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Oral Lichen Planus
Introduction
The name "lichen planus" was coined by British dermatologist Erasmus Wilson in 1869.[1] The term "lichen" originates from the Greek word leichen, referring to a moss, while planus is Latin for "flat." Lichen planus comprises a chronic inflammatory disease affecting the skin, hair follicles, nails, and mucosal surfaces, with predominant involvement of the skin and oral mucosa.[2][3] The oral variant, oral lichen planus (OLP), is a chronic condition characterized by periods of relapse and remission, requiring long-term symptomatic treatment and surveillance (see Image. Oral Lichen Planus). Approximately 15% of patients with OLP develop cutaneous lesions, and around 20% develop genital lesions.[4]
Cutaneous involvement is typically self-limiting and presents as violaceous, pruritic papules with overlying reticular white striae (Wickham striae), most commonly affecting the trunk or extremities, including the wrists and ankles.[5] Genital manifestations in women may include erythema, erosions, white reticulated plaques, labial resorption, or scarring.[6] In men, lesions may appear as annular, papulosquamous plaques on the glans penis, occasionally associated with dysuria and dyspareunia.[7]
Esophageal disease occurs in more than 1/4 of patients with OLP. Symptomatic individuals report dysphagia and odynophagia, with endoscopic examination revealing friable mucosa, white plaques, erythema, ulceration, erosions, or stricture formation.[8][9][10]
Etiology
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Etiology
The precise etiology of lichen planus is unknown. Multiple factors have been implicated in the pathogenesis of this condition, including genetic predisposition, microbial agents, allergies, psychological stress, intestinal disturbances, systemic diseases, and mucosal trauma from sharp teeth. Psychological stress is a significant trigger. Oral lesions frequently worsen during periods of heightened stress or depression, potentially due to elevated oxidative stress markers in oral mucosal cells, saliva, and serum. This increase in oxidative stress may amplify the local immunological response, aggravating existing lesions.
Associations between thyroid dysfunction and OLP have been reported, with elevated thyroid-stimulating hormone and reduced free thyroxine levels observed in affected individuals. These findings suggest that autoimmune thyroid disease may contribute to OLP pathogenesis. Studies have likewise identified a correlation between hepatitis C virus (HCV) infection and OLP.
Shifts in the oral microbiota have been associated with the onset of OLP, suggesting an interplay between microbial imbalance and immune dysregulation.[11] Alterations in the gut microbiota may compromise intestinal barrier integrity, permitting translocation of bacteria and their metabolites into the bloodstream, potentially activating T cells, and contributing to OLP pathogenesis.[12][13] Studies examining the oral microbiome in OLP have demonstrated dysbiosis within lesions compared to adjacent mucosa. However, the precise role of these microbial changes remains unclear. Research has also explored the salivary mycobiome, in which fungal imbalance may modulate bacterial communities and host immune responses. Overall, the relationship between microbial shifts and immune dysregulation in OLP requires further investigation.
Hormonal fluctuations, particularly during menopause, appear to influence OLP development. Endocrine alterations, including changes in sex steroid hormone levels, have been observed in affected individuals. Elevated estrogen levels have been correlated with increased lesion severity.[14] The specific contribution of hormonal variations to OLP pathogenesis remains uncertain, underscoring the need for further studies to clarify the complex interaction between hormones and disease expression.
Epidemiology
A 2020 meta-analysis reported that the estimated global prevalence of OLP is approximately 0.89% to 0.98%, with higher rates observed in clinical populations.[15] The condition occurs twice as frequently in women and is most often diagnosed between the 5th and 6th decades of life, although cases have also been documented in children and young adults.[16][17][18]
Pathophysiology
The pathophysiology of OLP is not fully understood. However, 2 primary mechanisms have been proposed: antigen-specific and nonspecific.[19]
The antigen-specific mechanism involves triggering events that expose OLP-specific antigens, leading to activation and recruitment of CD4+ helper T cells and subsequent release of pro-inflammatory T-helper 1 cytokines, including tumor necrosis factor α and interferon γ.[20] CD8+ T cell-mediated cytotoxicity targets the basal cell layer of the epithelium, resulting in basement membrane disruption, T-cell migration into the epithelium, and keratinocyte apoptosis.
