Non-homogenous leukoplakia is a lesion of non-uniform appearance. The color may be predominantly white or a. Homogeneous leukoplakias: the most common type, are uniformly white plaques – common in the buccal (cheek) mucosa and usually of low malignant potential. Oral leukoplakia (leuko=white, plakia=patch) is a white patch in the mouth that There are two main types: homogenous and non-homogenous leukoplakia.

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The main purpose of this paper was to assess the current state of science on oral leukoplakia. Nowadays there are no currently accepted markers to distinguish those that may progress to cancer from those that may not.

The current golden standard is considered the presence of epithelial dysplasia on the tissue biopsy of the lesion. Proliferative verrucous leukoplakia is a rare form of OL which has multiple recurrences, is refractory to treatment and has malignant transformation in a short period.

It is considered a true premalignant lesion. The management of oral leukoplakia varies from a “wait and see” attitude and topical chemopreventive agents to complete surgical removal. Oral leukoplakia OL is the most frequent potentially malignant disorder of oral mucosa. Although OL is mentioned in clinical reviews since 2it was first defined by World Health Organization in 3 as a white patch or plaque which cannot otherwise be characterized clinically or pathologically as any other disease.

Since then until now, the meaning of oral leukoplakia is not very much changed. In 4after an international symposium held in Uppsala, Sweden in the definition, was added that oral leukoplakia is not associated with any physical or chemical cause, excepting smoking and it can become cancer. In it was decided that the name of leukoplakia should be limited only to a clinical diagnosis defined by exclusion of other white lesions such as oral lichen planus, white sponge nevus, nicotine stomatitis, leukoedema etc 5.

In van der Waal 6 proposed a new definition which seems more oportune as it includes the histological confirmation “A predominantly white lesion or plaque of questionable behavior having excluded, clinically and histopathologically, any other definable white disease or disorder”. This one hasn’t been assessed yet by WHO but it has good chances for acceptance.

The pooled estimated prevalence rate of oral leukoplakia in varied between 1. For this estimated rate, the author- Stefano Petti, in a meta-analysis including 23 primary studies from all over the world published in the period found no difference between geographical areas and between younger and older patients. OL is often found among men, and its prevalence increases with age advancement.

It has been estimated that it mainly affects men over 40 years 8. The etiology of OL is considered multifactorial, but smoking is appreciated to be a frequently involved factor.

It is much more common among smokers than among non-smokers 5. Alcohol is thought to be an independent risk factor 4 but definitive data are still lacking. There are conflicting results of studies related to the possible role of human papillomavirus infection. As OL can mimic a large variety of lesions, in case a possible causal factor is suspected such as dental restoration, mechanical irritation.

In the later case a subsequent evaluation in 4 weeks is needed 6. OL is classified in two main types: Proliferative verrrucous leukoplakia is a subtype of verrucous leukoplakia characterized by an aggressive evolution, a multifocal appearance, resistance to treatment, higher degree of recurrence and a high rate of malignant transformation 9. Histological appearance of oral leukoplakia varies between no dysplasia and carcinoma.

Dysplasia reflects histological changes which are followed by the loss of uniformity or of the architecture of the epithelial cells. At the last world seminar of Oral Medicine about potentially malignant lesions, London 11it has been recommended a binary classification of histological changes without risk or low risk and moderate or severe risk.

This aims to reduce subjectivity in grading dysplasia, thus increasing the possibility of conformity between histological interpretations of different pathologists 5.


Lesions are classified as non-dysplastic and dysplastic mild dysplasia, moderate or severe. Some authors have already tested this system for grading dysplasia and confirmed these views Oral squamous cell carcinoma is a common malignancy worldwide and the most encountered oral malignant tumor 12 It has a multifactorial etiology but the most important factors are tobacco and alcohol, separately and synergically The cohort studies about oral leukoplakia are very rare, so it is difficult to appreciate its real malignant transformation rate due to various regional habits 6 The risk factors for malignancy of OL such as vicious habits smoking, alcohol intakeclinical form, location of lesions were studied.

Among them, tobacco cigarette smoking was reported to be the most important etiological factor for the development of oral premalignant lesions and to their progression into oral carcinoma Napier and Speight have recently revised predictive clinical factors -age, gender, location of lesions but results vary between different study populations In an Italian population oral premalignant lesions located on the tongue were more frequently dysplastic compared with the buccal mucosa.

Conversely in the Indian population oral leukoplakia of the buccal mucosa is more involved in malignisation. Despite enormous progress in molecular biology at present there is no certain marker to predict malignant transformation of oral leukoplakia in a particular patient. As it was 20 years ago, epithelial dysplasia is still currently considered “the gold standard” for determining the risk of malignant transformation However it is known that epithelial dysplasia is correlated with clinically heterogeneous lesions that are considered to have the greatest risk.

As histological examination has a degree of subjectivity, there is the need to improve its capacity to assess the dysplasia.

This can be done using other markers or by the cross examination of two pathologists. Identification of biomarkers for oral carcinogenesis is based on markers of proliferation Ki and component of cell cycle control such as tumor suppressor proteins p53, the retinoblastoma protein pRb and cycline D1.

