Oral yeast carriage correlates with presence of oral epithelial dysplasia M. McCullough a ,M.Jaber a , A.W. Barrett b ,L.Bain a , P.M. Speight b , S.R. Porter a, * a Department of Oral Medicine, Eastman Dental Institute for Oral Health Care Sciences, UCL, University of London, 256 Gray’s Inn Road, London WC1X 8LD, UK b Department of Oral Pathology, Eastman Dental Institute for Oral Health Care Sciences, UCL, University of London, 256 Gray’s Inn Road, London WC1X 8LD, UK Received 31 May 2001; accepted 21 June 2001 Abstract Previous studies have suggested a link between the presence of Candida albicans and the development of oral squamous cell carcinoma (OSCC). The aim of the present study was to assess the presence and level of colonisation of oral yeast in patients undergoing an incisional oral mucosal biopsy in order to assess whether the amount of oral yeast present correlated with the pres- enceanddegreeoforalepithelialdysplasticorneoplasticchange.Twohundredandtwenty-threepatientswhowereundergoingan incisional biopsy for the diagnosis of an oral mucosal lesion were enrolled in this study. Mouth swills were obtained from each patientforthepresenceandamountoforalyeastpresent.Someofthepatients(44.6%)hadahistopathologicaldiagnosisofeither oral epithelial dysplasia (OED) or OSCC and the frequency of oral yeast carriage was significantly greater (P < 0.001) in these patients than those without histopathologically detected dysplastic or neoplastic oral lesions. Furthermore, significantly (P < 0.001) more patients with OED or OSCC had a higher number of yeast (over 1000 cfu/ml) in their oral cavity than patients without any evidence of epithelial dysplasia or neoplasia histopathologically. The degree of epithelial dysplasia present in these patients also correlated with higher amounts of yeast in the oral cavity (P=0.017). The results of the present study reveal that there is an inter- action between oral carriage of yeast and oral epithelial dysplasia, however it remains unclear how yeast infection influences the development and progression of dysplasia. # 2002 Elsevier Science Ltd. All rights reserved. 1. Introduction Theprevalenceofdiseasescausedby Candida spp.has increased in recent years, mainly due to an increase in the number of patients who are immunocompromised. These yeasts are commensal organisms found in approximately 40% of individuals, the predominant species isolated being Candida albicans. C. albicans has the potential to infect virtually any tissue within the body, however, it is predominantly found on oral and vaginal mucosa. A spectrum of different oral mucosal lesions are associated with Candida including chronic hyperplastic candidiasis, also known as candidal leukoplakia. It has been suggested that this form of oral candidosis carries a significant risk of malignant transformation. The possible association between Candida spp. and oral neoplasia was first reported in the 1960s [1,2] with later reportssuggestingalinkbetweentheoralmucosalpres- ence of C. albicans and the development of oral squa- mous cell carcinoma (OSCC) [3–6]. In addition, it has recently been observed that C. albicans is much more frequentlydetectedinthebiofilmofOSCCtumoursites than control areas [7]. Sub-species differentiation by biotyping of C. albicans has revealed strain differences of C. albicans in leuko- plakic lesions compared with normal mucosa [8]. Of note C. albicans with very high potential to nitrosylate N-benzylmethylamine are more likely to be isolated from advanced, potentially malignant, oral mucosal lesions than early potentially malignant lesions or nor- maloralmucosa[9].Astudythatutilisedaratmodelof oral mucosal carcinogenesis revealed that the particular strain of Candida had the similar ability as phorbol- 12,13-didecanoate to promote neoplastic and mucosal changes [10]. 1368-8375/02/$ - see front matter # 2002 Elsevier Science Ltd. All rights reserved. PII: S1368-8375(01)00079-3 Oral Oncology 38 (2002) 391–393 www.elsevier.com/locate/oraloncology * Corresponding author. Tel.: +44-20-7915-1197; fax: +44-20- 7915-2341. E-mail address: s.porter@eastman.ucl.ac.uk (S.R. Porter).