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In this review article, the clinical and histopathological characteristics of oral premalignant lesions, and primarily oral leukoplakia, are noted and the risk factors for malignant transformation of oral leukoplakia are discussed. Malignant transformation rates of oral leukoplakia range from 0.13 to 17.5%. The risk factors of malignant transformation in the buccal mucosa and labial commissure are male gender with chewing tobacco or smoking in some countries such as India, or older age and/or being a non-smoking female in other countries. Some authors have reported that leukoplakia on the tongue or the floor of the mouth showed a high risk of malignant transformation, although others have found no oral subsites at high risk. In concurrence with some authors, the authors of this review view epithelial dysplasia as an important risk factor in malignant transformation; however, there are conflicting reports in the literature. Many authors believe that nonhomogeneous leukoplakia is a high risk factor without exception, although different terms have been used to describe those conditions. The large size of lesions and widespread leukoplakia are also reported risk factors. According to some studies, surgical treatment decreased the rate of malignant transformation; however, many review articles state that no definitive treatment including surgery can decrease the malignant transformation rate of oral leukoplakia because of the lack of randomized control trials of treatment. Tobacco chewing and smoking may be causative agents for cancerization of oral leukoplakia in some groups, and evidence for a role of human papilloma virus in the malignant transformation of oral leukoplakia is inconsistent. Further research to clarify its role in malignant transformation is warranted.

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This study evaluated the usefulness of cone-beam computed tomography (CBCT) during ultraselective transcatheter arterial chemoembolization (TACE) for hepatocellular carcinomas (HCC) that could not be demonstrated on angiography. Twenty-eight patients with 33 angiographically occult tumors (mean diameter 1.3 +/- 0.3 cm) were enrolled in the study. The ability of CBCT during arterial portography (CBCTAP), during hepatic arteriography (CBCTHA), and after iodized oil injection (LipCBCT) to detect HCC lesions was retrospectively analyzed. The technical success of TACE was divided into three grades: complete (the embolized area included the entire tumor with at least a 5-mm wide margin), adequate (the embolized area included the entire tumor but without a 5-mm wide margin in parts), and incomplete (the embolized area did not include the entire tumor) according to computed axial tomographic (CAT) images obtained 1 week after TACE. Local tumor progression was also evaluated. CBCTAP, CBCTHA, and LipCBCT detected HCC lesions in 93.9% (31 of 33), 96.7% (29 of 30), and 100% (29 of 29) of patients, respectively. A single branch was embolized in 28 tumors, and 2 branches were embolized in five tumors. Twenty-seven tumors (81.8%) were classed as complete, and 6 (18.2%) were classed as adequate. None of the tumors were classed as incomplete. Twenty-five tumors (75.8%) had not recurred during 12.0 +/- 6.2 months. Eight tumors (24.2%), 5 (18.5%) of 27 complete success and 3 (50%) of 6 adequate success, recurred during 10.1 +/- 6.2 months. CBCT during TACE is useful in detecting and treating small HCC lesions that cannot not be demonstrated on angiography.