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• W2776152832 abstract "Oral potentially malignant disorders (OPMDs) have a statistically increased risk of progressing to cancer, but the risk varies according to a range of patient- or lesion-related factors. It is difficult to predict the risk of progression in any individual patient, and the clinician must make a judgment based on assessment of each case. The most commonly encountered OPMD is leukoplakia, but others, including lichen planus, oral submucous fibrosis, and erythroplakia, may also be seen. Factors associated with an increased risk of malignant transformation include sex; site and type of lesion; habits, such as smoking and alcohol consumption; and the presence of epithelial dysplasia on histologic examination. In this review, we attempt to identify important risk factors and present a simple algorithm that can be used as a guide for risk assessment at each stage of the clinical evaluation of a patient. Oral potentially malignant disorders (OPMDs) have a statistically increased risk of progressing to cancer, but the risk varies according to a range of patient- or lesion-related factors. It is difficult to predict the risk of progression in any individual patient, and the clinician must make a judgment based on assessment of each case. The most commonly encountered OPMD is leukoplakia, but others, including lichen planus, oral submucous fibrosis, and erythroplakia, may also be seen. Factors associated with an increased risk of malignant transformation include sex; site and type of lesion; habits, such as smoking and alcohol consumption; and the presence of epithelial dysplasia on histologic examination. In this review, we attempt to identify important risk factors and present a simple algorithm that can be used as a guide for risk assessment at each stage of the clinical evaluation of a patient. Statement of Clinical RelevanceOral potentially malignant disorders may progress to oral cancer, but assessment of an individual patient's risk is difficult. This review describes the most important risk factors and presents an approach to risk assessment at each stage of the clinical evaluation of a patient. Oral potentially malignant disorders may progress to oral cancer, but assessment of an individual patient's risk is difficult. This review describes the most important risk factors and presents an approach to risk assessment at each stage of the clinical evaluation of a patient. The terminology for oral lesions that may have the potential to progress to malignancy has varied over the years. The term premalignant is commonly used and is widely understood, but it implies that an individual lesion may inevitably become malignant. However, the risk is only statistically increased, and therefore the term potentially malignant, which suggests that the progression to malignancy is only a potential risk, has become more widely accepted.1Warnakulasuriya S. Johnson N.W. van der Waal I. Nomenclature and classification of potentially malignant disorders of the oral mucosa.J Oral Pathol Med. 2007; 36: 575-580Crossref PubMed Scopus (505) Google Scholar Potentially premalignant is an alternative term that is in keeping with the concept that not all lesions—for example, leukoplakia—will have any potential to progress to malignancy and that the clinician is faced with a mucosal change that is only a potentially premalignant lesion. However, this may add confusion because the sentence may be tautologic and conceptually difficult to understand for nonexperts. At a World Health Organization (WHO) workshop in 2007, it was also recommended that the distinction between potentially malignant lesions and conditions be abandoned in favor of a common term, oral potentially malignant disorders (OPMDs),1Warnakulasuriya S. Johnson N.W. van der Waal I. Nomenclature and classification of potentially malignant disorders of the oral mucosa.J Oral Pathol Med. 2007; 36: 575-580Crossref PubMed Scopus (505) Google Scholar, 2Warnakulasuriya S. Reibel J. Bouquot J. Dabelsteen E. Oral epithelial dysplasia classification systems: predictive value, utility, weaknesses and scope for improvement.J Oral Pathol Med. 2008; 3: 127-133Crossref Scopus (284) Google Scholar and this has now been accepted in the latest WHO classification.3Reibel J. Gale N. Hille J. et al.Oral potentially malignant disorders and oral epithelial dysplasia.in: El-Naggar A.K. Chan J.K.C. Grandis J.R. Takata T. Slootweg P.P.J. WHO Classification of Head and Neck Tumours. 