Diagnosis and Management of Oral Lichen Planus
Complex and incurable, OLP demands careful, continuous attention
Nelson L. Rhodus, D.M.D., M.P.H.,*
Sandra Myers, D.D.S., M.S.,** and
Shanti Kaimal, B.D.S., M.D.S.***
It was Erasmus Wilson who coined the term "lichen planus" in 1869. He considered this to be the same disease as "leichen ruber", previously described by Hebra.Wickham noted the punctuations and striae atop the lesions that currently bear his name.2 Today, lichen planus, including the cutaneous form and oral lichen planus (OLP), is recognized as a chronic mucocutaneous
inflammatory condition of the stratified squamous epithelia.
Oral lichen planus (OLP) is a poorly defined and misunderstood chronic inflammatory condition involving the oral mucosal tissues. The condition is most often seen in middle-aged patients, and affects more women than men.3-4 Children are only rarely affected. 5 The etiology of lichen planus is most likely of multifactorial origin.6
OLP is believed to be a T-cell mediated autoimmune disorder, although the initial event in OLP lesion formation and the factors that determine OLP susceptibility are unknown.4 Others believe that OLP has a genetic predisposition and is initiated by a variety of factors, including emotional stress and hypersensitivity to drugs, dental materials, or food.5-8 Some of the potential contributors to OLP and its periodic exacerbations are listed in Table I.
The clinical presentation of OLP is variable, and it may present as any one of the following clinical forms: atrophic, bullous, erosive, papular, plaque-like, or reticular, with the reticular form the most common.3-4
Lesions of OLP are typically bilateral. Any location in the oral cavity may be involved, with the most common site being the posterior buccal mucosa.7 Other common locations cited for OLP include: tongue, gingiva, retromolar/ tuberosity area, vestibule, palate, floor of the mouth, and lip.8 Although OLP lesions generally have a distinct clinical morphology, they may also present a confusing array of patterns and forms. At least six clinical appearances have been described, and it is not uncommon to have more than one form in any individual patient. It is also not uncommon for the lesions to change not only in character and severity but also in intraoral anatomic locations.
Forms of Lichen Planus
This is the most common type. It consists of slightly raised slender whitish lines in an interlocking lace-like pattern ("Honiton lace" or "Wickham's striae") or in an annular arrangement. This lace-like network is often interspersed with papules or rings (Figure 1).
Minute white papules may be seen. These gradually enlarge and coalesce to form either a reticular, annular, or plaque pattern.
The plaque form may be difficult to distinguish from leukoplakia, but in OLP there is usually no change in the flexibility of the affected mucosa. Another distinguishing feature may be the presence of a reticular periphery.
Atrophic OLP presents as a diffuse red or erythroplakic lesion.
Erosive OLP often presents an amalgamation of erythematous and ulcerative areas surrounded by keratotic striae. Gingival involvement with this form produces desquamative
gingivitis (Figure 2).
This form of OLP is quite rare. The intraoral bullae rupture soon after they appear, resulting in the classic appearance of erosive OLP.
Significant pain and discomfort accompany the atrophic, erosive, and bullous forms.9 Typically there is a cycle of waxing and waning with respect to the symptoms. The cycles may vary, but usually occur about every three to four weeks.9 Cutaneous lesions occasionally accompany OLP in about 30% of cases.10 The characteristic cutaneous lesion is a flat-topped, erythematous or
violaceous pruritic papule typically involving the flexor surfaces of the legs and arms, especially the wrists. The papules occur either as isolated lesions or in aggregate patterns and may show a fine transparent superficial scale. Wickham's striae may be present on many papules. Hyperpigmentation may be a sequela, and is often quite marked but temporary. The nail beds may also be affected, resulting in ridging, thinning, and subungual hyperkeratosis. Scalp involvement, if untreated, can lead to scarring and permanent hair loss.10
Lesions of OLP often present a diagnostic dilemma. In addition to the patterns and forms enumerated above, a number of lesions can simulate OLP and are designated as "lichenoid".9 Oral lichenoid lesions can follow the administration of a systemic drug (non-steroidal anti-inflammatory drugs, beta blockers etc.), placement of a dental restoration, or provision for a denture.10-11 Flavorings, especially cinnamates in toothpaste, may also trigger lichenoid contact sensitivity reactions12-13 (Table I).
