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An Official Publication of the Indian Association of Oral and Maxillofacial Pathologists

  Table of Contents    
Year : 2011  |  Volume : 15  |  Issue : 2  |  Page : 127-132

Oral lichen planus: An update on pathogenesis and treatment

Department of Oral and Maxillofacial Pathology, Ragas Dental College and Hospital, Uthandi, Chennai, India

Date of Web Publication5-Sep-2011

Correspondence Address:
N Lavanya
Senior Lecturer, Department of Oral and Maxillofacial Pathology, Ragas Dental College, 2/102, East Coast Road, Uthandi, Chennai - 600 119
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0973-029X.84474

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Oral lichen planus (OLP) is a chronic inflammatory disease that affects the mucus membrane of the oral cavity. It is a T-cell mediated autoimmune disease in which the cytotoxic CD8+ T cells trigger apoptosis of the basal cells of the oral epithelium. Several antigen-specific and nonspecific inflammatory mechanisms have been put forward to explain the accumulation and homing of CD8+ T cells subepithelially and the subsequent keratinocyte apoptosis. A wide spectrum of treatment modalities is available, from topical corticosteroids to laser ablation of the lesion. In this review, we discuss the various concepts in the pathogenesis and current treatment modalities of OLP.

Keywords: Apoptosis, autoimmune, basal keratinocytes, corticosteroids, oral lichen planus

How to cite this article:
Lavanya N, Jayanthi P, Rao UK, Ranganathan K. Oral lichen planus: An update on pathogenesis and treatment. J Oral Maxillofac Pathol 2011;15:127-32

How to cite this URL:
Lavanya N, Jayanthi P, Rao UK, Ranganathan K. Oral lichen planus: An update on pathogenesis and treatment. J Oral Maxillofac Pathol [serial online] 2011 [cited 2023 Mar 25];15:127-32. Available from: https://www.jomfp.in/text.asp?2011/15/2/127/84474

   Introduction Top

Lichen planus is a chronic inflammatory disease that affects the skin and the mucus membrane. Oral lichen planus (OLP), the mucosal counterpart of cutaneous lichen planus, presents frequently in the fourth decade of life and affects women more than men in a ratio of 1.4:1. [1] The disease affects 1-2% of the population. [2],[3] It is seen clinically as reticular, papular, plaque-like, erosive, atrophic or bullous types. Intraorally, the buccal mucosa, tongue and the gingiva are commonly involved although other sites may be rarely affected. [4] Oral mucosal lesions present alone or with concomitant skin lesions. The skin lesions present as violaceous flat-topped papules in ankles, wrist, and genitalia, but characteristically the facial skin is spared.

The etiology and pathogenesis of OLP has been the focus of much research, and several antigen-specific and nonspecific inflammatory mechanisms have been put forward to explain the pathogenesis. Although mostly palliative, a spectrum of treatment modalities is in practice, from topical application of steroids to laser therapy. In this review, we discuss the recent concepts in the pathogenesis and current treatment modalities of OLP.

   Pathogenesis Top

OLP is a T-cell mediated autoimmune disease in which the auto-cytotoxic CD8+ T cells trigger apoptosis of the basal cells of the oral epithelium. [5] An early event in the disease mechanism involves keratinocyte antigen expression or unmasking of an antigen that may be a self-peptide or a heat shock protein. [1],[6] Following this, T cells (mostly CD8+, and some CD4+ cells) migrate into the epithelium either due to random encounter of antigen during routine surveillance or a chemokine-mediated migration toward basal keratinocytes. [1] These migrated CD8+ cells are activated directly by antigen binding to major histocompatibility complex (MHC)-1 on keratinocyte or through activated CD4+ lymphocytes. In addition, the number of Langerhan cells in OLP lesions are increased along with upregulation of MHC-II expression; subsequent antigen presentation to CD4+ cells and Interleukin (IL)-12 activates CD4 + T helper cells which activate CD8+ T cells through receptor interaction, interferon γ (INF - γ) and IL-2. The activated CD8+ T cells in turn kill the basal keratinocytes through tumor necrosis factor (TNF)-α, Fas-FasL mediated or granzyme B activated apoptosis.[1],[6]

