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| REVIEW ARTICLE |
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| Year : 2019 | Volume
: 8
| Issue : 11 | Page : 3504-3517 |
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Oral lichen planus and associated comorbidities: An approach to holistic health
Shamimul Hasan1, Sameer Ahmed2, Ravi Kiran2, Rajat Panigrahi3, Joseph Mathew Thachil4, Shazina Saeed5
1 Department of Oral Medicine and Radiology, Faculty of Dentistry, Jamia Millia Islamia, New Delhi, India
2 Department of Periodontology, Darshan Dental College and Hospitals, Udaipur, Rajasthan, India
3 Department of Oral Medicine and Radiology, Institute of Dental Sciences, SOA University, Bhubaneswar, Odisha, India
4 Private Practitioner, Paravur, Ernakulum, Kerala, India
5 Amity Institute of Public Health, Amity University, Noida, Uttar Pradesh, India
| Date of Submission | 08-Sep-2019 |
| Date of Decision | 08-Sep-2019 |
| Date of Acceptance | 23-Sep-2019 |
| Date of Web Publication | 15-Nov-2019 |
Correspondence Address:
Dr. Shazina Saeed
Amity Institute of Public Health, Amity University, Noida, Uttar Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jfmpc.jfmpc_749_19
Lichen planus (LP) is a chronic inflammatory disorder with involvement of skin, oral and genital mucosa, scalp, and nail appendages. Oral lichen planus (OLP) lesions demonstrate a number of morphologic presentations, persist for a long time with rare self-resolution, and undergo malignant changes. OLP has been associated with numerous systemic connotations such as metabolic syndrome, diabetes mellitus, hypertension, thyroid diseases, psychosomatic ailments, chronic liver disease, gastrointestinal diseases, and genetic susceptibility to cancer. The oral health physician should be aware of these systemic associations and should work in close connect with the primary healthcare physicians to rule out the predisposing factors for the associated comorbidities. This article aims to highlight the various systemic associations of OLP and warrants the screening of these ailments in OLP for prevention and effective management.
Keywords: Diabetes mellitus, hepatitis C virus, lichen planus, oral lichen planus, psychosomatic diseases, systemic diseases
How to cite this article:
Hasan S, Ahmed S, Kiran R, Panigrahi R, Thachil JM, Saeed S. Oral lichen planus and associated comorbidities: An approach to holistic health. J Family Med Prim Care 2019;8:3504-17 |
How to cite this URL:
Hasan S, Ahmed S, Kiran R, Panigrahi R, Thachil JM, Saeed S. Oral lichen planus and associated comorbidities: An approach to holistic health. J Family Med Prim Care [serial online] 2019 [cited 2021 Apr 11];8:3504-17. Available from: https://www.jfmpc.com/text.asp?2019/8/11/3504/270947 |
| Introduction | |  |
Lichen planus (LP) is a chronic autoimmune mucocutaneous condition, primarily affecting the oral and genital mucous membrane, skin, nails, and scalp. Although the condition has an obscure etiopathogenesis, an underlying immune dysfunction and multifactorial predisposing factors also play a role.[1]
Oral lichen planus (OLP) is the mucosal analog of LP of skin, although the two demonstrate marked clinical variability. OLP exhibits a more persistent course, propensity for malignant alterations with seldom undergoing self-remission. Isolated OLP cases are frequently seen in the dental setup, with only 20% of the OLP cases presenting with cutaneous manifestations.[2]
OLP has demonstrated numerous systemic connotations such as diabetes mellitus (DM), hypertension, metabolic syndrome (MS), thyroid diseases, psychosomatic ailments, chronic liver disease, gastrointestinal diseases, and genetic susceptibility to cancer.[3] Therefore, OLP should be regarded as a systemic disorder, and the dental surgeon should be aware of the various systemic associations of LP and should work in close connection with primary healthcare physicians to rule out the predisposing factors for the associated comorbidities.[1]
| Etiopathogenesis | | |
The exact etiology of OLP is not fully elucidated, although recent research suggests a key role of immunological mechanisms that may be implicated. LP is an autoimmune disease, mediated by T CD 8+ cells, macrophages, and Langerhan's cells. Immune mechanisms trigger apoptosis resulting in cell destruction and the appearance of characteristic histological changes.[2]
Systemic associations
Hepatitis C virus (HCV) infection: Prevalence of HCV infection in patients with OLP varies between 0.5% and 35% as reported by multiple authors for distinguished geographical areas.[4] Ulcerative/erosive OLP is most frequently seen in patients with chronic liver diseases.[5] Mokni et al.[6] were the first to suggest a possible link between chronic liver diseases and OLP.
