Controversies regarding oral lichen planus and lichenoid-dysplastic lesions.

Objective: Oral lichen planus (OLP) is an immune-mediated condition featuring chronic inflammation. The World Health Organization classifies OLP as potentially malignant, but it is believed that the malignant transformation of OLP occurs in lesions with both lichenoid and dysplastic features (LD). This review discusses the issues surrounding OLP and LD, including their malignancy, classification, and categorization, and whether lichenoid inflammation causes dysplastic changes in LD or vice versa. Methods: English full-text literature on OLP, LD and/or dysplasia was retrieved from PubMed, CINAHL, and Google Scholar. Results: Thirty-six publications including original research articles, reviews, meta-analyses, books, reports, letters, and editorials were selected for review. Discussion: Research suggests that OLP has malignant potential, although small, and that LD should not be disregarded, as dysplasia presenting with or without lichenoid features may develop into cancer. There is also disagreement over the classification and categorization of LD. Different terms have been used to classify these lesions, including lichenoid dysplasia, OLP with dysplasia, and dysplasia with lichenoid features. Moreover, in LD, it is not clear if dysplasia or lichenoid infiltration appears first, and if inflammation is a response to dysplasia or if dysplasia is a response to the persistent inflammation. The main limitation in the literature is the inconsistency and subjective nature of histological diagnoses, which can lead to interobserver and intraobserver variation, ultimately resulting in the inaccurate diagnosis of OLP and LD. Conclusion: Although further research is required to understand OLP and LD, both lesions should be considered potentially malignant and should not be disregarded.

Objectif: Le lichen plan buccal (LPB) est une pathologie auto-immune qui se présente sous la forme d'une inflammation chronique. Selon la classification de l'Organisation mondiale de la santé, le LPB est une pathologie potentiellement maligne. Toutefois, on soupçonne que la transformation maligne du LPB se produit dans des lésions présentant à la fois des caractéristiques lichénoïdes et dysplasiques (LD). Cet examen porte sur les questions relatives au LPB et aux LD, notamment leur malignité, leur classification et leur catégorisation, et pour savoir si l'inflammation du lichénoïde entraîne des changements dysplasiques des LD ou vice versa. Méthodes: On a utilisé le texte intégral de documents rédigés en anglais sur le LPB, les LD et la dysplasie issus de PubMed, de CINAHL et de Google Scholar. Résultats: Trente-six publications, notamment des articles sur des études originales, des revues, des méta-analyses, des livres, des rapports, des lettres et des éditoriaux, ont été sélectionnées aux fins d'examen. Discussion: Des études suggèrent que le LPB est potentiellement malin, bien que ce potentiel soit faible, et que les LD ne doivent pas être ignorés : en effet, une dysplasie peut évoluer en cancer, qu'elle présente des caractéristiques lichénoïdes ou non. On constate également un désaccord quant à la classification et à la catégorisation des LD. Différents termes ont été utilisés pour la classification de ces lésions, notamment « dysplasie lichénoïde ¼, « LPB dysplasique ¼ et « dysplasie à caractéristiques lichénoïdes ¼. De plus, dans le cas des LD, on ne sait pas avec certitude si la dysplasie ou l'infiltration lichénoïde apparaît en premier, ni si l'inflammation découle de la dysplasie ou si la dysplasie est une conséquence de l'inflammation persistante. La principale limite de la littérature est due aux incohérences et à la nature subjective des diagnostics histologiques, qui peut entraîner des variations d'un observateur à l'autre ou même avec un même observateur, ce qui entraîne à terme des diagnostics erronés de LPB et de LD. Conclusion: Bien que d'autres études soient nécessaires pour comprendre le LPB et les LD, les lésions de ces 2 catégories doivent être considérées comme potentiellement malignes et ne doivent pas être ignorées.

The ABO blood group antigens in patients with oral lichenoid reaction.

Evaluating the association of ABO blood group with different delayed hypersensitivity reactions, such as oral lichenoid reaction (OLR), can provide a new perspective for clinical practice. Therefore, this study designed to investigate ABO blood group antigens in OLR patients. In this case-control study, the ABO blood group of 112 OLR patients and 117 individuals without oral lesions were included. Gender, age, characteristics of the lesions, medications and restorative materials recorded. Chi-square test used to compare the frequency of ABO blood groups in OLR patients with controls. The O blood group was significantly higher in OLR patients and all its subtypes. Also, there were significant relation between O blood group, and severity of lesions. The frequency of dysplasia was non-statistically significant higher in OLR patients with O blood group than other blood group. Based on the results of the present study, O blood group was significantly more in patients with lichenoid reaction than control group, and AB blood group was the lowest. Also, O blood group showed a positive association with the more severe form of OLR lesions and frequency of dysplasia.