4th ed. IARC, Lyon, France2017: 112-115Google Scholar The term OPMD recognizes the fact that even in patients with a defined lesion, such as leukoplakia, malignancy may arise elsewhere in the oral cavity as a result of field change, even in clinically normal mucosa.4Napier S.S. Speight P.M. Natural history of potentially malignant oral lesions and conditions: an overview of the literature.J Oral Pathol Med. 2008; 1: 1-10Google Scholar, 5van der Waal I. Potentially malignant disorders of the oral and oropharyngeal mucosa: terminology, classification and present concepts of management.Oral Oncol. 2009; 45: 317-323Abstract Full Text Full Text PDF PubMed Scopus (355) Google Scholar Numerous disorders have been associated with an increased risk of squamous cell carcinoma (SCC), including leukoplakia, erythroplakia, oral lichen planus, oral submucous fibrosis, actinic cheilitis, palatal lesions of reverse cigar smoking, discoid lupus erythematosus, and some inherited disorders, such as dyskeratosis congenita and Fanconi anemia. From a clinical perspective, the vast majority of lesions of concern present as white patches, with or without a speckled or red component. Many patients with these lesions will not have a specific diagnosis, and the lesions must be managed as leukoplakia. Although these disorders have an increased statistical risk of malignant change, it is very difficult to predict the outcome for an individual patient. This review will focus on leukoplakia, but other disorders will be mentioned where there is evidence of any defined risk factors. The definition of leukoplakia remains unsatisfactory, but essentially, it refers to a white lesion of the oral mucosa that cannot be defined as a known disease or disorder and carries an increased risk of progressing to cancer.1Warnakulasuriya S. Johnson N.W. van der Waal I. Nomenclature and classification of potentially malignant disorders of the oral mucosa.J Oral Pathol Med. 2007; 36: 575-580Crossref PubMed Scopus (505) Google Scholar, 2Warnakulasuriya S. Reibel J. Bouquot J. Dabelsteen E. Oral epithelial dysplasia classification systems: predictive value, utility, weaknesses and scope for improvement.J Oral Pathol Med. 2008; 3: 127-133Crossref Scopus (284) Google Scholar, 3Reibel J. Gale N. Hille J. et al.Oral potentially malignant disorders and oral epithelial dysplasia.in: El-Naggar A.K. Chan J.K.C. Grandis J.R. Takata T. Slootweg P.P.J. WHO Classification of Head and Neck Tumours. 4th ed. IARC, Lyon, France2017: 112-115Google Scholar, 4Napier S.S. Speight P.M. Natural history of potentially malignant oral lesions and conditions: an overview of the literature.J Oral Pathol Med. 2008; 1: 1-10Google Scholar, 5van der Waal I. Potentially malignant disorders of the oral and oropharyngeal mucosa: terminology, classification and present concepts of management.Oral Oncol. 2009; 45: 317-323Abstract Full Text Full Text PDF PubMed Scopus (355) Google Scholar, 6Warnakulasuriya S. Ariyawardana A. Malignant transformation of oral leukoplakia: a systematic review of observational studies.J Oral Pathol Med. 2016; 45: 155-166Crossref PubMed Scopus (21) Google Scholar However, leukoplakia is a dynamic lesion that may vary in texture or color over time and is not always “white.” Indeed, leukoplakias deemed to be at highest risk are often speckled red and white lesions. Pure red lesions, or erythroplakia, are much rarer but have the greatest risk for malignant change.7Reichart P.A. Philipsen H.P. Erythroplakia—a review.Oral Oncol. 