Histopathology 2015, 66, 463–466.
Correspondence Oral lichen planus: a histopathological study DOI: 10.1111/his.12538 © 2014 John Wiley & Sons Ltd
Sir: Oral lichen planus (LP) is an immune-mediated disease.1 In 2005, the World Health Organization (WHO) classified it as a potentially malignant disorder,2 but this classification is controversial.3,4 Authors have discussed the criteria used for the diagnosis of oral LP in the cases of malignant transformation reported in the literature.3,4 In view of this controversy, archival cases diagnosed as LP were evaluated using Eisenberg’s histologic criteria3 in order to determine the possibility that cases of lichenoid dysplasia had been diagnosed as LP. A total of 121 archival cases stained with haematoxylin and eosin and diagnosed as LP between 2000 and 2009 were analysed individually by three experienced pathologists (A, B and C). Only those cases with clinical descriptions of symmetrical and bilateral reticular lesions on the buccal mucosa were considered in the study. Cohen’s kappa coefficient indicated that the examiners were calibrated (j for A and B = 0.9; for A and C = 0.95; and for B and C = 0.92). Eisenberg established the essential findings for the diagnosis of LP, as well as other features that could be present or not.3 Furthermore, the presence of two or more exclusion criteria rules out the diagnosis of LP and indicates that the case should be reclassified as lichenoid dysplasia. There was diagnostic agreement between at least two pathologists in all cases. Histological pictures illustrating a case of typical LP and one case diagnosed by the authors as lichenoid dysplasia can be seen in Figures 1 and 2. Forty-nine (40.5%) cases exhibited all essential findings for the diagnosis of LP. Two or more exclusion criteria for the diagnosis of LP were found in the remaining 72 (59.5%) cases. Malignant transformation of oral LP has been contested.3 The major problem of studies evaluating the potential for malignant transformation of LP is the lack of universal and specific criteria for the diagnosis of the disease.4 Eisenberg argues that most cases of malignant transformation described in the literature exhibited variable degrees of epithelial atypia at the time of initial diagnosis, and should therefore be diagnosed as a distinct histopathological entity, i.e.
lichenoid dysplasia.3 His histopathological criteria are important, and contribute to a more objective diagnosis of LP. However, in cases in which two or more exclusion criteria are present, van der Meij and van der Waal5 concluded that it would be more appropriate to refer to them as epithelial dysplasia in histology reports, and treatment would be the same as that recommended for any other epithelial dysplasia. Mignogna et al.6 argued that the inflammatory infiltrate can cause DNA damage, and suggested that the epithelium in LP is more sensitive to conventional environmental carcinogens such as tobacco and alcohol. The inflammatory process itself may cause cellular alterations similar to those found in epithelial dysplasia, which can make differentiation from lichenoid dysplasia difficult.6 On the basis of these arguments, rigorous longterm follow-up is recommended for both patients with LP and those with lichenoid dysplasia to permit the early identification of clinical alterations, particularly in smokers and alcohol drinkers. However, the diagnosis of lichenoid dysplasia requires closer clinical follow-up. Notwithstanding, the present study was a
Figure 1. Histological findings of typical lichen planus. A band-like lymphocytic infiltrate at the epithelial–stromal junction with obfuscation of the basal cell region.
464
Correspondence
1
2
Department of Biosciences and Oral Diagnosis, Department of Social Science and Pediatric Dentistry, Institute of Science and Technology, UNESP – Univ Estadual Paulista, S~ao Jose dos Campos, S~ao Paulo, Brazil, and 3Department of Stomatology, School of Dentistry, University of S~ao Paulo, S~ao Paulo, S~ao Paulo, Brazil
1. Anuradha CH, Reddy BV, Nandan SR, Kumar SR. Oral lichen planus. A review. NY State Dent. J. 2008; 74; 66–68. 2. Van Der Waal I. Potentially malignant disorders of the oral and orapharyngeal mucosa; terminology, classification and present concepts of management. Oral Oncol. 2009; 45; 317– 323. 3. Eisenberg E. Oral lichen planus: a benign lesion. J. Oral Maxillofac. Surg. 2000; 58; 1278–1285. 4. Ismail SB, Kumar SKS, Zain RB. Oral lichen planus and lichenoid reactions: etiopathogenesis, diagnosis, management and malignant transformation. J. Oral Sci. 2007; 49; 89–106. 5. Van der Meij EH, van der Waal I. Lack of clinicopathologic correlation in the diagnosis of oral lichen planus based on the presently available diagnostic criteria and suggestions for modifications. J. Oral Pathol. Med. 2003; 32; 507–512. 6. Mignogna MD, Fedele S, Lo Russo L, Lo Muzio L, Bucci E. Immune activation and chronic inflammation as the cause of malignancy in oral lichen planus: is there any evidence? Oral Oncol. 2004; 40; 120–130. Figure 2. Histological findings of lichenoid dysplasia. Submucosal extension of the lichenoid infiltrate beyond the superficial stroma, with perivascular infiltration.