   A Cytokine-Mediated Lymphocyte Homing Mechanism Top

Attraction of the lymphocytes to the epithelium-connective tissue interface has also been proposed to be due to cytokine-mediated upregulation of adhesion molecules on endothelial cells and concomitant expression of receptor molecules by circulating lymphocytes. In OLP, there is increased expression of the vascular adhesion molecules (CD62E, CD54, CD106) by the endothelial cells of the subepithelial vascular plexus. [7] The infiltrating lymphocytes express reciprocal receptors (CD11a) to these vascular adhesion molecules. This supports the above-explained hypothesis that the cytokine-mediated lymphocyte homing mechanism plays an important role in the pathogenesis of lichen planus. Some of the cytokines that are responsible for the upregulation of the adhesion molecules are: TNF-α, IFN-γ and IL-1. These are derived from the resident macrophages, Langerhans cells, lymphocytes and the overlying keratinocytes themselves, thus setting up a vicious cycle. [7]

The normal integrity of the basement membrane is maintained by a living basal keratinocyte due to its secretion of collagen 4 and laminin 5 into the epithelial basement membrane zone. In turn, keratinocytes require a basement membrane derived cell survival signal to prevent the onset of its apoptosis. Apoptotic keratinocytes are no longer able to perform this function, which results in disruption of the basement membrane. Again, a non-intact basement membrane cannot send a cell survival signal. This sets in a vicious cycle which relates to the chronic nature of the disease. [1],[8]

The matrix metalloproteinases (MMP) are principally involved in tissue matrix protein degradation. MMP- 9, which cleaves collagen 4, along with its activators is upregulated in OLP lesional T cells, resulting in increased basement membrane disruption. [9]

RANTES (Regulated on Activation, Normal T-cell Expressed and Secreted) is a member of the CC chemokine family which plays a critical role in the recruitment of lymphocytes and mast cells in OLP. CCR1, CCR3, CCR4, CCR5, CCR9 and CCR10, which are cell surface receptors for RANTES, have been identified in lichen planus. [1],[10] The recruited mast cell undergoes degranulation under the influence of RANTES, which releases chymase and TNF-α. These substances upregulate RANTES secretion by OLP lesional T cells. This again sets in a vicious cycle which relates to the chronic nature of the disease.[10]

60% mast cells have been found to be degranulated in OLP compared to 20% in normal mucosa. Mast cell degranulation releases a range of pro-inflammatory mediators such as TNF-α, chymase and tryptase. TNF-α upregulates the expression of endothelial cell adhesion molecules (CD62E, CD54 and CD106) in OLP, which is required for lymphocyte adhesion to the luminal surfaces of blood vessels and subsequent extravasation and stimulates RANTES secretion from T cells. Chymase, a mast cell protease, is a known activator of MMP-9, leading to basement membrane disruption in OLP. [1],[9]

Weak expression of transforming growth factor (TGF)-β1 has been found in OLP. TGF-β1 deficiency may predispose to autoimmune lymphocytic inflammation. The balance between TGF-β1 and IFN-γ determines the level of immunological activity in OLP lesions. Local overproduction of IFN-γ by CD4+ T cells in OLP lesions downregulates the immunosuppressive effect of TGF-β1 and upregulates keratinocyte MHC class II expression and CD8+ cytotoxic T-cell activity. [1],[8]

   Hepatitis C Virus Infection and Oral Lichen Planus Top

Epidemiological evidences from more than 90 controlled studies worldwide strongly suggest that Hepatitis C Virus (HCV) may be an etiologic factor in OLP. The association seems to be prevalent in Southern Europe, Japan and USA. However, countries with highest prevalence of HCV report negative or nonsignificant associations suggesting that the LP-HCV association cannot be explained on the basis of high prevalence in population alone. In OLP, HCV replication has been reported in the epithelial cells from mucosa of LP lesions by reverse transcription/polymerase chain reaction or in-situ hybridization; also, HCV-specific CD4 and CD8 lymphocytes were reported in the subepithelial band. These probably suggest that HCV-specific T lymphocytes may play a role in the pathogenesis of OLP. The characteristic band like lymphocytic infiltrate might thus be directed toward HCV infected cells. Whether HCV infected patients have increased risk of developing OLP or patients with OLP have enhanced risk of developing HCV infection is yet to be answered. The putative pathogenetic link between OLP and HCV still remains controversial and needs a lot of prospective and interventional studies for a better understanding. [11]

