Oral Lichen Planus

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Background

Oral lichen planus (OLP) is a chronic mucocutaneous disorder that presents in a wide range of clinical forms, including unilateral or bilateral white striations, papules, or plaques on the buccal mucosa, labial mucosa, tongue, and gingiva. (See the image below.) Erythema, erosion, and blisters may or may not be present.



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Plaquelike oral lichen planus on buccal mucosa on left side.

Pathophysiology

Evidence suggests that OLP is a T-cell–mediated autoimmune disease in which autocytotoxic CD8+ T cells trigger apoptosis of oral epithelial cells.[1, 2, 3]

The dense subepithelial mononuclear infiltrate in OLP is composed of T cells and macrophages, and there are increased numbers of intraepithelial T cells. Most T cells in the epithelium and adjacent to the damaged basal keratinocytes are activated CD8+ lymphocytes. Therefore, early in the formation of OLP lesions, CD8+ T cells may recognize an antigen associated with the major histocompatibility complex (MHC) class I on keratinocytes. After antigen recognition and activation, CD8+ cytotoxic T cells may trigger keratinocyte apoptosis. Activated CD8+ T cells (and possibly keratinocytes) may release cytokines that attract additional lymphocytes into the developing lesion.

OLP lesions contain increased levels of tumor necrosis factor (TNF)-α.[4] Basal keratinocytes and T cells in the subepithelial infiltrate express TNF in situ.[5] Keratinocytes and lymphocytes in cutaneous lichen planus (LP) express elevated levels of TNF receptor I (TNF-RI).[6] T cells in OLP contain mRNA for TNF and secrete TNF in vitro.[7] Serum and salivary TNF levels are elevated.[8, 9] TNF polymorphisms have been identified in OLP patients and may contribute to the development of additional cutaneous lesions.[10]  Successful treatment with thalidomide, a drug known to suppress TNF production, has been reported.[11, 12] These data implicate TNF in the pathogenesis of OLP.

Elevated concentrations of interleukin (IL)-6 and neopterin in saliva and serum of patients with the erosive-atrophic form of OLP suggest that these substances may be involved in the etiology of this variant.[13]  Some research has suggested that osteopontin, CD44, and survivin may be involved in the pathogenesis of OLP as well.[14] Additionally, microRNA 4484 (miR-4484) has been found to be significantly upregulated in the salivary exosomes of patients with OLP.[15]

Although the specific antigen that triggers LP is unknown, it may be a self-peptide (or altered self-peptide), in which case LP would be a true autoimmune disease. The role of autoimmunity in the pathogenesis is supported by many autoimmune features of OLP, including the following:

The expression or unmasking of the LP antigen may be induced by drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Köbner phenomenon), viral infection, or other unidentified agents.[16, 17, 18]

Etiology

OLP is believed to be a T-cell–mediated autoimmune disease in which autocytotoxic CD8+ T cells trigger the apoptosis of oral epithelial cells. However, its precise cause is unknown.

Reported associations between OLP and systemic diseases may be coincidental, given that (1) OLP is relatively common, (2) OLP occurs predominantly in older adults, and (3) many drugs used in the treatment of systemic diseases trigger the development of oral lichenoid lesions as an adverse effect.

In many patients, a cause for the oral lichenoid lesions cannot be identified; in these patients, the disease is called idiopathic OLP.

Oral lichenoid drug reactions may be triggered by systemic drugs including nonsteroidal anti-inflammatory drugs (NSAIDs), beta blockers, sulfonylureas, some angiotensin-converting enzyme (ACE) inhibitors, and some antimalarials. In patients with oral lichenoid lesions, it is important to be alert for any systemic drug as a cause.

Oral lichenoid contact-sensitivity reactions may be triggered by contact allergens, including dental amalgam composite resin and toothpaste flavorings, especially cinnamates. Skin patch testing may help in identifying contact allergens (see Other Tests). If an allergy is detected, lesions may heal when the offending material is removed.

