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Table of Contents
Year : 2019  |  Volume : 5  |  Issue : 1  |  Page : 19-23

Oral leukoplakia: Management protocol for primary health-care providers and family physicians

1 Department of Dentistry, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India
2 Department of Orthodontics, Nair Hospital Dental College, Mumbai, Maharashtra, India

Date of Web Publication4-Jul-2019

Correspondence Address:
Ashok Kumar Jena
Department of Dentistry, All India Institute of Medical Sciences, Sijua, Bhubaneswar, Odisha
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/IJCFM.IJCFM_9_19

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Oral cancer is very common in India. Most of the oral cancers develop on a potentially malignant (precancerous) lesion. Leukoplakia is the most common precancerous lesion in the oral cavity. The malignant transformation rate of oral leukoplakia is very high. There is no marker to distinguish those lesions that may transform to frank cancer from those that may not. Thus, early identification of oral leukoplakia and its proper treatment is important for best prognosis. This article highlights on the diagnosis and treatment protocol for oral leukoplakia.

Keywords: Family physicians, management protocol, oral cancer, oral leukoplakia, primary health-care providers

How to cite this article:
Jena AK, Sharan J, Ghodke S, Anusuya V, Barhate UH. Oral leukoplakia: Management protocol for primary health-care providers and family physicians. Indian J Community Fam Med 2019;5:19-23

How to cite this URL:
Jena AK, Sharan J, Ghodke S, Anusuya V, Barhate UH. Oral leukoplakia: Management protocol for primary health-care providers and family physicians. Indian J Community Fam Med [serial online] 2019 [cited 2022 Aug 8];5:19-23. Available from: https://www.ijcfm.org/text.asp?2019/5/1/19/262127

  Introduction Top

Majority of the oral cancers are preceded by asymptomatic clinical lesions together called oral potentially malignant disorders or a precancerous lesion. The prevalence of precancerous lesions in the oral cavity is about 2.5% in the general population.[1] About 15%–48% of the squamous cell carcinomas of the oral cavity are developed from innocent-appearing precancerous lesions,[2],[3] and approximately 60% are present as white keratotic lesions.[4] However, most of the precancerous lesions are diagnosed at a late stage. Early identification of the oral precancerous lesions, particularly in high-risk individuals, is important to prevent further morbidity and to improve the oral health-related quality of life. Although dentists screen their patients' oral mucosa for any early sign of oral cancer, the identification of any suspicious lesions by a primary health-care provider is paramount for their early treatment. Of all oral precancerous lesions, leukoplakia has a very high malignant transformation rate. This article highlights the oral leukoplakia management protocol for a primary health-care provider and family physician.

  Which Lesions Should Be Defined as Oral Leukoplakia? Top

The term “leukoplakia” was first described in 1877 by Schwimmer.[5] In 1978, the World Health Organization (WHO) defined leukoplakia as a white patch that does not rub off and cannot be characterized clinically or histopathologically as any other disorder.[6] In 1994, the WHO has modified the definition by adding “oral leukoplakia is not associated with any physical or chemical cause, except smoking and it can cause cancer” to the previous WHO definition.[7] However, in 2007, it was decided that the term leukoplakia should only be used for clinical diagnosis. However, any white patch in the oral cavity can be identified clinically as any other diseases such as candidiasis, white sponge nevus, lichen planus, or leukoedema. Then, the disorder cannot be called as leukoplakia. In certain clinical situation, a white patch may be diagnosed clinically as leukoplakia, but when histopathology reveals it as another specific diagnosis, the lesion should not be specified as a leukoplakia. Furthermore, white patches in the oral cavity due to chronic irritation by denture or cheek bite should not be categorized as leukoplakia, as these lesions are not premalignant and are reversible in nature if the irritation is withdrawn. Similarly, the nicotine stomatitis and tobacco pouch keratosis also should not be called as leukoplakia. In 2012, the latest definition of leukoplakia defines it as” a predominantly white lesion or plaque of questionable behavior having excluded clinically and histopathologically, any other definable white disease or disorder.[8]