   Differential Diagnosis Top

The diagnosis of reticular lichen planus can often be made based on the clinical findings alone. Interlacing white striae appearing bilaterally on the posterior buccal mucosa is often pathognomonic. Difficulties arise often when there is superimposed candidal infection which masquerades the classic reticular pattern and in eliciting the erosive and erythematous forms of OLP. The differential diagnosis can include cheek chewing/frictional keratosis, lichenoid reactions, leukoplakia, lupus erythematosus, pemphigus, mucus membrane pemphigoid, erythematous candidiasis and chronic ulcerative stomatitis. Lichenoid drug reactions are usually unilateral in distribution, accompanied by a history of new drug intake. The most reliable method to diagnose lichenoid drug reactions is to note if the reaction resolves after the offending drug is withdrawn, and returns if the patient is challenged again. Dental restorative material induced lichenoid reactions can be identified when OLP like lesions are confined to areas of the oral mucosa in close contact or proximity to restorative materials, usually amalgam. A positive patch test, a strong clinical correlation of proximity of a restoration and biopsy suggestive of diffuse lymphocytic infiltrate rather than a subepithelial band favor a diagnosis of oral lichenoid reactions. Clinically, lesions of lupus erythematosus (LE) most often resemble erosive lichen planus but tend to be less symmetrically distributed. The keratotic striae of LE are much more delicate and subtle than Wickham's striae and show a characteristic radiation from the central focus. Biopsy of LE shows a characteristic perivascular infiltrate.

Erosive or atrophic types that usually affect the gingiva should be differentiated from pemphigoid, as both may have a desquamative clinical appearance. Both pemphigus and pemphigoid occur as solitary erythematous lesions and are not associated with any white striae. This can aid in clinical differential diagnosis as erosive and atrophic forms of OLP usually show concomitant reticular form. Peeling of the epithelium from the epithelium-connective tissue junction on slight lateral pressure in nonaffected area (Nikolsky's sign) differentiates it from erosive and erythematous forms of lichen planus. A biopsy from the perilesional tissue can diagnose pemphigus or pemphigoid, which show intraepithelial or subepithelial split histologically. In some cases, erythema multiforme (EM) can resemble bullous lichen planus, but EM is more acute and generally involves the labial mucosa. Chronic ulcerative stomatitis (CUS) is an immune-mediated disorder affecting the oral mucosa which clinically and histopathologically resembles lichen planus. Diagnosis of CUS is based on direct immunofluorescence studies where autoantibodies are directed against p63 in the basal and parabasal layers of the epithelium. These lesions have to be differentiated from lichen planus because CUS does not respond to corticosteroid therapy and has to be treated using antimalarial drugs. [12]

   Recent Concepts In Treatment Top

Corticosteroids have been the mainstay of management of OLP; yet, other modalities like calcineurin inhibitors, retinoids, dapsone, hydroxychloroquine, mycophenolate mofetil and enoxaparin have contributed significantly toward treatment of the disease.Analysis of current data on pathogenesis of the disease suggests that blocking IL-12, IFN-γ, TNF-α, RANTES, or MMP-9 activity or upregulating TGF-β1 activity in OLP may be of therapeutic value in the future.[1],[13]


These are the most commonly used group of drugs for the treatment of OLP. [14] The rationale behind their usage is their ability to modulate inflammation and immune response. They act by reducing the lymphocytic exudate and stabilizing the lysosomal membrane. [15] Topical midpotency corticosteroids such as triamcinolone acetonide, high-potent fluorinated corticosteroids such as fluocinonide acetonide, disodium betamethasone phosphate, and more recently, superpotent halogenated corticosteroids such as clobetasol are used based on the severity of the lesion. The greatest disadvantage in using topical corticosteroids is their lack of adherence to the mucosa for a sufficient length of time. Although trials were done using topical steroids along with adhesive base, no study shows their superiority when compared to steroids without the base (carboxymethyl cellulose). [16] However, the same study also recommends the usage of adhesive paste used for dentures, which contains only inactive ingredients as a vehicle to carry the topical application. This has shown excellent bioadhesive properties, due to its high molecular weight (above 100,000) and the flexibility of the polymeric chain. Small and accessible erosive lesions located on the gingiva and palate can be treated by the use of an adherent paste in a made-to-measure tray (custom tray), which allows for accurate control over the contact time and ensures that the entire lesional surface is exposed to the drugs. [17] Patients with widespread forms of OLP are prescribed high-potent and superpotent corticosteroids mouthwashes and intralesional injections. Long-term use of topical steroid can lead to the development of secondary candidiasis which necessitates antifungal therapy. [15] The potential tachyphylaxis and adrenal insufficiency is high when using superpotent steroids like clobetaso l, especially when used for a longer period of time. Systemic corticosteroids are reserved for recalcitrant erosive or erythematous LP where topical approaches have failed. Systemic prednisolone is the drug of choice, but should be used at the lowest possible dosage for the shortest duration (40-80 mg for 5-7 days). [14]

