What are the histopathological features of psoriasis in early lesions, partially treated lesions, relapsed lesions after Koebner phenomenon (e.g., Morison salt‑water bath), relapsed lesions after discontinuation of risankizumab, and in scalp psoriasis or sebopsoriasis?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: February 22, 2026 • View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

Histopathological Features of Psoriasis Variants

Classic Plaque Psoriasis

The hallmark histopathological features of established plaque psoriasis include regular epidermal hyperplasia with club-shaped rete ridges (96%), hypogranulosis (96%), suprapapillary plate thinning (63%), Munro microabscesses (78%), spongiform pustules of Kogoj (53%), and dermal papillary capillary ectasia (90%). 1

Core Architectural Features

  • Epidermal changes: Regular acanthosis with uniform elongation and fusion of rete ridges, though irregular acanthosis occurs in 84% of clinically confirmed cases 1
  • Parakeratosis: Horizontally confluent but vertically intermittent pattern, alternating with orthokeratosis 2
  • Granular layer: Thinning or absence (hypogranulosis) in 96% of cases 1
  • Hyperkeratosis: Extensive, though least common in truncal lesions 3

Inflammatory Features

  • Neutrophilic collections: Munro microabscesses in stratum corneum (78%) and spongiform pustules of Kogoj in spinous layer (53%) 1
  • Dermal infiltrate: Perivascular lymphocytic infiltrate with significant correlation between degree of inflammation and epidermal hyperplasia 4
  • Vascular changes: Dilated capillaries with proliferation in papillary dermis (90%), showing strong correlation with inflammatory infiltrate 4

Early Psoriasis

Early psoriatic lesions demonstrate less pronounced epidermal hyperplasia with more prominent inflammatory infiltrate and vascular changes, reflecting the immunopathogenic cascade that precedes full keratinocyte hyperproliferation. 4

Distinguishing Features

  • Inflammatory predominance: More prominent perivascular lymphocytic infiltrate relative to epidermal changes 4
  • Vascular proliferation: Capillary dilation and proliferation appear early, correlating strongly with inflammatory grade 4
  • Incomplete architectural changes: Rete ridge elongation may be minimal or absent 2
  • Parakeratosis presence: May be focal rather than confluent 2

Partially Treated Psoriasis

Treated psoriatic lesions show resolution of neutrophilic collections, decreased inflammatory infiltrate, and normalization of epidermal thickness, though parakeratosis and vascular changes may persist. 5

Histological Evolution During Treatment

  • Neutrophil clearance: Munro microabscesses and Kogoj pustules resolve first 5
  • Inflammatory regression: Decreased lesional infiltration of T cells, dendritic cells, and neutrophils 5
  • Persistent features: Parakeratosis and capillary dilation may remain despite clinical improvement 2
  • Epidermal normalization: Gradual reduction in acanthosis and restoration of granular layer 2

Relapsed Psoriasis (Koebner Phenomenon)

Koebnerized psoriatic lesions developing after trauma (including salt-water baths) demonstrate the same histopathological features as spontaneous psoriasis, triggered by skin trauma in genetically susceptible individuals. 5, 6

Pathogenic Context

  • Trauma-induced: Skin injury triggers inflammatory cascade in predisposed patients 5
  • Identical histology: Shows full spectrum of psoriatic changes including regular acanthosis, hypogranulosis, and neutrophilic collections 2
  • Environmental trigger: Cold climate and physical trauma worsen disease severity 6

Relapsed Psoriasis After Risankizumab

Post-biologic relapse demonstrates reactivation of the IL-23/IL-17 inflammatory axis with return of classic psoriatic histopathology, including epidermal hyperplasia, neutrophilic infiltration, and vascular proliferation. 5

Immunological Rebound

  • Cytokine reactivation: Return of IL-12/23-dependent gene expression and TNF-α/interferon-γ pathways 5
  • Cellular infiltration: Re-accumulation of T cells, dendritic cells, and neutrophils in lesional skin 5
  • Full histological spectrum: All classic features recur, including Munro microabscesses, spongiform pustules, and capillary ectasia 2, 1

