Leukoplakia oral (overview) K13.2

White, non-wipeable mucous membrane area that cannot be assigned to a defined disease (WHO definition). Pathogenetically, every leukoplakia, regardless of the cause, is based on an increased or abnormal keratinization of the stratified (normally non-cornnifying) squamous epithelium of the oral mucosa. The resulting change in the refraction and reflection of light leads to a white discoloration of the mucosa.

Basically, oral leukoplakia is divided as follows:

I. Leucoplakia in the narrower sense(exogenous-irritant leukoplakia):

1. Leucoplakia due to physical effects (mechanical irritation caused by damaged teeth, malposition of teeth, morsicatio buccarum).
2. Leucoplakia due to chemical noxae (local contact with smoking or chewing tobacco).
3. Special position: Proliferative verrucous leukoplakia

II. leukoplakia in a broader sense (see Table 1):

1. Hereditary leukoplakia, e.g. nevus spongiosus albus mucosae, benign intraepithelial dyskeratosis, dyskeratosis follicularis, pachyonychia congenita and others
2. Endogenous irritant leukoplakia (inflammatory or infectious): e.g. lichen planus mucosae, drug reaction, fixed, pemphigus vulgaris, glossitis interstitialis syphilitica, viral papillomas.

Starting from the clinical appearance, it is useful to further differentiate leukoplakia in the strict sense (see above) according to appearance and surface. A distinction is made between:

1. Flat leukoplakia (mostly harmless)
2. verrucous leukoplakia
3. Erosive leukoplakia (urgent suspicion of precancerousness).

Oral erythroplakia is a precancerous special form, an analogue of erythroplasia of the genital mucosa, see below VIN and PIN.

Histologically, leukoplakia can be divided into:

1. Dysplastic leukoplakia
2. Non-dysplastic leukoplakia.

Frequency (Central Europe): 0.6-3.3% of the population. Men over 40 years of age are preferentially affected, frequency 1-5%. Men are affected 3-5 times more often than women.

Ubiquitous in the oral cavity; preferably retro-angular, floor of the mouth, edges of the tongue, vestibulum oris, edentulous alveolar ridge.

Uni- or multicentre, circumscribed or large, grey to rich white flocks with smooth or bumpy surfaces. S.a.u.

• speckled leukoplakia
• homogeneous leukoplakia
• erosive leucoplacia
• leucoplacia simplex
• Leucoplacia verrucosa.

Acanthosis, hyperkeratosis (ortho- or parakeratotic). Dysplastic epithelial changes of varying degrees.

• Of crucial importance for the therapeutic procedure is the question of the dignity of the lesion. Histological clarification and regular control biopsies are mandatory. A leukoplakia remains suspected of malignancy until the opposite is proven. In the case of dysplastic leukoplakia a surgical procedure is necessary.
• Electrodissection of the leukoplakic area (after histological confirmation of the findings), followed by curettage of the dissected area with a sharp curette, has proven successful.
• Ablation with_CO2 laser in defocused mode (diameter approx. 2-3 mm) can be attempted. The aim is ablation of the epithelium with subsequent secondary healing (healing time 6-8 weeks depending on the initial findings).
• Basically it is important to avoid causal external irritants such as defective teeth, poorly fitting dentures, smoking, alcohol, cheek chewing, UV damage (lip area), maceration in the vulva area.

Risk of carcinoma. Also exogenous-irritative and endogenous-irritative leukoplakias can transform into carcinomas. The average malignancy risk of a leukoplakia is 6-17.5% and is twice as high in the group of dysplastic leukoplakia as in non-dysplastic leukoplakia. Leucoplakias at the base of the mouth and in the area of the posterior lateral edges of the tongue show a higher rate of transformation, as does erythroleukoplakia.

Etiological classification of leukoplakia in the narrow and broader sense

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