Precancerous Conditions

According to WHO leukoplakia is defined as a predominantly white lesion of the oral mucosa that cannot be scraped off, and cannot be diagnosed as any other disease or definable lesion. The prevalence in Sweden of leukoplakia is 3.6 per cent; it is more common in men (6.1 %) than in women (1.2 %) [3].

Leukoplakia is the most common oral precancerous lesion. Within a time span of 10-20 years about four per cent of the leukoplakias transform to cancer [4]. They are categorized as homogenous leukoplakia, non-homogenous leukoplakia, and erythroplakia.

Homogenous Leukoplakia

Mainly white, flat and thin lesion, possibly with shallow furrows. The surface is smooth, wrinkled or corrugated, but has a homogenous texture throughout the lesion. *CASE*

Non-homogenous Leukoplakia

Mainly white or white and red lesion (erythroleukoplakia), which can be irregular, flat, nodular or exophytic. The nodular lesion displays slightly elevated, rounded, red or white papules or nodules, and the exophytic lesion has irregular, blunt or sharp projections. Fig--------

Leukoplakia has been the designated diagnosis for many white lesions. Several studies have shown, however, that white lesions in the oral cavity can have a variety of causes [5]. It is important to establish the etiology as it may pertain to the malignancy risk. White patches or plaques that have a local cause of origin, e g friction, dental restoration, or cheek bites, should not be included among leukoplakias. White patches or plaques that can be referred to, or is the result of, tobacco consumption or other physical or chemical agents are diagnosed as oral leukoplakias. In some of these lesions there is a great risk of malignancy , while other ones display more limited or unknown risks. Since this can be partly explained by local variations and habits attributable to these, it is particularly important to establish the etiology. *CASE*

Snuff Induced Lesions

Smokeless tobacco (snuff, chewing tobacco) is used all over the world. It is essential to have a clear picture of the content in various tobacco products to compare the mucosal changes that are the consequences of indulging in the habit of using snuff. In 1995 about 900 000 Swedes used snuff, which corresponds to 0.7 kilos per capita, a figure that makes Sweden the leading country in the world in this respect. Snuff lesions are graduated in a scale of four stages as introduced by Axéll et al in 1976 [6]. The scale is based on color and shape changes in the oral mucosa.

A comparative study [7] concerning loose vs portion-bag-packed moist snuff, indicated that the usage of the loose variety produced more pronounced clinical and histological changes compared to portion-bag-packs (Figs 3 and 4. KOMPLETTERING)*CASE*. The exposure time (h/day) is the most prominent factor for the degree of damage, followed by the quantity (g/day), and lastly, the number of years of use [7]. Snuff users who varied the location of their snuff displayed less pronounced damage than those who invariably put the snuff in the same location [7]. The snuff lesion is reversible - if the habit is stopped the mucosa regains its normal appearance. This also goes for more pronounced lesions that indicate histological signs of dysplasia [7].

Erythroplasia

Red areas that cannot be diagnosed as any other disease or definable lesion. Erythroplakia is a comparatively rare lesion of the oral mucosa. Early diagnostics is of the utmost importance [8,9], as it is the most serious precancerous change in the oral mucosa. In about 80 per cent of the erythroplakias grave epithelial dysplasias can be found. In most cases the erythroplakia is well demarcated and relatively small, but more extensive changes and interspersions of white papules and nodules can exist.
*CASE*

Oral Lichen Planus

The prevalence of oral lichen planus in Sweden is 1.9 per cent [3]. It is more frequent in women (2.2 %) than in men (1.6 %). The oral lichen planus lesions exhibit a varied pattern from which six main types can be discerned. Three of these are white and designated papular, reticular, and plaque, respectively; three are red and designated atrophic, ulcerous, and bullous, respectively [8,9]. More than one type can be found simultaneously in a patient. The skin disease lichen ruber planus can have intraoral manifestations in one and the same patient. However, it is more common for the intraoral lichen lesions to develop from immunological mechanisms connected to local factors [10].

Oral lichen is considered to be a precancerous condition. In investigations incorporating large patient groups the malignancy incidence varies between 0.4 to 12.3 per cent. The differences can in some studies be attributed to uncertainty regarding the original diagnosis and variations in the follow-up time span. In all, a couple of hundred cases have been reported in the literature about cancer evolving from lichen lesions of chiefly the atrophic, ulcerous or plaque varieties. *CASE*

Treatment of Precancerous Conditions

When the primary clinical diagnosis is homogenous leukoplakia, the treatment should be started by eliminating suspected etiologic factors. The time required for the white lesions to regress after the elimination can vary from one or two weeks to months. If no signs of regression can be detected within 2-4 weeks after the elimination of a suspected etiologic factor, a representative biopsy should be performed [5]. If possible, the whole lesion should be excised, otherwise a tissue specimen should be taken from the most transformed area, including the transition to normal mucosa. For more extensive lesions this may imply that more than one biopsy should be performed.

All intraoral lesions that are excised must be forwarded for histopathologic examination. If the histology analysis reveals signs of dysplasia the patient must without further delay be referred to maxillofacial surgery or the ENT department for specialist care.

The most common etiology for leukoplakias is some kind of tobacco-related habit. It is of the utmost importance to inform the patient explicitly on the relationship between this habit and the lesions in the oral cavity. The patient should preferably be persuaded to stop using tobacco. A reduction of the cigarette consumption only seems to have a marginal effect. Snuff users, on the other hand, can reduce their snuff damage by cutting down on the daily consumption, use portion-bag-packs or altering the location of the snuff.

Lesions in which a candida infection is present, is treated with antimycotics for a period of at least four weeks. In this way non-homogenous leukoplakias can be homogenized and follow-ups can thus be carried out as for the homogenous leukoplakias, where no further treatment is required. The first checkup should be after three months, and thereafter at intervals of six months.

Patients with erythroplakia must immediately be referred to specialist care. Excision of these lesions have to be performed with wide margins owing to the fact the transformation almost always unfolds grave epithelium dysplasias and frequently cancer in situ lesions.

Oral lichen lesions with red traces (atrophic, ulcerous, and bullous) in patients with subjective symptoms, or those who have findings directly attributable to some form of trauma, should be treated [8]. Elimination of the trauma, including careful mouth hygienic measures, and smoothing of dentures and/or tooth fillings, constitutes the initial treatment. A change of material can be necessary if there is a contact surface between the mucosal changes and a filling (usually amalgam, but also composite material, gold, or porcelain-fused-to-metal ceramics)*CASE*. Sometimes an allergy test of dental material is necessary. When required, a representative biopsy should be done. If there is a suspicion of malignancy the patient must immediately be referred to a specialist.

If there is no traumatical cause antimycotic treatment with Fungizone® (Amphotericin B) sucking tablets, one tablet four times a day, alternatively Mycostatin® (Nystatin) mixture, sugarfree, one ml four times a day, should be administered. The treatment should proceed for at least four weeks, but be re-evaluated after two weeks, when atrophies and ulcerations should have improved markedly. Otherwise complement with anti-inflammatory treatment , Kenacort ®- T (Triamcinolonacetonid) paste or ordinary ointment rubbed into the lesions and covered with a layer of Kenacort ®- T mouth ointment. This treatment, carried out 2-3 times a day, should go on for at least four weeks, after which it can be successively de-escalated . Ulcerations that do not respond to treatment should be excised [8].