2005; 41: 551-561Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar Although progression to cancer is the most significant outcome, only relatively few lesions progress to that stage; the remainder may persist unchanged, may enlarge or reduce in size, or may even resolve completely. Features that may be associated with increased risk of progression to malignancy, along with our estimate of the strength of the association, are listed in Table I. Explanatory notes and relevant references are found in the following sections.Table IFeatures associated with an increased risk of malignant progression of OPMDsFeatureParameterAssociationClinical featuresSize of lesion>200 mm2StrongTextureNonhomogeneousStrongColorRed (or speckled)StrongSiteTongue and floor of mouthStrongSexFemaleMediumAge>50 yearsMediumHabitsNonsmokerWeakHistologic featuresDysplasiaSevereStrongHigh-riskStrongHPV HPV-16 +MediumDNA contentAneuploidyMediumLOHMany genes involvedMediumSee text for discussion and references.HPV, human papillomavirus; LOH, loss of heterozygosity; OPMD, oral potentially malignant disorder. Open table in a new tab See text for discussion and references. HPV, human papillomavirus; LOH, loss of heterozygosity; OPMD, oral potentially malignant disorder. The location of a lesion within the mouth may influence the risk of malignant transformation, but this is almost certainly related to etiologic factors and therefore may vary by geographic location and local habits. For example, in betel quid chewers, the buccal mucosa is likely to be the most affected site, whereas in reverse smokers, it may be the palate. The lateral border of the tongue and the floor of the mouth are anatomically contiguous and, together, are the most common site for OPMDs and oral cancer in the developed world, where smoking of tobacco and alcohol consumption are the most important etiologic factors. In a UK study of 630 patients with dysplastic lesions, over 95% were leukoplakias; the most common sites (42% of lesions) were the lateral and ventral tongue and the floor of mouth.8Jaber M.A. Porter S.R. Speight P.M. et al.Oral epithelial dysplasia: clinical characteristics of western European residents.Oral Oncol. 2003; 39: 589-596Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar In addition, lesions at this site were more likely to show severe epithelial dysplasia. Conversely, only 21% of lesions arose on the buccal mucosa, and these were mostly mild dysplasia. In a similar study in Australia, Dost et al.9Dost F. Lê Cao K.A. Ford P.J. Farah C.S. A retrospective analysis of clinical features of oral malignant and potentially malignant disorders with and without oral epithelial dysplasia.Oral Surg Oral Med Oral Pathol Oral Radiol. 2013; 116: 725-733Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar found that 40% of lesions arose on the tongue and the floor of mouth and that these were more likely to be dysplastic or malignant (odds ratio [OR] 2.6; P = .005). Thirty-one percent of lesions were on the buccal mucosa, but these were less likely to be dysplastic, and none progressed to malignancy. In a cross-sectional study of 3256 leukoplakias in the United States, the highest prevalence of severe dysplasia or carcinoma in situ (CIS) was in the floor of mouth (13.5%) and tongue (5%).10Waldron C.A. Shafer W.G. Leukoplakia revisited. A clinicopathologic study of 3256 oral leukoplakias.Cancer. 1975; 36: 1386-1392Crossref PubMed Google Scholar These data suggest that these sites are at the highest risk, but studies of actual malignant transformation have shown variable findings. In Hungary, although only 8.2% of leukoplakias arose on the tongue, these accounted for 37.5% of the lesions that underwent malignant transformation, equivalent to a transformation rate of 27% for tongue leukoplakias.11Bánóczy J. Follow-up studies in oral leukoplakia.J Maxillofac Surg. 1977; 5: 69-75Abstract Full Text PDF PubMed Scopus (0) Google Scholar The floor of mouth also had a high transformation rate, with 13% of lesions developing into cancer. In contrast, although most of the leukoplakias (63%) were found on the buccal mucosa, only 4% of these lesions progressed.11Bánóczy J. Follow-up studies in oral leukoplakia.J Maxillofac Surg. 1977; 5: 69-75Abstract Full Text PDF PubMed Scopus (0) Google Scholar Similar data have been reported in England, where 2 studies showed high transformation rates of 24%12Kramer I.R.H. El-Labban N. Lee K.W. The clinical features and risk of malignant transformation in sublingual keratosis.Br Dent J. 1978; 144: 171-180Crossref PubMed Google Scholar and 16%13Pogrel P.A. Sublingual keratosis and malignant transformation.J Oral Pathol. 