   Other Immunosuppressants and Immunomodulatory Agents Top

Calcineurin inhibitors

Calcineurin is a protein phosphatase which is involved in the activation of transcription of IL-2, which stimulates the growth and differentiation of T-cell response. [18] In immunosuppressive therapy, calcineurin is inhibited by cyclosporine, tacrolimus and pimecrolimus . These drugs are called calcineurin inhibitors.


Cyclosporine, a calcineurin inhibitor, is an immunosuppressant used widely in post-allogenic organ transplant to reduce the activity of patient's immune system. This selectively suppresses T-cell activity, the main reason for transplant rejection, and hence enhances the uptake of the foreign organ. Cyclosporine binds to the cytosolic protein cyclophilin of immunocompetent lymphocytes, especially T-lymphocytes. This complex of cylosporine and cyclophilin inhibits calcineurin, which under normal circumstances induces the transcription of IL-2. They also inhibit lymphokine production and IL release, leading to a reduced function of effector T-cells. Cyclosporine is used as a mouth rinse or topically with adhesive bases in OLP. However, the solution is prohibitively expensive and should be reserved for highly recalcitrant cases of OLP. Systemic absorption is very low. [14] It is known to cause dose-related gum hyperplasia which reduces when the drug is withdrawn.


Tacrolimus, also a calcineurin inhibitor, is a steroid-free topical immunosuppressive agent approved for the treatment of atopic dermatitis. It is 10-100 times as potent as cyclosporine and has greater percutaneous absorption than cyclosporine. It has been successfully used in recalcitrant OLP cases. This substance is produced by Streptomyces tsukubaensis and belongs to the macrolide family. The immunosuppressive action of tacrolimus is similar to that of cyclosporine, although it has a greater capacity to penetrate the mucosa. It inhibits the first phase of T-cell activation, inhibiting the phosphatase activity of calcineurin. Burning sensation is the commonest side effect observed; relapses of OLP after cessation have also been observed. The US Food and Drug Administration has recently issued a potential cancer risk from the prolonged use of tacrolimus and has recommended its use for short periods of time and not continuously. [14],[18]


Pimecrolimus inhibits T-cell activation by inhibiting the synthesis and release of cytokines from T cells. Pimecrolimus also prevents the release of inflammatory cytokines and mediators from mast cells. 1% topical cream of pimecrolimus has been successfully used as treatment for OLP. Pimecrolimus has significant anti-inflammatory activity and immunomodulatory capabilities with low systemic immunosuppressive potential. [19],[20]


Topical retinoids such as tretinoin, isotretinoin and fenretinide, with their immunomodulating properties, have been reported to be effective in OLP. Reversal of white striae can be achieved with topical retinoids, although effects may only be temporary. Systemic retinoids have been used in cases of severe lichen planus with variable degree of success. The positive effects of retinoids should be weighed against their rather significant side effects like cheilitis, elevation of serum liver enzymes and triglyceride levels and teratogenicity. [8],[21]


As an antibacterial agent, dapsone inhibits bacterial synthesis of dihydrofolic acid and hence is used in the treatment of leprosy. When used for the treatment of skin diseases, it probably acts as an anti-inflammatory agent by inhibiting the release of chemotactic factors for mast cells. [22] The most common untoward effect of dapsone is hemolysis of varying degree, which is dose related and develops in almost every individual administered 200-300 mg of oral dapsone daily. Glucose-6-phosphate dehydrogenase (G6PD) deficiency can increase the risk of hemolytic anemia or methemoglobinemia in patients receiving dapsone. Screening for G6PD deficiency is required before prescribing dapsone. Hypersensitivity reaction to dapsone called Dapsone reaction is frequent in patients receiving multiple drug therapy. The symptoms of rash, fever and jaundice generally occur within the first 6 weeks of therapy and can be ameliorated by corticosteroid therapy. [23]