A recent meta-analysis by Alaizari et al. ascertained the association between OLP and HCV infection and further necessitated the screening of patients with OLP for the timely diagnosis of HCV infection [Table 1].[7] | Table 1: Studies showing LP association with hepatitis C virus infection
Click here to view |
LP has a long-established relationship with a multitude of comorbidities including MS, DM, thyroid dysfunction (hypothyroidism), and dyslipidemia (a risk factor for cardiovascular diseases).[1] The association of LP with one or two of these comorbidities has been published in the literature.[8],[9],[10],[11],[12] Current published literature has emphasized that chronic inflammation, endocrine dysfunction, and oxidative stress, frequently associated with mucocutaneous disorders, may serve as potential predisposing risk factors for the development of the MS.[13] According to a recent study by Sadr Eshkevari et al., a majority of patients with LP presented with features of DM, hypertension, MS, and dyslipidemia [Table 2].[14]
Hence, patients with OLP entail exceptional surveillance from skilled health professionals and should be meticulously investigated to rule out the predisposing factors for cardiovascular diseases. This will aid to avert the possible complications and the associated comorbidities.[15]
The linkage between DM and OLP was first reported by Grinspan et al.[16] This association of DM and OLP may be highlighted by two facts: (a) impaired endocrine function in DM may result in immune dysregulation which may predispose to the development of OLP lesions [17] and (b) few antidiabetic medications in patients with DM may evoke an allergic reaction and result in an oral lichenoid lesion.[18] A meta-analysis study by Mozaffari et al. showed a statistically significant difference between the occurrences of OLP in patients with DM when compared with the controls (1.37% in patients with DM and 0.75% in the control population).[19] Otero Rey et al. conducted a recent systematic review with a two-fold objective, wherein they demonstrated the prevalence of DM in patients with OLP (1.6%–37.7% DM in OLP) and also the prevalence of OLP in DM (0.5%–6.1% OLP in DM) [Table 3].[20]
The association of thyroid disease and OLP was first reported in 1994, and the published literature has strengthened this association.[21] The possible association of OLP and thyroid gland diseases (TGDs) can be partly strengthened by the fact that numerous autoimmune conditions tend to congregate with autoimmune TGDs.[10],[22],[23] A meta-analysis study by Li et al. showed a statistically significant difference in the prevalence of TGD between the OLP and the control population. The study showed that hypothyroidism and Hashimoto thyroiditis were the most common associated thyroid diseases with OLP [Table 4].[24]
A study by Dreiher et al. demonstrated that a majority of patients with OLP presented with dyslipidemia.[9] Studies by Arias-Santiago et al.[25] and Aniyan et al.[26] demonstrated a higher prevalence of dyslipidemia in both skin and oral LP patients. Chronic inflammatory components result in uncontrolled dyslipidemia, and thus, augment the atherosclerotic plaque formation and other predisposing factors for cardiovascular diseases [Table 5].