retrospective analysis of archival cases with a histopathological diagnosis of LP. Only cases described clinically as symmetrical and bilateral reticular lesions on the buccal mucosa were included. Unfortunately, clinical follow-up of all cases was not possible. A diagnosis of oral LP should be based on welldefined criteria in view of the difficulties discussed.
Ethics statement Informed, written consent was obtained. The study was performed according to the Declaration of Helsinki and was approved by the Ethics Committees on Human Research of the Institute of Science and Technology, UNESP - Univ Estadual Paulista (Protocol no. 045/ 2009-PH/CEP) and of the School of Dentistry of the University of S~ao Paulo (FOUSP) (Protocol no. 44/10). M^ onica G Oliveira Alves1 Ivan Balducci2 Yasmin Rodarte Carvalho1 F abio D Nunes3 Janete D Almeida1
p40 immunoperoxidase staining of anorectal carcinomas DOI: 10.1111/his.12470 © 2014 John Wiley & Sons Ltd
Sir: The distinction between squamous cell carcinoma and adenocarcinoma is one of increasing importance at many anatomical sites, not simply with respect to the selection of adjuvant therapy, but also with respect to ancillary testing of tissue from a molecular perspective. Various studies have looked at the sensitivity and specificity with which positive immunoperoxidase staining with p40 antibody can identify squamous cell carcinoma, as opposed to differential diagnoses such as poorly differentiated adenocarcinoma and, on occasion, high-grade lymphoma. These studies have tended to focus upon anatomical sites where both squamous cell carcinoma and adenocarcinoma are known to occur with frequency. These include lung,1,2 uterine cervix3 and gastro-oesophageal junction.4,5 Our study includes some cases from each of these sites and then extends the list of sites investigated by incorporating cases from the anorectal junction. Histopathology
Copyright of Histopathology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Correspondence Oral lichen planus: a histopathological study DOI: 10.1111/his.12538 © 2014 John Wiley & Sons Ltd
Sir: Oral lichen planus (LP) is an immune-mediated disease.1 In 2005, the World Health Organization (WHO) classified it as a potentially malignant disorder,2 but this classification is controversial.3,4 Authors have discussed the criteria used for the diagnosis of oral LP in the cases of malignant transformation reported in the literature.3,4 In view of this controversy, archival cases diagnosed as LP were evaluated using Eisenberg’s histologic criteria3 in order to determine the possibility that cases of lichenoid dysplasia had been diagnosed as LP. A total of 121 archival cases stained with haematoxylin and eosin and diagnosed as LP between 2000 and 2009 were analysed individually by three experienced pathologists (A, B and C). Only those cases with clinical descriptions of symmetrical and bilateral reticular lesions on the buccal mucosa were considered in the study. Cohen’s kappa coefficient indicated that the examiners were calibrated (j for A and B = 0.9; for A and C = 0.95; and for B and C = 0.92). Eisenberg established the essential findings for the diagnosis of LP, as well as other features that could be present or not.3 Furthermore, the presence of two or more exclusion criteria rules out the diagnosis of LP and indicates that the case should be reclassified as lichenoid dysplasia. There was diagnostic agreement between at least two pathologists in all cases. Histological pictures illustrating a case of typical LP and one case diagnosed by the authors as lichenoid dysplasia can be seen in Figures 1 and 2. Forty-nine (40.5%) cases exhibited all essential findings for the diagnosis of LP. Two or more exclusion criteria for the diagnosis of LP were found in the remaining 72 (59.5%) cases. Malignant transformation of oral LP has been contested.3 The major problem of studies evaluating the potential for malignant transformation of LP is the lack of universal and specific criteria for the diagnosis of the disease.4 Eisenberg argues that most cases of malignant transformation described in the literature exhibited variable degrees of epithelial atypia at the time of initial diagnosis, and should therefore be diagnosed as a distinct histopathological entity, i.e.