Originally used to treat psoriasis, mycophenolic acid (now reformulated as mycophenolate mofetil) has been reintroduced in dermatological medicine. Being a very well-tolerated immunosuppressive drug used in organ transplant, it has been successfully used to treat severe cases of OLP. Mycophenolates are quite expensive and effective with long-term usage. [24]

Low-dose, low molecular weight heparin (enoxaparin)

Low-dose heparin devoid of anticoagulant properties inhibits T lymphocyte heparanase activity which is crucial in T-cell migration to target tissues. This promises to be a simple, effective and safe treatment for OLP when injected subcutaneously as it has no side effects. [25]


It is a recombinant humanized monoclonal antibody which is used as an immunosuppressant in the treatment of psoriasis. Efalizumab, a monoclonal antibody to CD11a, binds to this adhesion molecule and causes improvement in OLP by decreased activation and trafficking of T lymphocytes. In vitro studies of mononuclear cells in OLP have demonstrated a decrease of 60% in migration by peripheral blood mononuclear cells after pretreatment with anti-CD11a antibodies. It is administered once a week as a subcutaneous injection. It is currently an approved drug for the treatment of plaque psoriasis. [26] [Figure 1] gives a schematic representation of the probable sites of action of drugs based on their property in OLP.
Figure 1: Proposed sites of action based on property of drugs in oral lichen planus

Click here to view

   Non-Pharmacological Modalities Top

PUVA therapy

This non-pharmacologic approach uses photochemotherapy with 8-methoxypsoralen and long wave ultraviolet light (PUVA). Psoralens are compounds found in many plants, which make the skin temporarily sensitive to UV radiation. Methoxypsoralen is given orally, followed by administration of 2 hours of UV radiation intraorally in the affected sites. It has been successfully used in the treatment of severe cases of OLP. [27] Two major disadvantages of PUVA therapy include the adverse effects of nausea and dizziness secondary to psoralen and 24-hour photosensitivity when this medicine is taken orally. Also, dosimetry can be difficult within the complicated geometry of the mouth, because PUVA is usually administered on skin over large, open surfaces. [28]

Photodynamic therapy

Photodynamic therapy (PDT) is a technique that uses a photosensitizing compound like methylene blue, activated at a specific wavelength of laser light, to destroy the targeted cell via strong oxidizers, which cause cellular damage, membrane lysis, and protein inactivation. PDT has been used with relative success in the field of oncology, notably in head and neck tumors. PDT is found to have immunomodulatory effects and may induce apoptosis in the hyperproliferating inflammatory cells which are present in psoriasis and lichen planus. This may reverse the hyperproliferation and inflammation of lichen planus. [29]

Laser therapy

In patients who are suffering from painful erosive OLP and are unresponsive to even topical superpotent corticosteroids, surgical management using cryosurgery and different types of laser have also been tried. A 980-nm Diode laser, [30] CO 2 laser evaporation, [31] biostimulation with a pulsed diode laser using 904-nm pulsed infrared rays [32] and low-dose excimer 308-nm laser with UV-B rays have been tried. [28] All types of laser destroy the superficial epithelium containing the target keratinocytes by protein denaturation. A deeper penetrating beam like the diode laser destroys the underlying connective tissue with the inflammatory component along the epithelium. The few studies documented show a lot of promise, but their effectiveness is yet to be proven.

No therapy for OLP is completely curative; the goal of treatment for symptomatic patients is palliation. The following [Figure 2] simple systematic protocol will aid in effective treatment.
Figure 2: Protocol/algorithm for treatment of oral lichen planus

Click here to view

Relief can be achieved in a majority of cases through topical application of corticosteroids, with or without the combination of other immunomodulators. Very rarely does the condition necessitate systemic therapy. Laser therapy and other recent modalities are tried as the final remedy.

   Conclusion Top

OLP is a very common oral dermatosis and one of the most frequent mucosal pathosis encountered by dental practitioners. It is imperative that the lesion is identified precisely and proper treatment be administered at the earliest. A proper understanding of the pathogenesis of the disease becomes important for providing the right treatment.

