title: 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.
authors.affiliation: Department of Pathology, School of Medicine, Adnan Menderes University, Aydin, Turkey. fkdoger@gmail.com
authors.forename: Furuzan K
authors.initials: FK
authors.lastname: Doger
authors.forename: Emel
authors.initials: E
authors.lastname: Dikicioglu
authors.forename: Filiz
authors.initials: F
authors.lastname: Ergin
authors.forename: Emel
authors.initials: E
authors.lastname: Unal
authors.forename: Neslihan
authors.initials: N
authors.lastname: Sendur
authors.forename: Meltem
authors.initials: M
authors.lastname: Uslu
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D017209:Apoptosis; D015415:Biomarkers / Q000378:metabolism; D002452:Cell Count; D049109:Cell Proliferation; D004817:Epidermis / Q000378:metabolism / Q000473:pathology*; D005260:Female; D019085:Fluorescent Antibody Technique, Direct; D006801:Humans; D007124:Immunoenzyme Techniques; D020287:In Situ Nick-End Labeling; D015603:Keratinocytes / Q000378:metabolism / Q000473:pathology*; D019394:Ki-67 Antigen / Q000378:metabolism; D007700:Kinetics; D008297:Male; D008407:Mast Cells / Q000473:pathology; D008875:Middle Aged; D016328:NF-kappa B / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011565:Psoriasis / Q000378:metabolism / Q000473:pathology*; D012189:Retrospective Studies; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D015415:Biomarkers; D019394:Ki-67 Antigen; D016328:NF-kappa B; D019253:Proto-Oncogene Proteins c-bcl-2; D014409:Tumor Necrosis Factor-alpha