Oral Lichen Planus Clinical Presentation

Updated: Sep 15, 2020
  • Author: Jaisri R Thoppay, DDS, MBA, MS; Chief Editor: Jeff Burgess, DDS, MSD  more...
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The clinical history of oral lichen planus (OLP) and oral lichenoid lesions varies. Complete history taking and physical examination by an oral medicine practitioner or a dermatologist may be required in patients with extraoral symptoms or signs associated with oral lichen planus. [38]

Lichen planus may arise in patients with other immunologically mediated disorders, including alopecia areata, dermatomyositis, lichen sclerosis et atrophicus, morphea, myasthenia gravis, primary biliary cirrhosis, ulcerative colitis, and vitiligo.

In many patients, the onset of oral lichen planus is insidious, and patients are unaware of their oral condition. In such instances, the referring medical or dental practitioner identifies the clinical changes in the oral mucosa.

Some patients report a roughness of the lining of the mouth, a sensitivity of the oral mucosa to hot or spicy foods or oral hygiene products, painful oral mucosa, sore gums, red or white patches on the oral mucosa, red gums, or oral ulcerations.

Approximately two thirds of patients with oral lichen planus report oral discomfort, especially in association with atrophic and erosive lesions. Erythematous and erosive lesions are often sensitive or painful. Symptoms vary from mucosal sensitivity to continuous debilitating pain.

Oral mucosal lichenoid lesions may occur after potential triggers. Such triggers are often the administration of systemic drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs), sulfonylureas, antimalarials, beta-blockers, and some angiotensin-converting enzyme (ACE) inhibitors. The period between the commencement of the drug therapy and the clinical appearance of oral lichen planus–like disease varies. Products such as cinnamon, mints, tooth-whitening products, or red wine can trigger oral lichenoid reactions. [34]

Occasionally, dental restoration may cause an oral lichenoid reaction often seen on soft tissues in opposition or proximal to the dental restoration. Such presentations may be localized to that area, unlike diffuse presentations of oral lichen planus. Patients with an associated allergy to metals or components of the appliance should be evaluated by means of patch testing. [39]

Up to 44% of patients with oral lichen planus develop coincident skin lesions. Conversely, more than 70% of patients with cutaneous lichen planus develop coincident oral lichen planus.

The genitals are involved in as many as 25% of women with oral lichen planus, compared with only 2-4% of men with oral lichen planus. The features are similar to those of the oral lesions. Patients do not often report pain or pruritus, although on questioning, they may admit to such symptoms. [40]

In patients with oral lichen planus, scalp involvement (lichen planopilaris) is rare.

Nail involvement in patients with oral lichen planus is uncommon.

In a small group of patients, lichen planus may involve the esophagus, the tympanic membrane, the larynx, or the conjunction.

Oral lichen planus may appear similar to chronic oral graft versus host disease, which is a frequent and significant complication of allogenic hematopoietic cell transplantation.


Physical Examination

Pertinent physical findings in oral lichen planus (OLP) are limited to the oral mucosa. Some patients present with coincident lesions on the skin, scalp, nails, genital mucosa, esophageal mucosa, larynx, and conjunctivae. Complete history taking and physical examination by a dermatologist may be required in patients with extraoral symptoms or signs associated with oral lichen planus. [38]

Patients with reticular lesions are often asymptomatic, whereas those with atrophic (erythematous) or erosive (ulcerative) disease commonly have significant local morbidity. The oral pain is variable and exacerbated by trauma and foods, particularly those that are hot, spicy, or acidic.

Oral mucosal lesions are variable and present as white striations (Wickham striae), white papules, white plaques, erythema (mucosal atrophy), erosions (shallow ulcers), or blisters. The lesions predominantly affect the buccal mucosa, tongue, and gingivae, although other oral sites are occasionally involved. The lesions are usually bilateral but may be unilateral.

The lesions may appear as a mixture of clinical subtypes. For example, white streaks and gray streaks may form a linear or reticular pattern on an erythematous background. Alternatively, a central area of shallow ulceration (erosion) may have a yellowish surface (fibrinous exudate) surrounded by an area of erythema.

In most patients, telltale white striations or papules are evident on the buccal mucosa or on the lateral margin of the tongue, either alone or in combination with other lesions.

