A man with a 30-year history of oral lesions
Identifieur interne : 000607 ( Istex/Corpus ); précédent : 000606; suivant : 000608A man with a 30-year history of oral lesions
Auteurs : Mark Drangsholt ; Edmond L. Truelove ; Thomas H. Morton Jr ; Joel B. EpsteinSource :
- Journal of Evidence-Based Dental Practice [ 1532-3382 ] ; 2001.
English descriptors
- KwdEn :
- Bone loss, Buccal mucosa, Cancer cases, Cancer development, Carcinoma, Cell carcinoma, Clin cancer, Clinical characteristics, Clinical practice, Clinical service, Cohort study, Dental practice october, Dental practice volume, Differential diagnosis, Drangsholt, Erosive, Erosive lichen planus, Future malignancy, General population, Gingiva, Hard palate, Histopathologic diagnosis, Incidence rate, Incidence rates, Lesion, Leukoplakia, Leukoplakia studies, Lichen, Lichen planus, Lichenoid dysplasia, Long history, Main question, Malignant, Malignant disease, Malignant transformation, Maxillary, Maxillary sinus, Mucosal changes, Neoplastic lesion, Normal limits, Oral cancer, Oral cavity, Oral disease, Oral erosive lichen planus, Oral lesions, Oral leukoplakia, Oral lichen planus, Oral maxillofac surg, Oral oncol, Oral pathol, Oral surg, Oscc, Other risk factors, Pathol, Periodontal, Periodontal bone loss, Periodontal disease, Periodontal therapy, Planus, Posterior teeth, Premalignant lesion, Prognosis, Prognostic factors, Proliferative, Proliferative verrucous leukoplakia, Radiol endod, Relative risk, Relative risks, Risk factors, Scenario, Several regions, Silverman, Specific criteria, Squamous cell carcinoma, Subsequent development, Surg, Time periods, Transformation percentage, Transformation percentages range, Treatment responses, True incidence rate, Verrucous.
- Teeft :
- Bone loss, Buccal mucosa, Cancer cases, Cancer development, Carcinoma, Cell carcinoma, Clin cancer, Clinical characteristics, Clinical practice, Clinical service, Cohort study, Dental practice october, Dental practice volume, Differential diagnosis, Drangsholt, Erosive, Erosive lichen planus, Future malignancy, General population, Gingiva, Hard palate, Histopathologic diagnosis, Incidence rate, Incidence rates, Lesion, Leukoplakia, Leukoplakia studies, Lichen, Lichen planus, Lichenoid dysplasia, Long history, Main question, Malignant, Malignant disease, Malignant transformation, Maxillary, Maxillary sinus, Mucosal changes, Neoplastic lesion, Normal limits, Oral cancer, Oral cavity, Oral disease, Oral erosive lichen planus, Oral lesions, Oral leukoplakia, Oral lichen planus, Oral maxillofac surg, Oral oncol, Oral pathol, Oral surg, Oscc, Other risk factors, Pathol, Periodontal, Periodontal bone loss, Periodontal disease, Periodontal therapy, Planus, Posterior teeth, Premalignant lesion, Prognosis, Prognostic factors, Proliferative, Proliferative verrucous leukoplakia, Radiol endod, Relative risk, Relative risks, Risk factors, Scenario, Several regions, Silverman, Specific criteria, Squamous cell carcinoma, Subsequent development, Surg, Time periods, Transformation percentage, Transformation percentages range, Treatment responses, True incidence rate, Verrucous.
Abstract
Abstract: J Evid Base Dent Pract 2001;1:123-35
Url:
DOI: 10.1016/S1532-3382(01)70023-1
Links to Exploration step
ISTEX:0CA8E54EB7710A466E209D357405273965C1CABDLe document en format XML
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development</term><term>Carcinoma</term><term>Cell carcinoma</term><term>Clin cancer</term><term>Clinical characteristics</term><term>Clinical practice</term><term>Clinical service</term><term>Cohort study</term><term>Dental practice october</term><term>Dental practice volume</term><term>Differential diagnosis</term><term>Drangsholt</term><term>Erosive</term><term>Erosive lichen planus</term><term>Future malignancy</term><term>General population</term><term>Gingiva</term><term>Hard palate</term><term>Histopathologic diagnosis</term><term>Incidence rate</term><term>Incidence rates</term><term>Lesion</term><term>Leukoplakia</term><term>Leukoplakia studies</term><term>Lichen</term><term>Lichen planus</term><term>Lichenoid dysplasia</term><term>Long history</term><term>Main question</term><term>Malignant</term><term>Malignant disease</term><term>Malignant transformation</term><term>Maxillary</term><term>Maxillary sinus</term><term>Mucosal changes</term><term>Neoplastic lesion</term><term>Normal limits</term><term>Oral cancer</term><term>Oral cavity</term><term>Oral disease</term><term>Oral erosive lichen planus</term><term>Oral lesions</term><term>Oral leukoplakia</term><term>Oral lichen planus</term><term>Oral maxillofac surg</term><term>Oral oncol</term><term>Oral pathol</term><term>Oral surg</term><term>Oscc</term><term>Other risk factors</term><term>Pathol</term><term>Periodontal</term><term>Periodontal bone loss</term><term>Periodontal disease</term><term>Periodontal therapy</term><term>Planus</term><term>Posterior teeth</term><term>Premalignant lesion</term><term>Prognosis</term><term>Prognostic factors</term><term>Proliferative</term><term>Proliferative verrucous leukoplakia</term><term>Radiol endod</term><term>Relative risk</term><term>Relative risks</term><term>Risk factors</term><term>Scenario</term><term>Several regions</term><term>Silverman</term><term>Specific criteria</term><term>Squamous cell carcinoma</term><term>Subsequent 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Truelove</json:string></persName><placeName><json:string>United States</json:string><json:string>US</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Drangsholt et al</json:string><json:string>June 2000</json:string><json:string>June 1992</json:string><json:string>Kleinman et al 1991</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-CF44M0MH-G</json:string></ark><categories><wos></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - dentistry</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Dentistry</json:string><json:string>3 - General Dentistry</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences biologiques fondamentales et appliquees. psychologie</json:string></inist></categories><publicationDate>2001</publicationDate><copyrightDate>2001</copyrightDate><doi><json:string>10.1016/S1532-3382(01)70023-1</json:string></doi><id>0CA8E54EB7710A466E209D357405273965C1CABD</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/0CA8E54EB7710A466E209D357405273965C1CABD/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/0CA8E54EB7710A466E209D357405273965C1CABD/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/0CA8E54EB7710A466E209D357405273965C1CABD/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">A man with a 30-year history of oral lesions</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>©2001 Mosby, Inc.</p></availability><date>2001</date></publicationStmt><notesStmt><note type="content">Section title: Evidence-Based Case Conference</note><note type="content">: Table. Studies of malignant transformation of oral lichen planus and leukoplakia into oral squamous cell carcinoma</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">A man with a 30-year history of oral lesions</title><author xml:id="author-0000"><persName><forename type="first">Mark</forename><surname>Drangsholt</surname></persName><roleName type="degree">DDS, MPHa,b</roleName><affiliation>From the Departments of Oral Medicine,a Dental Public Health Sciences,b and Oral Biology,c School of Dentistry, University of Washington, Seattle</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Edmond L.