| INTRODUC TI ONOral lichen planus and lichenoid lesions comprise a group of disorders of the oral mucosa that likely represent a common reaction pattern in response to extrinsic antigens, altered self-antigens or super antigens. 1 Historically, there have been unresolved debates and controversies around the oral lichen planus and lichenoid lesions terminology. The latter term has frequently been used to refer to oral lesions that have clinical and histopathological features similar to oral lichen planus but no risk of malignant transformation, or to indicate an uncertain diagnosis of oral lichen planus. However, definitive clinical and histological diagnostic criteria able to distinguish oral lichen planus from lichenoid lesions are still lacking. 1 Furthermore, there remains no consensus regarding the possible different clinical behavior of the disorders in the oral lichen planus and lichenoid lesions group with respect to cancer development. In dermatology, the concept of 'lichenoid tissue reaction/interface dermatitis' was introduced a long time ago to define a number of distinct inflammatory cutaneous diseases sharing common histopathological features, including liquefactive/vacuolar changes of the basal keratinocytes and a subepithelial band-like array of mononuclear inflammatory cells, including activated T lymphocytes, macrophages, and dendritic cells. 1,2 During the 2006 World Workshop in Oral Medicine IV, it was proposed to classify the oral lichen planus and lichenoid lesions group in 4 distinct disorders, including oral lichen planus, oral lichenoid drug reactions caused by systemic drug exposure, oral lichenoid contact lesions triggered by local hypersensitive reaction to dental materials, and oral lichenoid lesions of graft-vs.-host disease. 3 Although a step forward, this classification failed to provide clear and reliable clinical and histological criteria to properly differentiate these 3 types of lichenoid lesions from oral lichen planus. In addition, several other disease entities characterized by clinical and/or histological features of lichenoid tissue reaction/interface dermatitis were excluded from the classification. Other authors have proposed alternative classifications. 4-6 Overall, there remains no consensus on classification, diagnostic criteria, clinical behavior, and management of the oral lichen planus and lichenoid lesions. 7-9In this review, we have attempted to (i) update the classification of oral lichen planus and lichenoid lesions, (ii) suggest pragmatic diagnostic criteria, and (iii) define a management strategy. Table 1 lists the main disorders displaying histological and/or clinical characteristics of this oral lichen planus and lichenoid lesions group. | CL A SS IFIC ATI ONSome of these disorders are apparently uncommon whereas others are poorly defined or may simply represent a misnomer. | OR AL LI CHEN PL AN USOral lichen planus is the prototype disorder of the group. Despite the lack of reliable epidemiological data, oral lichen planus is thought to be relatively commo...

This guideline has been initiated by the task force Autoimmune Blistering Diseases of the European Academy of Dermatology and Venereology, including physicians from all relevant disciplines and patient organizations. It is a S3 consensus‐based guideline that systematically reviewed the literature on mucous membrane pemphigoid (MMP) in the MEDLINE and EMBASE databases until June 2019, with no limitations on language. While the first part of this guideline addressed methodology, as well as epidemiology, terminology, aetiology, clinical presentation and outcome measures in MMP, the second part presents the diagnostics and management of MMP. MMP should be suspected in cases with predominant mucosal lesions. Direct immunofluorescence microscopy to detect tissue‐bound IgG, IgA and/or complement C3, combined with serological testing for circulating autoantibodies are recommended. In most patients, serum autoantibodies are present only in low levels and in variable proportions, depending on the clinical sites involved. Circulating autoantibodies are determined by indirect IF assays using tissue substrates, or ELISA using different recombinant forms of the target antigens or immunoblotting using different substrates. The major target antigen in MMP is type XVII collagen (BP180), although in 10–25% of patients laminin 332 is recognized. In 25–30% of MMP patients with anti‐laminin 332 reactivity, malignancies have been associated. As first‐line treatment of mild/moderate MMP, dapsone, methotrexate or tetracyclines and/or topical corticosteroids are recommended. For severe MMP, dapsone and oral or intravenous cyclophosphamide and/or oral corticosteroids are recommended as first‐line regimens. Additional recommendations are given, tailored to treatment of single‐site MMP such as oral, ocular, laryngeal, oesophageal and genital MMP, as well as the diagnosis of ocular MMP. Treatment recommendations are limited by the complete lack of high‐quality randomized controlled trials.

Introduction: Salivary gland hypofunction is a common and permanent adverse