10: Malignant disease of the oral cavity

10 Malignant disease of the oral cavity


In global terms, oral/oropharyngeal cancer is the sixth most common malignancy. In the Western world it accounts for only 2–4% of all malignant tumours although there is now good evidence to show that the incidence is increasing, particularly in younger people. By contrast, in Asia oral/oropharyngeal malig-nancy is the most common malignant tumour, which in parts of India accounts for no less than 40% of all malignancy. It is estimated that globally nearly 500 000 new cases develop annually and that in the year 2000 there were 1.5 million people alive with oral cancer at any one time.

Oral/oropharyngeal cancer is an almost entirely preventable disease, being caused by use of tobacco (with or without alcohol). In the West this is mostly cigarette smoking combined with alcohol abuse; the risk caused by both in combination is greater than the summation of the risks of each individually. In Asia and the Far East the use of Pan in its various forms and reverse smoking are the major aetiologic agents: epidemiological evidence strongly suggests that it is the presence of tobacco in the betel quid which is the major agent, although there seems also to be some relationship to the source of slaked lime and the areca nut itself. In the West, the incidence in women appears to be increasing and there is a worrying increase in the number of young patients, mostly male and particularly with tongue cancer, after a gradual fall earlier this century. This recent trend seems not to be related to tobacco and alcohol consumption and has been observed throughout Europe and North America. The general dental practitioner has a major role in prevention by advising and helping patients to cease tobacco smoking or chewing and moderating alcohol consumption.

Local control of disease at the primary site and the management of neck disease has improved; yet, despite this, cure rates and survival rates have only improved marginally in 40 years, remaining at approximately 55% survival at 5 years. Both recurrence of local disease and failure to control lymphatic metastases in the neck are early events and are a major cause of death. There is no doubt, however, that during the past 20 years great advances have been made in the management of oral cancer, and persistence of local disease and lymphatic metastasis are now less common. Why then have cure rates not improved? Field changes in the upper aerodigestive tract result in the phenomenon of multiple primary cancers. The longer a patient survives a first tumour, the greater the risk of developing a second or third primary tumour either elsewhere in the oral cavity or in the larynx, bronchus or oesophagus.

Even a patient who does not develop a second primary tumour is at risk of developing distant metastatic disease. Metastasis via the bloodstream is a relatively early event in oral cancer, although until recently rarely recognized during life. Currently 20% of all cancer-related deaths in patients with a tumour in the oral cavity/oropharynx are due to distant metastasis with no evidence of disease in the head or neck. Thus oral cancer is a ‘systemic’ disease from an early stage.


Megavoltage X-ray beams or electron beams are able to penetrate tissues and can cause cell death by producing lethal damage to DNA. Irradiated cells die as they attempt to divide and because malignant cells generally divide more rapidly than normal cells there is differential cell death. With careful planning and adjustment of dosage and frequency of treatment the tumour cells can be destroyed whilst sparing sufficient normal tissues to allow healing and repair. A typical regimen for an oral carcinoma would be a total dose of 55 Gray given by daily treatments on Monday to Friday over a 6-week period. The daily dose (fraction) is therefore only small and allows for repair of normal tissues between treatments. In most centres, surgery is the primary modality for most patients. Radiotherapy is used as a supplement when the surgical margins of the tumour are not clear or there is extensive nodal metastasis in the neck.

Although treating a cancer with radiotherapy avoids major surgery it has disadvantages:

An alternative way of treating tumours with radiotherapy is to implant radioactive materials into the tumour (brachytherapy). Radioactive iridium wires are the most commonly used implants. There is a rapid fall-off of dose with distance, and the technique continuously delivers very high-dose local irradiation with very little damage to adjacent tissues. Therefore the adverse effects of conventional radiotherapy are largely avoided.


The association of oral carcinoma with other oral mucosal lesions has been recognized for many years. Often these lesions are in the form of white plaques (‘leukoplakia’) or bright red velvety plaques (‘erythroplakia’), which may be present for periods of months to years before the onset of malignant change and often will be present together with the carcinoma when the diagnosis of malignancy is made. Because of this association, it has been assumed that such lesions lead directly to invasive carcinoma and hence are themselves premalignant. Some white plaques do have a potential to undergo malignant transformation and an examination of established carcinomas will show many to exist in association with white plaques. However, most oral carcinomas are not preceded by, nor associated with, leukoplakia.

Although historically oral leukoplakia has been recognized as premalignant, the risk of malignant transformation is not as great as was previously thought. Early literature suggested a 30% or higher incidence of malignant transformation of these lesions whereas more recent authors quote an incidence of 3–6%. The following oral lesions are now considered to carry a potential for malignant change:

A further group of conditions, although not themselves premalignant, are associated with a higher than normal incidence of oral cancer:

There remains a further group of oral conditions about which there is still some doubt as to whether their association with oral cancer is causal or casual:

Leukoplakia (Fig. 10.1)

Using the term leukoplakia either in a histological or clinical context is a matter of defining what is meant by the term. The World Health Organization (WHO) has defined leukoplakia as ‘any white patch or plaque that cannot be characterized clinically or pathologically as any other disease’. This definition has no histological connotation.

Potential for malignant change

The incidence of malignant change in oral leukoplakia increases with the age of the lesion. One study showed a 2.4% malignant transformation rate at 10 years, which increased to 4% at 20 years. It also showed that as the age of the patient increased so did the risk of malignant transformation: for patients younger than 50 years it was 1%, whereas for those between 70 and 89 years it was 7.5% during a 5-year observation period. Kramer et al. (1978) have shown that in Southern England leukoplakia of the floor of the mouth and ventral surface of the tongue, so-called ‘sublingual keratosis’, has a particularly high incidence of malignant change. Their study suggested that this occurrence was due to pooling of soluble carcinogens in the ‘sump’ of the floor of the mouth.


In any patient presenting for the first time with oral leukoplakia a careful history—particularly looking for aetiological factors—and a detailed clinical examination should precede the histological examination of biopsies of any suspicious areas. Suspicion is aroused by any areas of ulceration, induration or where the underlying tissues are bright red and hyperaemic. Vital staining with toluidine blue can be used to guide the clinician to those sites most suspicious of malignant change.

If there is a history of tobacco consumption then the patient should be persuaded to stop immediately. It has been shown that if the patient stops smoking entirely for 1 year the leukoplakia will disappear in 60% of the cases.

Whenever severe epithelial dysplasia or carcinoma-in-situ is present, surgical excision or CO2 laser excision of the lesions is mandatory. Small lesions may be excised, the margins of the adjacent mucosa undermined and the defect closed by advancing the margins. For larger defects the area should be left to epithelialize spontaneously (alternatively the area can be skin-grafted). On the tongue the graft is quilted onto the raw area, whereas on the cheek, floor of the mouth or palate the graft can be retained in place by suturing a suitable pack overlying it.

When only mild to moderate epithelial dysplasia is present the patient should be followed up at 4-month intervals and details of the lesions recorded in the notes either photographically or diagrammatically.

Jan 14, 2015 | Posted by in Oral and Maxillofacial Surgery | Comments Off on 10: Malignant disease of the oral cavity
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