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290 Australian Dental Journal 2002;47:4.

Oral lichen planus: Causes, diagnosis and management

PB Sugerman,* NW Savage†

Abstract

Oral lichen planus (OLP) is a chronic inflammatorydisease of unknown etiology. In this paper we reviewthe clinical and histological features of OLP, processof OLP diagnosis, causes of OLP, management of OLP patients and medical treatment of OLP lesions.

Approximately 0.2 per cent OLP patients developintra-oral carcinoma each year compared withapproximately 0.005 per cent Australian adults.Possible mechanisms of increased oral cancer risk inOLP patients are presented. The aims of currentOLP therapy are to eliminate mucosal erythema andulceration, alleviate symptoms and reduce the risk of oral cancer. Patient education may improve theoutcomes of OLP therapy and further reduce the riskof oral cancer in OLP patients. Although OLP maybe diagnosed clinically, appropriate specialistreferral is required for: (i) histological diagnosis; (ii)assessment of causative/exacerbating factors,associated diseases and oral cancer risk; (iii) patienteducation and management; (iv) medical treatment;and (v) long-term review and re-biopsy as required.

Key words: Oral lichen planus, causes, management.

(Accepted for publication 30 January 2002.)

Clinical features of oral lichen planus

Oral lichen planus presents as white striations (Fig 1),white papules, white plaques, erythema, erosions (Fig 2)or blisters affecting predominantly the buccal mucosa,tongue and gingivae, although other sites areoccasionally involved. Oral lichen planus affects 1-2per cent of the general adult population and is the mostcommon non-infectious oral mucosal disease inpatients referred to oral medicine and oral pathologyclinics.1,2 Oral lichen planus affects women more thanmen (1.4:1). Oral lichen planus occurs predominantlyin adults over 40, although younger adults and childrenmay be affected. Lesions are typically bilateral andoften appear as a mixture of clinical subtypes. White orgrey streaks may form a linear or reticular pattern onan erythematous background. Alternatively, there maybe a central area of shallow ulceration (erosion) with ayellowish surface (fibrinous exudate) surrounded by an

area of erythema. Notwithstanding the multiple oralmanifestations that form the basis of most currentclinical classifications of OLP, the major issue is toarrive at a correct diagnosis. Almost all cases of OLPpresent with reticular keratotic striae in some area of the oral mucosa. Therefore, all cases of oral mucosaldisease should be examined carefully for fine striaeboth peripherally around atrophic and/or erosive sitesand on the buccal mucosa, ventral tongue, lateraltongue and gingivae (Fig 3). Gingival lesions frequentlypresent as fiery red erythema affecting the entire widthof the attached gingiva, a condition previously termed“desquamative gingivitis” (Fig 4). As discussed

previously, OLP lesions may be associated with patchybrown melanin deposits in the oral mucosa(inflammatory melanosis), although this is uncommonin fair-skinned people (Fig 5).3 The dorsal surface of thetongue also carries the striae in some patients but afrequent alternative is an annular pattern in which thekeratotic lines form circles of varying size (Fig 6).

Patients with OLP may have co-incident skin lesionsthat present frequently as pruritic flat-toppedviolaceous papules and plaques, predominantly on theflexor aspects of the wrists or ankles, extensor aspectsof the lower legs, the skin of the lower central back andthe natal cleft. Some patients report genital involvement

with features similar to skin lesions. Scalp involvement(lichen planopilaris) causes follicular and perifollicular

INTRODUCTION

Oral lichen planus (OLP) is a chronic inflammatoryoral mucosal disease of unknown etiology. The aim of this communication is to provide an update of theclinical and histological features of OLP, process of OLP diagnosis, causes of OLP, management of OLPpatients and medical treatment of OLP lesions. Themalignant potential of OLP is discussed and practicalsteps to reduce the risk of oral cancer in OLP patientsare presented. The need for OLP patient education ishighlighted. Although OLP may in many cases bediagnosed clinically, specialist referral is required forthorough patient investigation, management andreview.

*Senior Research Fellow, AstraZeneca R&D Boston, Waltham,Massachusetts, USA.†Reader in Oral Medicine and Pathology, School of Dentistry,The University of Queensland.

