Arthur Knight

Disorders of Keratinization

This term is used to describe disorders in which there is a primary fault in the process of epidermal differentiation and (or) desquamation. It includes the ichthyotic disorders and a number of other quite uncommon disorders in which there is scaling and hyperkeratosis.

Melanocytic Naevi and Malignant Melanoma

Alterations in the melanin pigmentation of the skin produce abnormal duskiness or whiteness and may be due to many factors. Lightening of the skin may be due to a deficiency of melanin, or a reduction in the number of melanocytes. In albinism there are normal numbers of melanocytes, whereas in vitiligo the number of melanocytes is reduced or absent. This change is difficult to judge in ordinarily stained histological sections but can be assessed by quantitative electron-microscopic studies1, or by performing a DOPA oxidase histochemical test. In a similar fashion, darkening of the skin may be caused by an increase in epidermal or subepidermal melanin or an increase in the number of melanocytes. Thus in Addison’s disease there is an increase of activity of the cutaneous melanocytes without an alteration in their number, whereas in naevi and melanoma the abnormal pigmentation is associated with melanocytic hyperplasia.

Atlas of Skin Pathology

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Other Inflammatory Diseases

This recently described condition1, also known as Sweet’s disease after its discoverer, consists of tender papules and plaques up to 2 cm in diameter. The papules are erythematous and are associated with the development of leukocytosis and fever. The face, neck and upper limbs are involved most. There may be an accompanying arthralgia or arthritis. The disorder rapidly responds to systemic corticosteroids but may relapse. Nothing is known of the aetiology or pathogenesis of Sweet’s disease although it may be related to erythema multiforme.

Scalp and Hair Disorders

This condition may be the end result of discoid lupus erythematosus, lichen planus, a deep fungus or bacterial infection and pseudopelade of Brocq, although there is some doubt as to whether the last is a separate entity. There is localized scarring atrophy of the scalp with permanent loss of hair follicles.

Eczema. Psoriasis. Lichen Planus

The terms eczema arid dermatitis are synonymous. The various types of eczema cannot be readily distinguished histologically. Histological classification therefore resolves simply into (a) acute, (b) chronic and (c) lichenification. In acute eczema the skin is red, swollen and may blister. Chronic eczema tends to be rather dry and scaly and lichenification is a reactive thickening partially due to scratching.

Connective Tissue Disease, Vasculitis and Erythemas

The syndrome of lupus erythematosus (LE) has a spectrum of disease activity from the purely cutaneous discoid type to the rapidly progressive systemic form with internal organ involvement. Antinuclear antibodies circulate in the systemic form but the demonstration of cutaneous immunological abnormalities by immunofluorescence is important to all types.

Bullous and Vesicular Skin Disorders

The skin can develop vesicles and bullae as a result of diverse causes through mechanisms affecting different levels of the epidermis and dermis1. Histological diagnosis of bullous skin disorders requires attention to several key points. These include:

Reactions to Trauma and Vascular Injury

The sequence of changes that occur in the skin after injury are similar regardless of whether the injury is caused by a knife, by a burn or by a disease process (Figure 2.1). Immediately after injury the extravasated blood clots, due to activation of the clotting cascade, and vasoconstriction occurs. Polymorphonuclear leukocytes accumulate at the site of injury and separate viable from damaged, non-viable tissue components. After some 12 to 24 hours the process of re-epithelialization begins1. In the initial stages, epidermal cells actively move over the wounded area. The migrating epidermal cells adopt a spindle- or ribbon-shaped profile, resembling fibroblasts (Figure 2.2). Ultrastructurally they lose their desmosomal apparatus and cell-to-cell contact reverts to primitive interdigitating microvilli. Some 48 hours after wounding, mitotic activity begins at a point behind the leading edge of the sheet of migrating epidermal cells, and on the third and fourth days maturation of the new epidermal cover begins. During the early stages of re-epithelialization the epidermal cells need no specialized dermo-epidermal apparatus, but burrow through the damaged tissue planes, isolating the viable deeper tissues from the superficial necrotic crust, which is eventually sloughed off. Later on, the new epidermis secretes its own junctional apparatus, restoring continuity with the dermis beneath2.

Tumours of the Dermis

The dermis is composed of connective tissue including collagen and elastic tissue, muscle, vessels, nerves and fat extending from the subcutis. All of these elements may give rise to tumours, either true neoplasms or congenital malformations.