par Heenen, Michel 
;Galand, Paul ;De Maertelaer, Viviane ;Heenen, Paul-Henri
Référence Cell proliferation, 20, 6, page (561-570)
Publication Publié, 1987
;Galand, Paul ;De Maertelaer, Viviane ;Heenen, Paul-Henri Référence Cell proliferation, 20, 6, page (561-570)
Publication Publié, 1987
Article révisé par les pairs
| Résumé : | Abstract A mathematical model of cell renewal in epidermis is proposed for describing how psoriatic lesions might develop, based on available cell kinetic data for normal and psoriatic epidermis. Our simulations clearly demonstrate that an increase in the turnover rate in the germinative cell population cannot alone induce the typical psoriatic tissue architecture (i.e. increased number of germinative cells). Two perturbations are needed to account for the morphology of clinically‐stable psoriatic lesions. The first corresponds to a temporary disturbance of the steady state of the germinative layer, resulting in limited growth of this compartment; the second perturbation corresponds to a reduction in transit time in the differentiated compartment. Moreover, our simulation, based on a widely‐accepted hypothesis of homeostatic control of tissue kinetics, demonstrates that the primary cause of typical psoriatic morphology is probably an alteration in epidermal maturation. In this view, depletion of differentiated cells at the surface is the stimulus for the increased cell production rate in the germinative population. Copyright © 1987, Wiley Blackwell. All rights reserved |