Oral lichenoid lesions may be triggered by mechanical trauma (Köbner phenomenon) from calculus deposits, sharp teeth, rough surfaces of dental restorations or prostheses, cheek or tongue biting, or oral surgical procedures. Any teeth associated with OLP lesions should be scaled to remove calculus deposits and reduce sharp edges. Dental restorations and prostheses that are associated with OLP lesions should be mirror-polished.

Some studies have shown an increased incidence of Candida albicans infection in OLP, an increase that is more notable in erosive OLP than in nonerosive OLP.[19] The nature of the relation between C albicans infection and OLP remains to be fully elucidated.

Some studies have revealed a prevalence of viral (eg, hepatitis C virus [HCV] infection) infections in OLP. Some studies have reported human papillomavirus (HPV) types 6, 11, 16, or 18.[20, 21] Dysplastic OLP lesions had a higher prevalence of HPV-16 than nondysplastic OLP lesions.

Some study findings have suggested an association between OLP and chronic hepatic diseases such as HCV infection, autoimmune chronic active hepatitis, and primary biliary cirrhosis.[22, 23] This association probably reflects the geographic distribution of HCV disease and lichenoid reactions to various drug therapies (eg, interferon alfa for HCV disease and penicillamine for primary biliary cirrhosis). OLP is associated with HCV infection and liver disease in parts of Japan and southern Europe. An association between OLP and HCV infection has not been detected in British, French, German, Scandinavian, or American patients.

Oral lichenoid lesions may arise in people who habitually chew betel quid. A causal role for betel quid in OLP has not been established.

Oral lichenoid lesions are part of the spectrum of chronic graft-versus-host disease that occurs after allogeneic hemopoietic stem cell transplantation.

No consistent association with human leukocyte antigen (HLA) has been reported in OLP. Thus, the patient's genetic background appears not to play a critical role in OLP pathogenesis.

Exacerbations of OLP have been linked to periods of psychological stress and anxiety.[24, 25]

There is little evidence to support a connection between diabetes mellitus (DM) and OLP. The oral lichenoid lesion in Grinspan syndrome (triad of OLP, DM, and hypertension) is probably an adverse effect of the drug therapy for DM and hypertension.

Epidemiology

US and international statistics

OLP has been estimated to affect approximately 1-3% of the general adult population, though in many areas, the precise prevalence of the disease is unknown. A 2020 systematic review and meta-analysis (46 studies; N = 654,956) by Li et al yielded estimated global prevalence figures of 0.89% in the general population (15 studies; n = 462,993) and 0.98% in clinical patients (31 studies; n = 191,963).[26]

Age-, sex-, and race-related demographics

OLP predominantly occurs in middle-aged adults; younger adults and children can be affected, but rarely.[27]  The meta-analysis by Li et al found that in five of the clinic-based studies providing age distribution data, the prevalence of OLP was 0.62% in patients younger than 40 years and 1.90% in patients aged 40 years or older.[26]  A multicenter European study (N = 565) found that the average age at diagnosis of OLP was 60.11 years.[28]

The female-to-male ratio for OLP has been estimated at approximately 1.4:1. In the previously cited meta-analysis, the prevalence of OLP in the population-based studies was 1.55% in women vs 1.11% in men, whereas the prevalence of OLP in the clinic-based studies was 1.69% in women vs 1.09% in men.[26]

OLP affects all racial groups.

Prognosis

OLP is a mucosal subtype of LP. Whereas cutaneous LP lesions typically resolve within 1-2 years, the reticular forms of OLP have a mean duration of 5 years, and erosive OLP lesions are long-lasting and persist for up to 15-20 years or, in some cases, even longer. Resolution of the white striations, plaques, or papules is rare. Symptomatic OLP (ie, atrophic or erosive disease) characteristically waxes and wanes, though the associated white patches rarely resolve. Patients with atrophic (erythematous) or erosive (ulcerative) disease commonly have significant local morbidity. This condition can be aggravated by stress and can have a significant negative impact on quality of life.[29]

Immunosuppressive therapies usually control oral mucosal erythema, ulceration, and symptoms in OLP patients, with minimal adverse effects. However, it may prove necessary to try a range of therapies.

