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Gheorghe C, Mihai L, Parlatescu I, Tovaru S Association of oral lichen planus with chronic C hepatitis. Review of the data in literature. Maedica (Bucur). 2014; 9:98-103
Alaizari NA, Al-Maweri SA, Al-Shamiri HM, Tarakji B, Shugaa-Addin B Hepatitis C virus infections in oral lichen planus: a systematic review and meta-analysis. Aust Dent J. 2016; 61:282-287 https://doi.org/10.1111/adj.12382
Elenbaas A, Enciso R, Al-Eryani K Oral lichen planus: a review of clinical features, etiologies, and treatments. Dent Rev. 2022; 2:(1) https://doi.org/10.1016/j.dentre.2021.100007
Arduino P, Karimi D, Tirone F Evidence of earlier thyroid dysfunction in newly diagnosed oral lichen planus patients: a hint for endocrinologists. Endocr Connect. 2017; 6:726-730 https://doi.org/10.1530/EC-17-0262
Siponen M, Huuskonen L, Läärä E, Salo T Association of oral lichen planus with thyroid disease in a Finnish population: a retrospective case-control study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2010; 110:319-324 https://doi.org/10.1016/j.tripleo.2010.04.001
Khudhur AS, Di Zenzo G, Carrozzo M Oral lichenoid tissue reactions: diagnosis and classification. Expert Rev Mol Diagn. 2014; 14:169-184 https://doi.org/10.1586/14737159.2014.888953
Al-Hashimi I, Schifter M, Lockhart P Oral lichen planus and oral lichenoid lesions: diagnostic and therapeutic considerations. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2007; 103 Suppl:S25.e1-12 https://doi.org/10.1016/j.tripleo.2006.11.001
Lucchese A, Dolci A, Minervini G Vulvovaginal gingival lichen planus: report of two cases and review of literature. Oral Implantol (Rome). 2016; 9:54-60 https://doi.org/10.11138/orl/2016.9.2.054
Olszewska M, Banka-Wrona A, Skrok A Vulvovaginal-gingival lichen planus: association with lichen planopilaris and stratified epithelium-specific antinuclear antibodies. Acta Derm Venereol. 2016; 96:92-96 https://doi.org/10.2340/00015555-2141
Sharma N, Malhotra SK, Kuthial M, Chahal KS Vulvo-vaginal ano-gingival syndrome: Another variant of mucosal lichen planus. Indian J Sex Transm Dis AIDS. 2017; 38:86-88 https://doi.org/10.4103/0253-7184.203432
González-Moles MÁ, Ruiz-Ávila I, González-Ruiz L, Ayén Á, Gil-Montoya JA, Ramos-García P Malignant transformation risk of oral lichen planus: a systematic review and comprehensive metaanalysis. Oral Oncol. 2019; 96:121-130 https://doi.org/10.1016/j.oraloncology.2019.07.012
Garcia-Pola MJ, Llorente-Pendás S, González-Garcia M, García-Martín JM The development of proliferative verrucous leukoplakia in oral lichen planus. A preliminary study. Med Oral Patol Oral Cir Bucal. 2016; 21:e328-e334 https://doi.org/10.4317/medoral.20832
Locca O, Sollecito T, Alawi F Potentially malignant disorders of the oral cavity and oral dysplasia: a systematic review and meta-analysis of malignant transformation rate by subtype. Head Neck. 2020; 42:539-555 https://doi.org/10.1002/hed.26006
Suter VGA, Warnakulasuriya S The role of patch testing in the management of oral lichenoid reactions. J Oral Pathol Med. 2016; 45:48-57 https://doi.org/10.1111/jop.12328
Montebugnoli L, Venturi M, Gissi DB, Cervellati F Clinical and histologic healing of lichenoid oral lesions following amalgam removal: a prospective study. Oral Surg Oral Med Oral Pathol Oral Radiol. 2012; 113:766-772 https://doi.org/10.1016/j.oooo.2011.12.007
