Medical expert of the article
New publications
Soft leukoplakia: causes, symptoms, diagnosis, treatment
Last reviewed: 07.07.2025
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Soft leukoplakia was first described by B. M. Pashkov and E. F. Belyaeva (1964), and differs from the usual forms of leukoplakia by the presence of slightly raised white lesions on the mucous membrane of the cheeks, lips, and tongue, covered with soft scales that can be easily removed with a spatula. Clinical lesions are narrow, very soft, whitish stripes that often occupy a significant portion of the mucous membrane of the oral cavity, slightly raised as a result of edema.
Pathomorphology of soft leukoplakia. Acanthosis, parakeratosis are observed in the epithelium, the granular layer is absent, there are light, unstained optically "empty" cells with pycnotic nuclei. Inflammatory reaction in the stroma is often absent. Histochemical and electron microscopic studies of soft leukoplakia foci have shown that RNA and SH-protein groups are practically absent in light cells, the activity of energy metabolism enzymes (LDH, G6-PGD, NaOH- and NADPH-tetrazolium reductases, cytochrome oxidase) is sharply reduced, and in some places is not detected at all. Electron microscopy revealed that these cells have few tonofilaments, mitochondria are vacuolated. Organelles are not detected in the cytoplasm around the nucleus, signs of lysis are expressed in the nuclei of some of them.
Histogenesis of soft leukoplakia. Histochemical and electron microscopic studies indicate that soft leukoplakia is a type of common leukoplakia, but complete keratinization with the formation of anuclear horny cells does not occur in soft leukoplakia. The stage of keratohyalin formation is absent. The basis of the process is dyskeratosis with the formation of functionally active cells and dystrophy of other cellular elements. In soft leukoplakia, unlike usual, there is no increase in the mitotic activity of basal cells and an inflammatory reaction in the stroma. This suggests that soft leukoplakia is not the result of an inflammatory process or trauma to the mucous membrane, but is dystrophic, possibly congenital. This is consistent with the data of K. Hashimoto (1966), who found a large number of light cells in embryos and children in normal conditions, similar in structure to those in soft leukoplakia. This is also evidenced by the appearance of this type of leukoplakia at a young age.
[ What do need to examine?
How to examine?