2018
DOI: 10.4317/jced.55145
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Oral lichen planus and its relationship with systemic diseases. A review of evidence

Abstract: Background Oral lichen planus (OLP) is one of the most common dermatological diseases which are present in the oral cavity. It is a chronic autoimmune, mucocutaneous disease that affects the oral mucosa as well as the skin, genital mucosa and other sites.ObjectiveReview the relevant information to OLP and its relationship with systemic diseases.Material and MethodsSearches were carried out in the Medline/PubMed, Lilacs, Bireme, BVS, and SciELO databases by using key-words. After an initial search that provided… Show more

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Cited by 36 publications
(46 citation statements)
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“…Its function is uncertain, but in the exacerbation and continuation of the oral lichen planus, a cytokine complex network(such as TNF-α, IFN-γ, TGF-β, IL-1, 2, 4, 5, 6, 8, 10, 12, 17, 18, and IL-22) plays an significant role 5,14,18,[20][21][22] . Other researchers suggest that the cellmediated immune system starts with the expression of keratinocytes antigen; this step is accompanied by the movement of T cell lymphocytes directly activated by an antigen binding to the main histocompatibility complex (MHC)-1 on keratinocytes or activated CD4 + lymphocytes 13 .In exchange, the activated CD8 + T cells kill the basal keratinocytes by tumor necrosis factor (TNF)-alpha, Fas-FasLmediated or granzyme B-activated apoptosis 13 . Researchers conclude that oxidative stress influences molecules and pathways involved in the recruitment of lymphocytic infiltrates in OLP lesions and apoptosis induction, including ICAM-1, p53, TNF-alpha,NF-κB, Fas / FasL and granzyme B pathways 7,13 .Others assume that OLP 's inflammatory pathways activate T-cells to release reactive oxygen species ( ROS) alone or to enhance ROS production by activating keratinocytes, causing damage to neighboring cells 7 .…”
Section: Pathophysiologymentioning
confidence: 99%
“…Its function is uncertain, but in the exacerbation and continuation of the oral lichen planus, a cytokine complex network(such as TNF-α, IFN-γ, TGF-β, IL-1, 2, 4, 5, 6, 8, 10, 12, 17, 18, and IL-22) plays an significant role 5,14,18,[20][21][22] . Other researchers suggest that the cellmediated immune system starts with the expression of keratinocytes antigen; this step is accompanied by the movement of T cell lymphocytes directly activated by an antigen binding to the main histocompatibility complex (MHC)-1 on keratinocytes or activated CD4 + lymphocytes 13 .In exchange, the activated CD8 + T cells kill the basal keratinocytes by tumor necrosis factor (TNF)-alpha, Fas-FasLmediated or granzyme B-activated apoptosis 13 . Researchers conclude that oxidative stress influences molecules and pathways involved in the recruitment of lymphocytic infiltrates in OLP lesions and apoptosis induction, including ICAM-1, p53, TNF-alpha,NF-κB, Fas / FasL and granzyme B pathways 7,13 .Others assume that OLP 's inflammatory pathways activate T-cells to release reactive oxygen species ( ROS) alone or to enhance ROS production by activating keratinocytes, causing damage to neighboring cells 7 .…”
Section: Pathophysiologymentioning
confidence: 99%
“…It is described by periods of remission and exacerbation. It is the furthermost well-known disease of dermatological origin that influences the oral mucosa [22]. OLP occurs in a prevalence that ranges between 0.2 and 5% around the world.…”
Section: Discussionmentioning
confidence: 99%
“…DIF findings in patients with OLP are typical and widely reported in the literature [1,17]. OLP alternates between periods of remission and exacerbation, thus a scheduled follow-up is strongly recommended [10]. Treatment is normally reserved only for symptomatic patients.…”
mentioning
confidence: 86%
“…The onset age is between the fourth and seventh decade, with very few cases reported in the paediatric population [1,3,4]. The prevalent theory regarding the aetiopathogenesis relies on a T-lymphocyte-mediated immuno-pathological reaction, probably induced by a series of various exogenous triggers as the cause of an alteration of endogenous and surface antigens of the oro-mucosal keratinocytes, which ultimately enter into apoptosis [1,[5][6][7][8][9][10][11][12]. Six clinical subtypes of OLP exist individually or in combination: reticular, papular, plaque, erosive/ulcerative, atrophic and bullous [1,13].…”
mentioning
confidence: 99%