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The malignant potential of oral lichen planus - reply
Vol. 115 No. 3 March 2013
LETTERS TO THE EDITOR The malignant potential of oral lichen planus— confusion galore To the Editor: We read with interest the article by Bombeccari et al.,1 titled “Oral lichen planus and malignant transformation: a longitudinal study.” This study is one of the few prospective studies on this subject and reports an annual malignant transformation of 0.36%, which is consistent with the data in the published literature.2 The authors state that the revised and modified inclusion criteria proposed by van der Meij et al.3 for oral lichen planus (OLP) was used in the study. On cross referencing, however, we find that these criteria are not reflected as such in the presentation of their results, as the authors fail to make a distinction between OLP and oral lichenoid lesions (OLLs).3 Van der Meij et al. observed a dissonance in the clinical and histopathological criteria in the diagnosis of OLP. They proposed modifications to the criteria for the diagnosis of OLP and OLL.3 Their hypothesis is that OLP does not undergo malignant transformation; it is OLL (as defined by their criteria) that undergoes malignant transformation.2 Moreover, because distinction between OLP and OLL is not well defined by the World Health Organization criteria, this malignant transformation of OLP tends to be overestimated.3 A similar study has found malignant transformation in OLL alone.2 Thus, if these criteria are used, it is important for the results to be presented accordingly to the readers. Furthermore, it would be interesting to review if those OLP cases that underwent malignant transformation were clinically more symptomatic or were recalcitrant to treatment compared with typical OLP. Likewise, it would be informative to identify the defining clinical features that had alerted the clinician that the lichen planus was undergoing malignant transformation. Some studies2,4 have attempted to identify these clearly, and future studies should aim to help develop well-defined criteria that may enable the clinician to better predict malignant transformation. It is time to develop a standard protocol and criteria for diagnosis and reporting of OLP. Venkatraman Sreenivasan, MDS Department of Oral Medicine and Radiology Subharti Dental College and Hospital Swami Vivekanand Subharti University Meerut, India
REFERENCES 1. Bombeccari GP, Guzzi G, Tettamanti M, Giannì AB, Baj A, Pallotti F, Spadari F. Oral lichen planus and malignant transformation: a longitudinal cohort study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2011;112:328-34. 2. van der Meij EH, Mast H, van der Waal I. The possible premalignant character of oral lichen planus and oral lichenoid lesions: a prospective five-year follow-up study of 192 patients. Oral Oncol 2007;43:742-8. 3. 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;32:507-12. 4. Mignogna MD, Fedele S, Lo Russo L. Dysplasia/neoplasia surveillance in oral lichen planus patients: a description of clinical criteria adopted at a single centre and their impact on prognosis. Oral Oncol 2006;42:819-24. http://dx.doi.org/10.1016/j.oooo.2012.08.459
The malignant potential of oral lichen planus - reply In reply: We read the correspondence letter by Venkatraman Sreenivasan1 about our article2 and welcome the opportunity to address the issues raised. Dr. Sreenivasan questions the validity of distinction between oral lichen planus (OLP) and oral lichenoid lesions (OLLs).1 We disagree. In the Materials and Methods section of our original article,2 we clearly stated that we excluded 78 of 493 patients from the study because of “ineligible microscopic appearance.”2 Therefore, these 78 patients were classified according to the differentiation criteria proposed by van der Meij et al.3 and were considered to have OLLs, and, thus, were ineligible for participation in the study. We wanted to focus solely on the incidence of malignant transformation of OLP among adults. We appreciate the questions1 regarding symptoms that precede the onset of malignant transformation of OLP and if the patients were unresponsive to drug treatment. An answer to these questions is beyond the scope of our article. Table I of our article, however, shows that 4 of 8 patients with OLP-OSCC (oral squamous cell carcinoma) who received topical steroids were treated with intraoral application of clobetasol propionate 0.05%.1 None of the patients with OLP-OSCC (n ⫽ 4)1 were unresponsive to topical steroid treatment. As compared with patients who have classical OLP, those who had OLP-OSCC tended to have similar symptoms. Gian Paolo Bombeccari, DDS Francesco Spadari, MD, DDS Department of Biomedical, Surgical, and Dental Sciences 415
