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Psoriasis: keratinocyte hyperproliferation and silvery plaques

Psoriasis is a long-term inflammatory skin disease in which keratinocytes (the main skin cells) multiply too fast; classic plaque psoriasis gives red plaques (thickened patches) with silvery scale (skin flakes).

Remember

Plaque psoriasis is keratinocytes being made and pushed to the surface far too quickly, together with immune inflammation, which gives sharply edged red plaques with silvery scale, classically over the elbows and knees.

Memory aid

picture the skin as a conveyor belt running far too fast

Cells reach the surface unfinished and flake off as scale.

The epidermis is the outer layer of the skin. Its main cells are keratinocytes, which are made by cell division in the basal layer (the deepest layer of the epidermis). They travel upwards, maturing on the way, until they reach the cornified layer (the outer layer of the epidermis), where they are shed. Normal keratinocytes take about 28 days to reach the surface.

In psoriasis the immune system drives hyperproliferation, which means the keratinocytes multiply too fast. Their turnover (the transit time to the surface) shortens to about 3 to 5 days, so immature cells pile up faster than they can be shed. The surface layer thickens and flakes off as silvery scale (flakes of the outermost skin layer that build up and shed). The small blood vessels in the dermis (the layer beneath the epidermis) also become more twisted and widened, which probably adds to the red colour.

The plaques are well-demarcated (sharply edged), red and thickened. They favour the extensor surfaces, meaning the outer sides of joints such as the elbows and knees, and also the scalp, lower back and buttocks. The nails can be pitted or dented.

Genetic susceptibility sets the scene. Triggers such as infection, injury to the skin, alcohol or stress can set off a flare (a spell when the rash worsens). The cause is not fully understood, but psoriasis runs in families. It is not an infection and is not contagious.

Key facts

Appearance
well-demarcated red plaques covered with silvery scale
Distribution
the extensor surfaces, for example the elbows and knees, plus the scalp, lower back and buttocks
Mechanism
hyperproliferation of keratinocytes together with inflammation
Turnover
keratinocyte maturation takes about 28 days normally but only 3 to 5 days in psoriasis
Nails
can be pitted or dented
Triggers
infection, skin injury, alcohol, stress and some medicines can provoke a flare in someone who is already susceptible
Not infectious
psoriasis is not contagious

Exam traps

  • Atopic eczema (a dry, itchy, inflammatory skin condition) is the classic confusion: in older children and adults it favours the flexures (the creases), such as the back of the knee, whereas sharply bordered plaques with thick silvery scale point to psoriasis, although the two overlap.
  • A filaggrin deficiency (filaggrin is a skin barrier protein) is linked to atopic eczema, not psoriasis, because a barrier defect does not explain the accelerated keratinocyte turnover of psoriasis.
  • Slowed turnover with delayed shedding points the wrong way: in psoriasis turnover is speeded up, from about 28 days to 3 to 5 days, and the scale comes from cells arriving at the surface too fast.

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Based on 8 SimpleMed+ questions written and peer-reviewed by UK doctors.

Last updated 30 October 2026. For medical education only, not clinical advice.