Psoriasis - Histopathology & Differential Diagnosis

Opening Orientation

Histopathological Features (Layer by Layer)

1. Stratum Corneum - The Most Diagnostic Layer

• Parakeratosis - the hallmark. Instead of anucleate cornified cells, you see retained nuclei in the stratum corneum. This reflects accelerated epidermal turnover - keratinocytes don't have time to complete normal maturation.
• Munro microabscesses - collections of neutrophils and their remnants within the parakeratotic stratum corneum, sitting on top of small foci of parakeratosis. These alternate rhythmically with areas of normal orthokeratosis, suggesting the underlying pustule formation happens in a cyclical, pulsatile fashion.
• The granular layer (stratum granulosum) is absent or markedly reduced (hypogranulosis) - focally, corresponding precisely to the areas of parakeratosis above.

2. Epidermis - Dramatic but Orderly Hyperplasia

• Regular psoriasiform acanthosis - the rete ridges are elongated, bulbous, and "squared-off" at their bases. Some bases even coalesce.
• The epidermis is thin over the tips of the dermal papillae - a critically diagnostic feature, the so-called "suprapapillary plate thinning." This is the morphological basis of the Auspitz sign (punctate bleeding when scale is removed - you're shearing off the thin suprapapillary plate and nicking the dilated papillary capillary beneath).
• Spongiform pustules of Kogoj - neutrophils accumulating within the spongiotic upper stratum spinosum, surrounded by and infiltrating between pale keratinocyte strands, creating a sponge-like pattern. Together with Munro microabscesses, these are pathognomonic for psoriasis (and AGEP).
• Spongiosis is otherwise scant (unlike eczema), except immediately around neutrophil collections.

3. Dermis - Vascular and Inflammatory Changes

• The papillary dermis shows elongated, tortuous, dilated capillaries - they extend upward into the elongated dermal papillae. These tortuous capillaries are the vessels that bleed when the scale is removed (Auspitz sign again).
• A perivascular mixed infiltrate of lymphocytes, histiocytes, and neutrophils surrounds these vessels.
• Edema is present at the tips of the dermal papillae, especially in active lesions.

Active vs. Stable Lesion

Summary of Key Histologic Hallmarks

• H - Hypogranulosis (absent granular layer)
• A - Acanthosis (regular, squared-off rete ridges)
• M - Munro microabscesses (neutrophils in SC)
• P - Parakeratosis (retained nuclei in SC)
• E - Elongated/tortuous papillary capillaries
• R - Rete ridge thinning over dermal papillae (suprapapillary plate)

Differential Diagnosis on Histology

Conditions that mimic psoriasis (psoriasiform pattern):

• Also shows acanthosis and parakeratosis.
• Key distinction: prominent spongiosis throughout the epidermis (not just around neutrophils). Munro microabscesses and spongiform pustules of Kogoj are absent. Rete ridges are irregular rather than regularly elongated.

• Clinically greasy yellow scale vs. dry silver-white psoriatic scale.
• Histologically shows similar parakeratosis, but parakeratosis is characteristically "shoulder parakeratosis" - perifollicular, draping over follicular ostia. Spongiosis is more prominent. Neutrophils in the follicular infundibulum ("follicular neutrophilic exocytosis") are a clue. Munro microabscesses can occur but are not as organized.

• Can look identical to psoriasis clinically and histologically.
• Histologic clues pointing away from psoriasis:
  • Rete ridges are long and slender (not squared-off)
  • Plasma cells in the dermal infiltrate (present in ~70% of cases - their absence does not exclude it)
  • Vacuolar interface dermatitis component
  • Dermal blood vessels appear lumenless due to endothelial cell swelling (endarteritis obliterans)
  • Disproportionate neutrophils above parakeratosis compared to plaque psoriasis pattern

• Can cause a psoriasiform reaction pattern with neutrophils in the stratum corneum.
• Key distinction: neutrophils sit within the SC but not rhythmically alternating with orthokeratosis as in psoriasis.
• PAS stain is mandatory - reveals fungal hyphae or arthrospores in the stratum corneum. Always do PAS when you see neutrophils in the SC.

• Classic histologic clue: alternating orthokeratosis and parakeratosis in both vertical and horizontal directions ("checkerboard pattern") - unique to PRP.
• Follicular plugging prominent.
• Lacks significant neutrophilic exocytosis and true Munro microabscesses.

• Psoriasiform acanthosis can be present.
• Key distinguishing features:
  • Epidermotropism of large, hyperchromatic, angulated lymphocytes (the lymphocytes in psoriasis are small and bland)
  • "Bare underbelly sign" - the superficial perivascular infiltrate hugs the epidermal underside asymmetrically
  • Papillary dermal fibrosis
  • Lymphocytes are larger and darker than any dermal lymphocytes

• Histologically shares the two pathognomonic features: spongiform pustules of Kogoj AND Munro microabscesses.
• Distinction: clinical context (drug history, acute onset, fever), and histologically often shows eosinophils in the infiltrate and evidence of interface damage/necrotic keratinocytes - not seen in psoriasis.

Quick Reference - DD at a Glance

Closing Key Points for the Slide

1. Psoriasis histology is dynamic - the same patient may show different features depending on where and when you biopsy (active edge vs. old stable plaque).
2. The combination of Munro microabscesses + spongiform pustules of Kogoj is pathognomonic - if you see both, you are looking at psoriasis or AGEP.
3. Always do a PAS stain when neutrophils are in the stratum corneum - tinea can be a perfect mimic.
4. The suprapapillary plate thinning + elongated tortuous papillary vessels = Auspitz sign morphology - a structural explanation of a clinical sign, which makes for excellent slide discussion.
5. In psoriasiform eruptions with plasma cells: think syphilis first.