Patients with OLP should be followed at least every 6 months for clinical examination and repeat biopsy as required, though patients should be advised to seek medical care whenever symptoms are exacerbated or the presentation of the lesions changes. OLP has a potential malignant transformation in the range of 0.04-1.74%, as reported in the literature,[28] though there has been controversy regarding the etiopathogenesis of this transformation. Careful, regular long-term follow-up is essential for early detection of malignant transformation.[30]

In the context of appropriate medical care, the prognosis for most patients with OLP is excellent; the condition typically is well controlled by topical or systemic therapies.

Patient Education

Patient education is important. Many patients with OLP are concerned about the possibilities of malignancy and contagiousness, and many are frustrated by the lack of available patient education concerning their condition.

Patients with OLP should be informed regarding the following:

Patient-oriented information and support can be accessed online (eg, from the Texas A&M School of Dentistry's International Oral Lichen Planus Support Group).

Patient education material is available in the Cancer Center, as well as Cancer of the Mouth and Throat.

History

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 OLP.

Lichen planus (LP) 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 OLP 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 OLP report oral discomfort, especially in association with atrophic and erosive lesions. Erythematous and erosive lesions are often sensitive or painful. Symptoms range 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 OLP-like disease varies. Products such as cinnamon, mints, tooth-whitening products, or red wine can trigger oral lichenoid reactions.[27]

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 OLP. Patients with an associated allergy to metals or components of the appliance should be evaluated by means of patch testing.[31]

OLP patients may have coincident skin lesions, and patients with cutaneous LP may have coincident OLP.

Genital involvement may occur (more frequently in females than in males). Patients do not often report pain or pruritus, though they may admit to such symptoms on questioning.[32]  Scalp involvement is rare. Nail involvement is uncommon. In a small subset of patients, the esophagus, the tympanic membrane, the larynx, or the conjunctivae may be involved.

OLP 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 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.

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



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Reticular oral lichen planus on buccal mucosa on left side.



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Ulcerative oral lichen planus on dorsum of tongue.

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



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Plaquelike oral lichen planus on buccal mucosa on left side.

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.[33]

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

OLP 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 OLP, which may manifest as faint white striations, papules, or plaques. Exacerbations of OLP have been linked to periods of psychological stress and anxiety.[24, 25, 34]

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

As many as 44% of patients with OLP 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. Conversely, more than 70% of patients with cutaneous LP develop coincident OLP.

The genitals are involved in as many as 25% of women with OLP, compared with only 2-4% of men with OLP. The clinical 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).



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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.

Complications

OLP and its treatment may predispose people to oral C albicans superinfection.

Patients with OLP 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 OLP is a feared complication and a controversial issue. In several retrospective studies, fewer than 5% of OLP patients who were not using tobacco products developed oral SCC.[35, 36, 37] A 2019 study suggested that OLP and oral SCC share multiple epigenetic alterations and hypothesized that OLP is a precursor lesion of oral SCC.[38] Atrophic, erosive, and plaque lesions may carry a greater risk of malignant change, though SCC may arise in the unaffected oral mucosa as well.

The most important risk factors for oral SCC remain the concomitant use of alcohol and tobacco products. Any additive effect of OLP is difficult to detect in patients who use both.[39]  It has been suggested, albeit controversially, that human papillomavirus (HPV) may play a role in malignant transformation.[40]

When OLP is asymptomatic, malignant transformation may not be predictable, because patients commonly seek treatment only 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 are often beneficial for early detection of malignant transformation.

One proposed explanation for the increased risk of oral SCC in patients with OLP is that in comparison with healthy mucosa, the oral mucosa affected by OLP 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 OLP, the chronic inflammatory response and the simultaneous healing response of epithelial wounds may increase the likelihood of cancer-forming gene mutations.

Laboratory Studies

The history, typical oral lesions, and skin involvement are usually sufficient for diagnosing oral lichen planus (OLP), though laboratory studies and biopsy may be required in some cases (see Procedures).

Direct immunofluorescence testing can help in distinguishing erosive or the rare bullous OLP from pemphigus vulgaris, benign mucous membrane pemphigoid, dermatitis herpetiformis, and linear immunoglobulin A (IgA) dermatosis. The most characteristic feature of OLP is shaggy linear fibrin distribution.