1979; 8: 176-178Crossref PubMed Google Scholar for leukoplakias in the floor of the mouth (sublingual keratosis). In contrast, some studies have been unable to establish a strong correlation between site and malignant transformation. Schepman et al.14Schepman K.P. van der Meij E.H. Smeele L.E. van der Waal I. Malignant transformation of oral leukoplakia: a follow-up study of a hospital-based population of 166 patients with oral leukoplakia in The Netherlands.Oral Oncol. 1998; 34: 270-275Abstract Full Text PDF PubMed Google Scholar studied 101 patients with lesions on the tongue or the floor of mouth; 15 (14.9%) developed oral cancer, compared with 5 of 65 (7.7%) whose lesions were located elsewhere, but this was not statistically significant. In a second study by Dost et al.,15Dost F. Lê Cao K. Ford P.J. Ades C. Farah C.S. Malignant transformation of oral epithelial dysplasia: a real-world evaluation of histopathologic grading.Oral Surg Oral Med Oral Pathol Oral Radiol. 2014; 117: 343-352Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar the malignant potential of 383 dysplastic lesions in 368 patients was determined. Although the tongue (48.8% of lesions) and the floor of mouth (11.5%) together were the most common sites and the tongue had the highest transformation rate of 1.4% per year, the relationship between site and transformation was not significant. Holmstrup et al.16Holmstrup P.P. Vedtofte P.P. Reibel J. Stoltze K. Long-term treatment outcome of oral premalignant lesions.Oral Oncol. 2006; 42: 461-474Abstract Full Text Full Text PDF PubMed Scopus (189) Google Scholar followed up 236 patients with 269 lesions and found a malignant transformation rate of 12% for lesions treated surgically and 4% for lesions only observed. The only significant prognostic factors were size and type of lesion (homogeneous vs nonhomogeneous). The site of the lesions was not significant. In summary, most studies and clinical papers do emphasize the lateral and ventral tongue and the floor of the mouth as areas of particular clinical concern, and this may be attributed to their overexposure to carcinogens as a result of pooling of saliva in alcohol and tobacco users.17Reibel J. Prognosis of oral pre-malignant lesions: significance of clinical, histopathological, and molecular biological characteristics.Crit Rev Oral Biol Med. 2003; 14: 47-62Crossref PubMed Scopus (326) Google Scholar In their systematic review, Warnakulasuriya and Ariyawardana6Warnakulasuriya S. Ariyawardana A. Malignant transformation of oral leukoplakia: a systematic review of observational studies.J Oral Pathol Med. 2016; 45: 155-166Crossref PubMed Scopus (21) Google Scholar found that on a global basis, the buccal mucosa was the most common site overall (18.4% of lesions) but had the lowest rate of malignant transformation (3.35%), whereas the tongue accounted for 16.14% of lesions but was the most common site for transformation, with a rate of 24.22%. The next most common was the combined “tongue and floor of mouth” site, at a rate of 14.85%. However, these data may hide some geographic variations because they may apply to populations with the most common habits of tobacco and alcohol use. In other populations, other sites may be more important and be associated with specific tobacco habits. For example, in Andhra Pradesh, India, 71% of leukoplakias were located on the palate and associated with reverse smoking; in Kerala, 65% were on the buccal mucosa and associated with chewed tobacco.18Gupta P.C. Mehta F.S. Daftary D.K. et al.Incidence rates of oral cancer and natural history of oral precancerous lesions in a 10-year follow-up study of Indian villagers.Community Dent Oral Epidemiol. 1980; 8: 287-333Crossref Google Scholar Oral leukoplakia varies in clinical appearance, and this has led to several definitions that may be complex and confusing. Some lesions are uniformly white or plaque-like, with a flat or wrinkled surface that may contain fine cracks or fissures (“homogeneous leukoplakia”) (Figure 1), whereas others are “nonhomogeneous.” Nonhomogeneous lesions may have various appearances, resulting in a number of clinical terms used. They may have a warty, nodular, or verrucous surface pattern (“nodular” or “verrucous” leukoplakia) or may contain red areas or be speckled (“speckled leukoplakia”) (Figure 2). Speckled lesions