FIGURE 18.1

Diagram depicting the various components of normal skin (A) and, in greater detail, the normal epidermis (B).

FIGURE 18.2

Immunohistochemical staining for S-100 protein demonstrates melanocytes amongst the basal keratinocytes of the epidermis (A). Highly dendritic Langerhans’ cells (shown immunohistochemically by staining for the CD1a antigen) are present throughout the epidermis (B).

FIGURE 18.3

Acute eczema. Note the blisters oozing oedema fluid (A). The hallmarks of acute eczema are spongiotic oedema (which pushes apart individual keratinocytes) and intraepidermal collections of lymphocytes and oedema fluid known as vesicles (B). Chronic eczema. Here, the skin shows markings resembling tree bark. This appearance is termed lichenification (C). In chronic eczema the epidermis is acanthotic with surface scale. Lymphocytic inflammation is present within the rather fibrotic dermis; however, there is now little evidence of epidermal inflammation and spongiosis (D).

FIGURE 18.4

Contact allergic dermatitis. In this case, the patient is sensitive to nickel in clothes fasteners.

FIGURE 18.5

Contact allergic dermatitis. The immunopathogenesis of this delayed-type hypersensitivity reaction is presented diagrammatically. Langerhans’ cells process antigens (pale blue triangles) applied to the epidermal surface. During processing, the antigen is modified (dark blue triangles) which enhances its immunogenicity before being presented to T lymphocytes (green discs) (A). T lymphocytes exposed to antigen then migrate to regional lymph nodes, where there is clonal expansion of specifically sensitized cells (B). Subsequent exposure to the antigen results in chemical signalling which stimulates the proliferation of specifically sensitized T lymphocytes. Cell adhesion molecules allow these lymphocytes to home into the area of re-exposed epidermis where they elaborate the cytokines responsible for eliciting spongiotic dermatitis (C).

FIGURE 18.6

Psoriasis. This well-defined scaly plaque is typical of psoriasis. Note the dystrophic nail changes.

FIGURE 18.7

Psoriasis. The epidermis is acanthotic with evidence of clubbing and fusion of rete ridges. Large numbers of neutrophil polymorphs are apparent within parakeratotic surface scale forming Munro microabscesses.

FIGURE 18.8

Lichen planus. Itchy, flat topped, polygonal and violaceous papules are typical of lichen planus.

FIGURE 18.9

Lichen planus. The epidermis shows hyperkeratosis, hypergranulosis and irregular acanthosis. Within the upper dermis there is a dense band-like infiltrate of lymphocytes lying in close association with the basal epidermis.

FIGURE 18.10

Chronic discoid lupus erythematosus (CDLE). This is a large plaque of chronic lupus, associated with marked scarring, on the cheek. Sometimes the lesions have a symmetrical ‘butterfly’ distribution involving the nasal bridge and both cheeks.

FIGURE 18.11

Chronic discoid lupus erythematosus (CDLE). In this active lesion of lupus the epidermis is atrophic and hyperkeratotic. Numerous lymphocytes are apparent close to the basal epidermis, and this is associated with striking liquefaction degeneration.

FIGURE 18.12

Erythema multiforme (EM). This is a classic ‘target’ lesion of EM. Note the central discrete area of blistering.

FIGURE 18.13

Erythema multiforme (EM). In EM, the lymphocytic infiltrate tends to obscure the dermoepidermal junction. Lymphocytes infiltrate the epidermis, and scattered eosinophilic cytoid bodies are evident within both the basal and suprabasal layers.

FIGURE 18.14

Cutaneous graft-versus-host disease (GVHD). The epidermis shows marked hyperkeratosis, and there is a sparse infiltrate of lymphocytes extending into the epidermis. Note the close relationship between the intrusive lymphocytes and the eosinophilic apoptotic keratinocytes (‘satellite cell necrosis’).

FIGURE 18.15

Gastrointestinal tract GVHD. In this section from the colon there is nuclear debris around the periphery of the glands. This debris originates from epithelial cells undergoing lymphocyte-associated apoptosis.

FIGURE 18.16

Hepatic GVHD. The bile ducts arrows in this portal tract are surrounded by lymphocytes. A few lymphocytes infiltrate between the ductal epithelial cells, some of which are undergoing apoptosis.

FIGURE 18.17

Diagram illustrating the mechanisms responsible for epidermal–epidermal adhesion (A) and epidermal–dermal adhesion (B).

FIGURE 18.18

Pemphigus vulgaris. The fragile blisters of pemphigus vulgaris are often disrupted, leaving shallow erosions.

FIGURE 18.19

Pemphigus vulgaris. In this bullous disorder the blister cavity lies above the basal layer, which remains attached to the basement membrane.

FIGURE 18.20

Bullous pemphigoid. In this condition the blister cavity lies beneath the full thickness of the epidermis. Note the large numbers of eosinophil leucocytes within the dermis and bulla.

FIGURE 18.21

Pemphigus vulgaris. (A) Direct immunofluorescence demonstrates a ‘chickenwire’ pattern of IgG deposition within the epidermis. The line drawing emphasizes the suprabasal site of bulla formation with preservation of the basal layer. (B) Bullous pemphigoid. Direct immunofluorescence demonstrates a linear band of IgG deposition along the basement membrane zone. The line drawing illustrates that the bulla is subepidermal; however, the basement membrane does remain attached to the dermis and forms the floor of the blister – this is not obvious on routine histology. Eosinophils are often the predominant cell type in the inflammatory infiltrate. (C) Dermatitis herpetiformis. Direct immunofluorescence shows coarse granules of IgA deposited in the papillary dermis. The line drawing shows a discrete focus of subepidermal blistering associated with an infiltrate of neutrophil polymorphs.

