Nature of cell kinetics in psoriatic epidermis
Article first published online: 12 FEB 2007
Journal of Cutaneous Pathology
Volume 34, Issue 3, pages 257–263, March 2007
How to Cite
Doger, F. K., Dikicioglu, E., Ergin, F., Unal, E., Sendur, N. and Uslu, M. (2007), Nature of cell kinetics in psoriatic epidermis. Journal of Cutaneous Pathology, 34: 257–263. doi: 10.1111/j.1600-0560.2006.00719.x
- Issue published online: 12 FEB 2007
- Article first published online: 12 FEB 2007
- Accepted for publication December 4, 2006
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-α) and nuclear factor kappa B (NF-κB). In addition, densities of mast cell infiltration were also investigated.
Results: Ki-67 and TUNEL indexes and TNF-α and NF-κB 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.