But none of these markers are used in routine diagnosis. Expression of p53 and loss of expression of p16 are bomogeneous to be the earliest events in the malignisation process. Another valuable predictive method is a morphometric computer-assisted analysis was used the measure the size of the cell perimeter and the nuclear perimeter of normal mucosa, oral leukoplakia and oral carcinoma.

This technique used computer images of histological stained sections.

Oral Leukoplakia – an Update

It showed that these dimensions increased gradually with significant difference from normal homogebeous, oral leukoplakia and the highest level in oral carcinoma Proliferative verrucous leukoplakia PVL was first described by Hansen has a high risk of transformation in oral carcinoma. PVL begins as one or more homogeneous leukoplakic areas and, in time it extends to more oral sites. It slowly grows and has a high tendency to recur after treatment.

It has been reported that most frequently it affects the gingivae But other authors also homogeneouss the buccal mucosa, gingiva, and alveola ridges Proliferative verrucous leukoplakia has an uncertain etiology. The association of PVL and presence of Human Papilloma Virus has been suggested previously but wasn’t confirmed by further studies so far Epstain-Barr virus is the proven etiologic cause of nasopharyngeal carcinoma, oral hairy leukoplakia, lymphoproliferative disease, B-cell lymphomas and lymphoepithelial carcinoma.

The diagnosis of PVL based on clinical data is usually late, as the progressive evolution of the lesions from homogeneous leukoplakia spreading too many different locations and with the appearance of erythroplastic and verrucous forms takes time.

Proliferative verrucous leukoplakia has a high rate of recurrences after treatment and a high rate malignant transformation. Multiple location lesions are more prone to finally develop with single location leukoplakia they found that widespread lesions have a higher potential for the cancer development than unique lesions.

The usual clinical examination of oral mucosa is most frequently visual.

It is the standard conventional method for oral cancer screening. It depends on the experience and skills of the clinician. But the risk level of the lesion is difficult to measure.


A digital manual for the early diagnosis of oral neoplasia

There are many variants of adjunctive techniques for the detection of potentially malignant disorders, including oral leukoplakia. Brush biopsy was designed for clinical lesions which initially based on clinical features did not require a biopsy. This is a noninvasive technique which collects the basal layer cells using a brush. It can be used for mass screening campaigns.

Oral Leukoplakia – an Update

It eliminates the leukolpakia for surgical procedure in doubtful lesions Since it was introduced inuntil now it shows great promise Toluidine blue is an intravital staining for nucleic acids and abnormal tissue. Initially was used for mucosal lesions of the cervix. In the oral cavity the method was used as guidance for biopsy site selection.

Chemiluminescence reflective tissue fluorescence was first applied for the detection of cervix dysplasia. It is based upon the normal fluorescence of the tissue when exposed to blue-white illumination. The technique has been adapted for oral mucosal inspection in the ViziLite homogeneus. It detects a variety of oral mucosa lesions including linea alba, hairy tongue, leukoedema traumatic ulcers Oral leukoplakia has a high degree of visibility and sharpness with proeminent and distinctive margins of the surrounding mucosa.

As the test does not accurately distinguish between high risk and low risk leukoplakia it should be used with caution The limit of all these methods or techniques is that they do not provide a definitive diagnosis.

They are useful in evaluating a multicentric lesion as well as in noncompliant patient for motivating them to return for further controls.

The main objective in oral leukoplakia’s management of care is to detect and to prevent malignant transformation. At the first, the ceasing of the risk activities such as smoking is leukoplalia. Further, the histopathological evaluation is needed. The degree of dysplasia will guide the choice of the hommogeneous. Oral leukoplakia presenting low malignant risk no dysplasia or simple displasia may be either completely removed or not, and the decision should consider other factors such as location, size and, in the case of smokers, the patient’s engagement in smoking cessation In the presence of moderate or severe epithelial dysplasia, surgical treatment is recommended 6.

The surgical treatment can use conventional surgery or laser ablation, electrocauterization, or cryosurgery Surgical excision of OL does not lower the risk of subsequent malignant transformation but it brings the opportunity for a complete histolopathological examination of the lesion. Cryotherapy is not considered to be a first line therapy of oral leukoplakia.

The risk of post-operative scarring, tissue contraction limit the use of the method The medical treatment uses local and systemic chemopreventive agents such as vitamin A and retinoids, systemic beta carotene, lycopene a carotenoidhomgeneous as mouthwashlocal bleomycin, and a mixture of tea used both topically and systemically with a reduced benefit Another possible choice is an attitude of “wait and see” to keep oral leukoplakia under clinical and histological surveillance with frequent visits and biopsies without other treatment.

This uomogeneous can observe an early malignant transformation and subsequent specific treatment The role of the dentist and general practitioner is important in the early diagnosis when leukoplakia is usually asymptomatic and leumoplakia is simple to remove possible factors involved in its etiology -smoking, thus reducing the rate of malignant transformation.

There is no satisfactory treatment for leukoplakia so far. It must be assumed that generally leukoplakia should be removed preferably totally, if possible and patients should be regularly monitored for any relevant mucosal change, and instructed to avoid the major risk factors of oral epithelial dysplasia, especially tobacco usage and alcohol consumption.

National Center for Leuioplakia InformationU.