Bowel diseases occasionally described concomitant with OLP including celiac disease, ulcerative colitis, and Crohn's disease.[27] The relationship between Helicobacter pylori and OLP has been suggested by various studies. A statistically significant difference in Helicobacter pylori infection between patients with LP and control groups has been observed according to studies by Morravvej et al.[28] and Vainio et al.[29]
Psychological stress and anxiety
OLP is regarded as a psychosomatic disorder,[30] and an increased rate of depression, anxiety, and psychic ailments has been associated with patients with OLP.[31] Stress accounts as the major attribute to the acute exacerbations in patients with OLP.[32] The relationship between OLP and stress is well-documented by frequent depressive and anxiety episodes and an elevated salivary cortisol level in patients with OLP.[33] Elevated salivary/urinary cortisol levels correspond to increased anxiety and depressive states.[34] A recent study by Radwan-Oczko et al. assessed the psychological and psychopathological aspects of patients with OLP. The study confirmed the interrelationship between OLP and stress, depression, anxiety, and the resultant compromised quality of patient's life.[30] Another systematic review by Cerqueira et al. strengthened the linkage between the prevalence of OLP in patients with psychological disorders [Table 6].[35]
Pharmacological and/or psychotherapeutic stress management may prove as a valuable additional approach in OLP therapy. Psychological assessment of patients should be an integral approach in the comprehensive OLP diagnosis.[30]
Oral lichenoid reactions
Lichenoid reactions have a recognizable etiology, and clinically and histopathologically mimic OLP. Lichenoid lesions are characteristically unilateral [36] and erosive.[37] The inflammatory infiltrate is primarily composed of plasma cells, eosinophils, and neutrophils, and with numerous Civatte bodies.[36],[38]
Dental restorative materials: Amalgams, composite resins, cobalt, and gold are the chief contributors to oral lichenoid reaction (OLR). Flavoring agents and plastics also play a role in the pathogenesis and management of patients with OLR.[39]
Drug-induced OLR: The most common drugs associated with OLR are nonsteroidal anti-inflammatory agents (NSAIDs) and angiotensin-converting enzyme inhibitors (captopril, enalapril).[37] In 1994, Thompson and Skaehill showed strong evidence that drugs such as beta-blockers, methyldopa, penicillamine, and NSAIDS are linked with lichenoid eruptions.[40] Withdrawing the offending drugs results in the resolution of the lichenoid reaction and this aids the diagnosis of OLR.
Genetic predisposition: Documentation of several familial cases have suggested genetic predisposition in the pathogenesis of OLP.[41] Lowe et al. were the first to report a significantly higher HLA-A3 frequency in a British family with cutaneous LP.[42]
Predisposing factors
Mechanical trauma
Dental procedures, sharp cusps, uncountoured dental restorations, ill-fitting prosthesis, and deleterious oral habits are the possible predisposing factors.[43] Koebner's phenomenon refers to the development of lesions at sites subjected to trauma. This suggests a possible explanation for erosive lesions being more common in trauma-prone sites (buccal mucosa and lateral aspect of the tongue).[33]
Plaque and calculus
Erosive/atrophic LP patients, especially with desquamative gingivitis, face difficulty in tooth brushing because of gingival pain and bleeding. Gingival lesions of LP may be worsened by dental plaque and calculus.[44]
| Clinical Manifestations | | |
OLP is a mucocutaneous disorder of unknown etiology. In a majority of cases, LP may affect only the oral cavity. The condition may also affect other mucosal sites such as skin, genitals, scalp, and nails.[45] OLP primarily affects perimenopausal females with a prevalence of 0.1%–4%. Most OLP patients are in the age range of 30–60 years; however, no age group is spared.[46]
Skin lesions: Cutaneous LP lesions are usually self-limiting, cause itching, and are delineated by the characteristic six P's – planar, polygonal, pruritic, purplish, papules, and plaques. The disease has an acute onset, and the commonly affected sites are flexor surfaces of the wrists, forearms, and legs. Interlacing, fine, reticular-white lines (Wickham striae) often surround the skin lesions [47] [Figure 1].
Oral manifestations: Oral lesions have a chronic course with infrequent spontaneous remission and are potentially premalignant. In addition, oral lesions are difficult to treat, and hence, a source of morbidity.