Australian Dental Journal 2002;47:(4):290-297REV I EW


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violaceous scaly pruritic papules, follicular plugging,

bottle-brush hair formation (multiple hair shafts exitingfrom a single follicular orifice) and atrophic scarringwith permanent patchy hair loss. Nail involvementcauses pitting, subungual hyperkeratosis, longitudinalmelanonychia, onychorrhexis (longitudinal ridging andgrooving), onychoschizia (distal splitting) andonycholysis (separation of the nail plate from the nailbed). Permanent damage to the nail matrix results inpterygium formation (raised central ridge) andpermanent nail loss (anonychia). Rarely, there islaryngeal, oesophageal and conjunctival involvement.4

General dental practitioners may reasonably examine apatient’s wrists, scalp and nails. The detection of lesions

at these sites may expedite appropriate referral andmanagement.

Approximately two thirds of OLP patients reportoral discomfort.5 Most cases of symptomatic OLP areassociated with atrophic (erythematous) or erosive(ulcerative) lesions. Symptoms vary from mucosalsensitivity to continuous debilitating pain. Oral lichenplanus lesions usually persist for many years withperiods of exacerbation and quiescence. During periodsof exacerbation, there is increased erythema or

ulceration with increased pain and sensitivity. Duringperiods of quiescence, there is a decrease in the extentof erythema or ulceration with decreased pain andsensitivity. Patients are often unaware of quiescent OLPthat presents typically as faint white striations, papulesor plaques. Exacerbation of OLP has been linked toperiods of psychological stress and anxiety, apredictable correlation with any condition that isrelated to an immune system imbalance.6

Oral mucosal lichenoid lesions may follow theadministration of a systemic drug, with a variable lagperiod. These lichenoid drug reactions (LDR) may beunilateral but usually appear as idiopathic OLP. Drugsthat have been implicated in oral LDR include non-steroidal anti-inflammatory drugs, angiotensin-

converting enzyme inhibitors and beta-blockers,although there are many others (Fig 7).7 Oral mucosallichenoid lesions may follow the placement of a dentalrestoration or provision of a denture, again with avariable lag period. These lichenoid reactions areusually the result of a contact sensitivity or irritantcontact response to an amalgam or composite resindental restoration or a denture component in closeproximity to the oral mucosa (Fig 8, 9). Toothpaste

Australian Dental Journal 2002;47:4. 291

Fig 1. Reticular pattern of fine white keratotic striae typical of orallichen planus (OLP) on the posterior buccal mucosa. This baselinepresentation is found in almost all OLP patients somewhere on the

oral or gingival mucosae.

Fig 3. A more extensive area of erosion overlying a delicate atrophicmucosa. The typical striae are seen anterior to the erosion.

Fig 2. Linear erosive lesion on the ventral surface of the tongue. Thesurrounding mucosa is atrophic and erythematous with very faint

reticular striae.

Fig 4. Gingival OLP may present with the typical fine reticular striaeor, as in this case, with generalized erythema and fragility. The striaecan usually be seen as a very fine pattern on the tips of the interdentalpapillae. This pattern is frequently and incorrectly referred to asdesquamative gingivitis and may be misdiagnosed as mucous

membrane pemphigoid.


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flavorings, especially cinnamates, may also triggerlichenoid contact sensitivity reactions. Oral mucosallichenoid lesions are also seen within the spectrum of

chronic graft-versus-host disease following allogeneicbone marrow transplantation.3 In many cases, a causefor the oral lichenoid lesions cannot be identified andthe diagnosis by exclusion is “idiopathic OLP”.

