Oral leukoplakia: a Clinicopathological review

Waal, I. van der; Schepman, K.P.; Meij, E.H. van der; Smeele, L.E.

doi:10.1016/s1368-8375(97)00002-x

Cited by 252 publications

(193 citation statements)

References 112 publications

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“…These data appear in agreement with the concept of field effect in oral carcinogenesis (Braakhuis et al, 2003;Bremmer et al, 2008;Tabor et al, 2001;Van der Waal, 1997). The data obtained for the nondysplastic OPMLs, in particular, were in agreement with previous literature reports including two studies from our group using an independent patient population (Donadini et al, 2010;Pentenero et al, 2009;Saito, 1995).…”

Section: Discussionsupporting

confidence: 92%

Model of Chromosomal Instability in Oral Carcinogenesis and Progression

Giaretti¹

2012

Oral Cancer

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Section: Discussionsupporting

confidence: 92%

Model of Chromosomal Instability in Oral Carcinogenesis and Progression

Giaretti¹

2012

Oral Cancer

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“…The disease definition has changed over time, 1,21 complex classifications are in use and leukoplakia may have varied appearances that contributes to misclassification of cases. Oral leukoplakia has a multifactorial aetiology 44 and different severities may be attributed to each case depending on the dysplasia grade. Based on these factors different management options may be indicated that are outside the trial design.…”

Section: Cancer Therapymentioning

confidence: 99%

Treatment of oral leukoplakia with a low‐dose of beta‐carotene and vitamin C supplements: A randomized controlled trial

Nagao

Warnakulasuriya

Nakamura

et al. 2014

Intl Journal of Cancer

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Management of oral leukoplakia-a potentially malignant disorder-is currently not evidence-based. Of the few randomized trials that have been reported, most have negative data. Therefore, a multi-centre, randomized, double-blind controlled trial (RCT) was undertaken to evaluate the use of low-dose beta-carotene combined with vitamin C supplements for the treatment and to prevent malignant transformation of oral leukoplakia. 46 Japanese participants with oral leukoplakia were allocated randomly either to an experimental arm (10 mg day 21 of beta-carotene and 500 mg day 21 of vitamin C) or placebo arm (50 mg day 21 of vitamin C). Current or ex-smokers within 3 months of cessation were excluded. The supplements were continued over a period of 1 year. The primary endpoint was clinical remission at 1-year and the likelihood of malignant transformation during a 5-year follow-up period as a secondary endpoint. The overall clinical response rate in the experimental arm was 17.4% (4/23) and 4.3% (1/23) in the placebo arm (p 5 0.346). During the median 60-month follow-up period, two subjects in the experimental arm and three in the control arm developed oral cancer. Under the intention-to-treat principle, relative risk by supplementing with beta-carotene and vitamin C was 0.77 (95%CI: 0.28-1.89) (p 5 0.580) by the Cox proportional hazards model. No unfavorable side-effects were noted. Beta-carotene (10 mg day 21 ) and vitamin C were neither effective for clinical remission, nor for protection against the development of cancer. Data from this RCT does not support the hypothesis that chemoprevention with this treatment is effective for oral leukoplakia.Oral leukoplakia-a potentially malignant disorder of the oral cavity-is associated with an increased risk of oral cancer. 1 Although a number of options for treatment of oral leukoplakia are available, 2 there is a lack of consensus on the most appropriate method of management and ways to minimize malignant transformation. 3 Tobacco and alcohol misuse are significant risk factors for the development of oral leukoplakia. 4 While it is possible to treat tobacco dependence, 5 the compliance of users and resources offered by healthcare delivery systems have been disappointing. Surgical and laser treatment of oral leukoplakia, although reducing the risk of malignant transformation, is at times associated with recurrences. 6 In this context, a medical treatment for leukoplakia is attractive, particularly if a chemopreventive agent that is effective and safe, and produces lasting benefit, can be found. 7,8 In 1981, Peto et al. hypothesized that high dietary intake of carotenoids may reduce cancer among humans. 9 Observational studies on diet suggest that its role in cancer prevention is mainly related to antioxidants in foods and/or beverages. 10,11 The incidence of a number of cancer types (i.e. lung, oral, pharyngeal and stomach) are inversely related to beta-carotene intake or blood concentrations. 12,13 A Japanese population study reported that high serum beta-carotene levels wer...

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“…Leukoplakia is the most common precancerous lesion [55]. The incidence and prevalence of oral leukoplakia in the UK are not known.…”

Section: Precancerous Lesions/conditions and Malignant Transformationmentioning

confidence: 99%

“…The risk of malignant transformation is reported to vary with gender (higher among women), type of leukoplakia (higher among those that are idiopathic, nonhomogenous, of a long duration, or situated on the tongue/¯oor of the mouth), presence of Candida albicans, and presence of epithelial dysplasia [55]. Hospitalbased series from Europe and USA have reported malignant transformation rates of 4.4±17.5% for leukoplakia, whereas in India, population-based studies report rates of 0.13±2.2% ( Table 2).…”

Section: Precancerous Lesions/conditions and Malignant Transformationmentioning

confidence: 99%

“…Tradati et al [84] suggest surgical excision of all persistent leukoplakias because of poor patient compliance with follow-up. Other authors [55] recommend active treatment for lesions showing moderate or severe dysplasia, with oral sub-site being the deciding factor in whether or not to treat mild dysplasia. In the UK, treatment of mild to moderate dysplasia varies, with 16% of oral and maxillofacial surgeons preferring no active treatment.…”

Section: Potentially Malignant Oral Lesionsmentioning

confidence: 99%

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Oral cancer in the UK: to screen or not to screen

1998

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Although oral squamous cell carcinoma accounts for only a small proportion of malignant neoplasms in the UK, oral cancer incidence and mortality rates have been rising in recent years. The natural history of oral cancer is not adequately understood at present and there is very little information about the epidemiology of precancerous lesions in the UK. There are also insucient data to provide ®rm evidence that the percentage of cases arising de novo is greater in the UK and the Western world as compared to the Indian subcontinent. Screening for oral cancer by visual examination is simple, inexpensive and causes little discomfort; however, there is no evidence for the eectiveness of screening for oral cancer either in reducing mortality from the disease or in reducing the incidence of invasive disease by detection and treatment of precancerous lesions. There is currently insucient evidence to recommend population screening for oral cancer in the UK. Measures aimed at primary prevention of the disease may be a more feasible method of disease control at present. #

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Oral leukoplakia: a Clinicopathological review

Cited by 252 publications

References 112 publications

Model of Chromosomal Instability in Oral Carcinogenesis and Progression

Model of Chromosomal Instability in Oral Carcinogenesis and Progression

Treatment of oral leukoplakia with a low‐dose of beta‐carotene and vitamin C supplements: A randomized controlled trial

Oral cancer in the UK: to screen or not to screen

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