an advancing border at the periphery.
Lupus erythematosus. Due to lichen planus occurring on the generally sun exposed upper extremity, one must rule out lupus erythematosus. Patients who present with only scalp or oral lesions are particularly difficult to differentiate and a biopsy is necessary. If there is a malar rash (i.e. the characteristic butterfly facial rash) or atrophic scarring occurs following the initial skin rash on the sun exposed areas, physicians should strongly consider systemic lupus erythematosus and discoid lupus erythematosus.
Pityriasis rosea and secondary syphilis. If the lesions began on the chest or back, and have begun to spread to the extremities, physicians should rule out pityriasis rosea. If the patient can remember a “herald patch” on the chest or back, that information is particularly helpful in diagnosing pityriasis rosea. Secondary syphilis is very similar in appearance to pityriasis rosea and is also a differential.
Drug reaction. Lichen planus itself can be a response to an exogenous medication. Lichenoid drug eruptions or drug-induced lichen planus can be virtually indistinguishable both clinically and pathologically from idiopathic lichen planus. The most common drugs that may lead to these reactions are ACE inhibitors, thiazide diuretics and antimalarials.
Onychomycosis. In the aforementioned patient case study, the nail disease was prevalent at the proximal nail plate and one could misdiagnose this as proximal subungual onychomycosis. It is important to look at all skin surfaces, ask pertinent questions and perform a nail culture/biopsy before placing a patient such as this on oral antifungals.
The oral, skin and nail disease in this case led to the diagnosis clinically. For the aforementioned patient, we utilized systemic corticosteroids (prednisone taper) and injections of triamcinolone acetonide into the proximal nail fold in order to target the matrix.7 I explained to the patient that the nails may be permanently scarred and the oral lesions may remain for years. I referred the patient to an ENT physician for further evaluation of the oral lichen planus.
Lichen planus can be a frustrating condition to treat as no truly efficient regimen has been described in the literature to date. Cutaneous lichen planus lesions generally have a life span of anywhere from six months to 18 months and have the potential to spontaneously regress. In my clinical experience, the lesions can last up to 24 months and can become a chronic relapsing phenomenon. If the skin eruption is caused by a drug, then the patient should obviously discontinue that medication.
The first line of treatment for both the nails and the skin is a super-potent topical corticosteroid. Researchers have described the use of intralesional steroids for the nail matrix and pruritic lesions. Systemically, oral prednisone, retinoids (acitretin), griseofulvin and metronidazole have had some success. Finally, phototherapy, such as PUVA or narrowband UVB, has offered some relief in this patient population.8
Dr. Vlahovic is an Associate Professor at the Temple University School of Medicine. She is a Fellow of the American Professional Wound Care Association and is board certified by the American Board of Podiatric Surgery.
Dr. Vlahovic pens a bimonthly blog for Podiatry Today. For more info, visit www.podiatrytoday.com/blogs 
For further reading, see “What You Should Know About Lichen Planus” in the June 2007 issue of Podiatry Today.
1. Boyd AS, Neldner KH. Lichen Planus. J Am Acad Dermatol. 1991; 25(4):593-619.
2. James WD, Berger TG, Elston DM. Lichen planus and related conditions. In: Andrews’ Diseases of the Skin: Clinical Dermatology, 10th ed. WB Saunders, Philadelphia, 2006, p. 217.
3. Silverman S, Gorsky M, Luzada-Nur F. A prospective follow-up study of 570 patients with oral lichen planus: persistence, remission, and malignant association. Oral Surg Oral Med Oral Pathol. 1985; 60(1): 30-4.
4. Bigby M. The relationship between lichen planus and hepatitis C clarified. Arch Dermatol. 2009; 145(9):1048-50.
5. Ingafou M, Leao JC, Porter SR, et al. Oral lichen planus: a retrospective study of 690 British patients. Oral Dis. 2006; 12(5):463-8.
6. Holzberg M. Common nail disorders. Dermatol Clin 2006; 24(3):349-54.
7. Grover C, Bansal S, Nanda S, et al. Efficacy of triamcinolone acetonide in various acquired nail dystrophies. J Dermatol 2005; 32(12):963-8.
8. Cribier B, Frances C, Chosidow O. Treatment of lichen planus. An evidence-based medicine analysis of efficacy. Arch Dermatol. 1998; 134(12):1521-30.