   References Top

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16.Lo Muzio L, della Valle A, Mignogna MD, Pannone G, Bucci P, Bucci E, et al. The treatment of oral aphthous ulceration or erosive lichen planus with topical clobetasol propionate in three preparations: A clinical and pilot study on 54 patients. J Oral Pathol Med 2001;30:611-7.  Back to cited text no. 16
17.Gonzalez-Moles MA, Ruiz-Avila I, Rodriguez-Archilla A, Morales-Garcia P, Mesa-Aguado F, Bascones-Martinez A, et al. Treatment of severe erosive gingival lesions by topical application of clobetasol propionate in custom trays. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003;95:688-92.  Back to cited text no. 17
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20.Swift JC, Rees TD, Plemons JM, Hallmon WW, Wright JC. The Effectiveness of 1% Pimecrolimus cream in the treatment of oral erosive lichen planus. J Periodontol 2005;76:627-35.  Back to cited text no. 20
21.Oral mucosal diseases in the office setting: Part II: Oral lichen planus, pemphigus vulgaris, and mucosal pemphigoid. Sciubba JJ. Academy of general dentistry.Available from: http://www.agd.org/support/articles/?ArtID=2013 [Last accessed on 2011 Apr 21].  Back to cited text no. 21
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23.Graham WR Jr. Adverse effects of dapsone. Int J Dermatol 1975;14:494-500.  Back to cited text no. 23
24.Liu V, Mackool BT. Mycophenolate in dermatology. J Dermatolog Treat 2003;14:203-11.  Back to cited text no. 24
25.Hodak E, Yosipovitch G, David M. Low dose, low molecualr weight heparin (enoxaparin) is beneficial in lichen planus-a preliminary report. J Am Acad Dermatol 1998;38:564-8.  Back to cited text no. 25
26.A Cheng. Oral erosive lichen planus treated with efalizumab.Arch Dermatol 2006;142:680-2.  Back to cited text no. 26
27.Lundquist G, Forsgren H, Gajecki M, Emtestam L. Photochemotherapy of oral lichen planus. A controlled study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995;79;554-8.  Back to cited text no. 27
28.Trehan M, Taylor CR. Low-dose excimer 308-nm laser for the treatment of oral lichen planus. Arch Dermatol 2004;140:415-20.  Back to cited text no. 28
29.Aghahosseini F, Arbabi-Kalati F, Fashtami LA, Fateh M, Djavid GE. Treatment of oral lichen planus with photodynamic therapy mediated methylene blue: A case report. Med Oral Patol Oral Cir Bucal 2006;11:E126-9.  Back to cited text no. 29
30.Soliman M, Kharbotly AE, Saafan A. Management of oral lichen planus using diode laser (980nm). A clinical study. Egypt Dermatol Online J 2005;1:3-12.  Back to cited text no. 30
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32.Cafaro A, Albanese G, Arduino PG, Mario C, Massolini G, Mozzati M, et al. Effect of low-level laser irradiation on unresponsive oral lichen planus: Early preliminary results in 13 patients. Photomed Laser Surg 2010;28 Suppl 2:S99-103.  Back to cited text no. 32