Gingival lesions commonly appear with a fiery-red erythema that affects the entire width of the attached gingiva, a condition previously called desquamative gingivitis. [41]

In patients predisposed to pigmentation, oral lichen planus lesions may be associated with patchy brown melanin deposits in the oral mucosa (inflammatory melanosis).

Oral lichen planus lesions usually persist for many years, with periods of exacerbation and quiescence. During periods of exacerbation, the area of erythema or erosion increases, with increased pain and sensitivity. During periods of quiescence, the area of erythema or erosion decreases, with decreased pain and sensitivity. Patients are often unaware of quiescent oral lichen planus, which may manifest as faint white striations, papules, or plaques. Exacerbations of oral lichen planus have been linked to periods of psychological stress and anxiety. [29, 30]

Lichenoid drug reactions have the same clinical features as those of idiopathic oral lichen planus. Lichenoid disease may be unilateral. Lichenoid reactions of the oral mucosa occur on the oral mucosa in contact with (or close to) an amalgam or composite resin dental restoration, or a denture component. Mechanical trauma (the Koebner phenomenon) may exacerbate lichenoid lesions, especially when it affects the midline of the buccal mucosa or the lateral margin of the tongue.

Up to 44% of patients with oral lichen planus develop coincident skin lesions. These typically appear as pruritic, flat-topped, violaceous papules and plaques that predominantly affect the flexor aspects of the wrists or ankles, the extensor aspects of the lower legs, the skin of the lower central part of the back, and the natal cleft.

The genitals are involved in as many as 25% of women with oral lichen planus, compared with only 2-4% of men with oral lichen planus. The features are similar to those of oral lesions.

Nail involvement (see the image below) causes pitting, subungual hyperkeratosis, longitudinal melanonychia, onychorrhexis (longitudinal ridging and grooving), onychoschizia (distal splitting), and onycholysis (separation of the nail plate from the nail bed). Permanent damage to the nail matrix can induce formation of a pterygium (scarring of the proximal nail fold to the nailbed), 20-nail dystrophy, or permanent nail loss (anonychia).

Lichen planus nail involvement. Lichen planus nail involvement.

Scalp involvement (lichen planopilaris) produces scarring alopecia with indurated erythematous areas of scalp or perifollicular scaly tender or pruritic papules, follicular plugging, doll’s hair formation (multiple hair shafts emerging from a single follicular orifice), or atrophic scarring with permanent patchy hair loss.

Rarely, laryngeal, esophageal, conjunctival, and tympanic membrane involvement occur.



Oral lichen planus (OLP) and its treatment may predispose people to oral C albicans superinfection.

Patients with oral lichen planus may have a slightly increased risk of oral cancer, which they may be able to reduce (see Prevention).

Oral squamous cell carcinoma (SCC) in patients with oral lichen planus is a feared complication and a controversial issue. In retrospective studies, less than 5% of patients with oral lichen planus who were not using tobacco products developed oral SCC. [42, 43, 44] A 2019 study suggests oral lichen planus and oral SCC share multiple epigenetic alterations and hypothesizes that oral lichen planus is a precursor lesion of oral SCC. [45] Atrophic, erosive, and plaque lesions may be at greater risk of malignant change, although SCC may arise in the unaffected oral mucosa as well. The most important risk factors of oral SCC remain the concomitant use of alcohol and tobacco products. Any additive effect of oral lichen planus is difficult to detect in patients who use both. [46] While controversial, human papillomavirus (HPV) has been suggested to possibly play a role in malignant transformation. [47, 48]

When oral lichen planus is asymptomatic, malignant transformation may be unpredictable as patients often seek treatment when the lesions are symptomatic. The base and lateral tongue are often reported as more susceptible areas. Hence, patient education and recommending a daily self-examination combined with a periodic examination by a specialist is often beneficial for early detection of malignant transformation. One proposed reason for the increased risk of oral SCC in patients with oral lichen planus is that compared with healthy mucosa, the oral mucosa affected by oral lichen planus may be more sensitive to C albicans and to the exogenous mutagens found in tobacco, alcohol, and betel quid. Another is that in patients with oral lichen planus, the chronic inflammatory response and the simultaneous healing response of epithelial wounds may increase the likelihood of cancer-forming gene mutations.