</forename><surname>Truelove</surname></persName><roleName type="degree">DDS, MSD</roleName><affiliation>From the Departments of Oral Medicine,a Dental Public Health Sciences,b and Oral Biology,c School of Dentistry, University of Washington, Seattle</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Thomas H.</forename><surname>Morton, Jr</surname></persName><roleName type="degree">DDS, MSDa,c</roleName><affiliation>From the Departments of Oral Medicine,a Dental Public Health Sciences,b and Oral Biology,c School of Dentistry, University of Washington, Seattle</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Joel B.</forename><surname>Epstein</surname></persName><roleName type="degree">DMD, MSD, FRCD(C)a</roleName><affiliation>From the Departments of Oral Medicine,a Dental Public Health Sciences,b and Oral Biology,c School of Dentistry, University of Washington, Seattle</affiliation></author><idno type="istex">0CA8E54EB7710A466E209D357405273965C1CABD</idno><idno type="DOI">10.1016/S1532-3382(01)70023-1</idno><idno type="PII">S1532-3382(01)70023-1</idno></analytic><monogr><title level="j">Journal of Evidence-Based Dental Practice</title><title level="j" type="abbrev">YMED</title><idno 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article"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 5.0.1//EN//XML" URI="art501.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="gr2"></istex:entity><istex:entity SYSTEM="gr3" NDATA="IMAGE" name="gr3"></istex:entity><istex:entity SYSTEM="gr4" NDATA="IMAGE" name="gr4"></istex:entity><istex:entity SYSTEM="gr5" NDATA="IMAGE" name="gr5"></istex:entity><istex:entity SYSTEM="gr6" NDATA="IMAGE" name="gr6"></istex:entity><istex:entity SYSTEM="gr7" NDATA="IMAGE" name="gr7"></istex:entity><istex:entity SYSTEM="gr8" NDATA="IMAGE" name="gr8"></istex:entity></istex:docType><istex:document><article docsubtype="fla" xml:lang="en"><item-info><jid>YMED</jid><aid>0010121</aid><ce:pii>S1532-3382(01)70023-1</ce:pii><ce:doi>10.1016/S1532-3382(01)70023-1</ce:doi><ce:copyright type="full-transfer" year="2001">Mosby, Inc.</ce:copyright></item-info><ce:floats><ce:table id="tab1" colsep="0" rowsep="0" frame="topbot"><ce:caption><ce:simple-para><ce:bold>Table.</ce:bold> Studies of malignant transformation of oral lichen planus and leukoplakia into oral squamous cell carcinoma</ce:simple-para></ce:caption><tgroup cols="10"><colspec colname="col1" colsep="0"></colspec><colspec colname="col2" colsep="0"></colspec><colspec colname="col3" colsep="0"></colspec><colspec colname="col4" colsep="0"></colspec><colspec colname="col5" colsep="0"></colspec><colspec colname="col6" colsep="0"></colspec><colspec colname="col7" colsep="0"></colspec><colspec colname="col8" colsep="0"></colspec><colspec colname="col9" colsep="0"></colspec><colspec colname="col10" colsep="0"></colspec><thead><row rowsep="1" valign="bottom"><entry>First author</entry><entry align="center">Pub. year</entry><entry align="center">No. of subjects</entry><entry align="center">Mean follow-up time (y)</entry><entry align="center">Outcome</entry><entry align="center">Malignant events</entry><entry align="center">Crude transformation rate (%)</entry><entry align="center">Calc. cancer incidence rate</entry><entry align="center">Rate per 1000 person-years</entry><entry align="center">Crude relative risk</entry></row></thead><tbody><row><entry>OLP</entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Mignogna</entry><entry align="center">2001</entry><entry align="center">502</entry><entry align="center">3.0*</entry><entry align="center">OSCC</entry><entry align="center">18</entry><entry align="center">3.6%</entry><entry align="center">0.01195</entry><entry align="center">12.0</entry><entry align="center">34.3</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Chainani-Wu</entry><entry align="center">2001</entry><entry align="center">229</entry><entry align="center">4.0*</entry><entry align="center">OSCC</entry><entry align="center">4</entry><entry align="center">1.7%</entry><entry align="center">0.00437</entry><entry align="center">4.4</entry><entry align="center">12.5</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Markopoulos</entry><entry align="center">1997</entry><entry align="center">326</entry><entry align="center">4.8</entry><entry align="center">OSCC</entry><entry align="center">4</entry><entry align="center">1.2%</entry><entry align="center">0.00256</entry><entry align="center">2.6</entry><entry align="center">7.3</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Silverman</entry><entry align="center">1997</entry><entry align="center">95</entry><entry align="center">6.1</entry><entry align="center">OSCC</entry><entry align="center">3</entry><entry align="center">3.2%</entry><entry align="center">0.00518</entry><entry align="center">5.2</entry><entry align="center">14.9</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Barnard</entry><entry align="center">1993</entry><entry align="center">241</entry><entry align="center">10*</entry><entry align="center">OSCC</entry><entry align="center">9</entry><entry align="center">3.7%</entry><entry align="center">0.00373</entry><entry align="center">3.7</entry><entry align="center">10.7</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Brown</entry><entry align="center">1993</entry><entry align="center">193</entry><entry align="center">4.5*</entry><entry align="center">OSCC</entry><entry align="center">0</entry><entry align="center">0.0%</entry><entry align="center">0.00000</entry><entry align="center">0.0</entry><entry align="center">na</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Voute</entry><entry align="center">1992</entry><entry align="center">113</entry><entry align="center">7.8</entry><entry align="center">OSCC</entry><entry align="center">3</entry><entry align="center">2.7%</entry><entry align="center">0.00340</entry><entry align="center">3.4</entry><entry align="center">9.8</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Silverman</entry><entry align="center">1991</entry><entry align="center">214</entry><entry align="center">7.5</entry><entry align="center">OSCC</entry><entry align="center">5</entry><entry align="center">2.3%</entry><entry align="center">0.00312</entry><entry align="center">3.1</entry><entry align="center">9.0</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Salem</entry><entry align="center">1989</entry><entry align="center">72</entry><entry align="center">3.2</entry><entry align="center">OSC</entry><entry align="center">4</entry><entry align="center">5.6%</entry><entry align="center">0.00730</entry><entry align="center">7.3</entry><entry align="center">21.0</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Holmstrup</entry><entry align="center">1988</entry><entry align="center">611</entry><entry align="center">7.5</entry><entry align="center">OSCC</entry><entry align="center">9</entry><entry align="center">1.5%</entry><entry align="center">0.00196</entry><entry align="center">2.0</entry><entry align="center">5.6</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Average</entry><entry align="center">5.8</entry><entry align="center">2.5%</entry><entry align="center">0.00436</entry><entry align="center">4.4</entry><entry