may also be called “erythroleukoplakia,” but this should not be confused with erythroplakia, a term that should only be used to describe lesions that are uniformly red.Fig. 2Nonhomogeneous leukoplakia on the lateral border of the tongue. The lesion shows irregular red and white areas and may be termed “speckled leucoplakia.” Histologic examination showed severe epithelial dysplasia.View Large Image Figure ViewerDownload Hi-res image Download (PPT) There is consensus in the literature that nonhomogeneous lesions have a greater risk of malignant transformation compared with homogeneous lesions,2Warnakulasuriya S. Reibel J. Bouquot J. Dabelsteen E. Oral epithelial dysplasia classification systems: predictive value, utility, weaknesses and scope for improvement.J Oral Pathol Med. 2008; 3: 127-133Crossref Scopus (284) Google Scholar, 3Reibel J. Gale N. Hille J. et al.Oral potentially malignant disorders and oral epithelial dysplasia.in: El-Naggar A.K. Chan J.K.C. Grandis J.R. Takata T. Slootweg P.P.J. WHO Classification of Head and Neck Tumours. 4th ed. IARC, Lyon, France2017: 112-115Google Scholar, 4Napier S.S. Speight P.M. Natural history of potentially malignant oral lesions and conditions: an overview of the literature.J Oral Pathol Med. 2008; 1: 1-10Google Scholar, 5van der Waal I. Potentially malignant disorders of the oral and oropharyngeal mucosa: terminology, classification and present concepts of management.Oral Oncol. 2009; 45: 317-323Abstract Full Text Full Text PDF PubMed Scopus (355) Google Scholar, 6Warnakulasuriya S. Ariyawardana A. Malignant transformation of oral leukoplakia: a systematic review of observational studies.J Oral Pathol Med. 2016; 45: 155-166Crossref PubMed Scopus (21) Google Scholar but it can be very difficult to compare studies because of the different locations and different ways of reporting malignant transformation. For example, most large studies in India are population or community based, often involving house-to-house surveys,18Gupta P.C. Mehta F.S. Daftary D.K. et al.Incidence rates of oral cancer and natural history of oral precancerous lesions in a 10-year follow-up study of Indian villagers.Community Dent Oral Epidemiol. 1980; 8: 287-333Crossref Google Scholar whereas most studies in the developed world are based on hospital populations or retrospective analyses of pathology records. However, a systematic review19Petti S. Pooled estimate of world leukoplakia prevalence: a systematic review.Oral Oncol. 2003; 39: 770-780Abstract Full Text Full Text PDF PubMed Scopus (118) Google Scholar found a global leukoplakia prevalence rate of 2.6% and a malignant transformation rate of 1.36% per year. Warnakulasuriya and Ariyawardana6Warnakulasuriya S. Ariyawardana A. Malignant transformation of oral leukoplakia: a systematic review of observational studies.J Oral Pathol Med. 2016; 45: 155-166Crossref PubMed Scopus (21) Google Scholar carried out a systematic review of 24 studies and found an overall malignant transformation rate of 1.5% to 34%, but there was wide variation in the location or type of study. They found 8 studies that compared homogeneous and nonhomogeneous lesions, and all showed that nonhomogeneous lesions had the highest rate of progression. In their summary analysis, Warnakulasuriya and Ariyawardana calculated an overall transformation rate of 3% for homogeneous lesions and 14.5% for nonhomogeneous lesions (P = .001). One of the largest series was published by Bánóczy,11Bánóczy J. Follow-up studies in oral leukoplakia.J Maxillofac Surg. 1977; 5: 69-75Abstract Full Text PDF PubMed Scopus (0) Google Scholar who summarized a series of reports20Bánóczy J. Sugár L. Longitudinal studies in oral leukoplakias.J Oral Pathol. 1972; 1: 265-272Crossref PubMed Google Scholar, 21Bánóczy J. Csiba A. Comparative study of the clinical picture and histologic structure of oral leukoplakia.Cancer. 1976; 29: 1230-1234Crossref Scopus (34) Google Scholar, 22Bánóczy J. Csiba A. Occurrence of epithelial dysplasia in oral leukoplakia.Oral Surg Oral Med Oral Pathol. 1976; 42: 766-774Abstract Full Text PDF PubMed Scopus (0) Google Scholar, 23Bánóczy J. Sugár L. Progressive and regressive changes in Hungarian oral leukoplakias in the course of longitudinal studies.Community Dent Oral Epidemiol. 