Treatment of Keratosis Lichenoides Chronica With Upadacitinib.

This case report describes a 30-year-old man presenting with 1-year history of nonitchy red papules and patches who was subsequently treated with upadacitinib.

Immune checkpoint inhibitor-induced lichenoid drug eruption-sparing scar burns.

The authors present a striking case of a patient experiencing a lichenoid drug eruption secondary to immunotherapy, curiously sparing scarred skin from past burns. We observed vastly higher amounts of inflammatory lymphoid cells staining for PD-1; 70% in skin with a lichenoid drug reaction and 50% in scarred skin. The lack of a lichenoid reaction at sites of scarred skin may indicate that a basement membrane component may be causative for a lichenoid drug eruption.

Oral Lichenoid Lesion following Dental Implant Placement and Successful Management with Free Gingival Graft: A Case Report with 10-Year Follow-Up.

Titanium and metal alloys are widely used in implants, crowns, and bridges in implant dentistry owing to their biocompatibility. In this case report of a 45-year-old female patient, multiple implants were placed in five different sextants at different time points. Notably, oral lichenoid lesions (OLL) occurred in three sextants following implant placement, strongly suggesting that the dental implants or prostheses were the causative factors for OLL. The lesion was of the reticular type with erythematous surroundings and was symptomatic. Although several conservative treatments, including repeated topical application of corticosteroids, were repeatedly continued, no discernible improvement or alleviation of symptoms was observed. Consequently, surgical excision and replacement of the lesion with a free gingival graft (FGG) harvested from the palatal soft tissue were performed. No clinical symptoms or recurrence of lesions were observed during 10 years of follow-up post-FGG.

ALDH1 immunoexpression in epithelial and stromal cells of oral lichen planus and lesions with lichenoid inflammatory infiltrate

Background: Oral Lichen Planus is a potential malignant disorder and shares clinical and histopathological features with other similar lesions. ALDH1 is a specific biomarker for stem cells identification, however its role in stromal cells of immune inflammatory infiltrate has not been explored. The aim of this study was to investigate the ALDH1 immunoexpression in epithelial and stromal cells of Oral Lichen Planus and other lesions with lichenoid inflammatory infiltrate. Material and Methods: 64 samples of Oral Lichen Planus, Oral Lichenoid Lesions, Oral Leukoplakia and Unspecific Chronic Inflammation were included. ALDH1 was evaluated in both epithelium and stromal cells. ALDH1+ cells ≥ 5% were considered positive in epithelium. Stromal cells were evaluated semi quantitatively. Fields were ranked in scores, according to criteria: 1 (0 to 10%); 2 (11 to 50%) and 3 (>50%). The mean value of the sum of the fields was the final score. Statistical differences among groups were investigated, considering p < 0.05. Results: ALDH1 expression in epithelium was low in all groups without difference among them. ALDH1+ cells in the lamina propria were higher for Lichen Planus [2.0], followed by Leukoplakia [1.3], Lichenoid lesions [1.2] and control [1.1] (p<0.05). Conclusions: ALDH1 immunoexpression in epithelium of lichenoid potential malignant disorders did not show a contributory tool, however ALDH1 in stromal cells of lichen planus might be involved in the complex process of immune regulation associated with the pathogenesis of this disease. (AU)

ALDH1 immunoexpression in epithelial and stromal cells of oral lichen planus and lesions with lichenoid inflammatory infiltrate.

BACKGROUND: Oral Lichen Planus is a potential malignant disorder and shares clinical and histopathological features with other similar lesions. ALDH1 is a specific biomarker for stem cells identification, however its role in stromal cells of immune inflammatory infiltrate has not been explored. The aim of this study was to investigate the ALDH1 immunoexpression in epithelial and stromal cells of Oral Lichen Planus and other lesions with lichenoid inflammatory infiltrate. MATERIAL AND METHODS: 64 samples of Oral Lichen Planus, Oral Lichenoid Lesions, Oral Leukoplakia and Unspecific Chronic Inflammation were included. ALDH1 was evaluated in both epithelium and stromal cells. ALDH1+ cells ≥ 5% were considered positive in epithelium. Stromal cells were evaluated semi quantitatively. Fields were ranked in scores, according to criteria: 1 (0 to 10%); 2 (11 to 50%) and 3 (>50%). The mean value of the sum of the fields was the final score. Statistical differences among groups were investigated, considering p < 0.05. RESULTS: ALDH1 expression in epithelium was low in all groups without difference among them. ALDH1+ cells in the lamina propria were higher for Lichen Planus [2.0], followed by Leukoplakia [1.3], Lichenoid lesions [1.2] and control [1.1] (p<0.05). CONCLUSIONS: ALDH1 immunoexpression in epithelium of lichenoid potential malignant disorders did not show a contributory tool, however ALDH1 in stromal cells of lichen planus might be involved in the complex process of immune regulation associated with the pathogenesis of this disease.