Andreason classified OLP into six clinical types: reticular [Figure 2]a and [Figure 2]b, papular, plaque-like [Figure 3], atrophic [Figure 4], ulcerative [Figure 5], and bullous [Figure 6].[48] OLP was further classified into reticular (reticular, plaque-like, and papular), erythematous (atrophic), and erosive type (ulcerative, bullous).[49] However, according to a few authors, OLP is of two types: reticular (reticular, plaque-like) and erosive (atrophic, ulcerative, and bullous).[50] | Figure 2: (a and b) Reticular lichen planus. Wickham's striae on the (a) lower labial mucosa and (b) buccal mucosa
Click here to view |
The reticular type is the most frequently encountered form and manifests as bilateral asymptomatic Wickham striae on the buccal mucosa, labial mucosa, tongue, palate, and gingiva. Atrophic and erythematous oral mucosa is seen in the atrophic LP. The vesicles filled with fluid are characteristically seen in bullous LP. Erosive LP presents as an ulcerated, erythematous, and painful lesion. These erosive lesions are frequently accompanied by secondary opportunistic candidal infections.[51]
Most of the OLP cases are seen on the buccal mucosa, followed by dorsum of tongue, gingiva, labial mucosa, and vermilion border of the lower lip.[33],[52] Exclusive gingival lesions are seen in about 10% of patients with OLP. Erythematous gingival lesions result in desquamative gingivitis, the most frequently seen form of gingival LP [Figure 7].[53] These lesions also manifest as a minute, raised, fine white interlacing papules or plaques and may mimic keratotic lesions (frictional keratosis or leukoplakia). Isolated OLP cases at sites other than the gingiva are rarely seen, although few isolated lip [54] or tongue [48] lesions have been reported.
Genital mucosa: Genital mucosa is the most commonly involved extraoral site in female patients, and about 20% of females with OLP develop genital lesions.[55] Vulvovaginal–gingival syndrome denotes the relationship of LP with the vulva, vagina, and gingiva.[56] Usually, genital lesions are primarily erosive. However, few patients may present with asymptomatic reticular genital lesions.[57]
The penogingival syndrome denotes the male analog of the vulvovaginal–gingival syndrome of LP.[58]
Skin appendages: Scaly, violaceous, pruritic papular lesions affecting the scalp are known as Lichen planopilaris. Untreated cases may result in scarring alopecia.[59]
Nails: Irregular, longitudinal grooving, ridging, and thinning of the nail plate are seen. This causes shedding of the nail plate with atrophy of the nail bed. Pterygium (i.e. cuticular overgrowth) is a characteristic finding.[60]
Esophageal LP may manifest as dysphagia, chronic pain, and strictures.[61]
| Diagnosis | | |
Bilaterally, symmetrical, white interlacing striae, and/or popular lesion is the most peculiar clinical manifestation of OLP.[62] The presence of bilateral, often symmetrical reticular lesions was also considered as an essential clinical criterion.
The following histopathological features are fundamental for OLP diagnosis [Figure 8]:
A distinct band-like lymphocytic infiltrate in the connective tissue zone.
Presence of epithelial basal layer liquefaction degeneration
No signs of atypia/epithelial dysplasia.[63]
Eisenberg [64] suggested the optional histologic diagnostic features, including saw-toothed rete ridges, colloid/civatte bodies, and parakeratotic epithelium.
