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      Pathophysiology, etiologic factors, and clinical management of oral lichen planus, part I: facts and controversies

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      Clinics in Dermatology
      Elsevier BV

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          Abstract

          Lichen planus (LP) is an inflammatory disease of the stratified squamous epithelia of unknown etiology. LP affects most frequently the oral mucosa, but it may also involve other mucosa and the skin. Oral LP (OLP) most frequently affects woman aged between 30 and 60 years. Histopathologic examination typically shows orthokeratotic hyperkeratosis, basal cell degeneration, and a dense well-defined infiltrate of lymphocytes in the superficial dermis. OLP lesions may result from the induction of keratinocytes apoptosis by cytotoxic CD8+ T cells stimulated by a yet unidentified self-antigen on a genetically predisposed patient. The association of OLP with hepatitis C virus (HCV) has been more consistently demonstrated in the Mediterranean area. Although HCV RNA and HCV-specific CD4+ and CD8+ T cells have been retrieved in the mucosal lesions of patients with chronic HCV infection and OLP, the eventual pathophysiology of HCV in OLP lesions remains unclear. Available treatments of OLP are not curative, and many have potentially prominent side effects. The objectives of OLP management should be to prevent and screen for malignant transformation and alleviate symptoms on the long-term. Avoidance of potential precipitating drugs, tobacco, alcohol, and local trauma, as well as strict oral hygiene, is essential. The first-line pharmacologic treatment relies on topical steroids. Systemic steroids should be limited to the short-term cure of severe refractory OLP. Life-long clinical follow-up, at least annually, is fundamental. Copyright 2010 Elsevier Inc. All rights reserved.

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          Author and article information

          Journal
          Clinics in Dermatology
          Clinics in Dermatology
          Elsevier BV
          0738081X
          January 2010
          January 2010
          : 28
          : 1
          : 100-108
          Article
          10.1016/j.clindermatol.2009.03.004
          20082959
          e40811af-7ec7-408d-a33d-5ef118f5f43f
          © 2010

          https://www.elsevier.com/tdm/userlicense/1.0/

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