Interventions for treating oral leukoplakia to prevent oral cancer

Abstract

cancer survival longer than five years after diagnosis are low. Drugs, surgery and other therapies have been tried for treatment of oral leukoplakia. Objectives This review aimed to evaluate whether treatments for oral leukoplakia are effective in preventing oral cancer, and safe and acceptable to patients. Study characteristics The evidence on which this review is based is up-to-date as of May 2016. We found 14 randomised controlled trials (RCTs) of medical and complementary treatments, which involved 909 participants in total. Treatments included herbal extracts, anti-inflammatory drugs, vitamin A, beta carotene supplements and others. Surgical treatment has not been compared with placebo or no treatment in an RCT. Key results Cancer development was measured in studies of three treatments: systemic vitamin A, systemic beta carotene and topical bleomycin. None of these treatments showed effectiveness in preventing cancer development, as measured up to two years for vitamin A and beta carotene, and seven years for bleomycin. Some individual studies of vitamin A and beta carotene suggested that these treatments may be effective for improving or healing oral lesions. However, some studies observed a high rate of relapse in participants whose lesions were initially resolved by treatment. Most treatments caused side effects of differing severity in a high proportion of participants. It seems likely that interventions were well accepted by participants because drop-out rates were similar between treatment and control groups. Quality of the evidence The available evidence is very limited. Most interventions were assessed by only one small study. Most studies had problems in the way they were conducted, making their results unreliable. We judged the quality of evidence for the outcome of cancer development to be very low. Author conclusions Larger, better studies of longer duration are required. As well as further studies of drug treatment and alternative treatments like vitamins, studies are needed to evaluate the effectiveness and safety of surgery, and of stopping risk factor habits such as smoking. * The risk in the intervention group (and its 95% conf idence interval) is based on the assum ed risk in the com parison group and the relative effect of the intervention (and its 95% CI) CI = conf idence interval; RR = risk ratio; vs = versus; d = day 4 Interventions for treating oral leukoplakia to prevent oral cancer (Review)

Malignant transformation rate of oral leukoplakia in an Australian population

“…A recent Cochrane review concluded that there was insufficient evidence to validate any intervention in the treatment of leukoplakia, including surgical modalities. This was due to the fact that there have been no randomised clinical trials assessing the effect of surgical excision on the development of oral cancer that include a control arm with no treatment, due to the associated ethical issues . The position can certainly be argued that lesions displaying any grade of OED should, where possible, be excised and this approach has mostly been taken with the current cohort under investigation …”

Oral leukoplakia remains a challenging condition

“…Often times, patients present with multifocal non‐contiguous lesions (PVL) with a histopathological diagnosis of “hyperkeratosis no dysplasia,” yet 70%–100% will develop cancer over time. Current strategies for oral leukoplakia include surgery, a “watch‐and‐see” approach, and medical treatment (Farah et al., ; Lodi et al, ; Ribeiro, Salles, da Silva, & Mesquita, ). Recurrence after surgical excision ranged from 0% to 35% (Holmstrup et al., ; Lumerman et al., ; Pindborg, Jolst, Renstrup, & Roed‐Petersen, ; Silverman et al., ; Vedtofte, Holmstrup, Hjorting‐Hansen, & Pindborg, ); 0%–15% when carbon dioxide laser was used; and 10%–25% in patients who underwent photodynamic therapy (Vohra et al., ).…”

Bibliometric analysis of a century of research on oral erythroplakia and leukoplakia

“…The incidence varies across the world and is high in Central and Eastern Europe, Hong Kong, India, and Brazil, and among African Americans in the USA . Although most OSCC develop de novo, with no preceding potentially malignant lesions, many cases of OSCC originate from oral erythroplakia and leukoplakia (OEL), the most common oral potentially malignant lesions (OPML) . Prevention of OEL malignant transformation may improve the outcome of OSCC, through the identification of OEL at high risk of malignant transformation, and the use of chemopreventive agents to address the field of cancerization .…”