align="center">12.5</entry><entry></entry><entry></entry><entry></entry><entry></entry></row><row><entry>Leukoplakia</entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Saito</entry><entry align="center">2001</entry><entry align="center">142</entry><entry align="center">4.0</entry><entry align="center">OSCC</entry><entry align="center">9</entry><entry align="center">6.3%</entry><entry align="center">0.0158</entry><entry align="center">15.8</entry><entry align="center">45.5</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Sudbo</entry><entry align="center">2001</entry><entry align="center">150</entry><entry align="center">8.6</entry><entry align="center">OSCC</entry><entry align="center">36</entry><entry align="center">24.0%</entry><entry align="center">0.0280</entry><entry align="center">28.0</entry><entry align="center">80.3</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Lee</entry><entry align="center">2000</entry><entry align="center">70</entry><entry align="center">7.0</entry><entry align="center">OSCC</entry><entry align="center">22</entry><entry align="center">31.4%</entry><entry align="center">0.0449</entry><entry align="center">44.9</entry><entry align="center">129</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Schepman</entry><entry align="center">1999</entry><entry align="center">166</entry><entry align="center">2.4</entry><entry align="center">OSCC</entry><entry align="center">20</entry><entry align="center">12.0%</entry><entry align="center">0.0498</entry><entry align="center">49.8**</entry><entry align="center">143</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Average</entry><entry align="center">6</entry><entry align="center">21.7%</entry><entry align="center">0.0362</entry><entry align="center">36.4</entry><entry align="center">104.0</entry><entry></entry><entry></entry><entry></entry><entry></entry></row><row><entry>PVL</entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Chang</entry><entry align="center">2000</entry><entry align="center">53</entry><entry align="center">3.5</entry><entry align="center">OSCC</entry><entry align="center">22</entry><entry align="center">41.5%</entry><entry align="center">0.1186</entry><entry align="center">118.6</entry><entry align="center">341</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Silverman</entry><entry align="center">1997</entry><entry align="center">54</entry><entry align="center">11.6</entry><entry align="center">OSCC</entry><entry align="center">38</entry><entry align="center">70.4%</entry><entry align="center">0.0607</entry><entry align="center">60.7</entry><entry align="center">174</entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Average</entry><entry align="center">7.6</entry><entry align="center">55.9%</entry><entry align="center">0.0896</entry><entry align="center">89.6</entry><entry align="center">258</entry><entry></entry><entry></entry><entry></entry><entry></entry></row><row><entry namest="col1" nameend="col2" align="center">General population in United States</entry><entry colname="col3" align="center"></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry><entry></entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Kleinman et al</entry><entry align="center">1991</entry><entry align="center">all adults</entry><entry align="center">1.0</entry><entry align="center">cancer of oral cavity</entry><entry align="center">0.0078%</entry><entry align="center">0.000078</entry><entry align="center">0.08</entry><entry align="center">0.22</entry><entry></entry></row><row><entry><ce:hsp sp="1.0"></ce:hsp>Kleinman et al</entry><entry align="center">1991</entry><entry align="center">adults aged 70-74</entry><entry align="center">1</entry><entry align="center">cancer of oral cavity</entry><entry align="center">0.035%</entry><entry align="center">0.000348</entry><entry align="center">0.35</entry><entry align="center">1.0***</entry><entry></entry></row><row><entry namest="col1" nameend="col10">*Estimated from study. **Incidence rate calculated in the study is 29.0 per 1000 person-years. ***Reference group: “unexposed” to OLP or PVL.</entry></row></tbody></tgroup><ce:legend><ce:simple-para><ce:italic>OLP,</ce:italic> Oral lichen planus; <ce:italic>OSCC,</ce:italic> oral squamous cell carcinoma; <ce:italic>PVL,</ce:italic> proliferative verrucous leukoplakia.</ce:simple-para></ce:legend></ce:table></ce:floats><head><ce:dochead><ce:textfn>Evidence-Based Case Conference</ce:textfn></ce:dochead><ce:title>A man with a 30-year history of oral lesions</ce:title><ce:author-group><ce:author><ce:given-name>Mark</ce:given-name><ce:surname>Drangsholt</ce:surname><ce:degrees>DDS, MPH<ce:sup>a,b</ce:sup></ce:degrees></ce:author><ce:author><ce:given-name>Edmond L.</ce:given-name><ce:surname>Truelove</ce:surname><ce:degrees>DDS, MSD</ce:degrees></ce:author><ce:author><ce:given-name>Thomas H.</ce:given-name><ce:surname>Morton</ce:surname><ce:suffix>Jr</ce:suffix><ce:degrees>DDS, MSD<ce:sup>a,c</ce:sup></ce:degrees></ce:author><ce:author><ce:given-name>Joel B.</ce:given-name><ce:surname>Epstein</ce:surname><ce:degrees>DMD, MSD, FRCD(C)<ce:sup>a</ce:sup></ce:degrees></ce:author><ce:affiliation><ce:textfn>From the Departments of Oral Medicine,<ce:sup>a</ce:sup> Dental Public Health Sciences,<ce:sup>b</ce:sup> and Oral Biology,<ce:sup>c</ce:sup> School of Dentistry, University of Washington, Seattle</ce:textfn></ce:affiliation></ce:author-group><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>J Evid Base Dent Pract 2001;1:123-35</ce:simple-para></ce:abstract-sec></ce:abstract></head><body><ce:sections><ce:para>A 70-year-old man was admitted to the clinical service with a complaint of oral lesions that had been present intermittently for more than 30 years. The mucosal changes had begun without specifically known triggering factors and had gradually involved several regions of the oral cavity, including the left and right buccal mucosa, the attached gingiva throughout all regions of his dentate mouth, part of the hard palate, and on the lateral borders of his tongue. Changes had not occurred in the tissue of the floor of the mouth, soft palate, or lips. His symptoms were mild and normally consisted of only slight discomfort during ingestion of salty, spicy, or acidic foods. Over the years, clinical assessment by his dentists had never demonstrated a significant or alarming progression of the lesions. His consultation with a local oral surgeon established a clinical diagnosis of erosive oral lichen planus (OLP), which was confirmed by means of a tissue biopsy. He was then followed up periodically. The patient described many episodes of flares and complete remission of the lesions over the years. In 1992, prior to being admitted to our service, changes on the maxillary attached gingiva in the region of tooth numbers 12 and 13 were observed and biopsied, and a histopathologic diagnosis of proliferative verrucous leukoplakia was established for that lesion. No evidence of malignant transformation was detected in the tissue samples, although mild dysplasia was noted.</ce:para><ce:para><ce:italic>Clinical and pathologic diagnoses, 1992: erosive lichen planus of the gingiva, palate, tongue and buccal mucosa, and proliferative verrucous leukoplakia (PVL) of the maxillary gingiva.