Immunofluorescence shows a linear pattern of fibrin and shaggy fibrinogen deposits at the epithelial basement membrane or cytoid bodies (Russell bodies), or both in the absence of deposition of fibrinogen [Figure 9].[65]
| Treatment | | |
Currently, OLP treatment intends at minimizing the ulcerations and mucosal inflammation, diminish the flare-up of the lesions, and possibly enhance the disease-free period. However, no single therapeutic regimen has proven valuable in the management of OLP.[66]
Usually, no treatment is warranted for the benign/asymptomatic form (reticular OLP), and periodic observation and evaluation is usually sufficient in such cases.[67] Patient education and motivation for maintaining oral hygiene and corrective dentistry may play a pivotal role in OLP management.[68] Topical high-potency corticosteroids comprise the cornerstone therapeutic regimen in patients presenting with severe pain and burning sensation.[67]
A range of therapeutic regimen is used for the management of OLP, including corticosteroids (topical, intralesional, and systemic), immunosuppressive agents (tacrolimus, cyclosporin, mycophenolate mofetil, azathioprine), retinoids, and immunomodulatory agents (thalidomide and levamisole).[69]
Mouth is a mirror of systemic diseases and oral manifestations of systemic disease may serve as an initial clue in the diagnosis and management of the primary systemic pathology. OLP is associated with numerous systemic manifestations (MS, chronic viral hepatitis, diabetes, hypertension, dyslipidemia, and psychosomatic disorders). The primary healthcare providers play an important role in the management of patients who have oral consequences of systemic disease, as they are often likely to be the first clinicians to observe such abnormalities. They will ensure that any potential oral manifestation of systemic disease is managed quickly and appropriately to improve the patient's quality of life.[70]
| Conclusion | | |
OLP has been associated with numerous systemic connotations and may necessitate a multidisciplinary treatment strategy. OLP should not be treated as an isolated entity, but utmost care should be taken to screen and treat the associated systemic manifestations. Hence, it is essential that the dental surgeon should be aware of the various systemic associations of LP and should work in close connect with physicians to rule out the predisposing factors for the associated comorbidities.
Financial support and sponsorship
Nil.
Conflict of interest
There is no conflict of interest.
| References | | |
| 1. | Hasan S. Lichen planus of lip – Report of a rare case with review of literature. J Family Med Prim Care 2019;8:1269-75.  [ PUBMED] [Full text] |
| 2. | Sugerman PB, Savage NW, Walsh LJ, Zhao ZZ, Zhou XJ, Khan A, et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;13:350-65. |
| 3. | Cassol-Spanemberg J, Rodríguez-de Rivera-Campillo ME, Otero-Rey EM, Estrugo-Devesa A, Jané-Salas E, López-López J. Oral lichen planus and its relationship with systemic diseases. A review of evidence. J Clin Exp Dent 2018;10:938-44. |
| 4. | Petti S, Rabiei M, De Luca M, Scully C. The magnitude of the association between hepatitis C virus and oral lichen planus: A meta analysis and case control study. Odontology 2011;99:168-78. |
| 5. | Gheorghe C, Mihai L, Parlatescu L, Tovaru S. Association of oral lichen planus with chronic C Hepatitis. Review of the data in literature. Maedica (Buchar) 2014;9:98-103. |
| 6. | Mokni M, Rybojad M, Puppin D Jr, Catala S, Venezia F, Djian R, et al. Lichen planus and hepatitis C virus. J Am Acad Dermatol 1991;24:792. |