Van der Meij EH, Van der Waal I Lack of clinicopathologic correlation in the diagnosis of oral lichen planus based on the presently available diagnostic criteria and suggestions for modifications. J Oral Pathol Med. 2003; 32:507-512 https://doi.org/10.1034/j.1600-0714.2003.00125.x
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Rudralingam M, Randall C, Mighell AJ The use of topical steroid preparations in oral medicine in the UK. Br Dent J. 2017; 223:633-638 https://doi.org/10.1038/sj.bdj.2017.880
Finn D, Randall C, Field EA UK Dental Medicines Advisory Service: questions asked by dentists – part 5: prescribing for oromucosal diseases and dry mouth. Br Dent J. 2021; 231:689-695 https://doi.org/10.1038/s41415-021-3681-9
Scottish Dental Clinical Effectiveness Programme. Drug prescribing for dentistry. 2025. www.sdcepdentalprescribing.nhs.scot/ (accessed March 2025)
Ioannides D, Vakirlis E, Kemeny L European S1 guidelines on the management of lichen planus: a cooperation of the European Dermatology Forum with the European Academy of Dermatology and Venereology. J Eur Acad Dermatol Venereol. 2020; 34:1403-1414 https://doi.org/10.1111/jdv.16464
Lajevardi V, Ghodsi SZ, Hallaji Z, Shafiei Z, Aghazadeh N, Akbari Z Treatment of erosive oral lichen planus with methotrexate. J Dtsch Dermatol Ges. 2016; 14:286-293 https://doi.org/10.1111/ddg.12636
Chauhan P, De D, Handa S, Narang T, Saikia UN A prospective observational study to compare efficacy of topical triamcinolone acetonide 0.1% oral paste, oral methotrexate, and a combination of topical triamcinolone acetonide 0.1% and oral methotrexate in moderate to severe oral lichen planus. Dermatol Ther. 2018; 31:(1) https://doi.org/10.1111/dth.12563
Yeshurun A, Bergman R, Bathish N, Khamaysi Z Hydroxychloroquine sulphate therapy of erosive oral lichen planus. Australas J Dermatol. 2019; 60:e109-e112 https://doi.org/10.1111/ajd.12948
Cheng S, Kirtschig G, Cooper S, Thornhill M, Leonardi-Bee J, Murphy R Interventions for erosive lichen planus affecting mucosal sites. Cochrane Database Syst Rev. 2012; 2012 https://doi.org/10.1002/14651858.CD008092.pub2
Wee JS, Shirlaw JS, Challacombe SJ, Setterfield JF Efficacy of mycophenolate mofetil in severe mucocutaneous lichen planus: a retrospective review of 10 patients. Br J Dermatol. 2012; 167:36-43 https://doi.org/10.1111/j.1365-2133.2012.10882.x
Didona D, Caposiena Caro RD, Sequeira Santos AM Therapeutic strategies for oral lichen planus: state of the art and new insights. Front Med. 2022; 9 https://doi.org/10.3389/fmed.2022.997190
Lodi G, Manfredi M, Mercadante V, Murphy R, Carrozzo M Interventions for treating oral lichen planus: corticosteroid therapies. Cochrane Database Syst Rev. 2020; 2 https://doi.org/10.1002/14651858.CD001168.pub3
Oral lichen planus (OLP) has an estimated global prevalence of 1% and is considered to be a disorder that requires lifelong surveillance. Clinical subtypes of OLP include reticular, atrophic, papular, plaque-like, ulcerative and bullous variants. OLP can present with desquamative gingivitis, and women may have associated vulval and/or vaginal involvement. Diagnosis of OLP is based on clinical and histopathological findings. Reticular and plaque-like OLP tends to be asymptomatic and seldom requires treatment. Ulcerative and atrophic OLP can generally be managed with topical corticosteroids. Severe and widespread ulcerative lesions may require systemic drugs.