[Lichenoid drug eruption with unfavorable evolution. Difficulties in diagnosis]. / Erupción liquenoide medicamentosa con evolución desfavorable. Dificultades en el diagnóstico.

We report the case of a woman who started with a lichenoid eruption, unfavorable evolution, for which a drug reaction was suspected. The final diagnosis was paraneoplastic pemphigus. Multidisciplinary care and evaluation by an Allergist is important in patients with severe skin reactions, suspected of drug reactions, due to the difficulty in establishing the diagnosis.

Se reporta el caso de una mujer que inició con erupción liquenoide, con evolución desfavorable, por lo que se sospechó una reacción medicamentosa. El diagnóstico final fue pénfigo paraneoplásico. Es importante la atención multidisciplinaria y la evaluación de un alergólogo en pacientes con reacciones cutáneas graves, por sospecha de reacciones farmacológicas, debido a la dificultad para establecer el diagnóstico.

Lichenoid dermatitis following PD-1 inhibitor-induced toxic epidermal necrolysis: a case report and literature review.

Immune checkpoint inhibitors such as anti-PD-1 receptor antibodies have been shown to be effective in patients with advanced gastric cancer. However, there is a growing concern about immune-related adverse events. A case of a patient with gastric adenocarcinoma who developed toxic epidermal necrolysis (TEN) induced by sintilimab and subsequently developed lichenoid dermatitis is reported. TEN was diagnosed according to a history of sintilimab use, clinical symptoms and physical examination. During hospitalization, the patient developed recurrent fever caused by bacteremia and recovered from TEN after anti-infection and anti-inflammatory treatments. However, when TEN was controlled, the patient developed the lesional manifestations of lichenoid dermatitis. To date, no cases of lichenoid dermatitis after TEN have been reported following the use of PD-1 inhibitors.

PD-1 inhibitors are drugs that help fight stomach cancer but can sometimes cause skin problems. Most skin problems are minor and do not have a serious impact on the patient's health. However, life-threatening skin problems such as toxic epidermal necrolysis (TEN) can sometimes happen. This case report describes a patient with stomach cancer who had lichenoid dermatitis (another skin problem) after TEN, following the treatment of his cancer with PD-1 inhibitors. To the best of our knowledge, it is very rare to experience both skin problems after treating cancer with PD-1 inhibitors. This rare phenomenon is reported to bring more attention to it. More research is needed to determine how to treat this problem better.

Cytotoxic dermatitis: Review of the interface dermatitis pattern in veterinary skin diseases.

Interface dermatitis or lichenoid interface dermatitis refers to a cutaneous inflammatory pattern in which keratinocyte cell death is the essential feature. These terms have evolved from the originally described lichenoid tissue reaction. These lesions are the basis for an important group of skin diseases in animals and people where cytotoxic T-cell-mediated epidermal damage is a major pathomechanism. Yet, for largely historical reasons these commonly used morphological diagnostic terms do not reflect the essential nature of the lesion. An emphasis on subsidiary lesions, such as the presence of a lichenoid band, and definitions based on anatomical features, such as location at the dermo-epidermal location, may cause confusion and even misdiagnosis. This review covers historical aspects of the terminology, including the origin of terms such as "lichenoid." The types of cell death involved and the histopathologic lesions are described. Etiopathogenesis is discussed in terms of aberrations of immune/inflammatory mechanisms focusing on cutaneous lupus erythematosus, erythema multiforme, and Stevens-Johnson syndrome/toxic epidermal necrolysis. Mechanisms have most extensively been studied in humans and laboratory animals and the discussion is centered on these species. As interface dermatitis is firmly entrenched in dermatological parlance, rather than using "cytotoxic" as its substitute, the terminologies "interface cytotoxic dermatitis" and "panepidermal cytotoxic dermatitis" are recommended, based on location and extent of epithelium affected.