PSORIASIS

• T-lymphocyte-driven immune process is central to the development

• Type I : young adults and includes guttate psoriasis is characterized by
a familial segregation involving HLA-Cw6.5,33
• Type II disease includes psoriasis vulgaris presenting at an older age
• (over 50 years) as well as palmoplantar pustulosis and shows no
familial segregation and no association with the PSORS1 locus.4,33,34
In the skin there is an increased epidermal proliferation rate: the
transit
time of keratinocytes through the epidermis in normal skin is 56
days; in psoriatic
skin it is shortened to 7 days
• Early lesions
early lesions, the histological features consist primarily
of dermal changes.75–79 The evolution of the psoriatic plaque consists initially
of the development of tortuous, dilated, and frequently congested capillaries
in the superficial papillary dermis accompanied by edema and a perivascular
mononuclear cell infiltrate

Lymphocytes then migrate into the

lower epidermis, which becomes spongiotic
Migration of neutrophils
from capillaries in the dermal papillae through gaps in the epidermal basement
membrane and hence to the stratum corneum completes the process.
Psoriasiform hyperplasia of the affected epidermis then follows
Classical plaque
• acanthosisof the epidermal ridges, which are evenly elongated and
club-shaped at their bases, alternating with long edematous papillae,
which are club-shaped at their tips
• Fusion of adjacent ridges
• diagnostic features of active lesions include the ‘Munro microabscess’
snd ‘spongiform pustule of Kogoj’.
Pustilar psoriasis
• particularly if the pustule has developed
• against a background of plaque-type disease, more often the features
• are much less well developed
• palmar/plantar pustular lesions, the initial changes are those of
spongiosis with lymphocytic exocytosis in the lower epidermis.80 As
the lesion progresses, neutrophils infiltrate the epidermis and a
macropustule develops