Some studies have shown an increased incidence of C albicans infection in patients with OLP. Periodic acid–Schiff (PAS) staining of biopsy specimens and candidal cultures or smears may be performed. However, these tests may be of limited clinical value, given that oral C albicans is present in more than 70% of the population as a common organism in oral flora. The presence of C albicans and the oral load of this organism do not aid either the diagnosis or the treatment of OLP.

Other Tests

Skin patch testing may be helpful in identifying a contact allergy in some patients with OLP.[31] The current recommendation is to use a standard series; a dental prosthesis series; and a metal salt series that includes gold, mercury, and palladium salts, as well as other salts of metals used in dental restorations. Late readings, or those obtained at 10 and 17 days after the application of the skin patch, may be required.

Although the assessment of hepatic function in the treatment of otherwise healthy southern European and Japanese patients with OLP may be warranted, similar screening in British and American patients appears to be of limited benefit. Formal studies continue. Hepatic biochemical testing should be considered only when patients have proven OLP and suspected liver disease.[41]

Procedures

Biopsy may be required to exclude malignancy or to differentiate between OLP and other white or chronic ulcerative oral lesions, including reactive keratoses, chronic hyperplastic candidosis, epithelial dysplasia, discoid lupus erythematosus, gastrointestinal disease (including oral Crohn disease), and anemic states.

Histologic Findings

Histopathologic examination of lesional tissue is the most relevant investigation in cases of OLP. It should be appreciated that good biopsy technique and appropriate handling are extremely important for achieving an accurate pathologic diagnosis.[42]

Consistent findings include a bandlike subepithelial mononuclear infiltrate consisting of T cells and histiocytes, increased numbers of intraepithelial T cells, and degenerating basal keratinocytes that form colloid (Civatte, hyaline, cytoid) bodies, which appear as homogenous eosinophilic globules. Variable findings include parakeratosis, acanthosis, and sawtooth rete pegs.

Degeneration of the basal keratinocytes and disruption of the anchoring elements of the epithelial basement membrane and basal keratinocytes (eg, hemidesmosomes, filaments, fibrils) weakens the epithelial-connective tissue interface. As a result, histologic clefts (ie, Max-Joseph spaces) may form, and blisters on the oral mucosa (bullous lichen planus) may be seen at clinical examination. B cells and plasma cells are uncommon findings.

Immunoglobulin or complement deposits are not a consistent feature of OLP, though fibrin is deposited in a shaggy linear pattern in the basement membrane zone. Colloid bodies contain fibrin, immunoglobulin M (IgM), C3, C4, and keratin. Laminin and fibronectin staining may be absent in areas of heavy fibrin deposition and colloid body formation. This finding suggests basement membrane damage in these areas.

In OLP, electron microscopy is used principally as a research tool. The ultrastructure of the colloid bodies suggests that they are apoptotic keratinocytes, and studies using the end-labeling method have revealed DNA fragmentation in these cells. Electron microscopy shows breaks, branches, and duplications of the epithelial basement membrane in OLP.[43]

Medical Care

Medical treatment of oral lichen planus (OLP) is essential for the management of painful, erythematous, erosive, or bullous lesions. The principal aims of OLP therapy are as follows:

In patients with recurrent painful disease, another goal is the prolongation of their symptom-free intervals.

The main concerns with available therapies are the local and systemic adverse effects and the possibility of lesion recurrence after treatment is withdrawn. No treatment of OLP is curative.

Local exacerbating factors should be eliminated. Any sharp teeth or broken restorations or prostheses that are likely to cause physical trauma to areas of erythema or erosion should be treated with conventional dental measures. The teeth should be scaled to remove calculus deposits and reduce sharp edges. If the patient has an isolated plaquelike or erosive OLP lesion on the buccal or labial mucosa adjacent to a dental restoration, and if an allergy is detected by means of skin patch testing, the lesion may heal if the offending material is removed or replaced. (However, most lichenoid lesions adjacent to dental restorations are asymptomatic.) Control of stress (eg, via relaxation training) may help in treatment.