Emotional stress has been considered to be a strong contributing factor by many investigators, especially for the exacerbation phases of OLP.2-11 Most of these lesions are unilateral and usually regress after removal of the causative (or precipitating) factor. In general, bilateral lesion distribution is a key clinical diagnostic feature of OLP, while unilateral distribution is a detractor rendering true OLP less likely.3, 13-14
Many of the clinical descriptions provided by clinicians contain generic terminology such as white/whitish, red and white, hyperkeratosis, and leukoplakia. These terms may describe lesions other than OLP, ranging from chronic cheek chewing to tobacco-pouch keratosis and verrucous carcinoma. Some clinicians, on the other hand, support their provisional clinical diagnosis by
providing definitive descriptions, such as striae of Wickham, and specifying a location for the oral lesions. The clinical appearance and location, in combination with medical and dental findings,are valuable clues for clinicians formulating and justifying provisional and differential clinical diagnoses. They are also valuable considerations for pathologists in rendering definitive final diagnoses. Approximately 30-50% of patients with OLP also have concomitant skin lesions. The presence of these characteristic cutaneous lesions can also aid in the diagnosis of OLP.
The diagnosis of OLP appears to have been extended by the use of modifying terminology to include lesions that have less than definitive features. The use of modifiers such as possible, probable, suggestive of, and consistent with OLP in definitive final diagnoses when the findings are less than classic may be misleading to clinicians formulating treatment options and follow-up care. Therefore the use of such confusing terminology should be restricted.8-9
In a recent study, it was reported that the ratio of females to males diagnosed with OLP was approximately two to one over a ten-year period, and the mean age for females increased by 5.2 years while the mean age for males decreased by 12.2 years. The percentage of all oral lesions biopsied over the time period which were diagnosed as OLP increased from 1.6% to 4.1%. However, the percentage of definitively diagnosed OLP lesions decreased from 100% to 42% over the same time period. These results indicate the difficulty with which OLP is diagnosed by histopathology alone. It is very important to include complete clinical information in the diagnosis of OLP.9
The histopathological features of OLP have been well established.14-15 The requisite features are liquefaction degeneration of the basal cells and a band-like infiltrate of lymphocytes within the lamina propria that intimately intermingles with the basal cell region of the surface epithelium. Additional features are the "saw-toothed" rete pegs, hyperkeratosis or parakeratosis, separation of surface epithelium from the underlying connective tissue, and the formation of "Civatte bodies"14 (Figure 3). These features are often present but are not a prerequisite for diagnosis.
The appearance of the classic histologic features makes the diagnosis of OLP fairly straightforward. It is only when the findings are variable and nonspecific that the diagnostic process is fraught with errors. The use of qualifying and disqualifying factors to rule in or rule out identifiable causes can substantially narrow the clinical and histopathologic diagnosis of lesions considered "true" OLP.9
Historically, both the histologic and clinical diagnoses of OLP have been enigmas. Histologic diagnostic criteria to separate OLP from lichenoid lesions and lichenoid dysplasia have been elucidated by several investigators 13-14 (Figure 3).
Relationship With Squamous Cell Carcinoma
Case studies16-18 have shown that some patients with a diagnosis of OLP also develop squamous cell carcinoma (SCC) within or adjacent to lichenoid lesions (Figure 4). Some investigators19-21 have attempted to demonstrate that OLP has premalignant potential and can progress to SCC. However, the question of whether the premalignant epithelial dysplasia or the OLP came first remains controversial. A significant problem in establishing a relationship between OLP and the development of SCC is the difficulty in differentiating histologically between the variable findings in OLP and those of dysplastic lesions with lichenoid features.13-14 In an effort to investigate these as two distinct and separate histopathologic entities, researchers are examining p53 a protein product of a tumor-suppressor gene involved in DNA repair and cell cycle as well as other arrest molecular biomarkers (Figure 3).22-24
No known cure exists for oral lichen planus. The treatment modalities in OLP are still empirical. The rationale for treatment is to provide oral comfort for the patient if the lesions are symptomatic, to improve function (eating, speaking, sleeping, wearing dental prostheses etc.), as well as to prevent or prolong the frequency and severity of exacerbations. Systemic and local relief with anti-inflammatory and immunosuppressant agents is often indicated. In some cases concomitant topical anesthetics, analgesics, and antifungal agents are also indicated. Identification of any precipitating factors including diet, dental materials, dental hygiene products, or medication (lichenoid drug reaction) (Table I) should be undertaken to ensure against a hypersensitivity reaction or exacerbation. Treatment or prevention of a secondary fungal infection with a systemic antifungal agent also should be considered in most cases.