  What are the Risk Factors of Oral Leukoplakia? Top

The exact etiology of oral leukoplakia is unknown and considered as multifactorial. Most important etiological factors are tobacco and alcohol, either separately or synergically.[9] However, tobacco smoking is considered as the most accepted risk factor of oral leukoplakia. Other physical agents such as chronic irritation, electro-galvanic reaction between unlike restorative metals, and ultraviolet radiation are also considered as risk factors for oral leukoplakia.[10],[11] There is a possible role of human papilloma virus infection in the origin of leukoplakia.[12] Further oral hairy leukoplakia has been considered as an early sign of HIV infections.[13]

  What are the Clinical Characteristics of Oral Leukoplakias? Top

Leukoplakia is common in the middle- and older-age group individuals and is more common in males. Buccal mucosa, alveolar mucosa, and lower lip are the most common sites for leukoplakia.[14] In the beginning stage, the lesions appear as slightly elevated grayish-white plaque [Figure 1]. Its margin may be either well defined or gradually blend into the surrounding normal mucosa.[15] Then, slowly, early lesions become thicker and whiter and leathery appearance with surface fissures [Figure 2]. Few lesions may develop surface irregularities and are called as granular or nodular leukoplakia [Figure 3]. Furthermore, few lesions develop a papillary surface and are called as verrucous leukoplakia. One occasional variety of leukoplakia is called as proliferative verrucous leukoplakia, [Figure 4] characterized by the widespread multiple sites of involvement and is developed without any known risk factors.[16] This proliferative verrucous leukoplakia has a high recurrence rate and very often transform into oral squamous cell carcinoma. In many patients, white patches are developed on the alveolar mucosa and buccal vestibule secondary to the use of mouthrinses containing herbal extract Sanguinaria.[17] However, Sanguinaria associated white patches are usually multifocal and should not be confused with early proliferative verrucous leukoplakia. Few leukoplakias develop in combination with red patches, i.e., erythroplakia. When both red and white patches are interproxed, the lesion is called speckled leukoplakia or speckled erythroplakia [Figure 5].
Figure 1: Early-stage leukoplakia on the left buccal mucosa which appears as slightly elevated grayish-white plaque

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Figure 2: A mature leukoplakia on the left lateral border of the tongue which is thicker and whiter and having leathery appearance with surface fissures

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Figure 3: Nodular leukoplakia on the left buccal mucosa

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Figure 4: Proliferative verrucous leukoplakia on the dorsum of the tongue

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Figure 5: Erythroleukoplakia on the right buccal mucosa having alternate white and red patches

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As the risk level of oral leukoplakia is difficult to measure clinically, few noninvasive methods that eliminate the need for surgical procedure can be used to detect the risk level. Brush biopsy can be done to collect the basal layer cells for microscopic evaluation. Toluidine blue which stains the nucleic acids and dysplastic cells can be applied clinically over the lesion to detect the level of risk. It is also used to select the best site for biopsy. These two methods are adjunctive diagnostic methods only and are not substitute to traditional scalpel biopsy.

  What is the Malignant Transformation Rate of Oral Leukoplakias? Top

The overall frequency of malignant transformation rate of oral leukoplakia varies between 15.6% and 39.2%.[18],[19] A speckled leukoplakia has maximum malignant transformation rate.[20] The annual average of malignant transformation rate of oral leukoplakia is 1% in various populations with the highest reported rate of 43%.[21] The location of the lesion has a significant correlation with the malignant transformation rate. Lesions on the floor of the mouth have the highest malignant transformation rate of 42.9% followed by 24.2% on the tongue and 24% on the lip.[18] The clinical appearance of the leukoplakia also has a correlation with their malignant transformation rate. In general, the thicker the lesion the greater the chance of having dysplastic changes.[15] The dysplastic changes are thus more with verrucous leukoplakia than a thick homogeneous lesion and which, in turn, is more than a thin homogeneous leukoplakia.[15] The malignant transformation rate of homogeneous leukoplakia is 6.5% and speckled leukoplakia is 23.4%.[22] Furthermore, 36.4% of the leukoplakia with microscopic evidence of dysplastic changes transformed into frank oral squamous cell carcinoma.[22] Almost 70.3% of the patients with proliferative verrucous leukoplakia change into oral squamous cell carcinoma.[16] In females, the malignant transformation rate is more compared to males.[11] Furthermore, the malignant transformation rate of leukoplakia among nonsmokers is more compared to smokers.[11],[22] The malignant transformation rate of oral leukoplakia is more when the size of the lesion is >200 mm2.[23] Furthermore, when there is the presence of invasive Candida albicans, the malignant transformation rate is more.[23]