The nonspecific mechanism involves mast cell activation, releasing pro-inflammatory mediators, such as proteases and upregulated matrix metalloproteinases (MMPs). This process promotes T-cell infiltration of the superficial lamina propria, basement membrane disruption, and subsequent keratinocyte apoptosis.
The chronic course of OLP has been linked to activation of nuclear factor κB and inhibition of the transforming growth factor β-Smad signaling pathway, contributing to hyperkeratosis and the formation of characteristic white lesions.[21][22] Genetic polymorphisms within the 1st intron of the interferon γ promoter gene have also been proposed as risk factors for OLP development.[23][24]
Histopathology
The first histopathologic diagnostic criteria for OLP were proposed by the World Health Organization Collaborating Centre for Oral Precancerous Lesions in 1978. OLP lesions may display the following microscopic features:
- Orthokeratosis or parakeratosis
- Sawtooth rete ridges
- Civatte bodies
- Narrow band of eosinophilic material in the basement membrane
- Band-like zone of lymphocytic infiltrate in the superficial lamina propria
- Liquefaction degeneration in the basal cell layer[25]
Many of these features were later recognized as nonspecific to OLP. A recent position paper by the American Academy of Oral and Maxillofacial Pathology proposed updated histopathologic criteria to exclude lichenoid mimics and improve diagnostic accuracy. The revised criteria include the following:
- Band-like zone of lymphocytic infiltrate at the epithelium-lamina propria interface
- Liquefactive degeneration in the basal cell layer
- Lymphocytic exocytosis
- Absence of epithelial dysplasia and verrucous epithelial architectural changes
Direct immunofluorescence (DIF) of OLP samples typically reveals fibrinogen deposition in a shaggy pattern along the basement membrane zone, without immunoglobulins or complement components.[26][27] Since histologic findings are not entirely specific, detailed patient history and clinical correlation are essential for a conclusive diagnosis.
History and Physical
Approximately 2/3 of patients with OLP are symptomatic, exhibiting alternating periods of exacerbation and quiescence. Symptom severity varies, but patients commonly report oral pain, sensitivity to spicy or acidic foods, and a sensation of mucosal roughness or tightness.[28]
OLP is classified into 6 clinical subtypes: reticular, papular, plaque, atrophic, erosive, and bullous.[29] These forms may occur independently or concurrently, with classification determined by the predominant subtype.
The reticular, erosive, and plaque forms are the most frequently encountered. Reticular OLP demonstrates the classic white lacy network of Wickham striae with hyperkeratotic plaques (see Image. Reticular Oral Lichen Planus). The erosive and atrophic OLP subtypes usually present with erythema and ulceration, often accompanied by pain and mucosal sensitivity. The peripheries of these lesions may show reticular keratotic striae. Papular and plaque variants manifest as white keratotic papules or plaques, potentially mimicking leukoplakia. In patients with darker skin tones, postinflammatory hyperpigmentation may be observed as diffuse brown or black discoloration in association with the lesions.[30]
OLP usually demonstrates bilateral distribution, most commonly affecting the buccal mucosa, tongue, and gingiva, followed by the labial mucosa and lower lip. The Koebner phenomenon, characterized by lesion development at sites of mechanical trauma such as friction from sharp teeth, rough dental restorations, or lip and cheek biting, may explain this predilection for trauma-prone sites.[31][32] Approximately 10% of patients present with lesions limited to the gingiva, typically manifesting as desquamative gingivitis.
Evaluation
Correct diagnosis of OLP requires comprehensive history taking, detailed clinical examination, and histopathologic confirmation. In patients with the characteristic reticular form, clinical features alone may be sufficiently diagnostic. However, oral biopsy may still be considered to confirm the diagnosis and exclude dysplasia or malignancy.
In cases presenting with desquamative gingivitis, DIF is valuable for excluding autoimmune vesiculobullous disorders such as pemphigus and pemphigoid. Shaggy fibrinogen and complement deposition may be observed along the basement membrane zone, although this finding is not pathognomonic for OLP. Indirect immunofluorescence has limited diagnostic utility in evaluating this condition.