LETTERS TO THE EDITOR
OOOO March 2013
416 University of Milan Milan, Italy Gianpaolo Guzzi, DDS Italian Association for Metals and Biocompatibility Research—A.I.R.M.E.B. Milan, Italy Mauro Tettamanti, PhD Laboratory of Geriatric Neuropsychiatry Istituto di Ricerche Farmacologiche “Mario Negri” Milano, Italy Aldo Bruno Giannì, MD Alessandro Baj, MD Complex Unit of Maxillofacial Surgery Fondazione IRCCS CA Granda Ospedale Maggiore Policlinico University of Milan Milan, Italy Francesco Pallotti, MD Unit of Anatomical Pathology Fondazione IRCCS CA Granda Ospedale Maggiore Policlinico University of Milan Milan, Italy REFERENCES 1. Venkatraman S. The malignant potential of Oral Lichen PlanusConfusion galore. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2013 [in press]. 2. Bombeccari GP, Guzzi G, Tettamanti M, Giannì AB, Baj A, Pallotti F, et al. Oral lichen planus and malignant transformation: a longitudinal cohort study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2011;112:328-34. 3. van der Meij EH, van der Waal I. Lack of clinicopathologic correlation in the diagnosis of oral lichen planus based on presently available diagnostic criteria and suggestion for modifications. J Oral Pathol Med 2003;32:507-12. http://dx.doi.org/10.1016/j.oooo.2012.09.089
The role of head and neck cancer anatomic subsites in evaluating the prevalence of human papillomavirus To the Editor: I read with great interest the recent article “Frequency and Genotype Distribution of Multiple Human Papillomavirus Infections in Cancer of the Head and Neck in a Mexican Population,” by Ibieta-Zarco et al.1 Their results were consistent with the current literature, with human papillomavirus (HPV) 16 being the most
prevalent genotype in oropharyngeal cancer. HPV positivity in oropharyngeal cancers was shown to correlate with improved survival (although not significantly) when compared with HPV-negative tumors. Interestingly, the paper highlighted the presence of HPV 56 in some of these cancers, either alone or as a coinfection. My criticism of this paper relates to the selection of their head and neck cancer patients for this study. The authors included 43 patients with various anatomical subsites (18 oropharyngeal, 15 oral cavity, 7 laryngeal, 1 pharyngeal, 1 parotid, 1 maxillary antrum). This sample is underpowered if one is attempting to determine the prevalence of HPV in head and neck cancers in the Mexican population in general. More centers in Mexico should have been included to gather a more representative sample or the patient base should have been larger. Head and neck cancer is a broad term that consists of a heterogenous group of various tumors. Different anatomical subsites may be influenced to varying extents by tobacco, alcohol, UV radiation, or other factors, including HPV. This study is composed of head and neck patients from various sites that have been pooled together. This includes the grouping of parotid tumors with maxillary antral tumors and oral or oropharyngeal tumors, among others. These groups are seldom compared on the basis of pathogenesis or behavior. For example, although lip cancer is anatomically part of the oral cavity, it is not comparable to oral cancer because it is related to UV radiation and sun exposure, whereas oral/oropharyngeal cancer is primarily related to tobacco and alcohol use. The use of these cancers as part of a collective is not appropriate for the purposes of this study. In an evaluation of HPV prevalence, anatomic subsites should be strictly divided because HPV positivity is higher in some anatomic locations (like the oropharynx, especially the tonsils), as emphasized previously in a large meta-analysis by Termine et al.2 Failing to appreciate this division could lead to inappropriate conclusions. Because oropharyngeal cancers were dominant in this study, it is logical to expect higher overall HPV positivity in this “head and neck cancer group” as a collective. Previous literature has shown the oropharynx to have the highest incidence of HPV involvement of these subsites.3 To extrapolate that all head and neck cancers have a high incidence of HPV is misleading when the majority of the cancers in this paper were oropharyngeal. The result biases in favor of this site in comparison with the other less frequently involved sites. To be more accurate, at the very least, equal numbers of patients with oral, oropharyngeal, or laryngeal cancer should have been included. This is in contrast to studies with inclusion of a single maxillary antral carcinoma patient and a solitary patient with pharyngeal cancer. Further, patients with lip cancer should have been
