Oral cancer is associated with significant morbidity, pain and death. Thus, prevention and early diagnosis is imperative. Recognition and control of pre-malignant oral lesions is an effective way to reduce the occurrence and thus, the morbidity and mortality of oral cancer. Oral pre-maglinancies are lesions with risk of uncontrolled cellular growth and transformation into cancer. Such lesions can occur in entire oral cavity and oropharynx. In the mouth, there are two main pre-cancerous lesions: leukoplakia and erythroplakia.

Leukoplakia is a white plaque that cannot be scraped off the mucosa. Those that are white, smooth and lack irregularities are homogeneous leukoplakias. Others show a rough corrugated surface and are referred to as verrucous leukoplakia. When these verrucous white lesions are diffuse or multifocal, they are termed proliferative verrucous leukoplakia. This form of leukoplakia is commonly found in elderly females, smoking habits are often absent, and they exhibit a high risk for malignant change.

Leukoplakia of the lips are associated with exposure to ultra-violet radiations. These white lesions are usually smooth, covering all or part of the vermilion lip border. Occasionally, they are crusted or thickened. When ulceration or induration is present, suspicion of dysplasia and early malignant change should be high.

Leukoplakia of the floor of mouth and ventral surface of the tongue (also known as sublingual keratosis) exhibit a high incidence of malignant transformation. Kramer et al reported up to 25% of malignant transformation in these lesions.

Another high-risk lesion is the red-appearing patch (Erythroplakia). Erythroplakia typically presents as a homogeneous velvety red diffuse macule and may also be associated with white lesions. Erythroplakia with multiple small white spots are referred to as speckled leukoplakia. These lesions are more likely to progress to carcinoma compared to the homogeneous leukoplakia.

Oral squamous cell carcinoma (OSCC) may arise in the site of pre-existing leukoplakia and erythroplakia or may arise de novo. Clinically, early carcinoma have the appearance of the aforementioned pre-cancerous lesions. Once there is substantial invasion of the submucosa by carcinoma cells, OSCC appear as indurated swellings or non-healing ulcers with raised borders.

The diagnosis of pre-malignant lesions depends upon clinical suspicion and biopsy followed by histological diagnosis. Visual inspection is largely inaccurate. Cellular markers and imaging modalities are being developed and tested to improve the accuracy of identifying malignant transformation in these lesions.

Risks factors for oral cancer and pre-malignancy are similarly. These include smoking, alcohol consumption, betel-nut chewing, etc. Smoking has been associated with hyperkeratosis and leukoplakia. The long-term usage of smokeless tobacco is associated with an increased risk for development of carcinoma. Alcohol consumption alone or in conjunction with tobacco usage increases the risk for carcinogenesis. Candida species is also associated with leukoplakia, since candidal hyphae are often seen in microscopic sections from oral leukoplakia. Candida is capable of producing carcinogenic nitrosamines through biochemical tissue reaction. Although the association with carcinogenesis is not clear, the presence of Candida must be considered to be a potential risk factor.

Frequently, biopsy is delayed because of patient of clinician’s decision to institute other treatment to rule out infection or local irritation. However, a definitive histological diagnosis should not be delayed until novel molecular markers or imaging modalities emerge. Pre-malignant lesions could be excised or treated with laser therapy.

Dr Raymond Peck		Dr Sandeep Rajan
Department Director &		Senior Consultant
Senior Consultant		Medical Oncology
National Dental Centre