</ce:italic></ce:para><ce:para>After the biopsy, the lesion was excised and the patient's name was placed on a recall program in our service. He was advised that his long history of erosive OLP and the recent development of PVL potentially increased his risk for oral cancer, and he agreed to be followed up on a regular basis and to return to our clinic immediately if other tissue changes developed. Over the next 6.5 years he was followed up, at least annually, and episodes of symptoms were treated with dexamethasone rinses and topical antifungal medications. No clinical changes were evident on each of 9 follow-up visits. The lesions continued to have the same classical clinical characteristics of oral erosive lichen planus as was seen before the surgical treatment, with no clinical evidence of progression or new lesion development.</ce:para><ce:section><ce:section-title>History and examination</ce:section-title><ce:section><ce:section-title>Medical and dental history</ce:section-title><ce:para>The patient reported that although he had been hospitalized several times in the past—including treatment of pneumonia at age 30, which resolved without residual complications, and for cataract removal—his health was excellent. Other prior health problems included arthritis (which he treated symptomatically with occasional use of naproxen), biopsy-confirmed benign prostatic hypertrophy, a cyst of the left kidney, and chronic nonspecific dermal changes on his shins. He also suffered from occasional bouts of back spasms. As a young adult, he had smoked a pipe but discontinued the use of tobacco 25 years earlier. He denied heavy use of alcohol but did report drinking 2 beers a day, with meals. For cardiac prevention, he took an aspirin each day without any adverse side effects. His past dental care had been episodic and included problems with caries and periodontal disease, which resulted in extensive dental treatment and extraction of all molars except for tooth #3 and placement of 2 implants replacing numbers 30 and 31. The remaining teeth had been restored with amalgam and cast restorations.</ce:para></ce:section><ce:section><ce:section-title>Psychosocial history</ce:section-title><ce:para>The patient was a retired engineer, married, with a positive attitude and no history of depression or other psychological problems. His life was very active in social, cultural, and physical activities that included remodeling and yard work. His major recreational activity was regular tennis matches.</ce:para></ce:section><ce:section><ce:section-title>Physical examination</ce:section-title><ce:para>The patient was pleasant, cooperative and articulate. His general appearance was that of a healthy and stable elder man with no obvious structural defects of the head, neck, or appendages. He weighed 66.1 kg and had a blood pressure of 139/78 mm Hg, a pulse of 64 beats/min, a respiration rate of 12 breaths/min, and a temperature of 36.5° C. His skeletal morphology was within normal limits, and no skin lesions were detectable on exposed facial or neck surfaces. Extraoral structures of the head and neck were examined and found to be normal, with no evidence of changes in the skin except for rosacea on the cheeks. The salivary glands and musculoskeletal structures were within normal limits, and no sensory or motor defects were evident during inspection and normal facial movements. Palpation of soft tissues of the face, neck, and floor of the mouth detected routine palpable, but not indurated or tender, lymph nodes. The lips were also within normal limits, as was the tissue of the maxillary and mandibular labial mucosa. The posterior right and left buccal mucosa exhibited a number of superficial changes, including patches of erythema with overlying white stria (Fig 1).
<ce:display><ce:figure><ce:label>Fig. 1</ce:label><ce:caption><ce:simple-para>Photograph of the right (<ce:bold>A</ce:bold>) and left (<ce:bold>B</ce:bold>) buccal mucosa taken when patient entered clinic show very mild inflammation and the presence of white stria on the right that are characteristic of lichen planus. On the left the stria are also clearly seen but the epithelium also demonstrates significant amount of inflammation that is common in erosive lichen planus.</ce:simple-para></ce:caption> <ce:link locator="gr1"></ce:link></ce:figure></ce:display>No areas of ulceration, induration, or tissue thickening could be detected. The hard palate was generally normal, except for a 1.5-cm zone of erythema with sparse white stria that covered the edentulous alveolar ridge and attached gingiva around the posterior teeth. Periodontal bone loss was evident, as was gingivitis, resulting from inadequate oral hygiene. A failing root canal was present in tooth #7. No residual verruciform lesions remained.</ce:para></ce:section><ce:section><ce:section-title>Radiographic examination</ce:section-title><ce:para>Panoramic and periapical radiographs of the mouth were ordered (Fig 2), as was a fine-cut CT scan.
<ce:display><ce:figure><ce:label>Fig. 2</ce:label><ce:caption><ce:simple-para>Photograph of gingival proliferative verrucous leukoplakia of the posterior maxillary region (example from another patient).</ce:simple-para></ce:caption> <ce:link locator="gr2"></ce:link></ce:figure></ce:display>The structures of the jaws were normal, with no evidence of osseous lesions or invasion of the tumor into underlying tissues. The posterior eden-tulous spaces and maxillary sinuses were visualized. Tooth #7 was failing and had periapical changes evident on the film. Periodontal bone loss was evident in several regions of the mouth. The pulp chambers in a number of teeth appeared to be obliterated but the implants replacing numbers 30 and 31 appeared to be well integrated.</ce:para></ce:section><ce:section><ce:section-title>Follow-up history and examination</ce:section-title><ce:para>In June 2000, the patient returned after a 26-month absence (which was 14 months later than the recommended follow-up date). He reported that 6 months earlier he had noticed that it “felt funny and rough” around his maxillary posterior teeth and that he had consulted his dentist, who thought that the changes were the result of advancing periodontal disease. The dentist treated the area with a chlorhexidine rinse and periodontal therapy, including curettage and scaling. But the lesion progressed, and the patient again sought evaluation in our clinic at the university. His medical history was generally unchanged, except for the notable additions of a diagnosis of colon cancer, which had been successfully treated with a colectomy, without radiation or chemotherapy. He also had a nasal operation performed to repair a deviated septum in 1999. He reported drinking a glass of wine with dinner, which had replaced his daily use of beer.</ce:para><ce:para>Physical examination revealed that the tissue around the maxillary bicuspids had undergone significant proliferative expansion and no longer had the clinical characteristics of OLP (Fig 3).
<ce:display><ce:figure><ce:label>Fig. 3</ce:label><ce:caption><ce:simple-para>First panoramic radiograph taken at the time the patient entered the clinical service (June 1992). Note the presence of bone loss, the retained root of #7, and missing posterior teeth.</ce:simple-para></ce:caption> <ce:link locator="gr3"></ce:link></ce:figure></ce:display>A biopsy specimen was taken from the area, and a histopathologic diagnosis of papillary squamous cell carcinoma was rendered by the pathologist (Figs 4 and 5).
