In 1893, Audry1 postulated that defective epidermal keratinization or cornification was the essential pathological feature of psoriasis. This hypothesis, based on histological studies, has been amply justified by recent biochemical investigations. However, before entering into a discussion of these recent findings, it would be well to reiterate Flesch's definition of the processes involved in cornification or rather in the maturation of the human epidermis.2 He has called the consolidation of fibrous keratin precursors keratinization and the decomposition of cellular proteins or the formation of nonkeratinous components, in the horny layer, differentiation. These terms will be used forthwith in this paper.
Concerning keratinization, it has been found that, in psoriasis, a fibrous protein can be extracted from the scales, which is similar or identical with tonofibrin, which has previously been isolated from normal cellular epidermis.3 This protein appears to be a fibrous, keratin precursor,
ROE DA. The Psoriatic Process. AMA Arch Derm. 1959;80(2):210–219. doi:10.1001/archderm.1959.01560200078010
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