Inflammatory skin diseases

1. Acute Inflammatory Skin Diseases

Overview

• Last days to weeks.
• Characterized by inflammatory cells (mononuclear), edema, and sometimes injury.
• Some persist → transition to chronic phase; others self-limited.

Acute Eczematous Dermatitis

• “Eczema” = clinical term for a group of conditions with red, papulovesicular, oozing, crusted lesions that develop into raised scaling plaques.

Clinical Types

Type	Cause
Allergic contact dermatitis	Topical exposure to allergen (e.g., poison ivy, nickel)
Atopic dermatitis	Keratinocyte barrier defect; associated with asthma + allergic rhinitis (atopic triad)
Drug-induced eczema	Hypersensitivity to a drug
Irritant contact dermatitis	Non-allergic skin reaction to direct damage (soap, solvent)
Stasis dermatitis	Venous insufficiency in lower limbs

Pathogenesis (Allergic Contact Dermatitis — #1)

• Type IV hypersensitivity (delayed, T-cell mediated).

1. Cutaneous exposure to sensitizing agent (e.g., poison ivy).
2. Self-proteins modified → processed by epidermal Langerhans cells.
3. Migrate to draining lymph node → present antigen to naïve T cells → immunological memory.
4. Re-exposure → T cells migrate to skin → cytokines → recruitment of inflammatory cells → epidermal damage.

Morphology

• Spongiotic pattern = accumulation of edema fluid within the epidermis (intercellular edema).
• Hallmark of eczematous dermatitis.

Clinical Features by Stage

• Lesions: itchy, edematous, oozing plaques; vesicles/bullae.
• Acute: preserved stratum corneum, intercellular edema, spongiotic microvesicles, papillary edema.
• Subacute: parakeratosis, spongiosis, acanthosis, papillary edema.
• Chronic: minimal parakeratosis + spongiosis, compact hyperkeratosis, superficial dermal fibrosis.

2. Chronic Inflammatory Skin Diseases

Overview

• Inflammation sustained over months to years.
• Skin surface often roughened from excessive shedding (desquamation).

A) Psoriasis

Definition

• Immunological disease with genetic susceptibility (HLA-Cw6) + environmental triggers.
• Well-demarcated pink plaques covered by loosely adherent silver-white scales.

Pathogenesis

• Inciting agent unknown.
• Sensitized T cells (Th17, Th1) enter skin → accumulate in epidermis → release cytokines (TNF, IL-17, IL-22) + growth factors → keratinocyte hyperproliferation → epidermal thickening.
• Koebner phenomenon: psoriasis induced at sites of trauma.

Morphology — Acanthotic Pattern

• Acanthotic pattern = epidermal hyperplasia (stratum spinosum).
• Elongation of rete ridges (extending into dermis).
• Loss of granular layer.
• Parakeratosis: retention of nuclei in stratum corneum.
• Munro microabscesses: neutrophils in stratum corneum.
• Auspitz sign: pinpoint bleeding when scale removed (capillaries at tips of dermal papillae).

Clinical Features

• Sites: extensor surfaces (elbows, knees, scalp), glans penis, lower back.
• Nail changes: yellow-brown discoloration, pitting, thickening, oil drop sign, crumbling, onycholysis.
• Associations: psoriatic arthritis, IBD, metabolic syndrome.

B) Lichen Simplex Chronicus (Acanthotic Pattern)

• Roughening of skin like “lichen on a tree”.
• Reaction to repetitive minor trauma (scratching) → epithelial hyperplasia + eventual dermal scarring.
• Histology: compact hyperkeratosis, irregular acanthosis, prominent granular layer, vertical streaks of dermal collagen, mild inflammation.
• Lesions: raised, erythematous, hyperpigmented with increased scale.
• Often masks another dermatosis (atopic dermatitis, lichen planus, etc.).

C) Lichen Planus (Lichenoid Pattern)

Definition

• Self-limited disease; characterized by 5 P’s:
  • Pruritic, Purple, Polygonal, Planar Papules / plaques.
• Chronic, T-cell mediated dermatosis (CD8⁺ T cells attack basal keratinocytes).
• Associated with hepatitis C.

Clinical Features

• Sites: wrists, elbows, oral + genital mucosa.
• Small, poorly demarcated, extremely itchy papules.
• Wickham striae: whitish lines visible on papules, especially oral mucosal lesions.

Histology

• Band-like (lichenoid) lymphocytic infiltrate at dermo-epidermal junction.
• Basal cell vacuolization + apoptotic keratinocytes (Civatte bodies).
• Saw-tooth rete ridges at dermo-epidermal junction.
• No parakeratosis; hypergranulosis.

3. Comparison Table

Pattern	Disease	Key features
Spongiotic	Eczematous dermatitis (contact, atopic)	Intercellular epidermal edema; itchy, oozing
Acanthotic (psoriasiform)	Psoriasis	Silver scales, extensor surfaces; parakeratosis + Munro abscess + loss of granular layer; Auspitz + Koebner; nail pitting
Acanthotic	Lichen simplex chronicus	Scratching → hyperplasia; compact hyperkeratosis + vertical dermal collagen
Lichenoid	Lichen planus	5 P’s; saw-tooth rete + band-like infiltrate + Civatte bodies; Wickham striae; HCV

💡 High-yield: Acute eczematous dermatitis = spongiotic pattern (intercellular edema); allergic contact dermatitis = type IV HS; atopic dermatitis = barrier defect + atopic triad. Psoriasis = acanthotic pattern; Th17/IL-17 + IL-22; silver scales on extensor surfaces, scalp, glans; parakeratosis + Munro microabscesses + loss of granular layer + elongated rete ridges; Auspitz sign (pinpoint bleeding), Koebner phenomenon; nail pitting + oil drop; HLA-Cw6; psoriatic arthritis. Lichen simplex chronicus = scratching-induced hyperplasia. Lichen planus = 5 P’s (Pruritic, Purple, Polygonal, Planar, Papules); saw-tooth rete + Civatte bodies + band-like infiltrate; Wickham striae (oral); HCV association.