1975; 3: 194-197Crossref PubMed Google Scholar on a cohort of 670 Hungarian patients. Over a 30-year follow-up period, 6% (40 cases) of leukoplakias progressed to cancer. They divided the lesions into 3 clinical variants: (1) simplex (homogeneous); (2) verrucous; and (3) erosive (speckled) (the latter 2 being nonhomogeneous). None of the homogeneous lesions (simplex) progressed to cancer, whereas the transformation rate for verrucous lesions was 4.6% and that for erosive lesions was 28%. The overall rate for the nonhomogeneous group was 13.4%. Expressing these data in a different way, there were 82 erosive lesions, which accounted for 74% of the oral cancers. The remaining 26% arose from 173 verrucous lesions. Although the actual data may vary, Bánóczy's finding that verrucous and, especially, speckled lesions have the highest rates of progression has been confirmed a number of times. In the largest Indian study to date,18Gupta P.C. Mehta F.S. Daftary D.K. et al.Incidence rates of oral cancer and natural history of oral precancerous lesions in a 10-year follow-up study of Indian villagers.Community Dent Oral Epidemiol. 1980; 8: 287-333Crossref Google Scholar the overall malignant transformation rates were very low (0.3%–2.19%), but homogeneous lesions were much less likely to become malignant. In California, Silverman24Silverman S. Gorsky M. Lozada F. Oral leukoplakia and malignant transformation. A follow-up study of 257 patients.Cancer. 1984; 53: 563-568Crossref PubMed Google Scholar showed that nonhomogeneous lesions (erythroleukoplakia) transformed in 23.4% of cases compared with 6.5% of homogeneous lesions. In a series of Norwegian patients,25Lind P.O. Malignant transformation in oral leukoplakia.Scand J Dent Res. 1987; 95: 449-455PubMed Google Scholar in 14 of 157 patients, leukoplakia developed into cancer, but only 1 of these arose in a homogeneous lesion (1.6%), whereas the remainder arose from nonhomogeneous lesions (13 of 97; 13.4%). Of these, 28 were described as nodular, and 8 became malignant (28.6%). In the study by Holmstrup et al.,16Holmstrup P.P. Vedtofte P.P. Reibel J. Stoltze K. Long-term treatment outcome of oral premalignant lesions.Oral Oncol. 2006; 42: 461-474Abstract Full Text Full Text PDF PubMed Scopus (189) Google Scholar nonhomogeneous lesions showed a 7-fold increase in the risk of progression to cancer compared with homogeneous lesions (OR = 7.0; 95% confidence interval [CI] 1.7-28.5). Of all the factors that they analyzed, the type of lesion was the most significant in predicting prognosis. A characteristic type of nonhomogeneous leukoplakia—proliferative verrucous leukoplakia—has been described and is discussed in the following sections. The use of the terms homogeneous leukoplakia and nonhomogeneous leukoplakia has been severely criticized because this may overemphasize the importance of white lesions and divert clinicians' attention away from the more significant and dangerous red lesions.26Mashberg A. Diagnosis of early oral and oropharyngeal squamous carcinoma: obstacles and their amelioration.Oral Oncol. 2000; 36: 253-255Abstract Full Text Full Text PDF PubMed Scopus (56) Google Scholar As noted earlier, the highest rates of malignant change were noted in lesions that were described as “speckled” or “erosive”11Bánóczy J. Follow-up studies in oral leukoplakia.J Maxillofac Surg. 1977; 5: 69-75Abstract Full Text PDF PubMed Scopus (0) Google Scholar or as “erythroleukoplakia”24Silverman S. Gorsky M. Lozada F. Oral leukoplakia and malignant transformation. A follow-up study of 257 patients.Cancer. 1984; 53: 563-568Crossref PubMed Google Scholar—in other words, emphasizing that these lesions are not, in fact, true “leukoplakias” (white plaques) but have a red component. The seminal work of Mashberg is well known, and although he did not primarily study OPMDs, he showed that most early oral cancers are red or have a significant red component (“erythroplasia”).27Mashberg A. Morrissey J.B. Garfinkel L. A study of the appearance of early asymptomatic oral squamous cell carcinoma.Cancer. 