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DYSKERATOSIS IN BOWEN'S DISEASE: THE ULTRASTRUOTURE AND FATE OF KERATINOCYTES WITH ALTERED TONO‐FILAMENT‐DESMOSOME COMPLEXES
Author(s) -
KARÁSEK JOSEF,
PIT́HA JAN,
OEHLERT WOLFGANG,
KONRAD BOHUSLAV
Publication year - 1971
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.1971.tb14029.x
Subject(s) - desmosome , keratinocyte , dyskeratosis , organelle , ultrastructure , epidermis (zoology) , intermediate filament , cytoplasm , acantholysis , bowen's disease , protein filament , chemistry , darier's disease , microbiology and biotechnology , biology , pathology , cell , basal cell , anatomy , medicine , hyperkeratosis , in vitro , immunology , disease , cytoskeleton , biochemistry , antibody , autoantibody
Summary.— The ultrastructure of dyskeratotic cells in Bowen's disease has been studied. It has been found that, in the suprabasal layers in some keratino‐cytes, all tonofilament‐desmosome complexes (TFDC), as well as many cytoplasmic organelles, are altered. The earliest stage of TFDG alteration con‐sisted in the separation and retraction of tonofilaments from the desmosomes. The consequence of this was the disappearance of the desmosomes and acantholytic separation of the involved keratinocyte. Our findings indicate that this was followed by the disintegration of the involved keratinocyte apart from the tonofilaments. These were released into the intercellular space and finally into the corium through breaks In the basal lamina. The Langerhans and some other dendritic epidermal cells are likely to play a role in the latter process.