Lichen planus may associate with other immune-mediated diseases including alopecia areata,dermatomyositis, lichen sclerosis et atrophicus,morphea, myasthenia gravis, primary biliary cirrhosis,ulcerative colitis and vitiligo. Oral lichen planus is alsoreported in association with hepatitis C infection andchronic active hepatitis. However, associations betweenOLP and systemic diseases may be co-incidental as OLPis relatively common, it occurs predominantly in older

adults and many drugs used in the treatment of systemic diseases trigger oral lichenoid lesions as a sideeffect. As an example, the oral lichenoid lesions in“Grinspan’s syndrome” (triad of OLP, diabetes mellitusand hypertension) may be a reaction to the drugs usedto treat diabetes mellitus or hypertension.7

Oral lichen planus and oral cancer

There is ongoing concern that OLP may bepremalignant, although the malignant transformation

data are currently under review and further prospectivestudies are required. Malignant transformation of OLPremains a very controversial issue. At least somereported cases diagnosed originally as OLP on clinicaland/or histological grounds were probably epithelialdysplasias (lichenoid dysplasias) that progressed

Fig 5. Oral lichen planus involving the lateral hard palate with typicalreticular striae and secondary melanosis. Fig 7. Extensive erosive OLP in a patient on long-term anti-

inflammatory medications. In this case the NSAIDS exacerbated apreviously existing OLP by introducing the erosive component thathad not previously been problematic. Withdrawal of the agent gaverapid resolution to the erosion although the original OLP remained.

Fig 6. Oral lichen planus lesions on the dorsum of the tongueshowing interlacing striae and, in particular, the annular keratoticstriae seen most frequently although not exclusively on the tongue.

Fig 9. Lichenoid reaction on the inner aspect of the lip to a compositeresin restoration in the adjacent incisor tooth. Replacement of the

restoration gave full resolution to the lesion.

Fig 8. Lichenoid reaction to the amalgam restoration on the buccalaspect of the molar tooth. This is an isolated response without the

symmetrical distribution seen in typical OLP.


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subsequently to overt squamous cell carcinoma (SCC).8

Approximately 0.2 per cent of OLP patients developoral SCC each year.7 In comparison, approximately

0.005 per cent of Australian adults develop intra-oral

SCC each year.9 Hence, it is clear that OLP patients are

at increased risk of oral cancer. However, less than

5 per cent of OLP patients who do not use tobaccoproducts develop oral SCC, most frequently in

atrophic, erosive and plaque lesions.7 It is therefore

unlikely that OLP is inherently premalignant.10,11 The

cause of increased oral cancer risk in OLP patients is

unknown, although the oral mucosa affected by OLP

may be compromised to the extent of being more

sensitive to exogenous mutagens in tobacco, alcohol,betel quid and Candida albicans. Alternatively, thechronic inflammatory response and simultaneous

epithelial wound healing response in OLP may increase

the likelihood of cancer-forming gene mutations. The

latter hypothesis is supported by recent important

findings that link chemical mediators of T cellinflammation to tumourigenesis. These studies showed

that macrophage migration inhibitory factor (MIF)

released from T cells and macrophages suppresses the

transcriptional activity of the p53 tumour suppressor

protein.12 As discussed previously, normal p53 functionis central to the prevention of many cancers including

oral SCC.13 Hence, blocking p53 function by MIF (and

possibly other inflammatory mediators) may underlie

the increased risk of oral cancer in OLP patients. The

increased risk of oral cancer underscores the need for

periodic clinical review of OLP patients and, where

indicated by the clinical appearance or previoushistology, further review by scalpel biopsy.

Diagnosis of oral lichen planus

A complete history and physical examination by a

multidisciplinary group of health care providers may be

required to investigate oral, skin, nail, scalp, genital,

oesophageal, laryngeal and conjunctival involvement.6

The history, typical oral lesions and skin or nail

involvement are usually sufficient to make a clinical

diagnosis of OLP. However, biopsy is required to

differentiate between OLP and other chronic white orulcerative oral lesions including reactive keratoses,

chronic hyperplastic candidosis, epithelial dysplasia,

discoid lupus erythematosus, gastro-intestinal disease

(including oral Crohn’s disease) or anemic states.

Malignancy must also be excluded. Direct

immunofluorescence can help distinguish erosive,

ulcerative or the very rare bullous form of OLP from

pemphigus vulgaris, benign mucous membrane

pemphigoid, dermatitis herpetiformis and linear IgA

bullous dermatosis. There are no consistent serological

changes associated with OLP but some patients do

present an elevated ANA titre.7 Blood biochemistry andFBE should also be included in the full patient workup.