Scalp Psoriasis and Sebopsoriasis

Scalp psoriasis shows classic psoriatic histopathology but may exhibit overlapping features with seborrheic dermatitis (sebopsoriasis), including shoulder parakeratosis, follicular involvement, and less pronounced neutrophilic collections. 2, 7

Scalp-Specific Features

  • Folliculocentric changes: Involvement of hair follicles more prominent than in non-scalp psoriasis 7
  • Parakeratosis pattern: May show "shoulder" parakeratosis around follicular ostia, overlapping with seborrheic dermatitis 2
  • Neutrophil distribution: Munro microabscesses may be less prominent compared to extensor surface lesions 7
  • Spongiosis presence: Can occur in 76% of psoriatic lesions, creating diagnostic overlap with eczematous conditions 1

Sebopsoriasis Overlap

  • Mixed features: Combination of psoriatic regular acanthosis with seborrheic dermatitis-like follicular involvement 7
  • Diagnostic challenge: Histopathological examination remains the main tool when clinical aspects are not definitive 7
  • Location-dependent variation: Histopathological findings vary by anatomic site, with scalp showing distinct patterns 3

Non-Classic Features That Do Not Exclude Psoriasis

The histopathological spectrum of psoriasis is broader than traditionally recognized, with several "non-classic" features frequently present in clinically confirmed cases. 1

Commonly Encountered Non-Classic Features

  • Irregular acanthosis: Present in 84% of confirmed cases 1
  • Spongiosis: Occurs in 76% of cases 1
  • Junctional vacuolar alteration: Found in 76% 1
  • Hypergranulosis: Present in 65% despite classic teaching of hypogranulosis 1
  • Dermal eosinophils: Seen in 49% of cases 1
  • Necrotic keratinocytes: Identified in 67% 1
  • Neutrophilic spongiosis: Present in 61% 1

Clinical Correlation Imperative

  • Biopsy limitations: Only non-classic or refractory cases tend to be biopsied, creating selection bias 1
  • Diagnostic approach: Presence of non-classic features does not exclude psoriasis when clinical criteria are met 1
  • Multiple biopsies: Consider if diagnosis remains uncertain, as this enhances diagnostic accuracy 8

References

5
Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

6
Guideline

Psoriasis – Definition, Clinical Features, Pathophysiology, Severity Assessment, and Systemic Implications

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

7
Research

Histopathological aspects of psoriasis and its uncommon variants.

Giornale italiano di dermatologia e venereologia : organo ufficiale, Societa italiana di dermatologia e sifilografia, 2018

8
Guideline

Differential Diagnosis of Psoriasiform Hyperplasia

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Related Questions

What are the typical findings of a skin biopsy in a patient with psoriasis?
How is a diagnosis of psoriasis confirmed?
What are the key differences between erythema multiforme (EM) and pustular psoriasis (PP) in terms of clinical presentation, diagnosis, and treatment?
How is psoriasis diagnosed and treated?
What are the key histopathological differences between psoriasis vulgaris and tinea corporis in a patient with a persistent skin lesion and a history of not responding to antifungal therapy?
What further diagnostic and therapeutic steps should be taken for a patient with a persistent thick‑walled right upper‑lobe cavitary lesion, increasing nodularity, new right lower‑lobe collapse with possible mucus plugging, and a moderate right pleural effusion after recent emergency‑department evaluation for cough, congestion, and right‑sided chest pain, treatment with antibiotics and a prednisone taper, and discharge home?
How should I interpret total, direct, and indirect bilirubin levels to determine the underlying cause?
What are the normal serum bilirubin reference ranges (total, direct, and indirect) for healthy adults?
Is a Waterlow score of 31 high risk for pressure ulcer in an older immobile patient with poor nutrition and incontinence?
What serum creatinine level requires a change in metformin dosing?
How should I manage community‑acquired cellulitis in a healthy adult, including antibiotic selection for non‑purulent versus purulent infection, dosing, duration, and criteria for hospital admission?

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.

Ask Question