LETTERS TO THE EDITOR The malignant potential of oral lichen planus— confusion galore To the Editor: We read with interest the article by Bombeccari et al.,1 titled “Oral lichen planus and malignant transformation: a longitudinal study.” This study is one of the few prospective studies on this subject and reports an annual malignant transformation of 0.36%, which is consistent with the data in the published literature.2 The authors state that the revised and modified inclusion criteria proposed by van der Meij et al.3 for oral lichen planus (OLP) was used in the study. On cross referencing, however, we find that these criteria are not reflected as such in the presentation of their results, as the authors fail to make a distinction between OLP and oral lichenoid lesions (OLLs).3 Van der Meij et al. observed a dissonance in the clinical and histopathological criteria in the diagnosis of OLP. They proposed modifications to the criteria for the diagnosis of OLP and OLL.3 Their hypothesis is that OLP does not undergo malignant transformation; it is OLL (as defined by their criteria) that undergoes malignant transformation.2 Moreover, because distinction between OLP and OLL is not well defined by the World Health Organization criteria, this malignant transformation of OLP tends to be overestimated.3 A similar study has found malignant transformation in OLL alone.2 Thus, if these criteria are used, it is important for the results to be presented accordingly to the readers. Furthermore, it would be interesting to review if those OLP cases that underwent malignant transformation were clinically more symptomatic or were recalcitrant to treatment compared with typical OLP. Likewise, it would be informative to identify the defining clinical features that had alerted the clinician that the lichen planus was undergoing malignant transformation. Some studies2,4 have attempted to identify these clearly, and future studies should aim to help develop well-defined criteria that may enable the clinician to better predict malignant transformation. It is time to develop a standard protocol and criteria for diagnosis and reporting of OLP. Venkatraman Sreenivasan, MDS Department of Oral Medicine and Radiology Subharti Dental College and Hospital Swami Vivekanand Subharti University Meerut, India
REFERENCES 1. Bombeccari GP, Guzzi G, Tettamanti M, Giannì AB, Baj A, Pallotti F, Spadari F. Oral lichen planus and malignant transformation: a longitudinal cohort study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2011;112:328-34. 2. van der Meij EH, Mast H, van der Waal I. The possible premalignant character of oral lichen planus and oral lichenoid lesions: a prospective five-year follow-up study of 192 patients. Oral Oncol 2007;43:742-8. 3. 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;32:507-12. 4. Mignogna MD, Fedele S, Lo Russo L. Dysplasia/neoplasia surveillance in oral lichen planus patients: a description of clinical criteria adopted at a single centre and their impact on prognosis. Oral Oncol 2006;42:819-24. http://dx.doi.org/10.1016/j.oooo.2012.08.459
The malignant potential of oral lichen planus - reply In reply: We read the correspondence letter by Venkatraman Sreenivasan1 about our article2 and welcome the opportunity to address the issues raised. Dr. Sreenivasan questions the validity of distinction between oral lichen planus (OLP) and oral lichenoid lesions (OLLs).1 We disagree. In the Materials and Methods section of our original article,2 we clearly stated that we excluded 78 of 493 patients from the study because of “ineligible microscopic appearance.”2 Therefore, these 78 patients were classified according to the differentiation criteria proposed by van der Meij et al.3 and were considered to have OLLs, and, thus, were ineligible for participation in the study. We wanted to focus solely on the incidence of malignant transformation of OLP among adults. We appreciate the questions1 regarding symptoms that precede the onset of malignant transformation of OLP and if the patients were unresponsive to drug treatment. An answer to these questions is beyond the scope of our article. Table I of our article, however, shows that 4 of 8 patients with OLP-OSCC (oral squamous cell carcinoma) who received topical steroids were treated with intraoral application of clobetasol propionate 0.05%.1 None of the patients with OLP-OSCC (n ⫽ 4)1 were unresponsive to topical steroid treatment. As compared with patients who have classical OLP, those who had OLP-OSCC tended to have similar symptoms. Gian Paolo Bombeccari, DDS Francesco Spadari, MD, DDS Department of Biomedical, Surgical, and Dental Sciences 415