| 7. | Alaizari NA, Al-Maweri SA, Al-Shamiri HM, Tarakji B1, Shugaa-Addin B. Hepatitis C virus infections in oral lichen planus: A systematic review and meta-analysis. Aust Dent J 2016;61:282-7. |
| 8. | Seyhan M, Ozcan H, Sahin I, Bayram N, Karincaoglu Y. High prevalence of glucose metabolism disturbance in patients with lichen planus. Diabetes Res Clin Pract 2007;77:198-202. |
| 9. | Dreiher J, Shapiro J, Cohen AD. Lichen planus and dyslipidemia: A case-control study. Br J Dermatol 2009;161:626-9. |
| 10. | 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;110:319-24. |
| 11. | Nagao Y, Myoken Y, Katayama K, Tanaka J, Yoshizawa H, Sata M. Epidemiological survey of oral lichen planus among HCV-infected inhabitants in a town in Hiroshima Prefecture in Japan from 2000 to 2003. Oncol Rep 2007;18:1177-81. |
| 12. | Carrozzo M, Gandolfo S, Carbone M, Colombatto P, Broccoletti R, Garzino-Demo P, et al. Hepatitis C virus infection in Italian patients with oral lichen planus: A prospective case-control study. J Oral Pathol Med 1996;25:527-33. |
| 13. | Garima PT. Metabolic syndrome and skin: Psoriasis and beyond. Indian J Dermatol 2013;58:299-305. |
| 14. | Sadr Eshkevari S, Aghazadeh N, Saedpanah R, Mohammadhosseini M, Karimi S Nikkhah N. The association of cutaneous lichen planus and metabolic syndrome: A case-control study. J Skin Stem Cell 2016;3:66785. |
| 15. | Kumar SA, KrishnamRaju PV, Gopal K, Rao TN. Comorbidities in lichen planus: A case-control study in Indian patients. Indian Dermatol Online J 2019;10:34-7. [ PUBMED] [Full text] |
| 16. | Grinspan D, Diaz J, Villapol LO, Schneiderman J, Berdichesky R, Palèse D, et al. Lichen ruber planus of the buccal mocusa. Its association with diabetes. Bull Soc Fr Dermatol Syphiligr 1966;73:898-9. |
| 17. | Petrou-Amerikanou C, Markopoulos AK, Belazi M, Karamitsos D, Papanayotou P. Prevalence of oral lichen planus in diabetes mellitus according to the type of diabetes. Oral Dis 1998;4:37-40. |
| 18. | Kaomongkolgit R. Oral lichenoid drug reaction associated with antihypertensive and hypoglycemic drugs. J Drugs Dermatol 2010;9:73-5. |
| 19. | Mozaffari HR, Sharifi R, Sadeghi M. Prevalence of oral lichen planus in diabetes mellitus: A meta-analysis study. Acta Inform Med 2016;24:390-3. |
| 20. | Otero Rey EM, Yáñez-Busto A, Rosa Henriques IF, López-López J, Blanco-Carrión A. Lichen planus and diabetes mellitus: Systematic review and meta-analysis. Oral Dis 2019;25:1253-64. |
| 21. | Kurgansky D, Burnett JW. Widespread lichen planus in association with Turner's syndrome and multiple endocrinopathies. Cutis 1994;54:108-10. |
| 22. | Garcia-Pola MJ, Llorente-Pendás S, Seoane-Romero JM, Berasaluce MJ, García-Martín JM. Thyroid disease and oral lichen planus as comorbidity: A prospective case-control study. Dermatol 2016;232:214-9. |
| 23. | Lavaee F, Majd M. Evaluation of the association between oral lichen planus and hypothyroidism: A retrospective comparative study. J Dent (Shiraz) 2016;17:38-42. |
| 24. | Li D, Li J, Li C, Chen Q, Hua H. The association of thyroid disease and oral lichen planus: A literature review and meta-analysis. Front Endocrinol (Lausanne) 2017;8:310. |
| 25. | Arias-Santiago S, Buendía-Eisman A, Aneiros-Fernández J, Girón-Prieto MS, Gutiérrez-Salmerón MT, Mellado VG, et al. Cardiovascular risk factors in patients with lichen planus. Am J Med 2011;124:543-8. |
| 26. | Aniyan KY, Guledgud MV, Patil K. Alterations of serum lipid profile patterns in oral lichen planus patients: A case-control study. Contemp Clin Dent 2018;9:S112-21. |