CPD/Clinical Relevance: General dental practitioners need to be able to recognize the different clinical presentations of oral lichen planus and refer appropriately.
Article
Lichen planus is a chronic inflammatory mucocutaneous disease that affects the skin and the oral and genital mucosae.1 It can also involve the nails, scalp and, more rarely, the oesophageal mucosa and eyes.1
Oral lichen planus (OLP) tends to be persistent and spontaneous resolution is uncommon. Disease activity fluctuates with periods of remission and exacerbation.1
OLP has an elevated risk of malignant transformation and is classified as an oral potentially malignant disorder (OPMD) by the World Health Organization (WHO).2 OLP therefore requires lifelong surveillance.
Aetiology
The aetiology of OLP is not known; however, it is considered to be a chronic T-cell mediated disease of the oral mucosa.3
Basal keratinocytes in the oral mucosa are recognized as being antigenically foreign, and an immune response is initiated with CD4+ and CD8+ T lymphocytes producing cytokines including interleukin-2 and tumour necrosis factor within the oral epithelium.4,5 This induces chronic inflammation, resulting in cell-mediated damage and keratinocyte apoptosis.4,5
Oral lichenoid lesions (OLL) clinically resemble OLP and are usually the result of drug reactions or close contact with dental restorative materials.2 OLLs may also occur in association with graft-versus-host disease.2
Prevalence
OLP has been reported to affect 1–2% of the population.5 A recent systematic review and meta-analysis revealed an estimated global prevalence of 1%, with notable geographical variation.6 The highest prevalence is in Europe (1.43%) and the lowest in India (0.49%), where it is postulated that keratosis associated with tobacco use may mask OLP detection.6 OLP predominantly affects women aged 30–60 years.7
Clinical presentation
OLP can have a wide range of clinical presentations and is classically bilateral, often symmetrical. Most commonly, it involves the buccal mucosae, but can also affect the dorsal and ventral surfaces of the tongue, vestibule, alveolar ridges and gingivae. Palatal and labial involvement can occur, but is less common.1
OLP manifests in six clinical presentations, which can occur alone or in combination:
Reticular;
Papular;
Plaque-like;
Atrophic;
Ulcerative or erosive;
Bullous.
Reticular OLP is the most common clinical presentation with a frequency of about 90%.8 White reticular striae classically present in a lace-like pattern, and can have a linear or annular arrangement (Figures 1 and 2). They are often compared to Wickman's striae on the skin, but are more defined in OLP.6 These white areas can be papular in appearance, but this is uncommon.
Figure 1. Buccal mucosa showing reticular oral lichen planus.Figure 2. Buccal mucosa and retromolar area showing reticular oral lichen planus.
Plaque-like OLP resembles oral leukoplakia so may involve diagnostic difficulties, which can potentially complicate management.6
Erythematous areas result from atrophic changes in the mucosal epithelium. Ulcers occur with epithelial loss from weak and oedematous basal areas.6 Shallow ulcers with a yellow sloughy covering are present in erosive OLP (Figures 3 and 4).
Figure 3. Buccal mucosa showing reticular and ulcerative areas.Figure 4. Lateral tongue showing reticular and ulcerative areas.
Rarely, bulla formation owing to epithelial separation can occur, but the fragility of bullae causes their rapid disintegration, resulting in ulceration.6
The presentation of full-width, erythematous and shiny attached gingivae is known as desquamative gingivitis (Figures 5–7). This is a descriptive term and is not specific to OLP. Desquamative gingivitis may also be a clinical manifestation of immunobullous pathology, particularly oral mucous membrane pemphigoid.9 OLP solely affecting the gingivae accounts for around 10% of cases.6
Figure 5. Oral lichen planus presenting as desquamative gingivitis.Figure 6. Oral lichen planus presenting as desquamative gingivitis.Figure 7. Oral lichen planus presenting as desquamative gingivitis with reticular areas in the labial sulcus.