LETTERS TO THE EDITOR
OOOO March 2013
416 University of Milan Milan, Italy Gianpaolo Guzzi, DDS Italian Association for Metals and Biocompatibility Research—A.I.R.M.E.B. Milan, Italy Mauro Tettamanti, PhD Laboratory of Geriatric Neuropsychiatry Istituto di Ricerche Farmacologiche “Mario Negri” Milano, Italy Aldo Bruno Giannì, MD Alessandro Baj, MD Complex Unit of Maxillofacial Surgery Fondazione IRCCS CA Granda Ospedale Maggiore Policlinico University of Milan Milan, Italy Francesco Pallotti, MD Unit of Anatomical Pathology Fondazione IRCCS CA Granda Ospedale Maggiore Policlinico University of Milan Milan, Italy REFERENCES 1. Venkatraman S. The malignant potential of Oral Lichen PlanusConfusion galore. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2013 [in press]. 2. Bombeccari GP, Guzzi G, Tettamanti M, Giannì AB, Baj A, Pallotti F, et al. Oral lichen planus and malignant transformation: a longitudinal cohort study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2011;112:328-34. 3. van der Meij EH, van der Waal I. Lack of clinicopathologic correlation in the diagnosis of oral lichen planus based on presently available diagnostic criteria and suggestion for modifications. J Oral Pathol Med 2003;32:507-12. http://dx.doi.org/10.1016/j.oooo.2012.09.089
The role of head and neck cancer anatomic subsites in evaluating the prevalence of human papillomavirus To the Editor: I read with great interest the recent article “Frequency and Genotype Distribution of Multiple Human Papillomavirus Infections in Cancer of the Head and Neck in a Mexican Population,” by Ibieta-Zarco et al.1 Their results were consistent with the current literature, with human papillomavirus (HPV) 16 being the most
prevalent genotype in oropharyngeal cancer. HPV positivity in oropharyngeal cancers was shown to correlate with improved survival (although not significantly) when compared with HPV-negative tumors. Interestingly, the paper highlighted the presence of HPV 56 in some of these cancers, either alone or as a coinfection. My criticism of this paper relates to the selection of their head and neck cancer patients for this study. The authors included 43 patients with various anatomical subsites (18 oropharyngeal, 15 oral cavity, 7 laryngeal, 1 pharyngeal, 1 parotid, 1 maxillary antrum). This sample is underpowered if one is attempting to determine the prevalence of HPV in head and neck cancers in the Mexican population in general. More centers in Mexico should have been included to gather a more representative sample or the patient base should have been larger. Head and neck cancer is a broad term that consists of a heterogenous group of various tumors. Different anatomical subsites may be influenced to varying extents by tobacco, alcohol, UV radiation, or other factors, including HPV. This study is composed of head and neck patients from various sites that have been pooled together. This includes the grouping of parotid tumors with maxillary antral tumors and oral or oropharyngeal tumors, among others. These groups are seldom compared on the basis of pathogenesis or behavior. For example, although lip cancer is anatomically part of the oral cavity, it is not comparable to oral cancer because it is related to UV radiation and sun exposure, whereas oral/oropharyngeal cancer is primarily related to tobacco and alcohol use. The use of these cancers as part of a collective is not appropriate for the purposes of this study. In an evaluation of HPV prevalence, anatomic subsites should be strictly divided because HPV positivity is higher in some anatomic locations (like the oropharynx, especially the tonsils), as emphasized previously in a large meta-analysis by Termine et al.2 Failing to appreciate this division could lead to inappropriate conclusions. Because oropharyngeal cancers were dominant in this study, it is logical to expect higher overall HPV positivity in this “head and neck cancer group” as a collective. Previous literature has shown the oropharynx to have the highest incidence of HPV involvement of these subsites.3 To extrapolate that all head and neck cancers have a high incidence of HPV is misleading when the majority of the cancers in this paper were oropharyngeal. The result biases in favor of this site in comparison with the other less frequently involved sites. To be more accurate, at the very least, equal numbers of patients with oral, oropharyngeal, or laryngeal cancer should have been included. This is in contrast to studies with inclusion of a single maxillary antral carcinoma patient and a solitary patient with pharyngeal cancer. Further, patients with lip cancer should have been