<ce:display><ce:figure><ce:label>Fig. 4</ce:label><ce:caption><ce:simple-para>Photograph of the maxillary alveolar mucosa around teeth #11 and #12 taken in 2000. The dentist of the patient had treated the lesion with periodontal therapy and chlorhexidine. Biopsy provided a diagnosis of papillary squamous cell carcinoma. Note the verrucous, exophytic appearance.</ce:simple-para></ce:caption> <ce:link locator="gr4"></ce:link></ce:figure></ce:display><ce:display><ce:figure><ce:label>Fig. 5</ce:label><ce:caption><ce:simple-para>Photograph of the same lesion distal to tooth #12 from a palatal view that was shown to be papillary squamous cell carcinoma.</ce:simple-para></ce:caption> <ce:link locator="gr5"></ce:link></ce:figure></ce:display>Due to the size of the lesion and close approximation to the maxillary sinus, a more aggressive surgical resection was scheduled. Working with the patient under general anesthesia, an oral and maxillofacial surgeon and a head and neck surgeon removed all the remaining teeth posterior to #9 and resected the soft tissue and maxillary alveolar bone in the area of the neoplasm, leaving an oral antral fistula that persists to the present time (Fig 6).
<ce:display><ce:figure><ce:label>Fig. 6</ce:label><ce:caption><ce:simple-para>Panoramic radiograph taken after wide surgical excision of the palatal lesion in 2000. Note the loss of all posterior teeth on the left side, the surgical defect into the maxillary sinus on the left side, and advancing bone loss in the mandibular left with reactive bone activity.</ce:simple-para></ce:caption> <ce:link locator="gr6"></ce:link></ce:figure></ce:display>Tissue from the resection also confirmed the diagnosis of papillary squamous cell carcinoma. The surgical margins showed no invasion into deeper tissues, and maxillofacial prosthodontic treatment was initiated to improve oral function.</ce:para><ce:para>The patient was followed up closely. At the 18-month follow-up, inflammatory, lichenoid, and other nonspecific tissue changes were detected around the lower left bicuspid. Periodontal pocket depth had increased significantly, and the tooth was mobile. The region was biopsied, and a diagnosis of lichen planus was established after the tissue was stained by using standard hematoxylin and eosin and immunofluorescent methods. No dysplastic or malignant changes were identified in the tissue specimens. The patient continues to be followed up, with no new tissue lesions having been found at the time of this report.</ce:para><ce:para><ce:italic>Final diagnoses: Papillary squamous cell carcinoma of the gingiva arising from PVL, and long-standing oral erosive lichen planus of the gingiva</ce:italic></ce:para></ce:section><ce:section><ce:section-title>Differential diagnosis</ce:section-title><ce:para>The differential diagnosis in this case must be assembled for both the lesions characterized as lichen planus and the tissue that underwent neoplastic proliferation. The lichenoid lesions could represent true lichen planus, which is considered to be one of the dermal and mucosal autoimmune diseases. The lesions could also represent a hypersensitivity response to dental restorative materials, including amalgam, nonprecious base metals, and precious metals. In addition, the lesions could have arisen as an idiosyncratic response to NSAIDs used by the patient for arthritis, or might have been significantly stimulated by the oral microflora, including bacteria and fungal organisms. Minor consideration could be given to including other autoimmune diseases in the differential diagnosis, including lupus erythematosus, since the patient reported problems with arthritis. The nature of his joint complaints and lack of other manifestations, however, make such a diagnosis unlikely. Consideration must also be given to including in the differential diagnosis any changes that may have been triggered from a long history of alcohol use, combined with a history of pipe smoking. The clinical and histologic nature of his lesions does not, however, support that diagnosis.</ce:para><ce:para>In approaching the neoplastic lesion as a separate entity, a differential diagnosis including lichenoid dysplasia is appropriate, as is a premalignant lesion secondary to heightened tissue susceptibility to chronic tobacco and alcohol use. Chronic fungal infection has been advocated by some as an etiologic cofactor in squamous cell carcinoma of the oral cavity, and in this case candidiasis was detected, making the addition of fungal infection as a cofactor a reasonable hypothesis. Viral infection has also been suggested to be associated with oral cancer, although this patient had no history of oral herpetic or other infections. Of interest is the development of a differential diagnosis focused on risk factors and cofactors, since their removal could potentially reduce the risk of neoplastic changes in other areas of the mouth.</ce:para></ce:section></ce:section><ce:section><ce:section-title>Discussion</ce:section-title><ce:para>The case of our older male patient identifies a series of challenging questions encountered in clinical practice, including at least the following:
<ce:list><ce:list-item><ce:label>•</ce:label><ce:para>Are mucosal diseases such as lichen planus significant risk factors for malignant transformation, and therefore should patients be treated completely differently than patients with other types of mucosal changes or should they be referred to specialists with broader experience in the management of such conditions?</ce:para></ce:list-item><ce:list-item><ce:label>•</ce:label><ce:para>How often should patients with oral or osseous changes that may represent serious disease be followed up?</ce:para></ce:list-item><ce:list-item><ce:label>•</ce:label><ce:para>For patients with generalized mucosal changes indicative of less serious disease, what are the best methods for determining when additional testing is indicated?</ce:para></ce:list-item><ce:list-item><ce:label>•</ce:label><ce:para>Are other risk factors in patients with lichen planus and other mucosal diseases more important in the development of malignant transformation than lichen planus itself, and therefore should they be addressed separately?</ce:para></ce:list-item><ce:list-item><ce:label>•</ce:label><ce:para>Does the overall effect of other risk factors for oral disease (periodontal disease, poor home care, chronic fungal infection, modest use of alcohol, history of tobacco use, history of other malignant disease) significantly alter the course of lichen planus?</ce:para></ce:list-item></ce:list></ce:para><ce:para>This patient had a long history of stable, but erosive, lichen planus that had gone through periods of remission and flare, requiring only the occasional use of topical medications. Generally, lesions of lichen planus are suggested to have a modest potential for malignant transformation (1%-4%) but in this case damaging progression of the lesion did occur. While it appears that in this case erosive lichen planus did directly undergo malignant change, it is also possible that the neoplastic lesion arose spontaneously in the same tissue and would have developed independent of the lichen planus. Whether the 2 lesions in this case were related—and the clinical question of risk of future malignancy and how to best follow up patients with lichen planus—deserves discussion. The decision of the patient to delay returning to the clinic for his annual checkup may have played an important role in a delayed diagnosis and the development of a larger lesion, necessitating a more aggressive surgical intervention. It is unlikely that the delay increased the likeli-hood that a malignant condition would develop. Other decisions contributing to the delay appear to include the patient's