Hyperplasia, keratosis, dysplasia and carcinoma in situ of the vocal cords?a follow-up study

Abstract

Comparison of reported series of laryngeal lesions is complicated by the inconsistency in the terminology. The classification of these lesions should logically be based on the degrees of dysplasia, as this has a bearing on the prognosis. The material for this study consisted of 193 patients with hyperplasia and/or keratosis, with or without mild dysplasia (Group I), moderate dysplasia (Group II), and severe dysplasia and carcinoma in situ (Group III). They were treated over a 14-year period (1966-1979) at Linköping University Hospital. Of the 98 patients in Group I available for follow-up, 23 had repeat excisions. Moderate dysplasia developed in 3 patients, severe dysplasia in 2, and invasive carcinoma in another 2 within 3 and 3.5 years; they both underwent laryngectomy. Among the 24 patients in Group II available for follow-up, severe dysplasia developed in 3 and invasive carcinoma in 3 up to 13 years after the initial diagnosis, all but one (with severe dysplasia) received a full course of radiotherapy, on one case total laryngectomy was subsequently performed for recurrent carcinoma. Of the 39 patients with severe dysplasia and carcinoma in situ 16 were given primary radiotherapy; 4 of these developed invasive carcinoma; 3 of them underwent total laryngectomy and one partial laryngectomy. Excision or stripping of the vocal cords was the primary treatment in 23 cases; 5 of these developed invasive carcinoma; 2 of them underwent total laryngectomy. Diffuse lesions and well differentiated forms of severe dysplasia caused most problems and had the highest incidence of invasive carcinoma irrespective of the form of treatment. Patients with hyperplasia, keratosis, dysplasia and carcinoma in situ should be carefully followed up, as invasive carcinoma may develop many years after the initial diagnosis.

Squamous Cell Carcinoma of the Upper Aerodigestive Tract: Precursors and Problematic Variants

“…This clinical concern is due to the fact that severe dysplasia is often multifocal and frequently occurs adjacent to or near synchronous foci of invasive carcinoma. Further, this form of dysplasia has a rate of progression to invasive carcinoma that is greater than that of "classic" CIS (20,23,25). A diagnosis of severe dysplasia requires therapeutic intervention, as well as clinical evaluation of the entire UADT to exclude the possible presence of additional foci of dysplasia or carcinoma.…”

Novel Markers for Diagnosis and Prognosis of Oral Intraepithelial Neoplasia

“…Evidence of the inability of pathologists to set up a single, unified classification of SILs was manifest in the WHO Classification of head and neck tumours, published in 2005, where the dysplasia system is presented as the 2005 WHO classification simultaneously with the classification of SIN and the Ljubljana classification (Gale et al 2005). The majority of current classifications, such as the traditional dysplasia system (Hellquist et al 1982;, keratosis without (KWA) and with atypia ⁄ in situ carcinoma (CIS) (Crissman 1979;Crissman 1982), Squamous Intraepithelial Neoplasia (SIN) (Crissman et al 1993;Crissman&Zarbo 1989) and Laryngeal Intraepithelial Neoplasia (LIN), (Friedmann&Ferlito 1993;Resta et al 1992) follow criteria similar to those commonly used for epithelial lesions of the uterine cervix. However, the different aetiology of oral lesions and their particular clinical and histological features require a grading system more appropriate to this region (Hellquist et al 1999).…”

“…The grades do not offer clear therapeutic guidelines to clinicians for appropriate management. For CIS at least, the WHO grading system diagnoses CIS showing maturation and differentiation as lower risk lesions, and these lesions account for a large proportion of cases in the oral mucosa (Hellquist et al 1982;Gillis et al 1983;Yoo et al 2004;Kleist&Poetsh 2004;Jeannon et al 2004;Chi et al 2004).…”

“…Particular attention has been directed to the analysis of the interrelationship between histological parameters and their biological behaviour (Gale et al 2005, Gale et al 2006Kambicˇ&Gale, 1986;Putney&O'Keefe 1953;Kambicˇ 1978;Crissman 1979;Henry 1979;Hellquist et al, 1982;Gillis et al, 1983;Grundmann 1983;Goodman 1984;Crissman&Fu 1986;Velasco et al 1987;Olde-Kalter et al 1987;Crissman&Zarbo 1989;Sllamniku et al 1989;Bouquot et al, 1991a;Kambic&Gale 1995;Hellquist et al 1999;Gallo et al 2001;Ricci et al 2003). These analyses have been recently further supplemented by molecular genetic investigations trying to include the molecular events involved in the pathogenesis of oral squamous cell carcinoma (OSCC) to improve the prognostic evaluation of OIN (Ha&Califano 2002;Somers et al 1992;Saglam et al 2007).…”

An Update on Precancerous Lesions of Oral Cavity

“…[20,21] 4. WHO system: low, moderate, severe and carcinoma in situ. [22,23,24] A Modified Classification and Staging System for Oral Leukoplakia: A proposal for a modified classification and staging system for oral leukoplakia (OLEP) has been presented by Van der Waal el al, 2000 in which the size of the leukoplakia and the presence or absence of epithelial dysplasia are taken into account. Altogether four stages are recognized: LI -Size of leukoplakia < 2 cm L2 -Size of leukoplakia 2-4 cm L3 -Size of leukoplakia >4cm Lx -Size not specified P -Pathology PO -No epithelial dysplasia PI -Distinct epithelial dysplasia Px -Dysplasia not specified in the pathology report.…”