OLP, particularly the reticular, papular and plaque-like types, is frequently asymptomatic, although patients are sometimes aware of a roughness in the affected areas of the mouth.6,10
Patients with symptomatic OLP report oral burning sensations and pain that can be spontaneous or associated with eating or drinking, particularly spicy, rough/sharp or salty foods and acidic/hot food or drinks.
Discomfort may occur with toothbrushing, especially in cases of desquamative gingivitis. Depending on the severity of symptoms, there can be significant impairment of oral hygiene and oral intake.
Associations
Hepatitis C infection
Hepatitis C (HCV) infection is associated with skin lichen planus and OLP.5 The varying prevalence of HCV infection between geographical regions globally means there is significant disparity in its association with OLP, which can range over 0.5–35%.11
The coexistence of OLP and HCV infection is more pertinent where HCV prevalence is higher (southern Europe, Southeast Asia, eastern Mediterranean) and less relevant in lower prevalence areas (North America and western/central Europe).5 Although OLP is frequently seen in the UK, an association with HCV is rare. A systematic review and meta-analysis of the prevalence of HCV infection in OLP showed that patients with OLP had a six-fold greater risk of HCV infection than controls.12
Thyroid dysfunction
An association between OLP and thyroid dysfunction, mainly hypothyroidism, has been suggested, but the evidence in the literature is conflicting.13,14 One study showed 15% of OLP patients to have a history of thyroid disease.15 Another demonstrated that, among OLP patients, almost half of thyroid diseases were of an autoimmune aetiology.14
Overall, however, there is no substantive evidence of an association of OLP with thyroid dysfunction.
Oral lichenoid lesions
Oral lichenoid contact reactions
Oral lichenoid contact reactions (OLCRs) tend to be unilateral and found in areas of direct mucosal contact with dental restorative materials, most commonly dental amalgam.2,16,17
The reaction is attributed to exposure to trace amounts of mercury, leading to delayed (Type IV) hypersensitivity reactions that result in immune-mediated damage of the basal epithelial keratinocytes.16
Rarely, similar reactions to composite and gold restorative materials may occur.17
Oral lichenoid drug reactions
Oral lichenoid drug reactions (OLDRs) result from exposure to medications or drugs and a high degree of suspicion is required to make the diagnosis.2,16,18 Substantial latent periods of months or years can occur between exposure to the drug and the development of associated lichenoid drug reactions.18 OLDRs commonly resolve within weeks of stopping the offending drug but this is not always the case.5
Medications associated with cutaneous lichenoid drug reactions have been implicated in OLDRs, and these include non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, oral hypoglycaemic drugs, beta-blockers, gold, methyldopa, penicillamine, thiazides, antimalarials, quinine and quinidine.16,18
A definitive diagnosis of an OLDR is histopathologically challenging as it cannot be confidently differentiated from OLP.19
Graft-versus-host disease
Acute and chronic graft-versus-host disease (GVHD) can manifest as oral lichenoid lesions but is more frequent in chronic GVHD.16
The oral cavity is the second most frequent site affected (after the skin) in chronic GVHD and is involved in 72–83% of patients.20 The condition commonly affects the buccal and labial mucosae and tongue; desquamative gingivitis can also occur.10,20
Skin involvement with lichen planus
The skin is the most commonly affected site of extra-oral lichen planus. The flexor surfaces of the wrists, trunk, lower back and limbs are most often involved.
The classic presentation on the skin is of purplish, shiny, flat papules on a background of white reticulations, known as Wickham's striae (Figure 8). Patients usually complain of an itchy rash.
Figure 8. Lichen planus on the skin presenting as Wickham's striae.