FIGURE 18.22

The typical excoriated papulovesicular rash of dermatitis herpetiformis.

FIGURE 18.23

Scanning magnification demonstrates a discrete focus of subepidermal vesiculation.

FIGURE 18.24

At higher magnification, large numbers of neutrophil polymorphs are apparent within the blister cavity and within the floor of the blister.

FIGURE 18.25

A biopsy of the distal duodenum demonstrates subtotal villous atrophy together with crypt hyperplasia and a marked increase in intraepithelial lymphocytes. These features are compatible with glutensensitive enteropathy.

FIGURE 18.26

Granuloma annulare. Within the dermis there is a zone of amorphous and eosinophilic collagen degeneration. A rim of histiocytes surrounds the area of collagen degeneration (forming a palisading granuloma).

FIGURE 18.27

Leucocytoclastic (allergic) vasculitis. The dermal capillary blood vessels are surrounded by an intense infiltrate of neutrophil polymorphs. Capillary endothelial cells appear swollen and the presence of abundant nuclear debris is in keeping with leucocytoclasis.

FIGURE 18.28

Numerous ulcerated vesicles are evident over the ankle.

FIGURE 18.29

Scanning magnification shows intense inflammation involving the dermis and epidermis. Loss of nuclear staining and multinucleation can be appreciated even at this power.

FIGURE 18.30

At higher magnification, the characteristic cytopathic effects of herpesvirus infection are clearly demonstrated. Margination of nuclear chromatin results in the nuclei appearing ‘empty’, and many of the keratinocytes are multinucleated.

FIGURE 18.31

Viral wart. The epidermis is thrown into folds (papillomatosis), and there is marked hyperkeratosis. Within the superficial layers of the epidermis many of the keratinocytes display nuclear pyknosis and perinuclear halos. These koilocytes indicate the presence of papillomavirus infection.

FIGURE 18.32

Molluscum contagiosum. Large eosinophilic intracytoplasmic viral inclusions are present within the superficial layers of the epidermis.

FIGURE 18.33

Superficial dermatophyte infection. Large numbers of fungal hyphae are present within the stratum corneum. (PAS.)

FIGURE 18.34

Scabies. A scabies mite (Sarcoptes scabiei) is apparent within the stratum corneum.

FIGURE 18.35

Seborrhoeic keratosis. This slightly raised and brownish benign skin tumour is common in late adult life. This particular example is only slightly raised and brownish; others are dark, broad-based papillomas.

FIGURE 18.36

Seborrhoeic keratosis. An exuberant proliferation of well-circumscribed sheets and strands of epithelium resulting in thickening of the involved skin is characteristic.

FIGURE 18.37

Actinic keratosis. The epidermis exhibits irregular orientation and increased variation in size and shape of keratinocytes. This is associated with parakeratosis (the presence of blue-staining nuclei in the stratum corneum) and an inflammatory infiltrate within the underlying dermis.

FIGURE 18.38

Basal cell carcinoma. This example manifests itself as a shiny, pigmented skin papule.

FIGURE 18.39

Basal cell carcinoma. Irregular strands of small darkly stained epithelial cells extend into the dermis. Although there may be a superficial resemblance to seborrhoeic keratosis, the strands are more irregular and the cellular details (not visible at this magnification) also differ.

FIGURE 18.40

Squamous cell carcinoma, manifesting itself as an irregular ulcer near the upper lip of an elderly patient.

FIGURE 18.41

Squamous cell carcinoma, forming highly irregular strands of atypical epithelial cells, invading the skin and inducing an inflammatory response.

FIGURE 18.42

Common acquired naevus. Round to oval nests of melanocytes are present at the dermoepidermal junction, and extend into the upper dermis. The epidermis shows a reactive lengthening of the rete ridges and slight hyperkeratosis.

FIGURE 18.43

Congenital naevus. Large numbers of naevus cells occupy almost the entire thickness of the dermis. Such deep penetration of tissues is common in congenital naevi, but rare in acquired naevi.

FIGURE 18.44

Superficial spreading melanoma. This lesion shows several of the key features of melanoma: irregular shape, marked variation in colour, and irregular surface with loss of skin lines in some places.

FIGURE 18.45

Superficial spreading melanoma. Atypical melanocytes are seen throughout the thickness of the epidermis, which contrasts with the more regular nests of melanocytes at the dermoepidermal junction, seen in most naevi (compare with Figure 18.42).

FIGURE 18.46

The skin lesion of this patient manifested itself as a raised, darkly pigmented, symmetrical nodule. Because of the pitch-black colour, there was some concern that the lesion could be a heavily pigmented nodular melanoma.

FIGURE 18.47

Histology of the lesion shows many confluent nests and sheets of melanocytes at the dermoepidermal junction, associated with epidermal hyperplasia and hyperkeratosis. The histology is characteristic of pigmented spindle cell naevus (PSCN), a benign lesion.

FIGURE 18.48

Skin tumour composed of endothelial cells. This haemangioma is a benign tumour characterized by an accumulation of regular vessels which may be small or large, and lined by (usually) flat endothelial cells.

FIGURE 18.49

Skin tumour composed of endothelial cells. Kaposi’s sarcoma, especially when it has progressed to the nodular phase, shows an irregular mass of elongated atypical endothelial cells alternating with slit-like spaces filled with blood.