lichenoid dysplasia.3 His histopathological criteria are important, and contribute to a more objective diagnosis of LP. However, in cases in which two or more exclusion criteria are present, van der Meij and van der Waal5 concluded that it would be more appropriate to refer to them as epithelial dysplasia in histology reports, and treatment would be the same as that recommended for any other epithelial dysplasia. Mignogna et al.6 argued that the inflammatory infiltrate can cause DNA damage, and suggested that the epithelium in LP is more sensitive to conventional environmental carcinogens such as tobacco and alcohol. The inflammatory process itself may cause cellular alterations similar to those found in epithelial dysplasia, which can make differentiation from lichenoid dysplasia difficult.6 On the basis of these arguments, rigorous longterm follow-up is recommended for both patients with LP and those with lichenoid dysplasia to permit the early identification of clinical alterations, particularly in smokers and alcohol drinkers. However, the diagnosis of lichenoid dysplasia requires closer clinical follow-up. Notwithstanding, the present study was a
Figure 1. Histological findings of typical lichen planus. A band-like lymphocytic infiltrate at the epithelial–stromal junction with obfuscation of the basal cell region.
464
Correspondence
1
2
Department of Biosciences and Oral Diagnosis, Department of Social Science and Pediatric Dentistry, Institute of Science and Technology, UNESP – Univ Estadual Paulista, S~ao Jose dos Campos, S~ao Paulo, Brazil, and 3Department of Stomatology, School of Dentistry, University of S~ao Paulo, S~ao Paulo, S~ao Paulo, Brazil
1. Anuradha CH, Reddy BV, Nandan SR, Kumar SR. Oral lichen planus. A review. NY State Dent. J. 2008; 74; 66–68. 2. Van Der Waal I. Potentially malignant disorders of the oral and orapharyngeal mucosa; terminology, classification and present concepts of management. Oral Oncol. 2009; 45; 317– 323. 3. Eisenberg E. Oral lichen planus: a benign lesion. J. Oral Maxillofac. Surg. 2000; 58; 1278–1285. 4. Ismail SB, Kumar SKS, Zain RB. Oral lichen planus and lichenoid reactions: etiopathogenesis, diagnosis, management and malignant transformation. J. Oral Sci. 2007; 49; 89–106. 5. Van der Meij EH, van der Waal I. Lack of clinicopathologic correlation in the diagnosis of oral lichen planus based on the presently available diagnostic criteria and suggestions for modifications. J. Oral Pathol. Med. 2003; 32; 507–512. 6. Mignogna MD, Fedele S, Lo Russo L, Lo Muzio L, Bucci E. Immune activation and chronic inflammation as the cause of malignancy in oral lichen planus: is there any evidence? Oral Oncol. 2004; 40; 120–130. Figure 2. Histological findings of lichenoid dysplasia. Submucosal extension of the lichenoid infiltrate beyond the superficial stroma, with perivascular infiltration.
retrospective analysis of archival cases with a histopathological diagnosis of LP. Only cases described clinically as symmetrical and bilateral reticular lesions on the buccal mucosa were included. Unfortunately, clinical follow-up of all cases was not possible. A diagnosis of oral LP should be based on welldefined criteria in view of the difficulties discussed.
Ethics statement Informed, written consent was obtained. The study was performed according to the Declaration of Helsinki and was approved by the Ethics Committees on Human Research of the Institute of Science and Technology, UNESP - Univ Estadual Paulista (Protocol no. 045/ 2009-PH/CEP) and of the School of Dentistry of the University of S~ao Paulo (FOUSP) (Protocol no. 44/10). M^ onica G Oliveira Alves1 Ivan Balducci2 Yasmin Rodarte Carvalho1 F abio D Nunes3 Janete D Almeida1
p40 immunoperoxidase staining of anorectal carcinomas DOI: 10.1111/his.12470 © 2014 John Wiley & Sons Ltd
Sir: The distinction between squamous cell carcinoma and adenocarcinoma is one of increasing importance at many anatomical sites, not simply with respect to the selection of adjuvant therapy, but also with respect to ancillary testing of tissue from a molecular perspective. Various studies have looked at the sensitivity and specificity with which positive immunoperoxidase staining with p40 antibody can identify squamous cell carcinoma, as opposed to differential diagnoses such as poorly differentiated adenocarcinoma and, on occasion, high-grade lymphoma. These studies have tended to focus upon anatomical sites where both squamous cell carcinoma and adenocarcinoma are known to occur with frequency. These include lung,1,2 uterine cervix3 and gastro-oesophageal junction.4,5 Our study includes some cases from each of these sites and then extends the list of sites investigated by incorporating cases from the anorectal junction. Histopathology
Copyright of Histopathology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
