Expression of survivin and p53 in oral lichen planus, lichenoid reaction and lichenoid dysplasia: An immunohistochemical study

Basheer, Shaini; Shameena, PM; Sudha, S; Varma, Sujatha; Vidyanath, S; Varekar, Aniruddha

doi:10.4103/jomfp.jomfp_39_15

Cited by 16 publications

(15 citation statements)

References 36 publications

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“…Its crucial role begins to emerge in the pathogenesis of autoimmune disorders in regard to persistent inflammation 6 . In fact, survivin overexpression has been identified in several autoimmune diseases 7‐12 . It has been postulated that survivin is associated with successful antigen presentation, differentiation of self‐reactive T‐ and B‐cell lines and the generation of autoantibodies.…”

Section: Introductionmentioning

confidence: 99%

Expression of survivin and p53 genes in patients with alopecia areata: A case–control study

2020

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Background Alopecia areata is a common non‐scarring hair loss disorder. It has been generally recognised as a loss of immune privilege leading to an autoimmune attack upon anagen hair follicles. Survivin is one of the apoptosis inhibitor proteins, responsible for apoptosis suppression and cell cycle regulation. Survivin expression has been demonstrated in the matrix and outer root sheath keratinocytes of anagen hair follicles. Survivin overexpression was shown in several autoimmune diseases, and it was postulated that it contributes to the survival of self‐reactive T and B cells. P53 is a tumour suppressor gene that was suggested to repress autoimmunity via induction of T regulatory cells. Survivin gene expression is transcriptionally suppressed by wild‐type p53. Aim The aim of this study was to investigate survivin and p53 genes expression in alopecia areata patients. Methods The mRNA tissue expression of survivin and p53 was measured by quantitative real‐time polymerase chain reaction in lesional and non‐lesional punch scalp biopsies of 25 alopecia areata patients and 25 healthy subjects. Results The study showed higher mRNA expression of survivin in lesional biopsies compared to non‐lesional (P < 0.001) and control biopsies (P = 0.001). In non‐lesional biopsies, the expression was significantly lower than in control biopsies (P < 0.001). The expression of p53 was lower in both lesional and non‐lesional biopsies relative to control biopsies. However, the difference was only significant in non‐lesional biopsies (P = 0.017). Conclusion Our results suggested that survivin and p53 genes expression was altered in patients with alopecia areata.

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Section: Introductionmentioning

confidence: 99%

Expression of survivin and p53 genes in patients with alopecia areata: A case–control study

2020

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“…IFN-α has also been reported as the causative agent of oral lichenoid lesions [25]. Unlike OLP, oral lichenoid reactions have distinct and detectable etiologies [8,11,24,53], which respectively include: 1. Dental materials: the main cause of oral lichenoid lesions is the reaction to dental materials [25,54,55], the most common of which are amalgam restorations containing mercury [22,41,56].…”

Section: Etiologymentioning

confidence: 99%

Oral Lichen Planus or Oral Lichenoid Reaction? A Literature Review

Agha‐Hosseini

Samami

Tavakol

et al. 2019

J Islam Dent Assoc Iran

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Background and Aim: Oral lichen planus (OLP) is a chronic, inflammatory, T-cellmediated autoimmune oral mucosal disease. Oral lichenoid lesions develop as a type IV hypersensitivity reaction. Both of these entities are potential precancerous conditions; this adds to their clinical significance. The purpose of this literature review was to detect the similarities and the differences of these lesions to enhance the information of colleagues in managing these groups of patients. Materials and Methods: For this review, we searched Cochrane, Medline, and Embase databases from January 1990 to the end of October 2018. A total of 96 published papers, including review papers, case reports, cohort studies, case-control studies, and meta-analysis studies, were included and analyzed. Results: OLP and oral lichenoid reactions are two distinct diseases. They can be clinically similar but they have different etiologic factors. A histopathological study is necessary to differentiate them. Conclusion: The definitive diagnosis of these conditions is extremely important given their potentially premalignant nature. A timely diagnosis probably results in proper management. Based on the present research, the final differentiation between OLP and oral Lichenoid reactions relies on both clinical and histopathological manifestations according to the modified World Health Organization (WHO) criteria.

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“…OLP, OLL, and OLD differ in etiology, pathogenesis and biological behavior, whereas all of them have close clinical and histopathological resemblances. Therefore, the malignant potency of these lesions is a greatly controversial issue [ 3 ]. In fact, the rate of malignant transformation of OLP patients varies considerably in the literature [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Intraepithelial Macrophage Expressing CD163 Is a Histopathological Clue to Evaluate the Malignant Potency of Oral Lichenoid Condition: A Case Report and Immunohistochemical Investigation

et al. 2020

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Oral lichenoid conditions (OLC), including oral lichen planus (OLP), oral lichenoid lesions and oral lichenoid dysplasia, differ in pathogenesis and biological malignancy. However, distinguishing them based on clinical or histological features is difficult. It is well known that CD163+ macrophages are associated with oral cancer aggressiveness. We recently demonstrated that CD163+ macrophages of noncancerous lesions infiltrate the stroma, not the intraepithelial area. In this report, we describe a case of OLC that was not detected as malignant by the first local biopsy. Furthermore, we evaluated the malignant potency of OLC by retrospectively comparing the histological findings between local biopsy and resected specimens focusing on CD163+ macrophages. A 72-year-old man with a white lesion in the unilateral buccal mucosa was diagnosed with OLP through the biopsy although invasive cancer was detected two years later. Intraepithelial CD163+ macrophages were found not only on the resected specimen but also biopsy. This is the first report to demonstrate that intraepithelial CD163+ macrophages may be noteworthy indicators to identify the malignant potency of OLC.

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Expression of survivin and p53 in oral lichen planus, lichenoid reaction and lichenoid dysplasia: An immunohistochemical study

Cited by 16 publications

References 36 publications

Expression of survivin and p53 genes in patients with alopecia areata: A case–control study

Expression of survivin and p53 genes in patients with alopecia areata: A case–control study

Oral Lichen Planus or Oral Lichenoid Reaction? A Literature Review

Intraepithelial Macrophage Expressing CD163 Is a Histopathological Clue to Evaluate the Malignant Potency of Oral Lichenoid Condition: A Case Report and Immunohistochemical Investigation

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