| 27. | Gupta S, Jawanda MK. Oral lichen planus: An update on etiology, pathogenesis, clinical presentation, diagnosis and management. Indian J Dermatol 2015;60:222-9. [ PUBMED] [Full text] |
| 28. | Morravvej H, Hoseini H, Barikbin B, Molekzdeh R, Razavi GM. Association of helicobacter pylori with lichen planus. Indian J Dermatol 2008;52:138-40. |
| 29. | Vainio E, Huovinen S, Liutu M, Uksila J, Leino R. Peptic ulcer and Helicobacter pylori in patients with lichen planus. Acta Daerm Venerol 2000;80:427-9. |
| 30. | Radwan-Oczko M, Zwyrtek E, Owczarek JE, Szcześniak D. Psychopathological profile and quality of life of patients with oral lichen planus. J Appl Oral Sci 2018;26:e20170146. |
| 31. | Rojo-Moreno JL, Bagan JV, Rojo-Moreno J, Donat JS, Milian MA, Jimenez Y. Psychologic factors and oral lichen planus. A psychometric evaluation of 100 cases. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;86:687-91. |
| 32. | McCartan BE. Psychological factors associated with oral lichen planus. J Oral Pathol Med 1995;24:273-5. |
| 33. | Eisen D. The clinical features, malignant potential, and systemic associations of oral lichen planus: A study of 723 patients. J Am Acad Dermatol 2002;46:207-14. |
| 34. | Manczyk B, Gołda J, Biniak A, Reszelewska K, Mazur B, Zając K, et al. Evaluation of depression, anxiety and stress levels in patients with oral lichen planus. J Oral Sci 2019;61:391-7. |
| 35. | Cerqueira JDM, Moura JR, Arsati F, Lima-Arsati YBO, Bittencourt RA, Freitas VS. Psychological disorders and oral lichen planus: A systematic review. J Investig Clin Dent 2018;9:12363. |
| 36. | Lamey PJ, McCartan BE, MacDonald DG, MacKie RM. Basal cell cytoplasmic autoantibodies in oral lichenoid reactions. Oral surg Oral Med Oral Pathol Oral Radiol Endod 1995;79:44-9. |
| 37. | Potts AJ. Hamburger J, Scully C. The medication of patients with oral lichen planus and the association of nonsteroidal anti-inflammatory drugs with erosive lesions. Oral Surg Oral Med Oral Pathol 1987;69:541-3. |
| 38. | Scully C, Eisen D, Carrozzo M. Management of oral lichen planus. Am J Clin Dermatol 2000;1:287-306. |
| 39. | Yiannias JA, el Azhary RA, Hand JH, Pakzad SY, Rogers RS III. Relevant contact sensitivities in patients with the diagnosis of oral lichen planus. J Am Acad Dermatol 2000;42:177-82. |
| 40. | Thompson DF, Skaehill PA. Drug induced lichen planus. Pharmacotherapy 1994;14:561-71. |
| 41. | Bermejo-Fenoll A, López-Jornet P. Familial oral lichen planus: Presentation of six families. Oral Surg Oral Med Oral Pathol Oral Radiol Endod2006;102:12-5. |
| 42. | Lowe NJ, Cudworth AG, Woodrow JC. HLA antigens in lichen planus. Br J Dermatol1976;95:169-71. |
| 43. | Conklin RJ, Blasberg B. Oral lichen planus. Dermatol Clin 1987;5:663-73. |
| 44. | Ramon-Fluixa C, Bagan-Sebastian J, Milian-Masanet M, Scully C. Periodontal status in patients with oral lichen planus: A study of 90 cases. Oral Dis 1999;5:303-6. |
| 45. | Scully C, Carozzo M. Oral mucosal disease-lichen planus. Br J Oral Maxilofac Surg2008;46:15-21. |
| 46. | Zakrzewska JM, Chan ES, Thornhill MH. A systematic review of placebo-controlled randomized clinical trials of treatments used in oral lichen planus. Br J Dermatol 2005;153:336-41. |
| 47. | Katta R. Lichen Planus. Am Fam Physician 2000;61:3319-24. |
| 48. | Andreason JO. OLP: A clinical evaluation of 115 cases. Oral Surg Oral Med Oral Pathol 1968;25:31-41. |
| 49. | Eisen D. The clinical manifestations and treatment of OLP. Dermatol Clin 2003;21:79-89. |