Although cytological changes may be detected in OLP,the use of exfoliative cytology is not recommended.14

Histology of oral lichen planus

The histology of OLP is characterized by a densesub-epithelial lympho-histiocytic infiltrate, increasednumbers of intra-epithelial lymphocytes anddegeneration of basal keratinocytes. Degenerating basalkeratinocytes form colloid (civatte, hyaline, cytoid)

bodies that appear as homogenous eosinophilicglobules. The ultrastructure of colloid bodies suggeststhat they are apoptotic keratinocytes and recent studiesusing the end-labeling method demonstrated DNAfragmentation in these cells.15-18 Epithelial basementmembrane changes are common in OLP and comprisebreaks, branches and duplications.19 In addition, thebasal keratinocyte anchoring elements(hemidesmosomes, filaments and fibrils) aredisrupted.20 Degeneration of basal keratinocytes anddisruption of the epithelial basement membrane andbasal keratinocyte anchoring elements produceweakness at the epithelial-connective tissue interface

which may result in histological cleft formation (Max- Joseph space) and clinical blistering of the oral mucosa(bullous lichen planus). Parakeratosis, acanthosis and“saw-tooth” rete peg formation may be seen.

B cells and plasma cells are infrequent in OLP andimmunoglobulin and complement deposits are not aconsistent feature. The presence of a mixed andsometimes more diffuse infiltrate should alert thepathologist that the condition may be drug related orperhaps lichenoid, rather than true idiopathic lichenplanus. Some cases show fibrinogen and fibrindeposition in a linear pattern in the basementmembrane zone. Colloid bodies may be positive forfibrin, IgM, C3, C4 and keratin. Laminin andfibronectin staining may be absent in areas of heavyfibrin deposition and colloid body formation,suggesting basement membrane damage in these areas.Immunofluorescent findings in OLP are not diagnostic.7

Pathogenesis of oral lichen planus

Current data suggest that OLP is a T cell-mediatedautoimmune disease in which auto-cytotoxic CD8+T cells trigger apoptosis of oral epithelial cells. However,the precise cause of OLP is unknown. The lymphocyticinfiltrate in OLP is composed almost exclusively of

T cells and the majority of T cells within the epitheliumand adjacent to damaged basal keratinocytes areactivated CD8+ lymphocytes.21,22 Our preliminarystudies showed that CD8+ T cells co-localize withapoptotic keratinocytes in OLP lesions.3 T cell lines andclones from lichen planus lesions were more cytotoxicagainst autologous lesional keratinocytes than T celllines and clones from clinically normal skin of lichenplanus patients. Lesional T cell clones were morecytotoxic against autologous lesional keratinocytes andnormal skin keratinocytes than against autologousB cell blasts. The majority of cytotoxic clones fromlichen planus lesions were CD8+ and the majority of

non-cytotoxic clones were CD4+. The cytotoxicactivity of CD8+ lesional T cell clones was partially



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blocked with anti-MHC Class I monoclonal antibody.23

Hence, early in OLP lesion formation, CD8+ lesionalT cells may recognize an antigen associated with MHCClass I on lesional keratinocytes. Following antigenrecognition and activation, CD8+ cytotoxic T cells maytrigger keratinocyte apoptosis. T cell activation and

subsequent clonal expansion may underlie restrictedT cell receptor Vß gene expression by infiltrating T cellsin OLP.24 Activated CD8+ T cells (and possiblykeratinocytes) may release cytokines which attractadditional lymphocytes into the developing lesion.

We hypothesize that keratinocytes express a lichenplanus antigen, but only at the lesion site, i.e., theclinical distribution of lichen planus lesions isdetermined by the distribution of the lichen planusantigen. In this context, an early event in lichen planuslesion formation may be keratinocyte antigenexpression or unmasking at the future lesion siteinduced by systemic drugs (lichenoid drug reaction),

contact allergens in dental restorative materials ortoothpastes (contact hypersensitivity reaction),mechanical trauma (Koebner phenomenon), viralinfection, bacterial products or an unidentified agent.The lichen planus antigen is unknown, although theantigen may be a self peptide thus making lichen planusa true autoimmune disease. The role of autoimmunityin disease pathogenesis is supported by manyautoimmune features of OLP including diseasechronicity, adult onset, female predilection, associationwith other autoimmune diseases, occasional tissue typeassociations, depressed immune suppressor activity inOLP patients and the presence of auto-cytotoxic T cell