Topical corticosteroids are the mainstay of medical treatment, though in rare cases, corticosteroids may be administered intralesionally for a focal lesion or systemically for diffuse recalcitrant lesions. Some topical corticosteroid therapies may predispose the patient to oral pseudomembranous candidosis; however, this condition is rarely if ever symptomatic, and it generally does not complicate healing of erosions related to OLP. Topical antimycotics (eg, nystatin, amphotericin) may be prescribed when an infection is present.

Erosive OLP that is unresponsive to topical corticosteroids may respond to topical tacrolimus.[44, 45, 46]  Other potential therapies for recalcitrant OLP include cyclosporine,[47]  hydroxychloroquine,[48]  azathioprine,[49]  dexamethasone elixir, mycophenolate mofetil,[50]  dapsone,[46]  systemic corticosteroids, and topical and systemic retinoids.[47]  OLP has been treated successfully with thalidomide,[11, 12]  but this is considered experimental and is associated with significant potential adverse effects; only clinicians trained thoroughly by the manufacturer can prescribe this agent.

Close monitoring of patients is essential when these medications are prescribed. Only practitioners completely familiar with the use of immunosuppressive drugs should attempt such treatment.

Platelet-rich plasma (PRP) and platelet-rich fibrin (PRF) have been suggested as possible alternatives to corticosteroids in the treatment of OLP. In a systematic review and meta-analysis comparing PRP and PRF with intralesionally administered corticosteroids, the three agents were found to be comparably effective.[51]

Some evidence suggests that topical curcumin may help palliate pain and promote clinical healing in patients with OLP.[52]

If systemic drug therapy (eg, treatment with nonsteroidal anti-inflammatory drugs [NSAIDs], antimalarials, or beta blockers) is suspected as the cause of oral lichenoid lesions, switching to another drug may be worthwhile. This change must be undertaken only by the patient's attending physician. However, the switch rarely resolves the erosion and almost never resolves the white patches of OLP.

All OLP patients should be informed of the slightly increased risk of oral squamous cell carcinoma (SCC), the most common of all oral malignancies.[53] They should be advised that this risk may be reduced by eliminating tobacco and alcohol consumption and by consuming a diet rich in fresh fruits and vegetables, among other measures. Erosive and atrophic lesions can be converted into reticular lesions by using topical steroids. Therefore, elimination of mucosal erythema and ulceration, with residual asymptomatic reticular or papular lesions, may be considered an endpoint of OLP therapy. With respect to plaque lesions, the effect of treatment on the risk of oral cancer is unclear.

A 2020 article outlined a potentially useful treatment algorithm for OLP, along with a staging system that may help facilitate management decisions.[54]

A 2025 study found that photobiomodulation (PBM; also referred to as low-level laser therapy [LLLT]) using an 810-nm diode was effective for treating OLP, though more so for erosive OLP than for keratotic OLP.[55]  The authors reported no complications and, as of the time of publication, were unaware of any cases of malignant transformation of OLP after PBM.

Diet

When OLP lesions are symptomatic, patients may avoid certain foods that may aggravate the symptoms. They are often on a soft diet, which may predominantly focus on carbohydrate diets.

Because OLP patients have a slightly increased risk of oral SCC (though the precise degree of risk has not been determined), they should be advised that a diet rich in fresh fruit and vegetables may help reduce this risk.

Activity

Patients with OLP should be advised to do the following:

Although OLP does not increase the risk of dental caries or gingival disease, painful lesions (particularly those on the gums) can limit the patient's ability to maintain good oral hygiene. Therefore, all patients with OLP should be informed regarding the appropriate methods of oral hygiene and advised to see their dentists often.

Prevention

The risk of oral cancer in patients with OLP may be reduced by means of the following:

Consultations

Typically, an oral medicine specialist or oral pathologist makes the primary diagnosis of OLP. Opinions may be sought from the following specialists if patients have relevant signs or symptoms:

Because exacerbations of OLP have been linked to periods of stress and anxiety, a psychological assessment may be beneficial in some OLP patients[34] ; however, objective data to support this link are limited.