| 50. | Edwards PC, Kelsh R. OLP: Clinical presentation and management. J Can Dent Assoc 2002;68:494-9. |
| 51. | Lodi G, Scully C, Carrozzo M, Griffiths M, Sugerman PB, Thongprasom K. Current controversies in oral lichen planus: Report of an international consensus meeting. Part 2. Clinical management and malignant transformation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;100:164-78. |
| 52. | Silverman Jr S, Gorsky M, Lozada-Nur F. A prospective follow-up study of 570 patients with oral lichen planus: Persistence, remission, and malignant association. Oral Surg Oral Med Oral Pathol 1985;60:30-4. |
| 53. | Scully C, Porter SR. The clinical spectrum of desquamative gingivitis. Semin Cutan Med Surg 1997;16:308-13. |
| 54. | Allan SJ, Buxton PK. Isolated lichen planus of the lip. Br J Dermatol1996;135:145-6. |
| 55. | Rogers RS III, Eisen D. Erosive oral lichen planus with genital lesions: The vulvovaginal-gingival syndrome and the peno-gingival syndrome. Dermatol Clin 2003;21:91-8. |
| 56. | Pelisse M. The vulvo-vaginal-gingival syndrome. A new form of erosive lichen planus. Int J Dermatol 1989;28:381-4. |
| 57. | Eisen D. The vulvovaginal-gingival syndrome of lichen planus. The clinical characteristics of 22 patients. Arch Dermatol 1994;130:1379-82. |
| 58. | Cribier B, Ndiaye I, Grosshans E. [Peno-gingival syndrome. A male equivalent of vulvo-vagino-gingival syndrome?]. Rev Stomatol Chir Maxillofac 1993;94:148-51. |
| 59. | Cevasco NC, Bergfeld WF, Remzi BK, de Knott HR. A case-series of 29 patients with lichen planopilaris: The Cleveland Clinic Foundation experience on evaluation, diagnosis, and treatment. J Am Acad Dermatol 2007;57:47-53. |
| 60. | James WD, Berger TG, Elston DM, Odom RB. Andrews' Diseases of the Skin: Clinical Dermatology. 10 th ed. Philadelphia, Pa.: Saunders Elsevier; 2006. |
| 61. | Souto P, Sofia C, Cabral JP, Castanheira A, Saraiva S, Tellechea O, et al. Oesophageal lichen planus. Eur J Gastroenterol Hepatol 1997;9:725-7. |
| 62. | Mattsson U, Jontell M, Holmstrup P. Oral lichen planus and malignant transformation: Is a recall of patients justified? Crit Rev Oral Biol Med 2002;13:390-6. |
| 63. | Larsson A, Warfvinge G. Malignant transformation of oral lichen planus. Oral Oncol 2003;39:630-1. |
| 64. | Eisenberg E. Clinicopathologic patterns of oral lichenoid lesions. Oral Maxillofac Surg Clin North Am 1994;6:445. |
| 65. | Helander SD, Rogers RS III. The sensitivity and specificity of direct immunofluorescence testing in disorders of mucous membranes. J Am Acad Dermatol1994;30:65-75. |
| 66. | Hasan S, Saeed S, Rai A, Kumar A, Choudhary P, Rajat Panigrahi R, et al. Thalidomide: Clinical implications in oral mucosal lesions – An update. Ann Med Health Sci Res 2018;8:21-8. |
| 67. | Scardina GA, Messina P, Carini F, Maresi E. A randomized trial assessing the effectiveness of different concentrations of isotretinoin in the management of lichen planus. Int J Oral Maxillofac Surg2006;35:67-71. |
| 68. | Miles DA, Howard MM. Diagnosis and management of oral lichen planus. Dermatol Clin1996;14:281-90. |
| 69. | Agha-Hosseini F, Sheykhbahaei N, SadrZadehAfshar Evaluation of potential risk factors that contribute to malignant transformation of oral lichen planus: A literature review. J Contemp Dent Pract 2016;17:692-701. |
| 70. | Porter SR, Mercadante V, Fedele S. Oral manifestations of systemic disease. Br Dent J 2017;10:683-91. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]
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