clones in lichen planus lesions.23,25,26 We identifiedupregulated heat shock protein (HSP) expression byOLP lesional keratinocytes in situ and HSP-reactivity of OLP lesional T cells in vitro.27 Upregulated HSPexpression by oral mucosal keratinocytes may be acommon final pathway linking a variety of exogenousagents (systemic drugs, contact allergens, mechanicaltrauma, viral infection, bacterial products) in thepathogenesis of OLP. Furthermore, HSP expressed byoral keratinocytes in OLP may be auto-antigenic.27

Antigen-presenting cells (APC) must undergo a processof terminal differentiation called “maturation” tostimulate a T cell response. Stimuli for APC maturationinclude mechanical trauma, various chemicals, e.g.,NiCl2, MnCl2, CoCl2, SnCl2, and allergens, e.g.,TNCB, DNCB, ion channel blockade, viral RNA,bacterial lipopolysaccharide and HSPs.28 Hence, orallichenoid lesions associated with mechanical trauma,dental restorations, toothpaste flavorings, systemicdrugs, viral infection or bacterial products may resultfrom APC maturation with subsequent T cellstimulation.

At this stage, the mechanisms used by the CD8+cytotoxic T cells to trigger keratinocyte apoptosis inOLP are unknown. Possible mechanisms include:

(i) T cell secreted TNF- binding the TNF- R1receptor on the keratinocyte surface; (ii) T cell surface

CD95L (Fas ligand) binding CD95 (Fas) on thekeratinocyte surface; or (iii) T cell secreted granzyme Bentering the keratinocyte via perforin-inducedmembrane pores. All of these mechanisms may activatethe keratinocyte caspase cascade resulting inkeratinocyte apoptosis.3 We identified elevated levels of

TNF- in the serum of OLP patients and showed thatOLP lesional T cells contained mRNA for TNF- andsecreted TNF- in vitro.29,30 These data suggested thatT cell-secreted TNF- may be involved in thepathogenesis of OLP. CD8+ cytotoxic T cells may secreteTNF- which triggers keratinocyte apoptosis in OLP.

Viruses in oral lichen planus

As discussed, CD8+ T cells are activated in OLP andCD8+ T cells co-localize with apoptotic keratinocytesin OLP lesions. CD8+ cytotoxic T cells are known totrigger apoptosis of virally infected cells.31 Hence, viralinfection of the oral mucosa may be involved in the

pathogenesis of OLP. Many DNA viruses are known toinfect the oral and peri-oral mucosa. Herpes simplexvirus (HSV: human herpesviruses types 1 and 2) causesan acute gingivostomatitis, herpes labialis (cold sores)and recurrent intra-oral herpes. Varicella-zoster virus(VZV: human herpesvirus 3) causes chicken pox withoral ulceration in children and shingles with pain andoral ulceration in adults. Epstein-Barr virus (EBV:human herpesvirus 4) causes glandular fever (infectiousmononucleosis) with associated sore throat andpetechiae on the soft palate. Cytomegalovirus (CMV:human herpesvirus 5) is associated with aphthous-typeoral ulceration. Human papillomavirus (HPV) 6 and 11

cause oral warts (squamous papilloma) and condylomaaccuminatum whereas HPV 16 and 18 are associatedwith some oral squamous cell carcinomas.32 Thecoxsackie RNA viruses may also infect the oralmucosa. Coxsackie A4 causes herpangina, coxsackieA10 causes acute lymphoreticular pharyngitis andcoxsackie A16 causes hand, foot and mouth disease. Jontell et al .33 identified HPV 11 in 6/20 OLP specimensusing southern blot hybridization. Humanpapillomavirus types 6, 16 and 18 were not detected.Using type-specific PCR, they identified HPV 11 in8/20 OLP (including the six positive by southern blothybridization), HPV 6 in 5/20 OLP and HPV 16 in3/20 OLP. Human papillomavirus 18 was not detected.Using PCR, 65 per cent OLP were positive for HPVDNA.33 However, the authors failed to examine healthyoral mucosa or other mucosal diseases. Hence, thespecificity of HPV infection in OLP is unknown. Thereare no reports of HSV, VZV, EBV, CMV or coxsackievirus in OLP.