In general, the quiescent, asymptomatic reticular and plaque forms do not warrant pharmacological intervention, while the erythematous and erosive forms are associated with a high degree of morbidity. Regardless of clinical type or presentation, lesions of OLP undergo periods of exacerbation and quiescence. Treatment is therefore aimed at reducing the severity and length of these episodic outbreaks.
Maintenance of oral hygiene with a non-abrasive dentifrice and avoidance of alcohol-containing mouthwashes is important since these have been observed to reduce severity of the symptoms.
Potential for Malignancy and Periodic Biopsies
Any chronic and/or refractory lesion should be considered for a biopsy, first to establish a diagnosis and subsequently to rule out malignancy. Periodic biopsies are indicated for persistent lesions as there is a potential for malignant transformation. The reported incidence of malignant transformation is approximately 2-5%. The mean length of time for OLP to transform to squamous cell carcinoma is 7.2 years.4,15,18,25 These figures indicate the need for long-term, appropriate follow-up and monitoring.
Stated again, there is no cure for OLP. Therapy should be individually tailored to the specific patient and is aimed at reduction of inflammation. Therapies with steroids and immunomodulating drugs are presented to inform the clinician that such modalities are available. There are several of these agents, and there is no single recommended therapy. Because of the potential for side effects, close collaboration with the patient's physician is recommended when these medications are prescribed. These modalities may be beyond the scope of clinical experience of general dentists, and referral to a specialist in oral medicine, a dentist with training and experience in this area, or to an appropriate physician may be necessary.26
Prolonged use of topical steroids (for a period of greater than two weeks continuous use) may result in mucosal atrophy and secondary candidiasis, and may increase the potential of systemic absorption. The concomitant prescribing of antifungal therapy along with the topical steroids may be necessary. Therapy with topical steroids, once the lichen planus is under control, should be tapered to alternate-day (or less) therapy depending on control of the disease and the tendency to recur. A usual course of steroid therapy should not exceed 10-14 days, with an interim period approximately the same before re-instituting the steroid therapy.
Steroid therapy may include any of the following.
Dexamethasone (Decadron) oral rinse, 0.5 mg/5 ml
Fluocinonide (Lidex) gel, 0.05%
Betamethasone valerate (Valisone) ointment 0.1%
Triamcinolone acetonide (Kenalog) ointment 0.1%
Hydrocortisone gel or ointment, 1.0%
Clobetasol propionate (Temovate) ointment, 0.05%
Halobetasol propionate (Ultravate) ointment, 0.05%
Examples of prescriptions for OLP would be:
Ç Fluocinonide (Lidex) gel 0.05%
Ç Disp: 30 gm tube
Ç Sig: Coat the lesion with a thin film after each meal and at bedtime.
Ç Dexamethasone (Decadron) elixir 0.5 ma/5 ml
Ç Disp: 100 ml
Ç Sig: Rinse with one teaspoonful for two minutes qid and spit out. Discontinue when lesions become asymptomatic.
In periods of remission and quiescence, OLP may be kept under control and the symptomatic exacerbation phase reduced in frequency by several interventions. First, elimination or avoidance of precipitating or perpetuating factors such as SLS-containing dentifrices, spicy or acidic foods,tissue trauma, and xerostomia-inducing agents (Table I). A "magic mouthwash" containing benadryl, kaopectate (or carafate), and milk of magnesia as a base to which nystatin and/or lidocaine may be added (depending upon the clinical indications) is quite effective as a therapy for mildly symptomatic cases or as maintenance therapy.
Oral candidiasis may result from topical steroid therapy. The oral cavity should be monitored for emergence of fungal infection on patients who are placed on steroid therapy. Most often oral candidiasis presents clinically as macular erythema, angular cheilosis, or pseudomembranous white plaques which can be scraped off the mucosa. However, significant candidiasis may be present with few clinical signs. Prophylactic antifungal therapy should be initiated in patients with a history of fungal infection and/or immunosuppressed patients and/or those with prior steroid administration.26,27
Phased and Combination Therapies
Due to the phasic nature of OLP alternating between symptomatic exacerbations and remissions, often a phased sequence of therapy is warranted and effective.26,27 In these cases, a more potent regimen of topical corticosteroid for a week or two followed by a second phase regimen of lesser potent topical corticosteroids will provide effective therapy. Additionally, often during periods of acute exacerbation, combinations of more than one topical corticosteroid may be effective
‹ for example, first the dexamethasone oral rinse followed by application of fluocinonide or triamcinolone ointment. There are many combinations which may be utilized, depending upon the individual clinical scenario.