and his dentist's decision that the probable cause for the tissue change around the tooth was periodontal inflammation rather than changes associated with neoplasia. In the early stages of change, differences in tissue characteristics could have resembled secondary periodontal infection and granuloma formation. The lack of appreciation by the general dentist in the risk for malignant disease must have influenced the decision to treat the condition conservatively. And the initial response to local therapy—the secondary infection was reduced—may have led both patient and dentist to believe that their decision was correct, further delaying effective follow-up. The long history of OLP without severe sequela also could have influenced the decision-making process, since both the dentist and the patient had followed the lesion for more than 30 years without catastrophic consequences. Additional “noise” in the decisionmaking process could have included the considerable debate about whether OLP is truly a premalignant lesion or is misdiagnosed as lichen planus in those cases that undergo malignant transformation and is really a much higher risk disease, such as lichenoid dysplasia or chronic lichenoid tissue change associated with a hypersensitivity reaction.</ce:para></ce:section><ce:section><ce:section-title>Determining the risk of oral cancer with PVL and OLP</ce:section-title><ce:section><ce:section-title>Two answerable clinical questions</ce:section-title><ce:para>What is the risk of the subsequent development of oral squamous cell carcinoma in patients with PVL? With OLP?</ce:para><ce:para>The main question arising from this report is one of prognosis: How can health care practitioners better estimate the risk of oral cancer in patients with specific oral lesions? The question could be phrased in PICO format as “In patients older than age 50 [<ce:italic>P</ce:italic>atient/problem], does the presence of OLP and/or proliferative verrucous leukoplakia [“<ce:italic>I</ce:italic>ntervention”] versus no oral lesions [<ce:italic>C</ce:italic>omparison “intervention”] increase the risk for oral squamous cell carcinoma [<ce:italic>O</ce:italic>utcomes]?”</ce:para></ce:section><ce:section><ce:section-title>Article searches</ce:section-title><ce:para>To answer the question of prognosis, the following 2 databases were searched: PUBMED (1965-August 2001), for scientific articles, and OCLC WorldCat (1950–August 2001), for books. We used the MeSH terms <ce:italic>oral lichen planus</ce:italic> and <ce:italic>oral leukoplakia</ce:italic> to search these databases during the indicated time periods. These searches resulted in locating 300 and 1175 articles, respectively, in PUBMED. We found that the indexing term <ce:italic>oral lichen planus</ce:italic> has only been used as a MeSH term since 1994, so the broader term <ce:italic>lichen planus</ce:italic> was needed to find articles published before this time. Since there were so many articles retrieved using these terms, we chose to restrict searches to the last 14 years (1987+, n = 351) for studies of <ce:italic>oral lichen planus,</ce:italic> to the last 3 years for studies of <ce:italic>leukoplakia, oral</ce:italic> (1999+, n = 107), and we did not restrict searches for studies of <ce:italic>proliferative verrucous leukoplakia</ce:italic> (n = 92). The Cochrane Collaboration was also searched for any information on clinical trials treating these conditions. One systematic review of treatment and 34 books or other materials were located for OLP, and 92 books on leukoplakia were found. We also read the reference lists of the pertinent articles that we found to search for other articles not indexed in this way. We limited our book searches to English-language books that were available at the University of Washington library but also searched recent textbooks on oral medicine, oral pathology, and dermatology.</ce:para></ce:section><ce:section><ce:section-title>Article selection</ce:section-title><ce:para>The titles, abstracts, and indexing terms of the retrieved articles were read to determine the relevance to our question and to initially screen for study quality. Since the main question is one of prognosis, the best study design to study this issue (although other designs can be used) would be to exclude any persons with oral cancer, and then observe all people in a defined population with and without the oral disease of interest (PVL, OLP) over a specified time period, and see how many develop oral cancer. Thus, only studies that were randomized trials, cohort or follow-up studies, that is, having data on more than a few subjects, and at least 2 points in time, with the exclusion at baseline of persons with the outcome of interest, were considered eligible.</ce:para></ce:section><ce:section><ce:section-title>Article evaluation</ce:section-title><ce:para>In addressing the validity of the located studies about prognosis, 4 specific criteria have been identified in evidence-based medicine<ce:cross-ref refid="bib4"><ce:sup>4</ce:sup></ce:cross-ref>:
<ce:list><ce:list-item><ce:label>1.</ce:label><ce:para>Was a defined, representative sample of patients assembled at a common (usually early) point in the course of their disease?</ce:para></ce:list-item><ce:list-item><ce:label>2.</ce:label><ce:para>Was patient follow-up sufficiently long and complete?</ce:para></ce:list-item><ce:list-item><ce:label>3.</ce:label><ce:para>Were objective outcome criteria applied in a “blind” fashion?</ce:para></ce:list-item><ce:list-item><ce:label>4.</ce:label><ce:para>If subgroups with different prognoses are identified, was there adjustment for important prognostic factors and validation in an independent group of “test set” patients?</ce:para></ce:list-item></ce:list><ce:display><ce:figure><ce:label>Fig. 7</ce:label><ce:caption><ce:simple-para>Schematic diagram of the spectrum of histologic changes in proliferative verrucous leukoplakia. Lesions slowly enlarge while progressing from the mildest form of hyperkeratosis through a stage of verrucous keratosis to verrucous carcinoma, with some lesions eventually becoming well-differentiated squamous cell carcinoma. (Reprinted from Sapp P, Eversole LR, Wysocki GP, editors. Contemporary oral and maxillofacial pathology. St. Louis: Mosby; 1997. By permission.)</ce:simple-para></ce:caption> <ce:link locator="gr7"></ce:link></ce:figure></ce:display></ce:para><ce:para>For OLP, we were able to find 10 studies from 1988 to present that had at least 200 person-years of follow-up time over at least 2 years.<ce:cross-refs refid="bib2 bib3 bib4 bib5 bib6 bib7 bib8 bib9 bib10 bib11"><ce:sup>2-11</ce:sup></ce:cross-refs> Three studies did not meet the criteria during this time period.<ce:cross-refs refid="bib12 bib13 bib14"><ce:sup>12-14</ce:sup></ce:cross-refs> For oral leukoplakia, we were able to find 4 studies from 1998 to present that had at least 200 person-years of follow-up for a minimum of 2 mean years.<ce:cross-refs refid="bib15 bib16 bib17 bib20"><ce:sup>15-17,20</ce:sup></ce:cross-refs> And with PVL, we found 2 studies that followed a minimum of 50 patients for at least 2 years.<ce:cross-refs refid="bib21 bib22"><ce:sup>21,22</ce:sup></ce:cross-refs> Two PVL studies did not meet the criteria for inclusion.<ce:cross-refs refid="bib23 bib24"><ce:sup>23,24</ce:sup></ce:cross-refs> These studies are listed in the Table, along with a population-based estimate of the incidence of oral cancer (>90% squamous cell carcinoma) in the US population for all adults, and older adults.