Management of oral lichen planus patients

Many systemic drugs may trigger oral LDRs andtherefore clinicians should be suspicious of anysystemic drug in patients with oral lichenoid lesions.7

Suspected oral LDRs should be managed, in part, bythe prescription of alternative drugs by the patient’s


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physician. A variable lag period prior to clinicalimprovement should be expected. In some cases, the

LDR is not a primary event but an exacerbation of a

true idiopathic OLP. Oral lichenoid contact sensitivityreactions may be triggered by many contact allergens.

Dental restorations and prostheses associated with oral

lesions should be replaced and cinnamate-flavoredtoothpaste should be discontinued if contact sensitivity

is suspected. Skin patch testing may help to identify

contact allergens in some OLP patients. The currentrecommendation is to use a standard series, a dental

prosthesis series and a metal salt series including gold,

mercury and palladium salts as well as other salts of metals used in dental restorations. Late readings (10

and 17 days after application of the skin patch) may be

required.34 Oral lichenoid lesions may be triggered bymechanical trauma (Koebner phenomenon) from

calculus deposits, sharp teeth, rough surfaces of dental

restorations or prostheses, cheek or tongue biting and

oral surgical procedures. Furthermore, circumstantialevidence implicates various bacteria in the pathogenesis

of OLP, although any causal role remains speculative.7

Hence, teeth associated with OLP lesions should be

scaled to remove calculus deposits and have sharpedges reduced. Dental restorations and prostheses

associated with OLP lesions should be mirror polished.

Oral lichen planus patients should be instructed inthorough oral hygiene.

Various HPVs have been identified in OLP.33

However, a causal role for viral infection in OLP has

not been identified and antiviral therapy in OLP is

currently not recommended. Some studies have shownan increased incidence of C. albicans infection in OLP.As discussed, OLP is associated with an increased risk

of oral cancer and chronic oral C. albicans infection isrecognized as an oral cancer risk factor.35 Hence,

candidal culture or smear should be undertaken

periodically and C. albicans superinfection should becontrolled with topical polyene or azole antimycotics.

Oral lichenoid lesions may arise in habitual chewers of

betel quid. Betel quid chewing is also recognized as anoral cancer risk factor and patients should be advised to

eliminate the habit.36 Some studies have shown an

association between OLP, hepatitis C virus (HCV)

infection, chronic active hepatitis and primary biliarycirrhosis.7 A causal role for HCV infection in OLP has

not been identified although liver function tests shouldbe considered in all OLP patients.

There are no consistent HLA associations reported in

OLP, suggesting that the genetic background does not

play a critical role in OLP pathogenesis.7 Exacerbationof OLP has been linked to periods of psychological

stress and anxiety.6 Psychological assessment may be

beneficial in some cases. Oral lichenoid lesions are seenwithin the spectrum of chronic graft-versus-host disease

following allogeneic bone marrow transplantation.

These lesions are usually effectively controlled withsystemic immunosuppressive therapy.

Medical treatment of oral lichen planus

The aims of current OLP therapy are to eliminatemucosal erythema and ulceration, alleviate symptomsand reduce the risk of oral cancer in OLP patients.37 Inthis context, medical treatment is restricted currently toatrophic (erythematous), erosive (ulcerated), bullous

(blilstering) or symptomatic OLP lesions.Corticosteroids are the mainstay of OLP therapybecause of their activity in dampening cell mediatedimmune activity and are administered topically, intra-lesionally or systemically. The combination of systemicand topical steroid therapy is often very effective.Localized oral lesions are treated with topical ointment,applied two to four times daily after meals. Thestrength and specific preparations used need to bebalanced carefully with the individual patient’s needs.Generalized oral lesions are often treated effectivelywith a steroid mouth rinse twice daily after meals.C. albicans superinfection, which may accompany any