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Jing Deng, Weiyi Pan, Ning Ji, Na Liu, Qian Chen, Jinhuan Chen, Yutong Sun, Liang Xie, Qianming Chen
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10 Automatic Detection of Image-Based Features for Immunosuppressive Therapy Response Prediction in Oral Lichen Planus
Ziang Xu, Qi Han, Dan Yang, Yijun Li, Qianhui Shang, Jiaxin Liu, Weiqi Li, Hao Xu, Qianming Chen
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11 Differential genotypes of TNF-a and IL-10 for immunological diagnosis in discoid lupus erythematosus and oral lichen planus: A narrative review
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12 Modulating the Antioxidant Response for Better Oxidative Stress-Inducing Therapies: How to Take Advantage of Two Sides of the Same Medal?
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13 Vitamin D in the Treatment of Oral Lichen Planus: A Systematic Review
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14 Efficacy and Safety of Topical Morphine: A Narrative Review
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15 DNA Fragmentation and mRNA Expression of Bcl-2, Bcl-xL, p53, p21 and HSP70 Genes in Nondysplastic and Dysplastic Oral Lichen Planus
Abhishek Jana, Jincy Thomas, Pratiti Ghosh
Contemporary Clinical Dentistry. 2022; 13(3): 249
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16 An improved scoring system for monitoring oral lichen planus: A preliminary clinical study
Ying Wu, Hao Xu, Yufeng Wang, Chunlei Li, Guoyao Tang, Hong Hua, Xiaoying Li, Xin Jin, Xin Zeng, Yu Zhou, Qianming Chen
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17 Salivary expression of lncRNA DQ786243 and IL-17 in oral lichen planus: case–control study
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18 Evaluation of the Efficacy and Safety of Apremilast in the Management of Lichen Planus
Vishalakshi Viswanath, Pradnya Joshi, Mayuri Dhakne, Dhiraj Dhoot, Namrata Mahadkar, Hanmant Barkate
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19 Comparative evaluation of the efficacy of Nigella sativa (75% v/v) cream and clobetasol propionate (0.05% w/w) gel in oral lichen planus—a double-blinded randomized control trial
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20 Reticular Oral Lichen Planus: A Clinical Experience of ENT Surgeons
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21 Experimental and clinical trial investigations of phyto-extracts, phyto-chemicals and phyto-formulations in the treatment of oral lichen planus: A systematic review
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22 JAK inhibitors in lichen planus: A review of pathogenesis and treatments
Ali Motamed-Sanaye, Yasaman Fatemeh Khazaee, Motahareh Shokrgozar, Maryam Alishahi, Najmeh Ahramiyanpour, Maliheh Amani
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23 A comprehensive summary of disease variants implicated in metal allergy
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24 Effective treatment of oral lichen planus with the JAK inhibitor baricitinib
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25 Application of mucous membrane dermoscopy (mucoscopy) in diagnostics of benign oral lesions - literature review and preliminary observations from International Dermoscopy Society study
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26 Combination of low dose corticosteroids and antioxidants in treatment of cutaneous lichen planus
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27 Are oral lichen planus patients at high risk of hepatitis C? A case-control study
Poramate Pitak-Arnnop, Keskanya Subbalekha, Nattapong Sirintawat, Chatpong Tangmanee, Prim Auychai, Chayawee Muangchan, Passanesh Sukphopetch, Jean-Paul Meningaud, Andreas Neff
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28 Review of the current evidence of non-HLA gene polymorphism in oral lichen planus
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29 Analysis of the psychopathological profile, quality of life, and cost-effectiveness of oral lichen planus patients treated with photobiomodulation
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30 An active surveillance program in oral preneoplasia and translational oncology benefit
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31 Immune mediated Lesions of the oral cavity: A scrupulously researched review
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International Journal of Oral Health Dentistry. 2021; 7(4): 238
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34 Hydrotherapy and Its Application in Oral Medicine
Riya Bhargava, Sindhuja D.S.V., Poorvi Poorvi
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35 Analysis of Treatment Response in Patients with Oral Lichen Planus
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36 Elevated Serum Interleukin-23 Levels in Patients with Oral and Cutaneous Lichen Planus
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Mediators of Inflammation. 2021; 2021: 1
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37 Effects of cold physical plasma on oral lichen planus: An in vitro study ( Effects of CAP on OLP )
Christian Seebauer, Eric Freund, Sybille Hasse, Vandana Miller, Maria Segebarth, Christian Lucas, Stefan Kindler, Tobias Dieke, Hans-Robert Metelmann, Georg Daeschlein, Katja Jesse, Klaus-Dieter Weltmann, Sander Bekeschus
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38 Analysis of the response to two pharmacological protocols in patients with oral lichen planus: A randomized clinical trial
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Oral Diseases. 2021;
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39 The effectiveness of topical forms of dexamethasone in the treatment of oral lichen planus— A systematic review
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Oral Diseases. 2021;
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40 Hydroxychloroquine- A new treatment option for erosive oral lichen planus
SubashChandra Raj, Debajani Baral, Lokanath Garhnayak, Annuroopa Mahapatra, Kaushik Patnaik, Shaheda Tabassum, JayantKumar Dash
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41 Non-Oncologic Applications of Nanomedicine-Based Phototherapy
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42 Approach to the aphthous lesions of the oral mucosa
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43 Genomic Analysis of Oral Lichen Planus and Related Oral Microbiome Pathogens
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44 A study on the pattern of oral cavity involvement in various dermatoses at tertiary care center
PragyaAshok Nair, Namrata Bhavsar, Dhruv Patel, Jinal Tandel
Indian Journal of Oral Health and Research. 2020; 6(1): 20
