pathogenesis of psoriasis

FREE subscriptions for doctors and students... click here
You have 3 more open access pages.

Hyperproliferation of keratinocytes in response to cytokines released by inflammatory cells produce characteristic changes in the epidermis and dermis, including:

  • reduced epidermal cell transit time - from 30 days to 2-3 days - causing:
    • acanthosis - epidermal thickening - 3-5 times normal
    • arrowheads - elongated epidermal rete ridges
    • hyperkeratosis - thickening of the cornified layer
    • parakeratosis - nuclei retained in stratum corneum (1)

  • increased expression of intercellular adhesion molecule 1 (ICAM-1) in the epidermis (1)

  • granular layer - thinned or absent (1)

  • infiltration of neutrophils and activated lymphocytes, extending from the dermis into the epidermis (1) (presence of neutrophils in the staratum corneum and mononuclear leucocytes in the papillary dermis are defining histopathological features of psoriasis) (2)

  • Munro's microabscesses - small aggregates of neutrophils transmigrate through the epidermis and forms microabscesse below the parakeratotic stratum corneum. Later these are moved towards the upper layers and sloughed off as the lesion progresses (1)

  • dilated, tortuous capillaries within outer dermal - papillary dermis; create minute bleeding points when scale removed - Auspitz sign

Current thinking is that endogenous or exogenous damage unmasks antigens in the corneum which fix complement and activate neutrophils. Neutrophils then release proteases which unmasks more antigen so repeating the cycle. Most likely, activation is assisted by arachidonic acid metabolites and leukotrienes, particularly B4.


Last edited 08/2019 and last reviewed 10/2021