immunosuppressive therapy, should be controlled withtopical antimycotics especially in risk groups such asxerostomics. Some patients should be managedprophylactically to prevent secondary candidalovergrowth and a careful examination should beundertaken in denture wearers to ensure they do nothave a pre-existing atrophic candidosis. Intralesionaland perilesional injection of steroids is useful forpersistent localized erosive OLP lesions but should beused with due caution. Most protocols using topicaland intralesional corticosteroids cause some adrenalsuppression and clinicians need to be aware of theprecise amounts of these medications being used on a

regular or irregular basis. Generalized atrophic orerosive oral lesions that do not respond to topicaltherapy may be treated with a short course of systemiccorticosteroids. Hypersensitivity, hypertension, viralinfection, tuberculosis, diabetes mellitus, pregnancy,stomach ulcers or a family history of early osteoporosismay contra-indicate the use of corticosteroidpreparations.3

Treatment of OLP with cyclosporin, azathioprine,levamisole, griseofulvin, retinoids, hydroxychloroquinesulphate, dapsone and psoralen/UVA has beenreported. The main concerns with these and other

current therapies are local and systemic side effects andlesion recurrence following withdrawal of treatment.4,7

A recent Cochrane review found only weak evidencefor the superiority of cyclosporin, retinoids, steroidsand phototherapy interventions over placebo forpalliation of symptomatic OLP.38 No treatment for OLPis curative. Oral lichen planus patients should bereviewed every month during active treatment andlesions monitored for reduction in mucosal erythemaand ulceration and alleviation of symptoms. Activetreatment should be continued and alternative therapiestried until erythema, ulceration and symptoms arecontrolled. The elimination of mucosal erythema and

ulceration leaving residual asymptomatic reticular orpapular lesions may be considered an end-point of



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current OLP therapy.37 Thereafter, due to the chronicityof OLP and the increased risk of oral cancer, OLP

patients should be reviewed at least six-monthly andlesions re-biopsied as indicated by their clinicalpresentation and previous histological findings. Orallichen planus patients should be advised to attendwhenever there is an exacerbation of symptoms or achange in lesion presentation.

Decreasing the risk of oral cancer in oral lichenplanus patients

As discussed, OLP patients are at increased risk of oral cancer. Patients with OLP should be advised toeliminate smoking and alcohol consumption. Most oralcancers arising in OLP patients are associated with

erosive, atrophic and plaque lesions.37

Erosive andatrophic lesions can be converted into reticular lesionsusing topical steroids. Hence, treatment of erosive andatrophic lesions with topical steroids may reduce therisk of oral cancer. With regard to plaque OLP lesions,the effect of treatment on the risk of oral cancer isunclear.37 Oral lichen planus patients should be advisedthat a nutritious diet including fresh fruit andvegetables may help reduce the risk of oral cancer. Dueto the potential role of C. albicans in the developmentof oral SCC, fungal superinfection should be eliminatedwith topical antimycotics.35 Oral lichen planus patientsshould attend whenever there is an exacerbation of

symptoms or a change in lesion presentation. Suchchanges most often indicate a phase of increased

disease activity, although neoplasia must be excluded.Oral lichen planus patients should be reviewed at leastsix-monthly and lesions re-biopsied as required.

Prognosis for oral lichen planus

Current immunosuppressive therapies usually

control oral mucosal erythema, ulceration andsymptoms in OLP with minimal side effects, although arange of therapies may need to be trialled. The typicalclinical course of OLP is lesion persistence with periodsof exacerbation and quiescence. Oral lichen planuspatients are at increased risk of oral cancer, althoughthe risk of oral cancer in OLP patients may be reducedas described. In this context, the prognosis for themajority of OLP patients is excellent.

Patient education in oral lichen planus

The importance of patient education in OLP hasbeen reported.39 Many OLP patients are concerned

about the possibilities of malignancy and contagionand patients are frustrated by the lack of availablepatient education.39 Suggested OLP patient informationis presented in Table 1. On-line OLP patientinformation is available currently, including a web-based OLP chat group.40 Patient education mayimprove the outcomes of OLP therapy and furtherreduce the risk of oral cancer in OLP patients.