Vulvo-vagino-gingival lichen planus
Vulvo-vagino-gingival lichen planus is a variant of lichen planus with erosive, mucous membrane involvement of the vulva, vagina and gingivae. Its prevalence is possibly underestimated because the affected areas are managed by different specialties and the absence of specific diagnostic criteria.21,22
Approximately 25% of women with OLP have vulvo-vaginal involvement.23,24 Diagnosis requires a biopsy from at least one affected site with immunofluorescence to exclude immunobullous disease.21
Histopathology
Histopathologically, OLP is characterized by a band-like lymphocytic infiltrate, predominantly of the T type, in the epithelium-lamina propria interface.1,6,17 Liquefactive degeneration of basal keratinocytes and distortion of the rete pegs occurs, with a flattened or a saw-tooth appearance.6,17
Other features include epithelial hyperkeratosis (parakeratosis or orthokeratosis), atrophy or acanthosis and the absence of epithelial dysplasia.1,6
Malignant potential
OLP is classified by the WHO as an OPMD, and has a variable risk of malignant transformation.2
A recent systematic review and meta-analysis showed a malignant transformation rate (MTR) of 1.1% for OLP.25 The MTR is high in erosive and atrophic lesions and the tongue is the site at highest risk.25 OLLs were recently added to the list of OPMDs by the WHO and their MTR has been reported as 1.9%.2, 25
There is limited evidence that OLP and OLLs, particularly those presenting as white plaques, may develop into proliferative verrucous leukoplakia, which has a rate of malignant transformation reported as 49.5%.26,27
Diagnosis
The diagnosis of OLP is based on clinical and histopathological findings. Although diagnosis can often be made clinically, especially in cases with a typical reticular appearance and concomitant skin involvement, a biopsy is usually undertaken to confirm clinical suspicion.7 This is particularly important if there plaque-like lesions that could represent leukoplakia with histological evidence of dysplasia or squamous cell carcinoma. If histopathology shows a significant degree of dysplasia, then excision of the lesion needs to be considered.
Immunofluorescence may be indicated in some atypical cases with ulceration or severe desquamative gingivitis to exclude immunobullous conditions, particularly oral mucous membrane pemphigoid.9
The authors recommend that a photographic record of suspected OLP is made, particularly if a decision is made not to refer to secondary care and/or undertake a biopsy.
In geographical areas with a higher prevalence of HCV, such as southern Europe and Southeast Asia, coexistence of OLP and HCV infection is relevant, so consideration should be given to testing for HCV infection, particularly if there is concern about previous exposure to the virus or if the patient is at high risk of infection.11,12
Patch testing may confirm the presence of OLCRs but its usefulness has been debated as positive patch testing has not been shown to predict resolution of OLCR when amalgam was replaced.28,29 The decision to patch test is best determined on a case-by-case basis, depending on whether results from such testing are likely to influence management.
In 2003, modified diagnostic criteria were produced based on the previous WHO criteria. These included clinical and histopathological aspects and appeared to foster more clinician and pathologist agreement – although they are not without their own limitations and are not universally agreed.30
Management
Regular monitoring of OLP and OLLs is required to check for any clinical changes suggestive of malignant transformation that may warrant re-biopsy. Reticular OLP with minimal or no erosive changes can be followed up by the patient's dental practitioner.
It is important to appreciate that the clinical manifestations of OLP are characteristically prolonged and may change spontaneously over months or years.
Patients with erosive and/or atrophic OLP often need to be monitored by a specialist in oral medicine or oral and maxillofacial surgery on a more frequent basis.
People with OLP should be given written information (for example, the leaflet at https://bisom.org.uk/clinical-care/patient-information/) and be warned that oral mucosal changes, such as persistent ulceration, induration and thickening, may warrant earlier review.31
Removal of amalgam or other restorations associated with OLCRs may lead to improvement or even resolution of the lesion, but this is not guaranteed. This uncertainty, combined with the associated dental costs and restorative complications (which can include loss of teeth), means that the routine removal of all amalgam restorations in patients with OLP or OLLs is not advised but should be considered on a case-by-case basis after thorough discussion with the patient.16
Some mild cases of OLP may be asymptomatic and not require any active treatment. Management includes topical and systemic medications dependent on the severity of the OLP.1
Topical treatments include antiseptic and analgesic preparations for symptomatic relief. Topical corticosteroids in the form of mouthwashes, oromucosal tablets and sprays are the mainstay of treatment (Table 1).32,33,34,35 Prescribing them for oromucosal conditions, including OLP, is off label and this may result in difficulties when GPs are requested to prescribe them.