  What are Microscopic Characteristics of Oral Leukoplakia? Top

Microscopic characteristics of oral leukoplakia vary between normal epithelial cellular architecture to dysplasia and carcinoma. The dysplasia may be mild, moderate, and severe types. The severity of the dysplasia can be assessed based on architectural disturbance accompanied by cytological atypia. According to the WHO, irregular epithelial stratification, loss of polarity of the basal cells, drop-shaped rete ridges, increased number of mitotic cells, dyskeratosis, and keratin pearls within rete ridges are the characteristics of epithelial dysplasia. There are no precise criteria to divide the dysplasia into mild, moderate, and severe categories.[24] In mild dysplasia, the cytological and architectural changes are confined to lower third of the epithelium thickness; in moderate dysplasia, the changes are up to the middle third of the epithelial thickness; and in severe dysplasia, the changes are more than middle two-third of the whole epithelium thickness.[24]

  How to Diagnose an Oral Leukoplakia? Top

A white lesion cannot be diagnosed clinically as any other disease of the oral mucosa (such as white sponge nevus, frictional lesions, candidiasis, chemical injury, leukoedema, hairy and leukoplakia) is a provisional diagnosis of leukoplakia. When any etiology such as tobacco, C. albicans and mechanical irritation, etc., is excluded and histopathologic examination cannot reveal that lesion as any other specific disease, then it is diagnosed as a definite leukoplakia. The tissue for the biopsy must be taken from most suspicious area. Toludine blue may be applied to select a suitable biopsy site. For a smaller size leukoplakia (<2–3 cm), excisional biopsy should be considered. For wide spread or multifocal leukoplakia, multiple incisional biopsies should be considered. Histopathology is considered to be the gold standard for the diagnosis of leukoplakia. When histopathology reveals typical characteristics, the lesion is confirmed as leukoplakia.

  What are the Treatment Options for Oral Leukoplakia? Top

The goal of leukoplakia treatment is to prevent its malignant transformation. Cessation of the smoking and alcohol habits is the first step in leukoplakia treatment. Usually, the degree of epithelial dysplasia and the location of the leukoplakia decide the choice of the treatment.[8] The ideal treatment for a leukoplakia is surgical excision. The commonly used surgical options for the excision are conventional scalpel surgery, carbon dioxide laser ablation, electrocauterization, and cryosurgery. However, there is no mention of the width of the margin that should be considered while excision. The recurrence rate following excision of the lesion varies between 0% and 30%.[8] Apart from surgical treatment, many chemoprevention treatment options such as topical or systemic use of antioxidant such as carotenoids (retinoids, beta-carotene, and lycopene); vitamins such as Vitamin A, C, and E; mouthwash containing an attenuated adenovirus; ketorolac mouthwash; local bleomycin; and mixture of tea are available in the literature.[25] However, the success of these chemoprevention treatments is not well documented.

  What is the Management Protocol for Oral Leukoplakia? Top

An outline for the management of oral leukoplakia is mentioned in [Figure 6]. The level of competency of a clinician to diagnose white lesions clinically is important. It is very critical to distinguish leukoplakia-like lesions from a true leukoplakia. Elimination of associated risk factors such as tobacco habit might need professional habit intervention, and 6–8 weeks are acceptable to observe a possible regression of the lesion. If the lesion does not regress within 6–8 weeks, a biopsy must be taken from the lesion. There is no quality scientific evidence showing that treatment of leukoplakia can prevent recurrence or further development of squamous cell carcinoma. It is always safe to treat a leukoplakia irrespective of the presence or absence of epithelial dysplasia.[26]
Figure 6: Oral leukoplakia management flowchart

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  Conclusion Top

An oral leukoplakia if left untreated may lead to frank oral cancer. The role of a primary health-care provider or a family physician is very important and crucial in the early identification of the leukoplakia. Elimination of associated habits can reduce the malignant transformation of a leukoplakia. There is no universally accepted standard treatment for the leukoplakia, but surgical excision of the total lesion is widely accepted treatment. These patients need lifelong follow-up at regular intervals.

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Conflicts of interest

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  References Top

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