<ce:cross-ref refid="bib25"><ce:sup>25</ce:sup></ce:cross-ref><ce:float-anchor refid="tab1"></ce:float-anchor></ce:para><ce:para><ce:list><ce:list-item><ce:label>•</ce:label><ce:para>Criterion 1, the most critical of all the criteria, was partially fulfilled by the listed studies, since all the subjects met specific criteria for OLP or leukoplakia, although the criteria differed. However, most studies did not list how long the subject may have had OLP or leukoplakia, or if they were referred from another practitioner. Thus, it is impossible to know if some subjects had their lesion for 20 years or for 3 months. This is a serious limitation of most of these prognostic studies.</ce:para></ce:list-item><ce:list-item><ce:label>•</ce:label><ce:para>Criterion 2—sufficiently long and complete follow-up—also appears to be partially met by all the studies, although the number of subjects lost to follow-up was not usually listed.</ce:para></ce:list-item><ce:list-item><ce:label>•</ce:label><ce:para>Criterion 3—whether objective criteria were used to assess the presence of oral cancer—was present in all the studies, although “blinding” was not indicated.</ce:para></ce:list-item><ce:list-item><ce:label>•</ce:label><ce:para>Criterion 4 is important only when attempting to find predictors, and this has not been done yet.</ce:para></ce:list-item></ce:list></ce:para><ce:para>The next step in evaluating these studies of prognosis is to determine how important these outcomes are. This can be assessed by answering 2 questions: First, how likely is the outcome of oral carcinoma over time? Usually, prognosis study results are listed in one of several ways: as a percentage of the outcome of interest (eg, 1-year survival rates), as a median time to survival (eg, length of time when 50% of subjects die, survive, or develop outcome), or as event curves (eg, survival curves). These results can illustrate, at specific time points, the part or proportion of the original sample that has not yet developed a specific outcome<ce:cross-ref refid="bib1"><ce:sup>1</ce:sup></ce:cross-ref>. In these studies, all but 1 study listed the outcome as a simple percentage of the number of patients in which oral cancer developed divided by the total number of patients followed up. The problem with this measure is that differing time periods of observations are not taken into account, thereby making the comparison of these percentages problematic. For example, in Fig 8, 4 different scenarios are presented: Scenarios 1 and 2, 3 and 4 have the same transformation percentages, 5% and 20%, respectively.
<ce:display><ce:figure id="fig8"><ce:label>Fig. 8</ce:label><ce:caption><ce:simple-para>An example of how incidence rates and relative risks are calculated. Scenarios 1 and 2 have the same percentage transformation “rate” to cancer, of 5%, but differ in the true incidence rate of cancer, since the time at risk varies between the two. Scenarios 3 and 4 also have the same transformation rate (25%), but the incidence rate is also shown to be different. Thus, transformation rates without a corresponding time period of the subjects at risk can be misleading. The last column in the <ce:cross-ref refid="tab1">table</ce:cross-ref> shows an example calculation of the relative risk using the incidence rates shown.</ce:simple-para></ce:caption> <ce:link locator="gr8"></ce:link></ce:figure></ce:display>However, their mean follow-up times are different, which is common in the literature. Instead, if a true incidence rate is calculated or at least approximated by multiplying the total time that each person is at risk by the number of subjects, a more accurate depiction of the transformation rate can be determined. In the example, scenarios 1 and 2 show substantially different incidence rates: scenario 1, 0.01 cases per person-year, and scenario 2, 0.05 cases per person-year. For ease of discussion, the denominators can be multiplied by 100 to yield 1 new cancer case per 100 person-years, and 5 new cancer cases per 100 person-years. Scenario 3 and 4 show a similar effect, instead of the same transformation percentage of 20%, the incidence rates are 0.02 cases per person-year, and 0.20 cases per person-year, or 2 new cases per 100 person-years, and 20 new cases per 100 person-years.</ce:para><ce:para>The <ce:cross-ref refid="tab1">Table</ce:cross-ref> shows the results of using the same methods for evaluating the existing studies of OLP, leukoplakia, PVL, and the subsequent development of sqaumous cell carcinoma. For the OLP studies, the transformation percentages range from 0.0% to 5.6%. The number of new cases per 1000 person-years, as estimated from the mean follow-up times, ranges from 0.0% to 12% new cancer cases per 1000 person-years.</ce:para><ce:para>For the leukoplakia studies, the transformation percentages range from 6.3% to 31.4%, and the incidence rates range from about 16 to 50 new cases per 1000 person-years. For the only 2 studies of PVL, the transformation percentage 41.5% to 70%, which is equal to 60 to 120 new cancer cases per 1000 person-years.</ce:para><ce:para>Because we are following only patients with oral lesions, how do these rates differ from what would be found in the general population, which is made up of mostly people without these lesions? These rates are available from studies that find all new oral cancer cases in a defined populations. For example, in the United States, the overall incidence rate for new cancer cases of all types of the oral cavity was 7.8 per 100,000 person-years in 1986-87. The second highest rates of all were among adults aged 70 to 74, and these rates were 5 times higher, at 34.8 per 100,000 person-years. These rates can be converted into a transformation percentage of 0.035%, or an incidence rate of 0.35 per 1000 person-years. We can compare these rates, using a measure called the relative risk, as defined in <ce:cross-ref refid="fig8">Fig 8</ce:cross-ref> as the incidence rate of the exposed (have oral lesions) divided by the incidence rate of the unexposed (general population). These rates are shown in the <ce:cross-ref refid="tab1">Table</ce:cross-ref>, and they illustrate that, although the incidence rates of oral cancer are low for OLP, they are many times higher than what might be seen in the general population. For example, for OLP, the relative risk using the category of one of the highest rates in the population, the 75- to 84-year-old men, varies from 5.6 to 34.3 in the OLP studies, from 45 to 143 in the leukoplakia studies, and 174 to 341 in the 2 studies of PVL. Relative risks greater than 2.0 are generally considered small to moderate in size, and risks greater than 10 are considered moderate to large, and are usually trusted to withstand the many biases that can result in such comparisons. Although the differences between our comparison groups likely exist (such as the exact ages, gender, and number of people smoking), since most OLP patients are non-smokers, adjustment for this factor would likely inflate the relative risks to even greater magnitude. Thus, these simple comparisons provide convincing evidence that people with OLP, leukoplakia, and PVL are at substantially greater risk for oral cancer. Even if two thirds of the cases were removed because they may not meet strict pathological criteria, as has been suggested by some pathologists, this increased risk would still be present.</ce:para><ce:para>Since not all cases of oral leukoplakia (and especially very few OLP patients) ultimately develop cancer, it would be valuable if we could predict which lesions will become cancerous. For example, recent studies have shown that dysplastic and malignant lesions may have molecular changes common in cancer persisting at the periphery of clinically and histologically normal tissue, and may explain recur-rence and, hence, prognosis.