Long-Term Monitoring

Patients with OLP should be reexamined during active treatment, and lesions should be monitored for reduction in mucosal erythema and ulceration and alleviation of symptoms. Active treatment should be continued (with alternative therapies tried as appropriate) until erythema, ulceration, and symptoms are controlled. Patients should be followed at least every 6 months.

Patients with OLP should be instructed to pay attention to any exacerbations of symptoms or changes in the features of the lesions. Such changes generally indicate a phase of increased erythematous or erosive disease.

In view of the potential association of OLP with oral SCC, an appropriate specialist should follow patients every 6-12 months. In addition, patients should be advised to examine their mouths regularly and to seek the help of a specialist if persistent red or ulcerative oral mucosal lesions develop.

Candidal cultures or smears may be obtained periodically. Infections can be controlled with topical antimycotic preparations. These tests may be of limited clinical value, because oral C albicans is present in at least 70% of all healthy persons.

Dapsone topical (Aczone)

Clinical Context: 

Tacrolimus ointment (Protopic)

Clinical Context: 

Cyclosporine (Gengraf, Neoral, Sandimmune)

Clinical Context: 

Prednisolone (FloPred, Millipred, Millipred DP)

Clinical Context: 

Dexamethasone (Baycadron, Decadron DSC, Dexamethasone Intensol)

Clinical Context: 

Betamethasone topical (Alphatrex, BetaVal, Dermabet)

Clinical Context: 

Fluocinolone (Capex, DermaSmoothe FS, Fluoderm)

Clinical Context: 

Clobetasol (Clobex, Clobex Spray, Cormax)

Clinical Context: 

Triamcinolone topical (Kenalog Orabase, Kenalog topical, Pediaderm TA)

Clinical Context: 

Hydroxychloroquine sulfate (Plaquenil)

Clinical Context: 

Azathioprine (Azasan, Imuran)

Clinical Context: 

Mycophenolate (CellCept, MMF, Myfortic)

Clinical Context: 

