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Objective@#To investigate the classification, clinical manifestations, diagnosis, differential diagnosis and treatment of oral lichenoid lesions and provide a reference for clinical practice.@*Methods@#Hospital ethical approval and patient informed consent were obtained. We report a case of oral lichenoid lesion in children and review the diagnosis and treatment of oral lichenoid damage in the literature.@*Results@#The patient experienced repeated rupture of the dorsal surface of the tongue with pain for more than 3 years. There was a large area of tongue back surface erosion with an irregular shape, surrounded by pearly-white lines. The left erosive area was accompanied by tissue hyperplasia, which was approximately 1.5 cm × 2.0 cm, with tough texture and broad masses. The pathological diagnosis of the patient was oral lichenoid lesion. After biopsy of the dorsal surface of the tongue, the pathological diagnosis of the patient was granulomatous inflammation. The final diagnosis of lichenoid granulomatous stomatitis was made on the basis of the patient's intraoral damage features, systemic history, medication history and histopathological findings. A review of the literature suggests that oral lichenoid lesions have an unknown etiology and need to be clinically differentiated from oral lichen planus, oral lichenoid drug reactions, oral lichenoid contact damage and chronic ulcerative stomatitis. The clinical treatment of oral lichen planus is based on the topical and/or systemic use of glucocorticoids.@*Conclusion@#There are still no uniform criteria for the classification and diagnosis of oral lichenoid lesions. They rely mainly on history taking, clinical manifestations and histopathological findings, and the treatment is mainly based on the topical and/or systemic use of glucocorticoids.
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Background@#Oral lichen planus is an idiopathic autoimmune inflammatory condition and oral lichenoid reactions are lesions that resemble oral lichen planus clinically and histopathologically, but develop secondary to various underlying causes. Oral lichenoid reactions have been reported to be caused by contact allergy to dental materials. This study aims to describe the characteristics of patients with a clinical and/or histopathological diagnosis of oral lichen planus who underwent patch testing in Hospital Kuala Lumpur, Malaysia.@*Methods@#This is a 5-year retrospective study of patients who had oral lichen planus and had undergone patch testing at the Department of Dermatology, Hospital Kuala Lumpur, Malaysia between January 2015 and Cecember 2019. Patch tests were performed with European Baseline Series and relevant extended series, which include dental and metal series as well as patients’ own products. Patch test results were recorded according to the International Contact Dermatitis Research Group recommendation.@*Results@#There were 41 patients with oral lichen planus who underwent patch test. The median age was 56 (range 21 to 73) with 70.7% of patients being female. There were 29 (70.7%) patients who developed at least one positive reaction. The most frequent sensitizing allergens were nickel sulfate (34.1%), gold(I)sodium thiosulphate dihydrate (22.0%), fragrance mix I (19.5%), cobalt chloride (14.6%), Peru balsam (12.2%) and sodium tetrachloropalladate (II) hydrate (12.2%). Current relevance was recorded in 16 patients (39.0%) and of these patients, 12 of them had positive patch test reactions to allergens found in dental materials such as dental fillings, dental implants, orthodontic braces, dentures and dental crowns.@*Conclusion@#Contact sensitization was detected in about 70% of our patients with oral lichen planus. The most common sensitizing allergen was nickel sulfate. Current relevance was found mainly towards dental materials.
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Dermatite Alérgica de ContatoRESUMO
Background: Dental restorative materials containing silver–mercury compounds have been known to induce oral lichenoid lesions. Objectives: To determine the frequency of contact allergy to dental restoration materials in patients with oral lichenoid lesions and to study the effect of removal of the materials on the lesions. Results: Forty‑five patients were recruited in three groups of 15 each: Group A (lesions in close contact with dental materials), Group B (lesions extending 1 cm beyond the area of contact) and Group C (no topographic relationship). Thirty controls were recruited in two groups of 15 individuals each: Group D (oral lichenoid lesions but no dental material) and Group E (dental material but no oral lichenoid lesions). Patch tests were positive in 20 (44.5%) patients. Mercury was the most common allergen to elicit a positive reaction in eight patients, followed by nickel (7), palladium (5), potassium dichromate (3), balsam of Peru, gold sodium thiosulphate 2 and tinuvin (2) and eugenol (1), cobalt chloride (1) and carvone (1). Seven patients elicited positive response to more than one allergen. In 13 of 20 patients who consented to removal of the dental material, complete healing was observed in 6 (30%), marked improvement in 7 (35%) and no improvement in 7 (35%) patients. Relief of symptoms was usually observed 3 months after removal. Limitations: Limited number of study subjects and short follow up after removal/replacement of dental restoration materials are the main limitations of this study. Conclusion: Contact allergy to amalgam is an important etiologic factor in oral lichenoid lesions and removal of restorative material should be offered to patients who have lesions in close proximity to the dental material.
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Introduction: Lichen planus is a chronic inflammatory mucocutaneous disease that clinically and histologically resembles lichenoid lesions, although the latter has a different etiology. Though criteria have been suggested for differentiating oral lichen planus from lichenoid lesions, confusion still prevails. Aims: To study the cellular and nuclear volumetric features in the epithelium of normal mucosa, lichen planus, and lichenoid lesions to determine variations if any. Materials and Methods: A retrospective study was done on 25 histologically diagnosed cases each of oral lichen planus, oral lichenoid lesions, and normal oral mucosa. Cellular and nuclear morphometric measurements were assessed on hematoxylin and eosin sections using image analysis software. Statistical Analysis: Analysis of variance test (ANOVA) and Tukey's post-hoc test. Results: The basal cells of oral lichen planus showed a significant increase in the mean nuclear and cellular areas, and in nuclear volume; there was a significant decrease in the nuclear-cytoplasmic ratio as compared to normal mucosa. The suprabasal cells showed a significant increase in nuclear and cellular areas, nuclear diameter, and nuclear and cellular volumes as compared to normal mucosa. The basal cells of oral lichenoid lesions showed significant difference in the mean cellular area and the mean nuclear-cytoplasmic ratio as compared to normal mucosa, whereas the suprabasal cells differed significantly from normal mucosa in the mean nuclear area and the nuclear and cellular volumes. Conclusions: Morphometry can differentiate lesions of oral lichen planus and oral lichenoid lesions from normal oral mucosa. Thus, morphometry may serve to discriminate between normal and premalignant lichen planus and lichenoid lesions. These lesions might have a high risk for malignant transformation and may behave in a similar manner with respect to malignant transformation.