Obviously, proper diagnosis and recognition of the nature of the OLP in the individual patient along with detailed patient information and self-therapy instruction are essential.
Systemic steroids and immunosuppressants prescribed for more severe cases would include:
Ç Dexamethasone (Decadron) elixir 0.5 mg/5 ml
Ç Disp: 320 ml
Ç Sig: 1. For 3 days, rinse with 1 tablespoonful (15 ml) qid and swallow. Then 2. For 3 days, rinse with teaspoonful (5 ml) qid and swallow. Then 3. For 3 days, rinse with 1 teaspoonful (5 ml) qid and swallow every other time. Then 4. Rinse with 1 teaspoonful (5 ml) qid and expectorate.
Ç Prednisone tablets 10 mg
Ç Disp: 26 tablets
Ç Sig: Take 4 tablets in the morning for 5 days, then decrease by 1 tablet on each successive day.
Ç Prednisone tablets 5 mg
Ç Disp: 40 tablets
Ç Sig: Take 5 tablets in the morning for 5 days, then 5 tablets in the morning every other day until
If oral discomfort recurs, the patient should return to the clinician for reevaluation.
Many studies suggest that oral lichen planus has an intrinsic property predisposing to malignant transformation. However, the etiology is complex, with interaction among factors including infectious agents, genetic variables, environmental influences, and lifestyle elements. Prospective studies have demonstrated that lichen planus patients have a slightly increased risk to develop oral squamous cell carcinoma. All patients exhibiting lichen planus intraorally, particularly those who have had the ulcerative form, should receive periodic follow-up.
Therapy with medications such as systemic steroids, immunosuppressants, and immunomodulators is presented to inform the clinician that such modalities have been reported effective for patients suffering from ulcerative lichen planus. Medications such as azathioprine, mycophenolate mofetil, tacrolimus hydro-xychloroquinesulfate, acitretin, and cyclosporine-A are used to treat patients with severe persistent ulcerative lichen planus but should not be routinely used because of the potential for side effects. Close collaboration with the patient's physician is recommended when these medications are prescribed.
Oral lichen planus is a complex and poorly understood clinical condition which cannot be cured. A definitive diagnosis and careful, conscientious follow-up are imperative. Symptoms and complications are common and challenging but may be managed with a variety of therapies including orally administered and systemic medications as well as lifestyle alterations and reduction of precipitating factors.
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16. Camisa, C., Hamaty, F.G., and Gay, J.D.: Squamous cell carcinoma of the tongue arising in lichen planus: a case report and review of the literature. Cutis 62: 175-178, 1998.
17. Duffey, D.C., Eversole, L.R., and Abemayor, E.: Oral lichen planus and its association with squamous cell carcinoma: an update on pathogenesis and treatment implications. Laryngoscope 106: 357-362, 1996.
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20. Lo Muzio, L., Mignogna, M.D., Favia, G. et al:The possible association between oral lichen planus and oral squamous cell carcinoma: a clinical evaluation on 14 cases and a review of the literature. Oral Oncol 34: 239-246, 1998.
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24. Schifter, M., Jones,A.M., and Walker,D.M.: Epithelial p53 gene expression and mutational analysis, combined with growth fraction assessment, in oral lichen planus. J Oral Pathol Med 27: 318-324, 1998.
25. Onofre, M.A., Sposto, M.R., Navarro, C.M. et al: Potentially malignant epithelial oral lesions: discrepancies between clinical and histological diagnosis. Oral Dis 3: 148-152, 1997.
26. Clinician's Guide to the Treatment of Common Oral Conditions, Fourth Edition, by Rosenberg, S.W., Arm, R.N., Bottomly, W.K., Rhodus, N.L. et al. New York, New York: American Academy of Oral Medicine, Inc., 1997.
27. Rhodus, N.L.: Clinical observations from approximately 300 patients, 2002.
*Dr. Rhodus is Professor and Director of Oral Medicine, University of Minnesota School of Dentistry, Minneapolis, Minnesota 55455.
**Dr. Myers is Associate Professor of Oral Pathology, University of Minnesota School of Dentistry, Minneapolis, Minnesota 55455.
***Dr. Kaimal is Research Fellow, University of Minnesota School of Dentistry, Minneapolis, Minnesota 55455.
Copyright 2003. Minnesota Dental Association.
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