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In this study, the clinical and histopathological aspects of 50 plantar warts are reported in relation to the type of papillomavirus present in the lesions, as detected by immunofluorescence tests, using specific guinea pig fluorescein-labelled IgG. Warts of plantar localization are not caused by the same human papillomavirus (HPV) since they are found to be associated with both HPV type 1 (HPV-1) and HPV type 2 (HPV-2). HPV-1 is always associated with deep and painful plantar warts (myrmecia), whereas HPV-2 is found to be associated with superficial, painless plantar warts (vulgaris or often mosaic type). Histologically, these two types of plantar warts are quite different. In myrmecia (HPV-1), characterized by an endophytic growth, large eosinophilic, keratohyaline-like granules are observed in the cytoplasm and nucleus of infected, often vacuolated cells. These granules appear early in stratum spinosum and are very numerous in stratum granulosum. In the mosaic type (HPV-2), the histopathological aspect is not different from that of common warts; these lesions have an exophytic growth and are characterized by foci of clear vacuolized cells which are found in stratum granulosum. Their cytoplasm contains round, basophilic keratohyalin granules which often have a heterogenous aspect. These differences are observed in other localizations of morphologically related warts associated with HPV-1 and HPV-2 and seem to be related to a specific cytopathogenic effect of HPV-1 an HPV-2 in human papillomas.

Are Epidermodysplasia verruciformis (E.V.) and disseminated flat warts different diseases? Are there any diagnostic criteria between them? In order to attempt answering these 2 questions, fundamental for prognosis and nosology, a comparative ultrastructural study was made of epidermal clear cells of 2 cases of E.V. and 4 flat warts from 4 patients of whom 3 were under immunosuppression drugs. The reason of cytoplasmic electron translucency was mainly a reduction in tonofilaments and keratohyalin amounts in E.V. and a centrifugal edema and vacuolization in flat warts. On the other hand, the number of ribosomes was raised in E.V. and reduced in flat warts. These findings allow differentiation between the 2 diseases and suggest a possible different host-virus relationship.

Estrone (E1)-sulfatase and dehydroepiandrosterone (DHEA)-sulfatase activities were studied in human female epidermis. Skin specimens were obtained by abdominal or plantar biopsies. The apparent Michaelis-Menten constants for E1 and DHEA sulfatases were 35.2 microM and 8.7 microM, respectively. A substrate inhibition was only observed for DHEA sulfatase. Both sulfatases had an elevated temperature optimum (65 degrees C). The effect of inorganic salts was also tested. In normal epidermis, E1-sulfatase activity was constantly higher than DHEA-sulfatase activity, but no correlation between these activities was observed. On the other hand, E1- and DHEA-sulfatase activities were lower in plantar than in abdominal epidermis. In plantar epidermis of palmoplantar keratoderma, large variations in E1-sulfatase activity, but no significant variation in DHEA-sulfatase activity, were observed. In human epidermis, the findings were consistent with the existence of two different sulfatases: E1 sulfatase and DHEA sulfatase. It would also appear that sulfatase activities are not linked to the abnormal shedding of plantar stratum corneum in palmoplantar keratoderma.

Incubation of human plantar stratum corneum (SC) with trypsin at various pH suppressed the typical "keratin pattern" in the cytoplasm of the horny cells and disclosed tonofilaments and desmosomal attachment plates as they are seen in living keratinocyts. Tonofilaments were 62-75 A wide and showed a 100-120 A periodicity. This effect was non-specific since it was also obtained by incubation of SC with citric acid or sodium citrate, but it was not due to hydration alone. Partial acantholysis was obtained by incubation with trypsin followed by citric acid. After simultaneous action of trypsin in sodium citrate and in citric acid, cell membranes were separated from the cytoplasm and many of them were broken around desmosomes with subsequent isolation of desmosomes. The role of trypsin in this effect was uncertain. These findings strongly suggest that the filamentous network built up by living keratinocytes remains almost unchanged during the keratinization process although no longer visible under E.M.

We report the results of an ultrastructural study of the hyperkeratotic epidermis in 23 cases of palmoplantar keratoderma (PPK) comprising 8 inherited keratoderma, 8 keratoderma climactericum in menopausal women and 7 symptomatic keratoderma. In all but one of the cases of inherited PPK and keratoderma climactericum, composite keratohyalin (KH) granules were found in granular cells of the interductal epidermis, which were similar to those found in the rat and in some other conditions. In the cases of symptomatic keratoderma, e.g. secondary to eczema, the appearance of the KH granules did not differ from that of granules observed in two normal plantar skin samples. While the real role played by these granules is unknown, they could constitute a differentiation marker of intraepidermal duct cells, and their abundance in PPK suggest that intraepidermal sweat ducts may play a part in PPK histogenesis.

The heterogenecity of keratohyalin (KH) has been demonstrated in rats, then in human warts where similar morphological features have been found and among them, dense homogeneous ovoïd single granules (SG) and composite granules (CG) apparently made up of single granules "coated" with a matrix. This work compares the ultrastructure of the KH of the tongue of newborn rats with that of common warts with and without post-fixation by OsO4, after oxydation by H2O2 and after pepsin treatment. The osmiophily of the SG is confirmed as well as the absence of osmiophily of the matrix of the CG. In man, however, the SG are resistant to oxydation by H2O2 and the CG matrix is oxydation sensitive whereas the opposite is observed in the case of rats. These differences show that it is impossible to deduce the composition of the KH in human warts from that of the rat despite their close ultrastructural resemblance but that important modification of the keratogenesis and KH formation are induced in the cells parasited by the virus of common warts.