What is oral lichen planus (OLP) and what is its presentation?What is the pathophysiology of oral lichen planus (OLP)?What is the cause of oral lichen planus (OLP)?What are the triggers for oral lichen planus (OLP)?What is the role of Candida albicans infection in the etiology of oral lichen planus (OLP)?What is the role of betel quid in the etiology of oral lichen planus (OLP)?What is the role of graft vs host disease in the etiology of oral lichen planus (OLP)?What is the role of genetics in the etiology of oral lichen planus (OLP) pathogenesis?What is the role of stress and anxiety in the etiology of oral lichen planus (OLP)?What is the role of diabetes mellitus in the etiology of oral lichen planus (OLP)?What is the prevalence of oral lichen planus (OLP)?What are the racial predilections of oral lichen planus (OLP)?How does the prevalence of oral lichen planus (OLP) vary by sex?Which age groups are at highest risk for oral lichen planus (OLP)?How long does it take for oral lichen planus (OLP) to resolve?What is the treatment for oral lichen planus (OLP)?What should patients be told about the prognosis of oral lichen planus (OLP)?What should be included in long-term follow-up for oral lichen planus (OLP)?What is the prognosis of oral lichen planus (OLP)?How information about oral lichen planus (OLP) should patients be given?What is the focus of clinical history for suspected oral lichen planus (OLP)?Which patients are at an increased risk for oral lichen planus (OLP)?How is the onset of oral lichen planus (OLP) characterized?What are the signs and symptoms of oral lichen planus (OLP)?What are potential triggers for oral lichen planus (OLP)?What is the prevalence of coincident skin lesions in oral lichen planus (OLP)?What is the prevalence of genital involvement in oral lichen planus (OLP)?How common is scalp involvement in oral lichen planus (OLP)?How common is nail involvement in oral lichen planus (OLP)?What is the possible otolaryngological involvement in oral lichen planus (OLP)?Which condition should be included in the differential diagnoses of oral lichen planus (OLP)?Where are the physical findings of oral lichen planus (OLP) most evident?Which physical findings are characteristic of in oral lichen planus (OLP)?How are the oral mucosal lesions of lichen planus characterized?How are the gingival lesions of lichen planus characterized?What is the appearance of oral lichen planus (OLP) lesions in patients predisposed to pigmentation?Which physical exam findings of oral lichen planus (OLP) suggest exacerbation?How are lichenoid drug reactions differentiated from idiopathic oral lichen planus (OLP)?How are skin lesions characterized in oral lichen planus (OLP)?What is the prevalence of genital lesions in oral lichen planus (OLP)?What are the physical findings of nail involvement in oral lichen planus (OLP)?What are the physical findings of scalp involvement in oral lichen planus (OLP)?How common is otolaryngological involvement in oral lichen planus (OLP)?What are possible complications in oral lichen planus (OLP)?Which conditions should also be included in the differential diagnoses for oral lichen planus (OLP)?What are the differential diagnoses for Oral Lichen Planus?What is the role of lab studies in the diagnosis of oral lichen planus (OLP)?Which tests are performed in the evaluation of oral lichen planus (OLP)?What is the role of biopsy in the evaluation of oral lichen planus (OLP)?What is the role of histology in the diagnosis of oral lichen planus (OLP)?Which histological findings are characteristic of oral lichen planus (OLP)?What is the role of electron microscopy in the diagnosis of oral lichen planus (OLP)?What are the treatment goals for oral lichen planus (OLP)?Which treatment for oral lichen planus (OLP) is curative?What are the treatment options for oral lichen planus (OLP)?Which dietary restrictions are beneficial in the treatment of oral lichen planus (OLP)?Which lifestyle changes are beneficial in the treatment of oral lichen planus (OLP)?What is the increased risk of oral cancer in patients with oral lichen planus (OLP) and how can the risk be mitigated?Which specialist consultations are needed for the treatment of oral lichen planus (OLP)?What is included in long-term monitoring of patients with oral lichen planus (OLP)?What is the mainstay of medical treatment for oral lichen planus (OLP)?What are the treatment options for recalcitrant oral lichen planus (OLP)?Which medications in the drug class Calcineurin Inhibitors are used in the treatment of Oral Lichen Planus?Which medications in the drug class Acne Agents, Topical are used in the treatment of Oral Lichen Planus?

Author

Jaisri R Thoppay, MS, DDS, MBA, President, Center for Integrative Oral Health, Inc

Disclosure: Nothing to disclose.

Specialty Editors

Michael J Wells, MD, FAAD, Dermatologic/Mohs Surgeon, The Surgery Center at Plano Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Jeff Burgess, DDS, MSD, (Retired) Clinical Assistant Professor, Department of Oral Medicine, University of Washington School of Dental Medicine; (Retired) Attending in Pain Center, University of Washington Medical Center; (Retired) Private Practice in Hawaii and Washington; Director, Oral Care Research Associates

Disclosure: Nothing to disclose.

Additional Contributors

Gregory J Raugi, MD, PhD, Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle School of Medicine; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle

Disclosure: Nothing to disclose.

Philip B Sugerman, MDS, PhD, Senior Clinical Science Manager, Abbott Immunology, Abbott Laboratories

Disclosure: Nothing to disclose.

Stephen R Porter, MD, PhD, FDSRCS(Eng), FDSRSE, Professor of Oral Medicine, University College London; Academic Head, Director of Research Strategy, Oral Medicine/Special Needs Unit, Division of Maxillofacial Diagnostic, Medical and Surgical Sciences, Eastman Dental Institute for Oral Health Sciences, UK

Disclosure: Nothing to disclose.

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Plaquelike oral lichen planus on buccal mucosa on left side.

Reticular oral lichen planus on buccal mucosa on left side.

Ulcerative oral lichen planus on dorsum of tongue.

Plaquelike oral lichen planus on buccal mucosa on left side.

Lichen planus nail involvement.

Plaquelike oral lichen planus on buccal mucosa on left side.

Reticular oral lichen planus on buccal mucosa on left side.

Ulcerative oral lichen planus on dorsum of tongue.

Lichen planus nail involvement.