The early stage consists in elongation and dilatation of blood vessels of the papillary derma, with associated aedema and lymphocytic infiltrate (perivascular cuffing). Vessels are dilated and tortuous, with some neutrophils in their lumen. Lymphocytes and neutrophils emerge from the vessel reaching the epidermis (“squirting” papilla). Rare erythrocytes extravasated may be found. Epidermis during this phase, is quite normal.Shortly after, there is a thickening of epidermis with loss of granular cell layer and formations of mounds of parakeratosis, which is thought to result from a markedly shortened cellular turnover time. Keratinocytes proliferate and mature rapidly, so that terminal differentiation is incomplete. Thus, squamous keratinocytes aberrantly retain intact nuclei and release few extracellular lipids that normally cement adhesion of corneocytes.
The resulting poorly adherent stratum corneum leads to the characteristic scales or flakes of psoriasis lesions. Scattered neutrophils are seen at the edge of mounds of parakeratosis: they represents the earliest manifestation of Munro microabscesses.
The advanced stage is characterized by regular acanthosis (thickening of stratum spinosum) and epidermal “psoriasiform hyperplasia” with regular elongation of the rete ridges and thinning of suprapapillary plates . Mitotic activity is often quite marked, a further indicator of the hyperproliferative nature of this condition. Parakeratosis become confluent, with loss of granular layer. There is transmigration of inflammatory cells through epidermis into parakeratotic scale resulting in intracorneal collections of neutrophils, the so called “Munro microabscesses” . Similar accumulation in the stratum spinosum are defined as “spongiform pustule of Kogoj”. When subcorneal abscesses are prominent the disease is designated as pustular psoriasis .
Munro microabscesses and Kogoj micropustoles are diagnostic clues of psoriasis, but they are notalways present. All other features can be found in numerous eczematous dermatitis, such as allergic contact dermatitis and atopic dermatitis. However, in these lesions spongiosis and “oozing” (presence of coagulated serum in cornified layer) are marked. Moreover, in allergic contact dermatitis there is a characteristic eosinophilic infiltrate which is normally absent in psoriasis.
Dermal inflammatory infiltrate is heavier than in early lesions, it is composed by T lymphocytes, containg a few Langherhan cells with occasional neutrophils. Under the epidermal basement membrane, macrophages CD11c positive are present. In addition to neutrophils, T lymphocytes are also found interspersed between keratinocytes throughout the epidermis and in larger quantities in the dermis. With immunohistochemical analysis it has been shown that epidermal lymphocytes are chiefly CD8+ T cells, while dermic lymphocytes are a mixture of CD4+ and CD8+ T cells, with a CD4+ predominance, similar to that seen in peripheral blood. Later lesions there is orthokeratosis, an intact granular layer and mild exocytosis of inflammatory cells .
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