<ce:cross-refs refid="bib27 bib28 bib29 bib30"><ce:sup>27-30</ce:sup></ce:cross-refs> Although specific histologic or other markers of malignancy have been explored, such as the presence of HPV, few of these studies use multivariable analyses that indicate if a specific factor, independently from other variables, is useful for predicting development into oral cancer. The most methodologically rigorous paper that we could find to help answer this question supports the long-held clinical impression that the degree of dysplasia is the single best predictor of future malignancy in patients with oral leukoplakia while controlling for other covarates,<ce:cross-ref refid="bib16"><ce:sup>16</ce:sup></ce:cross-ref> while a new paper with multivariable analysis indicates that DNA content, or ploidy, a rarely used histopathologic marker, is correlated with malignant transformation.<ce:cross-ref refid="bib15"><ce:sup>15</ce:sup></ce:cross-ref> But neither of these papers currently fulfill criterion 4, which requires the validation of the marker on another group of patients.</ce:para><ce:para>Finally, the precision of these estimates of risk should be assessed. For the sake of simplicity, we will not delve into this discussion, and since we restricted the discussion to the studies with relatively large number of subjects, except for the PVL subtypes, the interpretation will not be substantially different if confidence intervals are calculated for the incidence and relative risk estimates.</ce:para></ce:section><ce:section><ce:section-title>Evidence summarization</ce:section-title><ce:para>The evidence presented helps to answer the question, In patients with OLP or PVL, what is the risk for transformation to oral squamous cell carcinoma? This risk for OLP appears to be roughly 10 times higher than that seen in the general population, although only some patients with this condition will likely have squamous cell carcinoma develop. The risk for PVL appears much higher, and is approximately 100 times higher than in the general population, and it appears from 2 studies that most, if not all, subjects with this condition will ultimately have oral squamous cell carcinoma.</ce:para><ce:para>The question of how often patients with these oral lesions at risk for malignant transformation should be examined should be answered using risk-benefit and cost-benefit analyses, and this is beyond the scope of the current discussion. Suffice it to say that the benefits of active survelliance are probably worth any potential risks and side effects from observation and minor surgery, or from inaccurately labeling a person as having a potentially malignant disease. However, much more work needs to be done in this area to best assess this question, and the economic costs for examining all persons with OLP can be staggering.</ce:para><ce:para>Finally, the issue of how these patients should best be treated for their specific lesion is a question of therapy, and this could best be answered with a randomized controlled trial, or at least a cohort study of patients with the same diagnosis who are treated with different modalities. Many experts in the field believe that PVL is at such a high rate for malignant transformation that aggressive local excision is needed with the first histopathologic evidence of the lesion,<ce:cross-ref refid="bib22"><ce:sup>22</ce:sup></ce:cross-ref> although this guideline is not supported by such a study. However, a new cohort study of HPV-associated PVL lesions shows a clear advantage of surgical excision along with the use of an antiviral/immunomodulatory agent compared to surgery alone.<ce:cross-ref refid="bib32"><ce:sup>32</ce:sup></ce:cross-ref></ce:para></ce:section><ce:section><ce:section-title>Strength of evidence</ce:section-title><ce:para>The level of evidence presented is an intermediate 2b out of 5 levels (1 is the highest), since it is based on evidence from multiple summarized retrospective cohort studies.<ce:cross-ref refid="bib31"><ce:sup>31</ce:sup></ce:cross-ref> Because some of the methodological conditions for prognosis studies could not be met, there is still some uncertainty about the overall validity of the incidence of transformation. Nevertheless, because of the estimates of incidence, and because the relative risks are so great, large systematic errors from referral bias, improper case definitions, and confounding would have to be present to change the conclusions.</ce:para><ce:para>Clearly, studies are needed that employ commonly used epidemiological analytic techniques, such as multivariable regression, so that prognostic factors for OLP lesions can be better elucidated. Reanalysis of data from previously published studies using these methods would likely yield new useful information about prognostic factors for malignant transformation in OLP.</ce:para></ce:section><ce:section><ce:section-title>Summary</ce:section-title><ce:para>Proliferative verruciform leukoplakia is an uncommon oral lesion that has been shown to be at high risk for malignant transformation into squamous cell carcinoma from 2 follow-up studies. Oral lichen planus is a common oral lesion that also appears to be at risk for transformation, although at a lower rate. This article has presented the case of an older man in whom both conditions progressed into papillary squamous cell carcinoma. 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type="given">Edmond L.</namePart><namePart type="family">Truelove</namePart><namePart type="termsOfAddress">DDS, MSD</namePart><affiliation>From the Departments of Oral Medicine,a Dental Public Health Sciences,b and Oral Biology,c School of Dentistry, University of Washington, Seattle</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas H.</namePart><namePart type="family">Morton, Jr</namePart><namePart type="termsOfAddress">DDS, MSDa,c</namePart><affiliation>From the Departments of Oral Medicine,a Dental Public Health Sciences,b and Oral Biology,c School of Dentistry, University of Washington, Seattle</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joel B.</namePart><namePart type="family">Epstein</namePart><namePart type="termsOfAddress">DMD, MSD, FRCD(C)a</namePart><affiliation>From the Departments of Oral Medicine,a Dental Public Health Sciences,b and Oral Biology,c School of Dentistry, University of Washington, Seattle</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2001</dateIssued><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: J Evid Base Dent Pract 2001;1:123-35</abstract><note type="content">Section title: Evidence-Based Case Conference</note><note type="content">: Table. Studies of malignant transformation of oral lichen planus and leukoplakia into oral squamous cell carcinoma</note><relatedItem type="host"><titleInfo><title>Journal of Evidence-Based Dental Practice</title></titleInfo><titleInfo type="abbreviated"><title>YMED</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">200110</dateIssued></originInfo><identifier type="ISSN">1532-3382</identifier><identifier type="PII">S1532-3382(05)X7002-6</identifier><part><date>200110</date><detail type="volume"><number>1</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue-pages"><start>2A</start><end>154</end></extent><extent unit="pages"><start>123</start><end>135</end></extent></part></relatedItem><identifier type="istex">0CA8E54EB7710A466E209D357405273965C1CABD</identifier><identifier type="ark">ark:/67375/6H6-CF44M0MH-G</identifier><identifier type="DOI">10.1016/S1532-3382(01)70023-1</identifier><identifier type="PII">S1532-3382(01)70023-1</identifier><accessCondition type="use and reproduction" contentType="copyright">©2001 Mosby, Inc.</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Mosby, Inc., ©2001</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/0CA8E54EB7710A466E209D357405273965C1CABD/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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