1973; 32: 1436-1445Crossref PubMed Google Scholar, 28Mashberg A. Samit A. Early diagnosis of asymptomatic oral and oropharyngeal squamous cancers.CA Cancer J Clin. 1995; 45: 328-351Crossref PubMed Google Scholar In his first major study on this subject,27Mashberg A. Morrissey J.B. Garfinkel L. A study of the appearance of early asymptomatic oral squamous cell carcinoma.Cancer. 1973; 32: 1436-1445Crossref PubMed Google Scholar Mashberg identified 158 asymptomatic, early lesions in 125 patients. One hundred and twelve lesions were invasive SCCs, and 46 were CIS. His major finding, which formed the basis of his later work and opinions,26Mashberg A. Diagnosis of early oral and oropharyngeal squamous carcinoma: obstacles and their amelioration.Oral Oncol. 2000; 36: 253-255Abstract Full Text Full Text PDF PubMed Scopus (56) Google Scholar, 28Mashberg A. Samit A. Early diagnosis of asymptomatic oral and oropharyngeal squamous cancers.CA Cancer J Clin. 1995; 45: 328-351Crossref PubMed Google Scholar was that greater than 90% of the lesions had a red component and that only 14 (9%) were described as white (of which 9 were located on the lips). Sixty lesions (38%) were entirely red, and an additional 98 (62%) were red and white (speckled, stippled, or patchy). In later studies (reviewed by Mashberg and Samit28Mashberg A. Samit A. Early diagnosis of asymptomatic oral and oropharyngeal squamous cancers.CA Cancer J Clin. 1995; 45: 328-351Crossref PubMed Google Scholar), Mashberg confirmed these findings in a cohort of 236 asymptomatic cancers, of which only 6% were white. The remainder were entirely red (32%), had a predominant red component (32%), or were mixed (29%). In his reviews,26Mashberg A. Diagnosis of early oral and oropharyngeal squamous carcinoma: obstacles and their amelioration.Oral Oncol. 2000; 36: 253-255Abstract Full Text Full Text PDF PubMed Scopus (56) Google Scholar, 28Mashberg A. Samit A. Early diagnosis of asymptomatic oral and oropharyngeal squamous cancers.CA Cancer J Clin. 1995; 45: 328-351Crossref PubMed Google Scholar Mashberg emphasized the importance of redness as an early sign of cancer and expressed dismay at the overemphasis of “leukoplakia” as a premalignant condition, which, he claimed, is a major cause of the lack of progress in early diagnosis of cancer. Erythroplakia is a well-defined clinical lesion,3Reibel J. Gale N. Hille J. et al.Oral potentially malignant disorders and oral epithelial dysplasia.in: El-Naggar A.K. Chan J.K.C. Grandis J.R. Takata T. Slootweg P.P.J. WHO Classification of Head and Neck Tumours. 4th ed. IARC, Lyon, France2017: 112-115Google Scholar, 7Reichart P.A. Philipsen H.P. Erythroplakia—a review.Oral Oncol. 2005; 41: 551-561Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar but Mashberg's opinion is correct in that erythroplakia is often not included in studies of OPMDs4Napier S.S. Speight P.M. Natural history of potentially malignant oral lesions and conditions: an overview of the literature.J Oral Pathol Med. 2008; 1: 1-10Google Scholar, 6Warnakulasuriya S. Ariyawardana A. Malignant transformation of oral leukoplakia: a systematic review of observational studies.J Oral Pathol Med. 2016; 45: 155-166Crossref PubMed Scopus (21) Google Scholar, 10Waldron C.A. Shafer W.G. Leukoplakia revisited. A clinicopathologic study of 3256 oral leukoplakias.Cancer. 1975; 36: 1386-1392Crossref PubMed Google Scholar, 11Bánóczy J. Follow-up studies in oral leukoplakia.J Maxillofac Surg. 1977; 5: 69-75Abstract Full Text PDF PubMed Scopus (0) Google Scholar, 17Reibel J. Prognosis of oral pre-malignant lesions: significance of clinical, histopathological, and molecular biological characteristics.Crit Rev Oral Biol Med. 2003; 14: 47-62Crossref PubMed Scopus (326) Google Scholar—probably because it is relatively uncommon and therefore more difficult to study. In their survey of 50,915 Indian patients, Mehta et al.29Mehta F.S. Pindborg J.J. Gupta P.C. Daftary D.K. Epidemiologic and histologic study of oral cancer and leukoplakia among 50,915 villagers in India.Cancer. 1969; 24: 832-849Crossref PubMed Google Scholar found 881 leukoplakias (1.73%) but only 9 cases of erythroplakia (0.02%). In the United States, only 58 cases were ident" @default.
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• W2776152832 title "Oral potentially malignant disorders: risk of progression to malignancy" @default.
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