*Advise patient to take care with application to avoid producing anaesthesia of the pharynx before meals because this might lead to choking.
GSL: general sales list; POM: prescription only medicine; P: pharmacy medicine; DPF: available through Dental Practitioners' Formulary (UK).
Dental practitioners, working in NHS practice, are restricted in what they can prescribe in the UK for OLP; these topical preparations are listed in the Dental Practitioners' Formulary and by the Scottish Dental Clinical Effectiveness Programme (Table 1).34,35
Patients should be given instructions regarding the optimum use of topical corticosteroids and warned not to swallow mouthwashes.33 Frequent use of topical corticosteroids may result in oral candidal infections, which, depending on their severity, may require topical or systemic antifungal treatment.33,35 Adrenal suppression may occur, particularly with prolonged or excessive use of topical corticosteroids.32 Topical steroid ointments (e.g. clobetasol propionate 0.025–0.05%) mixed with an oral adhesive paste has been suggested for application to more localized areas of OLP.13,32
Patents with desquamative gingivitis may find toothbrushing painful and need assistance from a dental professional to maintain their oral hygiene. For more severe and widespread ulcerative cases of OLP, which do not respond to topical corticosteroids, systemic medication may be indicated.32 Corticosteroids (prednisolone 30–40 mg/day) can be prescribed for short courses, but long-term use should be avoided if possible.36
Recalcitrant cases of severe OLP may require systemic agents including mycophenolate mofetil, azathioprine, hydroxychloroquine, methotrexate, ciclosporin and dapsone.36,37,38,39,40,41,42
However, a Cochrane review has concluded that there is no strong evidence for the effectiveness of any treatment for erosive OLP.40
Use of systemic agents for treating OLP in the long term is best restricted to secondary care so that appropriate checks before starting medication and monitoring with blood tests can be undertaken.
The authors are part of a multidisciplinary team, consisting of specialists in oral medicine and dermatology. The majority of patients started on systemic medications are seen in a joint clinic. Table 2 summarizes the role of the general dental practitioner in the diagnosis and management of OLP.
Undertake a systematic, oral mucosal examination for all patients, preferably at each recall appointment
Record oral mucosal abnormalities, with specific reference to the site, clinical appearance and patient symptoms, if any. If feasible, make a photographic record
If there is a suspicion of malignancy, refer to secondary care via the 2-week, urgent head and neck pathway
Refer cases of suspected oral lichen planus (OLP) to secondary care with all clinical details and indicate the severity of symptoms, particularly if impacting on oral intake and quality of life
Advise patients to see their GP if skin and/or genital lesions are reported
Provide symptomatic relief for patients with erosive, ulcerative and atrophic presentations of OLP by prescribing topical preparations (Table 1)
Arrange for advice and support to be provided for the maintenance of oral hygiene, particularly if there is gingival involvement with OLP
Liaise with secondary care concerning the long-term arrangements for surveillance of patients with OLP. If there are concerns about changes in the clinical appearance of OLP, refer back to secondary care
Conclusion
OLP is a common inflammatory condition that is sometimes associated with cutaneous lesions. The pathogenesis is not completely understood but is believed to be autoimmune in nature.
Overall, severe OLP can be a challenging condition to manage owing to its chronic nature and potential for discomfort. A variety of topical and systemic agents may be beneficial to reduce inflammation and reduce symptoms. OLP is classified as an OPMD and long-term follow-up is required for all patients.
