Nature of cell kinetics in psoriatic epidermis.

Abstract:

BACKGROUND:Psoriasis vulgaris is a common chronic inflammatory dermatosis. Disorders in keratinocyte proliferation, differentiation, inflammation and immune dysregulation are the major factors implicated in the pathogenesis of psoriasis vulgaris. METHODS:The study was performed in skin specimens of 25 patients with psoriasis vulgaris and a control group of 10 individuals without a skin disease. Biopsy specimens from lesional and normal skin were analyzed by immunohistochemical method for expressions of Ki-67, Bcl-2, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL), tumor necrosis factor alpha (TNF-alpha) and nuclear factor kappa B (NF-kappaB). In addition, densities of mast cell infiltration were also investigated. RESULTS:Ki-67 and TUNEL indexes and TNF-alpha and NF-kappaB expressions were significantly higher in psoriatic epidermis than in normal epidermis (p < 0.05). There was no significant difference at Bcl-2 reactivity between the normal and the psoriatic epidermis (p > 0.05); however, Bcl-2 staining intensity of lymphocytes was higher in psoriatic lesions than in normal dermis (p < 0.05). Additionally, the number of mast cells was significantly higher in psoriatic dermis than in normal skin (p < 0.05). CONCLUSIONS:There were several complex factors involved in the pathogenesis of psoriasis. We conclude that cellular damage and apoptosis temporarily coincide with epidermal proliferation during the course of psoriatic hyperplasia.

journal_name

J Cutan Pathol

authors

Doger FK,Dikicioglu E,Ergin F,Unal E,Sendur N,Uslu M

doi

10.1111/j.1600-0560.2006.00719.x

subject

Has Abstract

pub_date

2007-03-01 00:00:00

pages

257-63

issue

3

eissn

0303-6987

issn

1600-0560

pii

CUP719

journal_volume

34

pub_type

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