CONCLUSIONS

Systemic drugs, contact allergens, bacterial products,mechanical trauma and psychological stress may triggeror exacerbate oral lichenoid lesions. The risk of oralcancer in OLP patients may be reduced by theelimination of exogenous carcinogens, effectivetreatment of atrophic, erosive and plaque OLP lesionsand consumption of a nutritious diet including freshfruit and vegetables. Oral lichen planus patients shouldbe reviewed at least six-monthly and lesions re-biopsiedas required. Oral lichen planus patients should beadvised to attend whenever there is an exacerbation of symptoms or a change in lesion presentation. Patienteducation may improve the outcomes of OLP therapyand further reduce the risk of oral cancer in OLPpatients. Although OLP may in many cases be

diagnosed clinically, appropriate specialist referral isrequired for: (i) histological diagnosis; (ii) assessment of causative/exacerbating factors, associated diseases andoral cancer risk; (iii) patient education andmanagement; (iv) medical treatment; and (v) long-termreview and re-biopsy as required.

ACKNOWLEDGEMENTS

Philip Sugerman is supported by a National Healthand Medical Research Council (Australia) IndustryResearch Fellowship (#143125).

REFERENCES

1. Axell T, Rundqvist L. Oral lichen planus - a demographic study.Community Dent Oral Epidemiol 1987;15:52-56.

Table 1. Oral lichen planus (OLP) patient information

1. Oral lichen planus (OLP) is a mouth rash of unknown cause2. OLP is not contagious and not inherited3. OLP presents as white lines or spots, redness or ulceration,

often in combination4. OLP may be painless or cause mucosal sensitivity or pain5. OLP may be more severe at times of psychological stress6. OLP may eventually disappear, although this can take many

years7. The skin, nails and scalp may be affected8. Lesions similar to OLP may be caused or aggravated by

medicines, tooth filling materials or toothpastes9. A biopsy is usually necessary to confirm the diagnosis

10. The aims of OLP treatment are to eliminate mucosal redness,ulceration, pain and sensitivity

11. OLP is usually effectively treated with steroids, althoughresponses vary and several treatments may need to be trialled

12. The teeth should be scaled and patients instructed in thoroughoral hygiene

13. It may be necessary to have teeth, fillings and denturessmoothed and polished

14. OLP patients are at increased risk of oral cancer15. Oral cancer develops in less than 5 per cent of OLP patients

who do not use tobacco products16. OLP patients should eliminate smoking and alcohol

consumption17. OLP patients should eat a nutritious diet including fresh fruitand vegetables

18. OLP patients are reviewed at regular intervals and lesions mayoccasionally require re-biopsy

19. OLP patients should attend whenever there is a change in thelook or feel of lesions

20. On-line OLP patient information, including a web-based OLPchat group, is available currently at URL:‘http://www.tambcd.edu/lichen/’. Accessed January 2002.


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2. Bowers KE, Sexton J, Sugerman PB. Commentary. Clin Dermatol2000;18:497-498.

3. Sugerman PB, Savage NW, Zhou X, Walsh LJ, Bigby M. Orallichen planus. Clin Dermatol 2000;18:533-539.

4. Eisen D. The evaluation of cutaneous, genital, scalp, nail,esophageal, and ocular involvement in patients with oral lichenplanus. Oral Surg Oral Med Oral Pathol Oral Radiol Endod1999;88:431-436.

5. Eisen D. The therapy of oral lichen planus. Crit Rev Oral BiolMed 1993;4:141-158.

6. Rojo-Moreno JL, Bagan JV, Rojo-Moreno J, Donat JS, MilianMA, Jimenez Y. Psychologic factors and oral lichen planus. Apsychometric evaluation of 100 cases. Oral Surg Oral Med OralPathol Oral Radiol Endod 1998;86:687-691.

7. Scully C, Beyli M, Ferreiro MC, et al. Update on oral lichenplanus: etiopathogenesis and management. Crit Rev Oral BiolMed 1998;9:86-122.

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40. International Lichen Planus Support Group Web at BaylorCollege of Dentistry, a member of The Texas A&M UniversitySystem. URL: ‘http://www.tambcd.edu/lichen/’. Accessed October2002.

Address for correspondence/reprints:Philip B Sugerman

Senior Research FellowAstraZeneca R&D Boston

35 Gatehouse DriveWaltham, Massachusetts, 02451, USA

Email: [email protected]


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