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45 Ulcerated oral lichen planus of the lower lip, common disease with the uncommon presentation: A case series
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46 Oral lichen planus in an 8-year-old child: A case report with a brief literature review
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47 The current understanding on langerhans' cells and its role in oral lesions
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Contemporary Clinical Dentistry. 2020; 11(3): 211
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48 A comparative evaluation on the effect of oral zinc 50 mg with or without 0.1% triamcinolone orabase on oral lichen planus
Chintada Suvarna, NallanC S K Chaitanya, Shaik Ameer, Himabindu Mannava, Parinita Bontala, JabarSadan Alyami, Humaira Samreen, Jayasurya Kondapaneni
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49 A multicenter experience using adipose-derived mesenchymal stem cell therapy for cats with chronic, non-responsive gingivostomatitis
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50 Burning mouth syndrome caused by xerostomia secondary to amlodipine
Tengku Natasha Eleena Binti Tengku Ahmad Noor
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51 Extended Erosive Oral Lichen Planus Treated with a very Low-Level Laser Therapy: A Case Report
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52 Treatment of lichen planus-induced desquamative gingivitis
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53 Renin Promotes STAT4 Phosphorylation to Induce IL-17 Production in Keratinocytes of Oral Lichen Planus
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54 Photodynamic therapy in oral lichen planus: A prospective case-controlled pilot study
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55 Oral lichen planus interactome reveals CXCR4 and CXCL12 as candidate therapeutic targets
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56 Efficacy of 1064 Q switched Nd:YAG laser in the treatment of oral lichen planus
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57 Clinical safety and efficacy of curcumin use for oral lichen planus: a systematic review
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58 Oraler Lichen planus — eine interdisziplinäre Herausforderung
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59 Features of immune status in patients with various clinical forms of oral lichen planus
S. V. Chuykin, G. M. Akmalova, I. A. Mirsayapova, G. I. Ron, N. D. Chernysheva, R. M. Khairullina
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60 Self-perceived Oral Health, Satisfaction with Overall Health and Quality of Life Comparisons between Patients with Oral Lichen Planus and their Matched Controls
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61 Oral Lichen Planus–A Brief Review on Treatment Modalities
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62 Oral Manifestation in Patients diagnosed with Dermatological Diseases
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63 Looking Beyond the Cyclosporine “Swish and Spit” Technique in a Recalcitrant Case of Erosive Lichen Planus Involving the Tongue
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64 Therapeutic Efficacy of Fresh, Allogeneic Mesenchymal Stem Cells for Severe Refractory Feline Chronic Gingivostomatitis
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65 Possible alternative therapies for oral lichen planus cases refractory to steroid therapies
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66 The Effects of NBF Gingival Gel Application in the Treatment of the Erosive Lichen Planus: Case Report
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67 Therapeutic Efficacy of Fresh, Autologous Mesenchymal Stem Cells for Severe Refractory Gingivostomatitis in Cats
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69 Lichen Planus of Larynx Manifesting as Airway Compromise: A Rare Presentation
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70 Immunohistochemical Expression of Perforin in Lichen Planus Lesions
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71 Efficacy of topical tacrolimus for oral lichen planus: real-life experience in a retrospective cohort of patients with a review of the literature
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72 Interleukin-6 and neopterin levels in the serum and saliva of patients withLichen Planusand oralLichen Planus
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73 Adverse drug events in the oral cavity
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74 Oral Mucosal Diseases
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75 HBO: A possible supplementary therapy for oral potentially malignant disorders
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76 Lichen ruber mucosae
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77 The relationship between oral lichen planus and blood group antigens
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78 Oral Lichen Planus and Lichenoid Mucositis
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79 The recognition and classification of lymphoproliferative disorders of the gut
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80 Proliferation and apoptosis of peripheral blood mononuclear cells in patients with oral lichen planus
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81 In vitro culture system for keratinocytes obtained from oral lichen planus lesions
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82 Clinical variants of lichen planus [Der Lichen ruber planus und seine klinisch-morphologischen Varianten]
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83 Photodynamic treatment of oral lichen planus
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Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology. 2013; 115(1): 62-70
84 Lichen planopilaris is characterized by immune privilege collapse of the hair follicleæs epithelial stem cell niche
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85 Efficacy of intralesional betamethasone for erosive oral lichen planus and evaluation of recurrence: a randomized, controlled trial
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87 Current treatment options in challenging oral diseases: Oral lichen planus, oral leukoplakia [Zorlu oral hastaliklarda güncel tedavi: Oral liken planus, oral lökoplaki]
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88 A comparative study of apoptosis in reticular and erosive oral lichen planus
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89 Altered expression of HSP70 in oral lichen planus
Tyagi, N. and Shetty, D.C. and Urs, A.B.
Journal of Oral and Maxillofacial Pathology. 2012; 16(2): 189-194


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