Treatment / Management
Mild OLP is frequently asymptomatic. When discomfort occurs, topical corticosteroids constitute the 1st-line treatment. Analgesic mouthwashes such as benzydamine provide pain relief, particularly before meals. Corticosteroids may be applied as an adhesive gel or administered as a mouth rinse. Topical therapy is preferred because of its efficacy and lower risk of systemic adverse effects. Although triamcinolone acetonide gel is widely used, higher-potency corticosteroids such as clobetasol propionate demonstrate superior symptomatic relief.[33]
Patients using topical gel should dry the oral mucosa before application and avoid eating or drinking for at least 30 minutes to ensure adequate mucosal contact. Dexamethasone mouth rinses are especially useful for patients with widespread or anatomically inaccessible lesions.[34][35](A1)
Intralesional corticosteroid injections may be administered for persistent erosive OLP.[36] Oropharyngeal candidiasis is one of the most common adverse effects of topical corticosteroids. Adjunctive topical or systemic antifungal therapy may be warranted when clinically indicated.[37] (A1)
Systemic corticosteroids are reserved for recalcitrant OLP unresponsive to topical treatment, severe disease with extensive ulceration and erythema, or lichen planus with multisite extraoral involvement. Short courses of systemic corticosteroids may achieve rapid control of persistent lesions. Dosage and frequency should be tapered as lesions resolve or symptoms improve to minimize adverse effects.
Second-line therapies may be considered for recalcitrant OLP unresponsive to topical corticosteroids. Options include calcineurin inhibitors (eg, cyclosporine, tacrolimus), retinoids, and steroid-sparing agents such as azathioprine, hydroxychloroquine, or mycophenolate mofetil. Transient burning sensation is the most frequently reported adverse effect associated with retinoids and cyclosporine, often limiting use in patients with erosive OLP.[38](A1)
Use of newer calcineurin inhibitors, including tacrolimus, requires caution because of the U.S. Food and Drug Administration's black box warning citing a potential increased risk of squamous cell carcinoma and lymphoma. Retinoids are contraindicated in pregnancy owing to teratogenicity.[39] Steroid-sparing agents must be prescribed with care, as azathioprine carries a risk of bone marrow aplasia, and hydroxychloroquine is associated with retinal toxicity.(A1)
Differential Diagnosis
Several conditions mimic OLP both clinically and histologically, including oral lichenoid drug reactions, oral lichenoid contact hypersensitivity, mucous membrane pemphigoid, chronic graft-versus-host disease, lupus erythematosus, lichen planus pemphigoides, chronic ulcerative stomatitis, proliferative verrucous leukoplakia, and oral epithelial dysplasia.[40] Key clinical and histopathologic distinctions between OLP and its most significant differential diagnoses are outlined below.
Oral Lichenoid Drug Reaction
Numerous medications can precipitate oral lichenoid reactions, producing reticular or atrophic-erosive lesions with an onset ranging from several weeks to over a year after drug initiation. Frequently implicated medications include nonsteroidal anti-inflammatory drugs, antihypertensives, anticonvulsants, antimalarials, and antiretrovirals.[41][42] Additional agents include oral hypoglycemics, dapsone, gold salts, penicillamine, and phenothiazines. Diagnosis is challenging and relies heavily on a detailed medication history. Collaboration with the prescribing clinician may be warranted to determine the feasibility of replacing the suspected drug, followed by careful monitoring for lesion resolution, which may require several months.
Oral Lichenoid Contact Hypersensitivity Reaction
Oral lichenoid contact hypersensitivity reactions develop on mucosal surfaces in direct contact with the triggering agent. Implicated agents include dental restorative materials (eg, metals, composites, glass ionomer cement) and flavoring agents (eg, menthol, eugenol).[43] Amalgam restorations are the most frequently associated cause.[44][45][46] Lesions commonly occur on the buccal mucosa or lateral tongue adjacent to the restoration. Clinical resolution is typically observed within several months after replacement of the restoration or discontinuation of the flavoring agent.[47]
Chronic Graft-Versus-Host Disease
Oral involvement occurs in approximately 80% of patients undergoing allogeneic bone marrow transplantation. Lichenoid lesions may affect any oral mucosal site, typically developing around 6 months posttransplantation. Diagnosis requires careful clinical correlation with transplantation history and systemic manifestations.
Lichen Planus Pemphigoides
Lichen planus pemphigoides is a rare mucocutaneous blistering disorder that exhibits both clinical and histopathologic features of OLP and mucous membrane pemphigoid. Oral involvement is reported in approximately 24% of patients, most commonly affecting the gingiva and buccal mucosa. DIF findings are indistinguishable from those of mucous membrane pemphigoid.
