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Article
January 1973

Alterations of Cell Surfaces as a Pathogenetic Factor in PsoriasisPossible Loss of Contact Inhibition of Growth

Author Affiliations

Cologne, Germany; Boston; Cologne, Germany; Boston

From the Department of Dermatology, University of Cologne, Cologne, Germany (Drs. Orfanos and Mahrle), and the Department of Dermatology, Tufts University Medical School, Boston (Drs. Schaumburg-Lever and Lever). During this study, Dr. Orfanos was Research Associate in Dermatology at Tufts University, Boston.

Arch Dermatol. 1973;107(1):38-46. doi:10.1001/archderm.1973.01620160010002
Abstract

The plasma membrane, surface and glycoprotein-rich surface coat of psoriatic keratinocytes are significantly altered, showing: (1) microvillous transformation of plasma membranes, (2) decreased adhesiveness of extradesmosomal membrane regions, (3) nearly complete absence of glycoprotein-rich surface coats in the malpighian layer and thickening of these coats in the horny layer, and (4) incomplete marginal bands and irregular spatial architecture of horny cell surfaces.

These findings indicate decreased capability of psoriatic keratinocytes to participate in an intracellular adhesive system, and suggest loss of "contact inhibition of growth" in psoriatic epidermis in vivo, as known from in vitro models. This loss may be responsible for the increased mitotic rate in psoriasis.

Changes are limited to the involved skin in psoriasis and show good response to treatment with corticosteroids locally or methotrexate systemically.

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