Chronic Ulcerative Stomatitis
This condition predominantly affects women in the 5th and 6th decades of life. Patients present with chronic oral ulcerations involving the gingiva, tongue, and buccal mucosa. Gingival involvement may manifest as desquamative gingivitis. Histopathologic findings closely resemble those of OLP, but perilesional tissue demonstrates deposition of immunoglobulin G autoantibodies within the nuclei of basal and parabasal epithelial cells in a characteristic speckled pattern.
Lupus Erythematosus
Both discoid and systemic lupus erythematosus can involve the oral mucosa. Lesions demonstrate central ulceration and atrophy with surrounding erythema and radiating white striae. The buccal mucosa, hard palate, and gingiva are common sites of involvement. Cutaneous lesions may coexist, and serologic evaluation frequently reveals positive antinuclear antibody titers.[48]
Prognosis
Lifestyle modifications and pharmacologic therapy can relieve symptoms and improve quality of life. Long-term clinical surveillance facilitates early detection of malignant transformation and supports a more favorable prognosis.
Complications
The malignant potential of OLP remains a subject of debate. Reported rates of transformation to squamous cell carcinoma range from 0% to 12.5%, reflecting substantial variability in study inclusion and exclusion criteria.[49][50][51][52][53] Most cases of malignant transformation are reported in patients with atrophic or erosive OLP.
A meta-analysis estimated the malignant transformation rate at 0.44%. Risk is increased in patients who smoke, consume alcohol, are seropositive for HCV, or present with the red subtypes of OLP.[54] Despite variability in reported rates, evidence consistently supports routine long-term follow-up for symptom management and surveillance for malignant change.
Several molecular and cellular factors have been associated with malignant transformation in OLP. Overexpression of MMPs (MMP-1, MMP-2, and MMP-9) and the c-Myc protein, altered salivary cortisol and nitric oxide levels, and dysregulated interleukin expression have been implicated in disease progression. Viral agents, including HCV, human papillomavirus, and Epstein–Barr virus, along with environmental carcinogens such as tobacco and alcohol, act as cofactors. At the molecular level, alterations in p16, p21, p53, and mRNA26 may contribute to malignant transformation. Whether malignant transformation develops as an intrinsic consequence of OLP or is primarily driven by these associated risk factors remains debated.
Chronic inflammation, similar to that seen in colitis-associated cancer, is considered a key driver of malignant transformation in OLP.[55] Inflammatory mediators can induce DNA damage, promote cell proliferation, inhibit apoptosis, and trigger protein alterations within oral epithelial cells.
Deterrence and Patient Education
Patients with OLP should be counseled that treatment primarily targets symptomatic relief. Lifestyle modifications, including avoidance of acidic or spicy foods, can reduce symptom severity.[56] Eliminating potential local exacerbating factors, such as adjusting sharp teeth or defective dental restorations, along with patient education on optimal oral hygiene and stress management, is essential for long-term disease control.[57] Discussing the low but clinically significant risk of malignant transformation is important to underscore the need for ongoing clinical surveillance. Regular follow-up facilitates early detection of concerning changes, including persistent ulcerations or mucosal growths.
Enhancing Healthcare Team Outcomes
OLP can pose a diagnostic challenge, as patients often present with nonspecific features that resemble other mucosal disorders. Accurate diagnosis requires a comprehensive history, clinical examination, and histopathologic assessment. Management is generally coordinated by a dentist, oral medicine specialist, or oral surgeon. Interprofessional collaboration with dermatologists, gynecologists, gastroenterologists, otorhinolaryngologists, or ophthalmologists may be warranted in patients with extraoral involvement. Pharmacotherapy, patient education, and lifestyle modification remain the cornerstone of OLP management and are critical for optimizing outcomes. Ongoing research is needed to elucidate the condition's pathogenesis and clinical course further.
Media
(Click Image to Enlarge)
Reticular Oral Lichen Planus. Characteristic Wickham striae are seen on the buccal mucosa, forming a lacy white network typical of the reticular subtype.
Contributed by H Olmo, DDS, MS
(Click Image to Enlarge)
Oral Lichen Planus. Classic reticular white lesions at the lateral tongue and buccal mucosa are seen, reflecting chronic inflammatory mucosal disease.
Contributed by S Munakomi, MD, and S Shah, MD
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